SURGICAL INTENSIVE CARE: FLUIDS AND ELECTROLYTES AND ANTIBIOTICS

AX Gxobole, S Parthab, K Kabongo

Moderator: Ms S Naidoo 23rd February 2019

Safe and effective prescribing of intravenous fluids requires understanding of the physiology of fluid and
electrolyte homeostasis, physiological responses to injury and disease, as well as knowledge of the properties
of intravenous fluids (IVF). Challenges, such as limited resources impact the practitioner’s choice of fluid - the
best fluid available may not be the best fluid for the individual patient.
IVFs should be prescribed as any other drug: we should consider the indications and contraindications for
different types of IVFs. In practice, we should consider the “four D’s” of fluid therapy: drug, dosing, duration
and de-escalation.
Problems arising from inappropriate fluid therapy can increase morbidity and prolong hospital stays.

Indications4
There are only 3 indications:
Resuscitation
Replacement
Maintenance
IVF therapy is used to maintain homeostasis when enteral intake is insufficient and to replace any additional
losses. These losses may occur from the gastrointestinal tract or the urinary tract; or be caused by blood loss
from trauma or surgery; insensible losses can increase during fever or after suffering from burns; accumulation
into spaces that normally contain minimal fluid volumes (e.g., the peritoneal or pleural cavities) or as a result
of inflammatory conditions (e.g., sepsis).
Achieving balance in the resuscitation period is challenging, particularly the volume administered. More fluid is
not always better, in fact, quite the contrary. Much of the literature on fluid resuscitation focuses on critically
ill patients with sepsis, or elective peri-operative patients. Extrapolation of data to the initial resuscitation
phase of the trauma patient is not possible.

Stages of fluid resuscitation 3,4

Fluid management differs in the four phases of resuscitation according to the ROSE concept. After the initial
resuscitation (R) phase comes organ support (O) and stabilization (S), and finally evacuation (E) of excess fluids
may be needed in some patients. Administration of fluid boluses is appropriate in the rescue and optimization
phases, but each bolus should be followed by reassessment of the need for ongoing fluid administration.
Resuscitation phase (R)
Rescue treatment with fluids administered quickly as a bolus (4 mL/kg over 10–15 min)
The goal is early adequate goal-directed fluid management (EAFM), fluid balance must be positive, and
the suggested resuscitation targets are: MAP > 65 mm Hg, CI > 2.5 L/min/m2, PPV < 12%, LVEDAI > 8
cm/m2

Optimization phase (O)

Occurs within hours; degree of positive fluid balance may be a marker of severity in this phase; risk of
polycompartment syndrome.
Unstable, compensated shock state requiring titrating of fluids to cardiac output
Targets: MAP > 65 mm Hg, CI > 2.5 L/min/m2, PPV < 14%, LVEDAI 8-12 cm/m2, IAP (<15 mm Hg) are
monitored, and APP (>55 mm Hg) is calculated. Preload optimized: GEDVI 640-800 mL/m2

Stabilization phase (S)

Evolves over days; fluid therapy only for normal maintenance and replacement; absence of shock or
threat of shock
Monitor daily body weight, fluid balance and organ function
Targets: neutral or negative fluid balance; EVLWI < 10-12 mL/kg PBW, PVPI < 2.5, IAP < 15 mm Hg, APP
> 55 mm Hg, COP < 16-18 mm Hg and CLI < 60

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Evacuation phase (E)
Patients who do not transition from the ‘‘ebb’’ phase of shock to the ‘‘flow’’ phase after the ‘‘second
hit’’ develop global increased permeability syndrome (GIPS). Fluid overload causes end-organ
dysfunction
Requires late goal-directed fluid removal (‘‘de-resuscitation’’) to achieve negative fluid balance
Once haemodynamic stabilization has been achieved, fluid should be administered primarily in or with food,
and preferably by the enteral route.

Most critically ill patients develop salt and water overload during stabilization, which is addressed in the
evacuation phase. Recovering critically ill patients with adequate renal function and fluid excretion undergo
spontaneous diuresis. If spontaneous diuresis is insufficient, excess fluid is removed by drug- induced diuresis
or ultrafiltration.

Electrolytes must also be considered and should be replaced as needed according to serum levels and
monitored appropriately – usually using formal blood results or blood gas analysis. Ionized calcium is the best
measurement to assess calcium levels.

Clear Fluid Resuscitation4

There is still an ongoing debate regarding crystalloid vs colloids in the acute phase of resuscitation. In the
resource-limited environment, the use of cheaper crystalloid solutions is still recommended due to lack of data
showing significant outcome benefits of more expensive synthetic colloids.
Balanced salt solutions are preferred as these are more physiological in nature. The high chloride load
(resulting in hyperchloraemic metabolic acidosis) must be considered and the effects thereof e.g. increasing
need for blood transfusions, prolonged ventilatory support and kidney injury.
Excessive IVF administration results in a dilutional coagulopathy and diffuse tissue oedema. This negatively
impacts organ function at both a macroscopic and cellular level by increasing the distance over which
electrolyte, elements and oxygen must move. The consequence is worsening renal, hepatic and cardiac
function. Therefore, until such time as blood and blood products are available, clear fluid resuscitation should
be limited to only that which is necessary to maintain adequate organ perfusion.

Albumin may be a used as a resuscitation fluid in patients with hypoalbuminaemia and should be avoided in
other patients (eg septic shock, major trauma etc). It is beneficial in patients with cirrhosis that require large
amounts of fluid and may be beneficial in hepato-renal syndrome, post heart, lung or liver transplants
(treatment of anasarca).

Haemoglobin Solutions4
Modified haemoglobin solutions are not substitutes for blood as they do not possess the metabolic functions
of erythrocytes. They act purely as oxygen carriers. Large scale investigation and experimentation in this field
has occurred, with uses not only limited to trauma patients but also general surgical patients, oncology
patients and Jehovah’s Witnesses suffering from severe anaemia. The only product that was registered for use
in South Africa is Hempure® used in isolation as well as in combination with blood products, or as a bridge to
blood transfusion. Further studies are required before these therapies become widely used.

Monitoring and Assessment 1,3,4

The purpose of monitoring intravascular volume status is to guide fluid administration in order to maintain
tissue perfusion. Hypovolemia typically reduces tissue perfusion. However, tissue oedema can also reduce
tissue perfusion.
Initial response is monitored using clinical and haemodynamic parameters, however once stabilised more
specific parameters are used.

Static parameters
Blood pressure and heart rate: BP and HR responses to changes in intravascular volume status are not
predictable in individual patients.

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 Central venous pressure: Range 8 -12 mmH2O. Dependant on cardiac and lung mechanics, however, this is
only reliable in the spontaneously breathing patient and trends are more important than the absolute
values.
Urine output: Oliguria (U.O <0.5 ml/kg/hr in adults or <1ml/kg/hr in children)
Mixed venous oxygen saturation: Measurements have limited utility to guide fluid therapy

Dynamic hemodynamic parameters

Dynamic parameters provide superior assessment of response to a fluid challenge (i.e., volume
responsiveness) compared with traditional static parameters.
Indices based on respiratory variation (arterial pressure waveform): e.g., pulse pressure variation [PPV],
stroke volume variation [SVV], systolic blood pressure variation [SPV], or change in inferior vena cava
diameter
Stroke volume estimates: SV using oesophageal Doppler technology or arterial wave form
Left ventricular size estimates (echocardiography): Underfilling evidenced by hyperdynamic systolic
function and decreased end-diastolic and end-systolic LV cavity dimensions.
Passive leg raise test: Mimics the effect of a fluid bolus. Positive result – Increase in SV by
Fluid Challenge: Assess responsiveness to a fluid bolus
Measurement of laboratory values: An ischemic insult to a specific organ, increased creatinine, increased
serum lactate levels or lactic acidosis

Fluids in Sepsis (Surviving Sepsis Guidelines 2016):2

IVFs for resuscitation in sepsis is the cornerstone of modern therapy.
Crystalloids at 30ml/kg within the first 3 hours have been recommended as the initial fluid of choice for
resuscitation and subsequent intravascular volume replacement in sepsis and septic shock.
Use of albumin in addition to crystalloids for initial resuscitation in patients who require substantial
amount of crystalloids.
Hydroxyethyl starches should not be used for intravascular volume replacement in sepsis.

Strategies of fluid resuscitation in trauma patientsb1, 3, 4

Fluid resuscitation in trauma is constantly being reviewed due to challenges with clear fluid overload-related
complications. Long distance transfers and non-availability of blood pose additional challenges. More fluid is
not always better3. The restrictive fluid policy applicable to penetrating injuries (thoraco-abdominal) is also
applied in the blunt trauma setting although no large trials available comparing restrictive and liberal fluid
strategies in the latter.

The ATLS management approach is applied in all trauma scenarios; current (2019 10th Edition)
recommendation is 1 litre IVI only (not 2litres) and, if non- responsive, then for blood & blood products
immediately.
It is imperative to identify risk factors and priorities in trauma patients early eg. Traumatic brain injury (TBI),
penetrating injury, etc. In the restrictive fluid policy for penetrating, thoraco-abdominal injuries, a systolic BP
between 60-70 mmHg is permitted, until the patient can be taken to the operating theatre. Once
haemorrhage controlled, with blood products available, higher blood pressure values may be targeted.
This fluid restriction minimises intra-abdominal bleeding while maintaining adequate organ perfusion.
In the context of polytrauma with associated head injury, MAP >80 mmHg is targeted in order to preserve
adequate cerebral perfusion (cerebral perfusion pressure of approx. 60 mmHg).

Clinical scenarios are often complicated, and blood pressure goals should be individualized according to patient
physiology, comorbidities and physiological compensation to shock during the resuscitation.1

Clear fluid resuscitation 1, 4, 7

Ongoing debate about the “best” fluid between crystalloids and synthetic colloids to use in the resuscitation
phase of trauma remains unanswered.
Excessive fluid, particularly crystalloids, results in dilutional coagulopathy and diffuse oedema.
Chloride load, potential contribution to metabolic acidosis and renal injury are a concern

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 Balanced salt solutions closely resemble human plasma with lower Na and Cl content compared to
0.9% saline, with the addition of a buffer such as acetate or lactate
Balanced salt solutions have a physiological pH and the electrolyte profile closely resembles that of
plasma therefore less effect on serum pH eg Ringer’s lactate , Hartman’s solution
There is no value of 0.9% saline over balanced salt solution in TBI; however in the context of
polytrauma, to avoid the above complications, Ringer’s lactate is recommended.
Synthetic Colloids: Research suggests that toxicity of Hydroxyethyl starch (HES) is attributed to tissue
storage and coagulopathy. HES-induced coagulopathy increases need for blood products in critically ill.
In our setting of resource limitation, crystalloids are still an appropriate and feasible recommendation;
however, the available solution may not be the best choice1.
Hypertonic saline - limited to use in patients with TBI as a bridge to neurosurgical intervention1.
Until blood and blood products are available, goal for clear fluid resuscitation is to maintain adequate
organ perfusion with earlier initiation of inotropic/vasopressor therapy if required. Improvements in
MAP, HR, metabolic acidosis & clearance of lactate denote responsiveness to fluid therapy.
Point of care testing for trauma-induced coagulopathy can guide component therapy

Damage Control Resuscitation (DCR) 1, 5, 6, 8

Early identification of trauma patients who will require massive transfusion is difficult but essential. Blood
consumption score can be used to predict patients who will require it. In severely injured patients DCR in
conjunction with damage control surgery, is associated with improved survival. Plasma restores volume as well
as corrects hypo-perfusion shock and coagulopathy.
Major principles include:
minimising crystalloid use
permissive hypotension
haemostatic resuscitation with balanced ratio of blood products (as per the PROPPR trial in which a ratio
of 1:1:1 resulted in reduced mortality from exsanguination within the 1st 24 hours, with similar
complication rates to a lower ratio protocol) and goal-directed correction of coagulopathy, rewarming,
correction of acidosis, and arrest of haemorrhage by surgical and non-surgical techniques.

Best current practices

Fluid response assessment1 Fluid responsive Patient types1, 4
Bedside ultrasonography- IVC compressibility Responders demonstrate physiological improvements
Increase in MAP with fluid boluses Transient responders improve then deteriorate further
+/-improving urine output Non-responders show continued clinical deterioration
PLR test despite initial fluid resuscitation.

The distinction between these patient types requires vigilance and repeated clinical assessment to identify
those patients with re-bleeding or ongoing bleeding in order to initiate blood and blood product resuscitation
together with surgical intervention.

Special Groups 1, 2, 4
Paediatrics
Children are not small adults and restoring circulating volume is paramount via appropriate intravenous or
interosseous access.
Blood volume 80ml/kg in a term neonate, decreases with age up to 70ml/kg in an adult.
Fluids should be administered with flow control to avoid fluid overload; total volume should not be >40mg/kg
ATLS: Damage control resuscitation for pediatric trauma patients is defined as an attempt to limit the use of
crystalloid resuscitation, as in adults. An initial bolus of 20 ml/kg bolus of fluid is followed by 10–20 ml/kg of
packed RBCs and 10–20 ml/kg of fresh frozen plasma and platelets as part of a massive transfusion protocol.
The use of colloids such as human plasma and albumin is preferred due to the smaller volumes required
compared to clear fluids.
Clear fluids must be isotonic and balanced. Maintenance fluids that may be hypotonic should be given in
limited volumes (max. 2ml/kg/hr) via a flow controller to prevent rapid transmission.

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Elderly
WHO defines elderly as a chronological age >65yrs. Advanced chronological as well as biological age render
increased risk of morbidity and mortality after trauma. The vascular system is less compliant thus hypo- and
hypervolemia are poorly tolerated. Assessment of fluid requirements is best done with echocardiography as
measurements based on pressure and pulse contour analysis, may vary due to age-related cardiovascular
system changes. Be cautious of possible underlying heart disease. Haemoglobin is best kept above 9g/dl and
MAP >70mmhg particularly if underlying co-morbidities are unknown.
ATLS: The 4th edition of the Brain Trauma Foundation’s Guidelines for the Management of Severe Traumatic
Brain Injury that are applicable to the early management of the brain-injured patient have been included in
the new edition of the ATLS course. These guidelines include avoiding prolonged hyperventilation with PC02
<25 mm Hg; maintaining systolic blood pressure >100 mm Hg for patients 50–69 years and >110 mm Hg or
higher for patients ages 15–49 or older than 70 years old to decrease mortality and improve outcomes

Crush injury/crush syndrome

Fluid loading needs to be exercised with caution. Muscle perfusion is maintained so reperfusion does not
occur. Fluid loading with initial 20-40ml/kg followed by 10-20ml/kg/hr.Traditionally, 0.9% saline is used for
loading. Alternatives to limit the occurrence of hypernatremia and hyperchloremic acidosis, include 0.45%
saline and 5% Dextrose. Balanced salt solutions such as modified Ringer’s lactate are not recommended due to
concerns regarding hyperkalaemia, but risk may be offset by hyperchloremic acidosis seen with large volume
saline administration. Third space loss has adverse effects. Dialysis is best opted for earlier. Pulmonary
oedema will result in hypoxia requiring intubation and ventilation. There is no role for loop or osmotic
diuretics and use of sodium bicarbonate to induce alkaline diuresis is also not supported.

Pregnancy
Pregnancy > 20 weeks’ gestation carries the risk of aorto-caval compression therefore maintain 20o left lateral
tilt. Standard principles of fluid resuscitation apply. The hyperdynamic state of pregnancy in 2nd and 3rd
trimester may result in under-estimation of blood loss and underlying injuries.

Burns
Deeper and more extensive burns require greater fluids, but excessive fluid administration will also increase
morbidity by generation of oedema. The role of colloids is controversial.
Enteral resuscitation can be combined with IV route and is effective if commenced within 6 hours.

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 FLOW DIAGRAM OF INITIAL FLUID RESUSCITATION OF TRAUMA PATIENTS1

Antibiotics in intensive care1, 9

Infections in critically ill patients are a major burden to the healthcare system. Of concern, neither the
incidence of these infections over the past years nor the mortality rates appear to be improving. This
challenging dilemma has led to 70% of all intensive care unit (ICU) patients being prescribed antibiotics at any
one time. Appropriate use of antibiotics is an integral part of good clinical practice. The pivotal points are to
prescribe the correct antibiotic, for the correct patient, at the correct time, at the correct dose & for the correct
duration. Unfortunately, appropriate antimicrobial prescribing practices are often inadequate with gap
between clinical practice & best evidence.

Principles of prescribing antibiotics include11

An accurate diagnosis of infection
Understanding differences between prophylaxis, empiric & targeted therapy
Prescribing antibiotics for the shortest duration
Understanding antibiotic characteristics: pharmacokinetics & pharmacodynamics due to the altered
physiology of the critically ill
Recognizing adverse effects of antimicrobial agents on the host
Accounting for host characteristics influencing antimicrobial activity

Antimicrobial prophylaxis 11,12

These are administered for operative procedures that have a high rate of surgical site infection or when
implants are used. The antimicrobial chosen should be effective against the aerobic & anaerobic pathogens
most likely to contaminate the surgical site, a single dose administered within 30 to 60 minutes before skin
incision to ensure adequate serum & tissue concentrations during the period of potential contamination. This
dose may be repeated intra-operatively if the procedure is more than 2-4 hours in duration or if there has
been significant blood loss. There is no evidence to advocate continuation postoperatively.

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Empiric therapy 8,10,12
Empiric regimens are considered when a treatable infection has been recognized or when there is high degree
of suspicion for infection but timeous culture report is impossible to obtain, due to severity of illness, such as
septic shock.
The timing of initiation of antibiotic treatment is the single strongest predictor of outcome; inappropriate &
delayed initial empiric antibiotic therapy is associated with greater morbidity & mortality10.

The Surviving Sepsis Campaign recommends broad spectrum empiric IV antimicrobials with adequate tissue
penetration to source of infection, to be commenced within the first hour of onset of sepsis/septic shock.
Choice of drug is based on most likely pathogens at identified infection site/source, local epidemiology which
may vary between units and health facilities, individual risk factors for MDR bacteria and candida species,
whether community- or hospital-acquired infection and individual susceptibility to potential drug adverse
events.

An optimal response to therapy can be achieved by using these strategies8

Early source control procedure
Early initiation of therapy
Correct dosing
Considering the risk factor for multidrug resistance
Avoiding use of identical antibiotic and the same antibiotic class administered in the preceding 3 months
Narrowing therapy once culture & sensitivity results available

Dosing 10,12
This is dependent on host factors and antimicrobial properties. The dosing of antibiotics has to be
adequately adjusted in order to achieve an effective drug level above the minimum inhibition
concentration (MIC) but avoiding toxic side effects e.g. In those with known renal impairment, renal dosing
is required.
Importantly, patients undergoing renal replacement therapy do not require renal dosing of antimicrobials.
Route should be intravenous for the critically ill and frequency is increased in order to achieve PK-PD
targets.
An appropriate initial loading dose is required and the regimen reviewed daily. Higher than standard
dosages of renally excreted drugs may be required for optimal exposure in patients with glomerular
hyperfiltration. Infusions have not been shown to be superior to bolus dosing in randomised control trials.

Monitoring response 2,3,12

Clinical progress:
Shock resolution / Decrease in vasopressor requirement.
Vital parameters: PR, Temp, RR.
Biomarkers:
Procalcitonin, WCC, CRP (trend).

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Duration2
Duration should be shortened as much as possible unless there is a specific need for prolonging therapy
and a daily assessment for de-escalation of antibiotics is recommended.
3-5 days is acceptable for stable patients who have shown improvement clinically & biochemically.
Conversion to oral dosing once patient is tolerating an oral diet if patient is stable.
If signs of sepsis persist beyond 5-7 days of appropriate treatment, aggressive diagnostic investigation is
required; the concern being uncontrolled source of infection or failure of antimicrobial therapy/resistance

Antimicrobial stewardship in intensive care 4,5,8, 12

The massive consumption of antibiotics in the ICU is responsible for substantial ecological side effects that
promote the dissemination of multidrug-resistant bacteria in this environment. Up to half of ICU patients
receiving empirical antibiotic therapy have no definitively confirmed infection.
Antimicrobial stewardship describes hospital-based interdisciplinary strategies dedicated to improving the use
of antimicrobials, reducing adverse events associated with its use e.g. resistance and adverse events
The core principles include:
Use of prophylaxis only when there is proven efficacy.
Use of the narrowest spectrum of antimicrobial with proven efficacy.
Use of the least number of agents and for the shortest length of therapy to achieve efficacy.
Appropriate antimicrobial dosing to maximize efficacy and limit complications.

An association between a stewardship programme and a decrease in antimicrobial resistance has been shown.

Resistance 6,7.8,12.
Drug resistance poses a challenge in the ICU setting and the entire health care sector.
The main mechanisms of resistance to antibiotics can be caused by:
Inactivation or modification of the antibiotic.
An alteration or the protection of the target site of the antibiotics that reduces its binding capacity.
The modification of the metabolic pathways to circumvent the antibiotic effects.
Reduced intracellular antibiotic accumulation by decreasing permeability and/or increasing active efflux of
the antibiotic.

The antimicrobial stewardship program, which is not yet definitely established in many facilities and is most
likely to vary based on local culture, policy and routine clinical practice, has proven to be a valuable tool to
fighting antimicrobial resistance however, the onus resides with each clinician to adhere to its core principles.

Conclusion
The critically ill patient poses many complex challenges to clinicians, the pharmaceutical industry and burdens
the healthcare system significantly.

A goal directed, evidence based, systematic and multidisciplinary approach in the care of the critically ill
patient is recommended in order to ensure reduction in morbidity & ultimately survival. In addition, post- ICU
quality of life, the emerging problems of antimicrobial resistance and the cost of health care have to be
considered.

A systematic approach with unit-driven protocols and consideration of the humanity of every critically ill or
injured patient is likely to improve patient care and provide better outcomes.

References
1. Vincent JL, DeBacker D. Circulatory shock. N Engl J Med 2013 ;369: 1726–34
2. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016
3. Finfer S, Myburgh J, Bellomo R. Intravenous fluid therapy in critically ill adults. Nature Reviews
Nephrology (2018) 14:541–557
4. Wise R, Faurie M, Malbrain MLN, Hodgson E. Strategies for Intravenous Fluid Resuscitation in trauma
Patients. World J Surg (2017) 41:1170–1183

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5. Chang R, Holcomb JB. Optimal fluid therapy for traumatic haemorrhagic shock. Crit. Care Clinics
(2017)33: 15-36
6. Mizushima Y, Nakao S, Idoguchi K, Matsuoka T. Fluid resuscitation of trauma patients: How much fluid
is enough to determine patient’s response? American Journal of Emergency Medicine 35 (2017): 842-
845
7. American College of Surgeons Committee on Trauma. ATLS® 9th Edition (2012).
8. Giannoudi M, Harwood P. Damage control resuscitation: lessons learned. Eur J Trauma Emerg Surg
(2016) 42:273–282
9. Mizobata Y. Damage control resuscitation: a practical approach for severely hemorrhagic patients and
its effects on trauma surgery. Journal of Intensive Care (2017) 5:4
10. Haase N, Perner A, Hennings LI. Hydroxyethyl starch 130/0.38-0.45 versus crystalloid or albumin in
patients with sepsis: systematic review with meta-analysis and trial sequential analysis. BMJ (2013)
;346:f839
11. Holcomb JB, Tilley BC, Baraniuk S. Transfusion of Plasma, Platelets, and Red Blood Cells in a 1:1:1 vs a
1:1:2 Ratio and Mortality in Patients with Severe Trauma, The PROPPR Randomized Clinical Trial.
JAMA(2015); 313(5):471-482
12. Roberts JA, Paul SK, Akova M, Bassetti M, De Waele JJ, Dimopoulos G, et al. DALI: defining antibiotic
-lactam antibiotic doses sufficient for critically ill
patients? Clinical infectious diseases. 2014;58(8):1072-83.
13. Rhodes A, Evans LE, Alhazzani W, Levy MM, Antonelli M, Ferrer R, et al. Surviving sepsis campaign:
international guidelines for management of sepsis and septic shock: 2016. Intensive care medicine.
2017;43(3):304-77.
14. Pepper D, Sun J, Rhee C, Welsh J, Powers JH, Danner RL, et al. Impact of Procalcitonin (PCT)-Guided
Antibiotic Therapy on Mortality in Critically Ill Patients: A Systematic Review and Meta-Analysis of 18
Randomized Controlled Trials. 2017.
15. Barlam TF, Cosgrove SE, Abbo LM, MacDougall C, Schuetz AN, Septimus EJ, et al. Implementing an
antibiotic stewardship program: guidelines by the Infectious Diseases Society of America and the
Society for Healthcare Epidemiology of America. Clinical Infectious Diseases. 2016;62(10):e51-e77.
16. Timsit JF, Bassetti M, Cremer O, Daikos G, de Waele J, Kallil A, et al. Rationalizing antimicrobial therapy
in the ICU: a narrative review. Intensive care medicine. 2019.
17. Zachariah P, Freedberg DE. Vancomycin use in surrounding patients during critical illness and risk for
persistent colonization with vancomycin-resistant Enterococcus. The Journal of hospital infection.
2019.
18. Logan LK, Weinstein RA. The epidemiology of carbapenem-resistant Enterobacteriaceae: the impact
and evolution of a global menace. The Journal of infectious diseases. 2017;215(suppl_1):S28-S36.
19. Sartelli M, Weber DG, Ruppé E, Bassetti M, Wright BJ, Ansaloni L, et al. Antimicrobials: a global alliance
for optimizing their rational use in intra-abdominal infections (AGORA). World journal of emergency
surgery. 2016; 11(1):33.
20. Sartelli M, Chichom-Mefire A, Labricciosa FM, Hardcastle T, Abu-Zidan FM, Adesunkanmi AK, et al. The
management of intra-abdominal infections from a global perspective: 2017 WSES guidelines for
management of intra-abdominal infections. World Journal of Emergency Surgery. 2017; 12(1):29.
21. Simone B, the role of the surgeon in the management of intra-abdominal infections, taken from
https://infectionsinsurgery.org/115-2/
22. https://infectionsinsurgery.files.wordpress.com/2019/01/antibiotic-prescribing-practices-in-surgery-
definitive-1.pdf).
23. Global Alliance for Infections in Surgery Working Group. A global declaration on appropriate use of
antimicrobial agents across the surgical pathway. Surgical Infections. 2017; 18(8):846-53.

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 SURGICAL NUTRITION AND ALIMENTARY TRACT FISTULAE
MZ Khan, A Mthethwa, N Mabaso
Moderator: Mr R Deonarain 2nd March 2019

In practice, adequate nutritional support is often not well managed. Many surgical patients are at risk of
under or malnutrition.
Malnutrition increases morbidity and mortality. Effects of malnutrition include immunodeficiency,
increased risk of infection, poor wound healing, increased bedsores, GIT bacterial overgrowth, increased
nutrient losses through the stool.
Feeding helps to attenuate the metabolic response to stress, prevents oxidative cellular injury, and
favourably modulates immune responses.

Nutritional Requirements
The methods available to determine a patient’s nutritional requirement include:
Indirect calorimetry
A published predictive equation
A weight-based equation (25-30 kcal/kg/day)1
Total energy is made up of protein (1.2-1.5g/kg/day), lipids (2g/kg/day), carbohydrates (3-6g/kg/day).
Suggested ratio is 20% protein, 30% lipids and 50% carbohydrates.
Whether measured by indirect calorimetry or estimated by predictive equations, energy expenditure
should be re-evaluated more than once a week.

Nutritional assessment
Clinical Assessment
History: Personal habits, eating patterns, drugs, alcohol
Examination: Muscle weakness, fatigue, depression, wasting, skin and hair changes, oedema,
weakness. Calculation of BMI (normal 20-25, obesity > 30, borderline underweight 18.5-20.
Undernutrition < 18.5.
Nutrition risk screening (NRS 2002) – see ESPEN guidelines below
Includes grading of severity of disease as a reflection of increased nutritional requirements. Includes 4
questions as a pre-screening for risk patients.
NUTRIC Score (see below)2
Designed to quantify the risk of critically ill patients developing adverse events that may be modified
by aggressive nutrition therapy. The score of 1-10, is based on 6 variables
Laboratory Markers: Albumin, pre-albumin, transferrin, retinol-binding protein: All are a reflection of
the acute-phase response and thus not accurate as markers of nutrition
Anthropometrics: Not reliable
Ultrasound: Measure muscle mass and determine changes in muscle tissue

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Elective surgery
ERAS Principles
A “bundle” of interventions. Its multimodal, multidisciplinary, integrated and standardized.
From a metabolic and nutritional point of view, the key aspects of perioperative care include:
Integration of nutrition into the overall management of the patient
Avoidance of long periods of preoperative fasting
Re-establishment of oral feeding as early as possible after surgery
Start of nutritional therapy early, as soon as a nutritional risk becomes apparent
Metabolic control e.g. of blood glucose
Reduction of factors which exacerbate stress-related catabolism or impair GIT function
Minimized time on paralytic agents for ventilator management in the postoperative period
Early mobilisation to facilitate protein synthesis and muscle function.
Prehabilitation
Preparing patients for surgery
Perioperative nutritional therapy to the malnourished and those at risk. Also, if anticipated that
the patient will be unable to eat for more than five days perioperatively.
Perioperative nutritional therapy to patients expected to have low oral intake and who cannot
maintain 50% of recommended intake for more than seven days.
Carbo-loading
To reduce pre-operative discomfort including anxiety
oral preoperative carbohydrate treatment the night before and two hours before surgery should
be administered (instead of overnight fasting).
Oral carbohydrates have been reported to improve post-operative well being

Early feeding
Oral intake, including clear fluids shall be initiated within hours after surgery in most patients.
Immunonutrition
This is the administration of supra-normal doses of nutrients considered to have immune-modulatory,
anti-inflammatory, anabolic and tissue protective effects. The usual substances involved are Glutamine,
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Omega-3 Fatty acids, Arginine and Nucleotides. Studies have shown a decrease in infective complications
and possibly length of hospital stay. However, none of these have been shown to have a decrease in
mortality.
Glutamine
Usually a non-essential fatty acid
In critical illness, it becomes depleted and in effect becomes an essential amino acid
Functions
Vital for gut barrier function
Nitrogen transport
Acid-base haemostasis
Need for T-cell function as well
Deficiency is associated with increased bacterial translocation which increases
Arginine
Precursor for nitrous oxide
Thought to assist with post-operative cardiac stability
Stimulates t-cell function
Omega-3 Fatty Acids
Precursors of eiconasoids : pro-inflammatory effects
Decrease levels: SIRS and ARDS
High levels: anti-thrombotic effects

Feeding strategies
Orally: This is the most natural way of feeding. There are a variety of oral supplements available
Enteral:
1. Nasogastric /Orogastric tubes: If anticipated feeding duration is 4-6 weeks.
2. Post pyloric feeding: In patients with a high risk of aspiration not tolerating gastric feeds.
3. Gastrostomy: If the anticipated duration of feeding is greater than 4-6 weeks or to facilitate
transfer to a rehabilitation facility.
4. Jejunostomy tube: With gastric outlet obstruction for feeding of an elemental diet.

Parenteral Nutrition
Parenteral nutrition is a means of giving feeds intravenously in patients who otherwise have contra-
indications to having enteral / trophic feeds.
Some benefits, amongst other have been described in literature for PN, and these include:
Rapid improvement of nitrogen balance, allowing better wound healing and lymphocyte recovery
Achievement of caloric goals
Decreased risk of conditions due to aspiration for ileus

During the first week of PN, fluid Intake should be limited to approximately 800 ml/day plus
compensation for insensible losses avoids both fluid overload and dehydration. Daily monitoring of body
weight can aid in determining the necessary fluid volume. A weight gain of >0.25 kg/day or 1.5 kg/week is
typically indicative of fluid accumulation and not of an improved nutritional state.
Carbohydrates administered daily should not exceed 2–3 g/kg body weight/day and blood glucose
concentration should be strictly monitored because of the high risk of hyperglycaemia.
Patients with normal renal function should be generously substituted with phosphate, potassium and
magnesium with appropriate laboratory checks. It is necessary to check also the fluid balance (fluid
intake, urine production) on a daily basis

Complications of parenteral nutrition can be catastrophic; can be divided into early and late. Early
complications are usually as a result of procedures used to gain vascular access. Late complications can be
divided into catheter related sepsis, metabolic abnormalities, hepatobiliary, and GIT complications.
Patients with central catheters who are not receiving parenteral nutrition have lower rates of sepsis.
3
Complications of parenteral feeding:

Early complications Late complications

Haemo-, chylo-, or pneumothorax Catheter related sepsis
Venous thrombosis Metabolic
Arrhythmias Hyperglycaemia
Tracheal puncture Serum electrolyte derangements
Brachial plexus injury Macro and micronutrient excess or
Haemopericardium deficiency
Cardiac tamponade Refeeding syndrome
Air embolism Wernicke’s encephalopathy
Arterial puncture Hyperlipidaemia
Catheter embolism

Gastrointestinal
Gastroparesis
Intestinal villous atrophy

Hepatobiliary
Hepatic steatosis (fatty liver)
Cholestasis (resulting in cholecystitis)
Gallstone and biliary sludge formation
Hyperlipidaemia (causing acute
pancreatitis)

Serum electrolytes and triglycerides as well as additional monitoring measures are necessary in altered
renal function, electrolyte-free substrate intake, lipid infusions, and in ICU patients3

Refeeding Syndrome3
Refeeding syndrome (RFS) is a condition where a change in the metabolic function of the patient as a
result of re-introduction of feeding in a previously starved patient.
The criteria, according to the NICE guidelines is as follows:
Criteria from the guidelines of the National Institute for Health and Clinical Excellence 4 for identifying
patients at high risk of refeeding problems; the patient has one or more of the following:
Body mass index (kg/m2) <16
Unintentional weight loss >15% in the past three to six months
Little or no nutritional intake for >10 days
Low levels of potassium, phosphate, or magnesium before feeding
Or the patient has two or more of the following:
Body mass index <18.5
Unintentional weight loss >10% in the past three to six months
Little or no nutritional intake for >5 days
History of alcohol misuse or drugs, including insulin, chemotherapy, antacids, or
Diuretics
Risk factors for Refeeding Syndrome
Severely malnourished
Decreased intake:
Anorexia
Dysphagia
Chronic alcohol abuse
Starved
Decreased absorption:
Inflammatory bowel disease
Coeliac disease
4
 Increased metabolic demands:
surgery
malignancy
Critically ill

Pathophysiology of refeeding syndrome

Refeeding regime for patients at risk of refeeding syndrome (as per the National Enteral Nutrition
Practice Guidelines: South Africa 2016)
Day Calorie intake (all feeding routes) Supplements
Day 1:
- 10 kCal/kg/day
- For extreme cases (BMI < 14kg/m2 or no food > 15 days):
- 5 kCal/kg/day
- Carbohydrate: 50-60%
- Fat: 30-40%
- Protein: 15-20%
- Prophylactic supplement
- PO4 : 0.5-0.8mmol/kg/day
- K+: 1-3mmol/kg/day
- Mg2+: 0.3-0.4 mmol/kg/day
- Na+: <1 mmol/kg/day (restricted)
- IV fluids: restricted, maintain “zero” balance
- IV thiamine + vitamin B complex 30 minutes prior to feeding
Day 2-4:
- Increase by 5 kCal/kg/day If low or no tolerance stop or keep minimal feeding regime
- Check all biochemistry and correct any abnormality
- Thiamine and vitamin B complex orally or IV till
Day 3: Monitoring as required
Day 5-7:
5
 - 20-30 kCal/kg/day -Check electrolytes, renal and liver functions and minerals
- Fluid: maintain zero balance
- Consider iron supplement from day 7
Day 8-10: 30 kCal/kg/day or increase to full requirement

Short Bowel Syndrome

Extensive resection of the intestinal tract frequently results in inadequate digestion and/or absorption of
nutrients, a condition known as short bowel syndrome (SBS). This challenging condition demands a
dedicated multidisciplinary team effort to overcome the morbidity and mortality in these patients
Short bowel syndrome results in:
1. Loss of absorptive surface area
2. Loss of site-specific transport processes
3. Loss of site-specific endocrine cells and gastrointestinal (GI) hormones
4. Loss of ileocecal valve
The mainstay of treatment for these patients is control of sepsis, maintenance of fluid and electrolyte
balance and initiation of nutritional support in the early management.

Intestinal failure
An adjunct of short bowel syndrome, Intestinal failure (IF) occurs when the body is unable to sustain its
energy and fluid requirements without support, due to loss of functional small bowel. Prolonged IF is
seen after large intestinal resection
Drugs that are thought to enhance bowel adaptation to enteral feeds are Growth hormone, Glucagon –
like peptide 2 and glutamine.
Intestinal failure can be classifies according to:
Speed of onset
Underlying pathology
Duration
Localisation

It can further be subtyped into:

Type I: Self-limiting and reversible. Normally occurs with post-operative ileus
Type II: occurs in patients with hostile abdomens, fistulae and adhesions
Type III: A type of chronic intestinal failure where patients require long term parenteral nutrition

The mainstay of medical management for both intestinal failure and short bowel syndrome is appropriate
resuscitation at onset and nutritional support. Surgical techniques such as serial transverse enteroplasty
procedure (STEP) and Intestinal transplantation have been identified as possible means to increase the
absorptive surface are of the intestine affected.

Alimentary Tract Fistulae

A fistula is defined as a pathological connection between two epithelialized surfaces. Enterocutaneous
fistulae involve communication between the bowel and the skin. The majority of these fistula occur as a
result of operative procedures. Approximately one third of these fistula will close with medical
management; remaining two thirds will require surgical reconstruction. Management involves a stepwise
approach, but is nevertheless challenging and time consuming with a high morbidity and mortality.
Classification
Aetiology: Iatrogenic /post-operative (80%) vs Spontaneous (20%)
Anatomical/Organs affected: large bowel, small bowel, bladder
Skin/ visceral involvement:
External – involving hollow viscera and skin
Internal – Involving two hollow viscera
Output
High > 500ml/ day
6
 Intermediate 200-500ml/ day
Low < 200ml/day
Character: Simple (single tract) vs complex (multiple tracts and defects in bowel)
Fistulae associated with Crohn’s Disease
Type 1: no active disease
Type 2: complex fistulas with active disease
Risk Factors for Post-operative Fistulae
Emergency laparotomy, damage control procedures and open abdomen
Type of procedure: oncologic surgery, appendicectomy, stoma reversal, adhesinolysis
Technical errors during bowel anastomosis (leading to suture line ischemia/ breakdown)
Intra-operative haemorrhage, Shock & Large volume crystalloid resuscitation

Causes of Spontaneous fistulae

Inflammatory: Crohn’s disease, diverticulitis, pancreatitis
Infective: Tuberculosis, appendicitis, amoebiasis
Ischemic colitis
Malignancy (GIT, gynaecological), Post radiation
Foreign bodies/ Bezoars

Clinical Presentation
Clinical presentation depends on the degree of control of the fistula.
1. Uncontrolled fistula: signs of systemic sepsis, localized guarding or a frank peritonitis.
2. Controlled fistula: drainage of enteric content through an abdominal wound or via a new sinus.
3. Early features: failing to recover from, abdominal distension, nausea and pyrexia.
4. Internal fistulation depend on the viscera involved. Small to large bowel fistulae present with
diarrhoea. Bladder to bowel fistula may present with pneumaturia or faecaluria. Faecal drainage from
the vagina will point towards a rectovaginal fistula.

Management
The stepwise approach is designed to create conditions favourable for spontaneous closure while also
optimising patients should they require surgery. The detection and management of sepsis is a continuous
process that is included in all steps.
1. Patient resuscitation (Fluids and electrolyte replacement)
2. Diagnosis/ control of fistula
3. Control of sepsis
4. Nutritional support
5. Definitive management strategy – conservative vs surgical treatment

Patient resuscitation
Present acutely unwell, septic, dehydrated and with various electrolyte derangements.
Resuscitation with balanced crystalloid fluids such as Ringers Lactate or Isotonic Saline i
Endpoints of resuscitation include adequate urine output, normalisation of vital signs and
biochemistry including urea and creatinine.

Diagnosis and control of fistula

Complicated fistula tracts, internal fistulas and pancreatic fistulas may require investigation
1. A fistulogram will confirm the diagnosis, allow for delineation of the anatomy and provides
information on distal patency or obstruction.
2. Contrast studies also confirm the diagnosis by demonstrating communication between hollow
viscera as well as perforation or vascular communication.
3. Endoscopy (with biopsy) can be used to diagnose fistulae involving the proximal GIT.

7
 4. Contrast enhanced CT is useful to diagnose a fistula, but also provides information on its relation
to surrounding viscera and gives information regarding distal bowel. Furthermore it allows
detection of intraabdominal collections and aids in planning percutaneous drainage.

Control of fistula
Involves accurate quantification and protection of skin.
Accurate quantification guides fluid resuscitation, nutritional therapy and provides prognostic
information regarding chance of spontaneous closure 5.
Vacuum-assisted closure been shown to be useful 6. They allow for accurate charting of output
and less corrosive damage to surrounding skin and do not increase the risk of further fistula
formation. However they do restrict patient mobility.

Reducing fistula output

Reducing fistula output reduces fluid requirements, allows for enteral feeding and creates a more
favourable environment for spontaneous closure. Pharmacologic agents include loperamide, codeine
phosphate and somatostatin. Current evidence suggests that somatostatin is effective in reducing effluent
output especially in high output fistulas but does little with respect to aiding spontaneous closure.

Control of sepsis
Sepsis (in all systems) has been found to be the leading cause of mortality in both pre- and post-op
patient groups. Intra-abdominal sepsis should be aggressively treated as this is a preventative factor
against spontaneous closure.

Nutritional therapy
Malnutrition is due to poor oral intake, high output losses and sepsis. The assessment of nutritional state
in these patients still remains complex. Biochemical markers such as albumin, prealbumin, transferrin and
retinol binding protein provide useful prognostic information but inaccurate nutritional information.
Enteral feeding remains the preferred method of nutrition. Fistuloclysis is a feeding technique that
involves the administration of enteral feeds and effluent via the distal limb. This method has been shown
to decrease TPN requirements, in-hospital mortality rates and hospital stay. Indications for TPN include
the resuscitative phase, high output fistula, ileus or bowel obstruction.

Definitive management
While 30-70% of fistulas will close spontaneously, those that do not will require definitive treatment.
Factors preventing spontaneous closure can be summarized by the mnemonic FRIEND.
Foreign bodies, Radiation, Ongoing infection/ inflammation or sepsis
Epithelialisation of tract, Neoplasia, Distal obstruction
Favourable factors for spontaneous closure (in the absence of the FRIEND criteria):
Location – oesophageal, pancreas, biliary tree, colon, duodenal stump
< 1cm enteric defect, > 2cm tract length
Intestinal continuity
Absence of diseased bowel
No adjacent/ associated abscess
Low output fistula, Simple fistula
Adequate nutrition

The principles of surgical management of fistulae are noted below. 6

1. Preoperative optimisation of nutrition and physiology.
2. Adequate preparation for a potentially long case.
3. Experienced surgeon and anaesthetist.
4. Skin incision should be made away from existing scars to avoid adhesions.
5. Meticulous, patient Adhesinolysis from ligament of Treitz to rectum to rule out distal obstruction.
6. Sharp dissection using a scalpel or dissecting scissors & avoidance of diathermy.
8
 7. Careful identification of fistula segment with resection and primary end to end anastomosis
8. In the case of a entero-atmospheric fistulae, attempt to achieve fascial closure
9. Duodenal fistulae requiring operative management are better treated with gastro-jejunostomy
rather than resection.

Novel therapies 8, 9, 10
Novel therapies have been born out of the high morbidity and mortality rates as well as the prolonged
hospital stays associated with Enterocutaneous Fistulae.
1. Fibrin glue is a sealant derived from human pooled plasma (sealer protein) and a thrombin mimic.
This patch works as a biological adhesive agent and promotes haemostasis. After 2-4 weeks the
patch is replaced with collagen fibers. The advantages of fibrin include biocompatibility,
biodegradation of the patch and reduced time to closure.
2. Cyanoacrylate plugs are synthetic compounds that are instilled into the fistula tract, solidify and
obliterate the tract. Solidifcation occurs in 30-45 seconds and induces an inflammatory response
which enhances fibrosis, granuloma formation and ultimately epithelialisation.
Case studies and trials reveal these therapies are successful in closing low output, long tract fistulae but
have not yet shown to replace surgery in its entirety.

Enteroatmospheric Fistula (EAF)

Unlike enterocutaneous fistulae, EAFs have neither overlying soft tissue nor a real fistula tract. This makes
their management more challenging and reduces the likelihood of their spontaneous closure, warranting
surgical closure. They occur in up to 25% of open abdomens, due to compromised physiologic state and
bowel manipulation, and carry a mortality rate of 42%. The management of EAF’s follows the same
principles of care as for an ECF, with a few additions, as mentioned below.

In the acute setting, the patients may have uncontrolled fistulae with peritonism, warranting urgent
laparotomy. Proximal diversion may be impossible in this acute setting due to a frozen abdomen, and
effluent isolation may be required. Placement of drains is controversial in this setting as they may erode
into the fistula, widening the defect. Control of content at the fistula site is challenging due to the lack of
overlying skin. Options include stoma bags, floating stomas, wound managers, and vacuum-assisted
closure (VAC) devices.

VAC devices have been found to be safe and effective in controlling fistula effluent and improving wound
healing. Additional benefits include: protection of skin, protection of underling bowel to manipulation
from repeated dressing changes and reduced risk of further fistula formation. Continuous negative
pressure up to 125mmHg has been found to be most effective. Intermittent pressure causes manipulation
and deformation of the bowel, increasing the risk of fistula formation.

Timing to surgical correction of the defect is usually withheld to a minimum of 6 weeks, as is done with
ECF. Definitive surgery and abdominal closure is often delayed by a minimum of 3 months or more.
Simultaneous closure of the intestinal tract and abdominal wall is associated with a higher complication
rate, and a staged procedure should be considered. A simple manual test can be used to determine the
timing of definitive surgery in these patients. By pinching the skin graft between the index finger and
thumb, the surgeon can assess if the graft lifts freely from the underlying bowel. Usually, this is found to
be present at approximately 3 months.

Conclusion
Despite advances in healthcare, the management of alimentary tract fistula remain challenging. A
structured stepwise approach with a keen eye for sepsis is vital in the management of these patients in
order to provide them with the greatest chance of spontaneous closure. Failure of conservative
management warrants surgical closure, a task that is considerably challenging for even the most
experienced surgeons. Intense and meticulous pre-operative optimisation will yield more favourable
outcomes.

9
References
1. Gurunand A,Ngcobo Q ,Wain H; Seminar (2017): Surgical Nutrition and Alimentary Tract Fistulae, UKZN
Department of Surgery
2. Heyland DK, Dhaliwal R, Jiang X, Day AG. Identifying critically ill patients who benefit the most from
nutrition therapy: the development and initial validation of a novel risk assessment tool. Critical Care.
2011;15(6):R268.
3. German Medical Science 2009, Vol. 7, ISSN 1612-3174, Complications and monitoring- guidelines for
parenteral nutrition
4. Hearing SD.BMJ. 2004 Apr 17;328(7445):908-909
5. Stein SL. (2017) Overview of enteric fistulas. [online] UpToDate. Available at:
https://www.uptodate.com/contents/overviewofentericfistulas. [Accessed 13 Jan. 2017]
6. Fischer JE, Evenson AR. Chapter 126. Gastrointestinal-Cutaneous Fistulae. Mastery of Surgery 5th
Edition. Lipincott Williams and Wilkins. 2007
7. Badrasawi M, Shahar S, Sagap I. Nutritional Management in Enterocutaneous Fistula: What is the
Evidence? Malays J Med Sci 2015; 22(4): 6-16
8. Stevens P, Delicata RJ. Evidence for using somatostatin analogues in the treatment of enterocutaneous
fistula. British Journal of Surgery. 2011; 98: 1682–1684
9. Ravindran P et al. Definitive surgical closure of enterocutaneous fistula: outcome and factors predictive
of increased postoperative morbidity. Colorectal Disease 2013. 16, 209–218
10. Martinez JL et al. Systematic Management of Postoperative Enterocutaneous Fistulas: Factors Related
to Outcomes. World J Surg. 2008. 32:436–443

10
 SHOCK AND MULTIPLE ORGAN DYSFUNCTION SYNDROME
KN Boolaky, M Kadwa, S Naidu
Moderator: Ms TN Shangase 9th March 2019

Introduction 1, 2
Circulatory shock is the final pathway of cardiovascular failure and although it may initially be reversable,
morbidity and mortality remain high. It is a life-threatening medical condition that requires emergency
medical treatment.

Definition
It may be defined as a state in which tissue perfusion is inadequate to meet cellular metabolic
requirements. It is clinically manifested by symptoms of organ hypoperfusion, namely altered mental
state, cool and clammy extremities, bradycardia, oliguria and hypotension.

Pathophysiology
The mechanism of shock lies in alteration of one or more components of the circulatory system.
Intravascular volume is the first component which determines mean circulatory pressures and venous
return to the heart with a decrease resulting in a lower cardiac output.
The heart itself is the second component with cardiac output being determined by heart rate,
contractility and loading conditions. Aberrations in any of these components will limit cardiac output.

The arteriolar bed makes up the resistance circuit and is the third component of shock. Ventricular
loading conditions, arterial pressure and distribution of systemic blood flow are determined by arteriolar
tone with decreases producing hypotension and increases impeding cardiac ejection.

Capillaries are the fourth component and are the site of nutrient and fluid exchange. Increases in capillary
permeability will result in loss of intravascular volume and tissue oedema. Obstruction or endothelial
dysfunction decrease the capillary cross-sectional area which may result in opening of arteriovenous
connections, leading to a bypass of the capillary network(known as shunting), and play a role in tissue
hypoperfusion.

The lowest site of shear stress in the circulatory system are the venules, which are the fifth component of
shock, this lends to them being susceptible to occlusion. Capillary hydrostatic pressure is increase by a
rise in venular tone and this will promote the movement of fluid into the extravascular space.

The sixth component is the venous capacitance circuit with more than 80% of total blood volume in the
large capacitance vessels. Venous capacitance is decreased by an increase in venous tone, this increases
venous return to the heart with the converse being true for decreases in venous tone.
The last component is mainstream patency. Ventricular ejection if impeded by obstruction to the
systemic or pulmonary circuits whilst venous obstruction limits venous return to the heart.

Classification of shock
When the mechanism by which shock occurs are reviewed it is easy to understand why Hinshaw and Cox
derived the classification of shock into 4 main types.
These are namely:
1. Hypovolaemic Shock: Loss of blood or fluid
2. Cardiogenic Shock: Reduced cardiac function(pump failure)
3. Obstructive Shock: Due to extracardiac causes of pump failure(TPT/Tamponade and VTE)
4. Distributive Shock: Arteriolar and venular dilatation caused by loss of vasomotor tone
(Anaphylactic, septic and neurogenic subtypes)

1
Progression and Stages of Shock
All the above mechanisms result in the activation of a complex set of reflexes to maintain cardiac output
and arterial pressure.
The sympathetic nervous system increases heart rate and contractility. Catecholamines, angiotensin,
vasopressin and endothelins increase arteriolar and venous tone which in turn redirect blood volume
centrally leading to an increase in arterial pressure. Vasopressin and the RAAS augment water and
sodium retention to protect the intravascular blood volume.
Progression of the shock state is marked by a decline in blood pressure that compromises coronary
perfusion and performance.
The terminal phase of shock is characterised by loss of arteriolar tone and paradoxical increase in venular
resistance. This brings about loss of intravascular volume due to an increase in capillary hydrostatic
pressure and increased microvascular permeability.
However, this pathophysiology is altered in patient with hyperdynamic forms of circulatory shock, viz
septic shock. Inflammatory mediators play a significant role in septic shock bringing about vascular
dilation and increased cardiac output.
This will be expanded on later in the seminar.

Stages of Shock

Stage Pathogenesis Effects

Compensated Shock Widespread vasoconstriction Cool clammy skin
Fluid conservation by kidney Tachycardia
Stimulation of adrenal medulla
Progressive Pulmonary hypoperfusion Decreased cardiac output
Decompensated Tissue ischaemia Mental confusion
Shock Decreased urine output
Tachypnoea
Irreversible Progressive vasodilatation Brain: hypoxic encephalopathy
Decompensated Increased vascular permeability CVS: focal myocardial necrosis
Shock Myocardial depressant factor Lungs: ARDS
Pulmonary hypoperfusion Kidney: ATN
Anoxic damage Adrenals: necrosis
Hypercoagulability GI: haemorrhagic
gastroenteropathy
Liver: Necrosis
Haematological: DIC

Haemorrhagic Shock2
This is the most common type of shock in trauma patients. Haemorrhage is defined as an acute loss of
circulating blood volume of approximately 7% of ideal body weight in the adult and 8-9% in children.
The division of haemorrhagic shock into 4 classes are used as a guide for initial therapy, although the
changes outlined in each class represent a continuum rather than a static model. Subsequent volume
replacement must be guided by the patient’s response to initial therapy.

2
Estimated Blood Loss Based of Patient’s Initial Presentation– 10th Ed ATLS updated

Class I Class II Class III Class IV

Blood Loss (% blood volume) 15 15-30 30-40 >40
Pulse Rate <100 100-120 120-140 >140
Systolic Blood Pressure Normal Normal Decreased Decreased
Pulse Pressure Normal or Decreased Decreased Decreased
Increased
Respiratory Rate 14-20 20-30 30-40 >35
Urine output (ml/hr) >30 20-30 5-15 Negligible
Mental State Slightly Mildly anxious Anxious, Confused,
anxious confused lethargic
Base deficit 0 to –2 mEq/L 2 to –6 mEq/L –6 to –10 -10 mEq/L or
mEq/L less
Need for blood products Monitor Possible Yes Massive
Transfusion
Protocol

The following factors must be considered as they confound the classic haemodynamic response to the
acute loss of circulating blood volume and are namely:
Patient age
Severity of injury, type of injury and anatomic location of injury
Time lapse between injury and initial or treatment
Prehospital fluid therapy
Medication used for chronic conditions

Initial Management of Haemorrhagic shock

The diagnosis of shock and institution of treatment are done simultaneously.
The basic tenant of treatment is to stop bleeding and replace blood volume.
The standard most up to date ATLS protocol should be practiced when approaching a patient in
haemorrhagic shock, with care taken to prevent hypothermia which will exacerbate blood loss by
contributing to coagulopathy and worsening acidosis.
Initially the ATLS guidelines recommend a 1 litre warmed fluid bolus of isotonic fluid to be given
in adults (20ml/kg bolus for children weighing less than 40kg).
The patient is then reassessed, and fluid administered accordingly, with early blood product
administration advised currently.
Imaging (ultrasound or CT Scan) may be necessary to identify the source of bleed but should not
delay surgical intervention in the unstable patient.
Blood sampling should be done to assess that patient’s haemoglobin, acid-base, coagulation and
lactate status.

3
Responses to Initial Fluid Resuscitation

Rapid Response Transient Response Minimal or No

Response
Vital Signs Return to normal Transient Remain abnormal
improvement,
recurrence of
decreased blood
pressure and
increased heart rate
Estimated Blood Loss <15% 15-40% >40%
Need for Blood Low Moderate to High Immediate
Blood Preparation Type and crossmatch Type-specific Emergency unit
Need for Operative Possibly Likely Highly likely
Intervention
Early Presence of Yes Yes Yes
Surgeon

Measuring Patient Response to Therapy

The signs and symptoms used to diagnosis shock are also used to assess response to therapy,
however these do not provide insight into organ perfusion and tissue oxygenation.
Urine output is a prime indicator of response to resuscitation provided that it is not altered by
kidney injury, marked hyperglycaemia or diuretics it is a sensitive indicator of renal perfusion.
A urine output of 0.5ml/kg/hr in adults and 1ml/kg/hr in children (2ml/kg/hr in children <1year of
age) should be used as a goal. Decreasing urine output with an increase in specific gravity suggest
an inadequate resuscitation.
Evaluation of acid-base status is another measure by which resuscitation is gauged. A mild
metabolic acidosis from tachypnoea does not require treatment, however severe acidosis can
develop from long-standing or severe shock.
Metabolic acidosis is caused by anaerobic metabolism as a result of inadequate tissue perfusion
and production of lactic acid.
Acidosis is treated with fluids and blood as well as measures to control haemorrhage.
Base deficit and lactate values are used to determine presence and severity of shock and serial
measurements can be used to gauge response to therapy.

Septic shock3,4
Sepsis-3 task definitions focus on the fact that sepsis is a multifaceted patient response to infection
resulting in organ dysfunction. The new definitions focus on organ dysfunction and hypo-perfusion in the
presence of infection rather than on inflammation (SIRS).

Sepsis is defined as life threatening organ dysfunction caused by a dysregulated host response to
infection.

Septic shock is seen in patients with sepsis who develop circulatory and metabolic abnormalities resulting

4
Early Recognition of Sepsis
The sequential organ failure assessment (SOFA) is the organ dysfunction assessment tool used to
identify patients with sepsis, mostly in ICU. SOFA is effective in quantifying the severity of organ
dysfunction, morbidity and estimating mortality risk.
The quick SOFA (qSOFA) relies on only three variables: systolic blood pressure, respiratory rate
and mentation. In non-ICU patients, the qSOFA score predicts elevated risk of death and
extended ICU stay but is not designed to stand alone as an early warning of sepsis or to identify
which patients should be transferred to ICU– it is a screen in cases of suspected infection.
Additional information imparted by serum lactate levels can guide the resuscitations, a lactate of
-perfusion of tissues. Normalization of previously elevated lactate
levels remains a recommendation in the current SSC guidelines.
The impaired energy metabolism in septic shock is not a result of inadequate tissue perfusion but
is caused by a defect in oxygen utilization in mitochondria, cytopathic hypoxia. This causes
increased production of pyruvate and inhibition of pyruvate dehydrogenase and hence results in
an increase of lactate levels.

qSOFA Score

Any change in mental status

Patients are assigned one point for each abnormal parameter. Non-ICU patients with a total score
of 2 or 3 are considered at elevated risk for an extended ICU stay or death and should be assessed
for evidence of organs dysfunction using the SOFA.

5
Management (Surviving Sepsis Guidelines Update 2018)

Hour- 1 bundle
Measure lactate level, re-
Blood cultures prior to antibiotics administration
Administer broad spectrum antibiotics
B
A
65mmHg

Initial fluid resuscitation

30mL/kg crystalloid fluids should be initiated at time zero
Choice of fluids still under study but crystalloids are favoured for the time being
Colloids increase the risk of nephrotoxicity in septic shock
If a colloid is needed albumin can be used because the latter doesn’t increase the risk of
nephrotoxicity
Ringer’s lactate is the fluid of choice compared to saline as there are some evidence for chloride
restrictive resuscitation strategy

Source control
Observational data showed that inadequate early source control was associated with an increase
in 28-day mortality from 26.7% to 42.9%
Must be within 6-12hours post diagnosis

Antibiotic therapy
Regarding patients with hypotension there is a strong association between delay of initiating
antibiotics and death, with an increase of 7% risk of death for every hour of delay
Should be initiated within first hour after blood cultures have been taken
Broad spectrum antibiotics must be used, assess the need to combination agents

6
 Antibiotic spectrum should be narrowed down once cultures are available
De-escalation of antibiotics should be considered daily

Vasopressors
Asfar et al., showed that a higher MAP (80 – 85 mmHg) is not associated with higher survival
compared with a lower target (65 – 70 mmHg)
Noradrenaline is the first line of choice for its reduced risk of arrhythmias compared to dopamine
Vasopressin reduces the dose of catecholamine vasopressors but does not appear to affect
patient mortality
Two new vasopressors have been introduced, selepressin and angiotensin II
Both drugs have been shown to increase blood pressure and reducing the noradrenaline dose
hence reducing the use of catecholamine in septic shock

Glycaemic control and nutritional support

Tight glycaemic control is not recommended due to the number to death from hypoglycaemia, a
glucose level of around 180 mg/dl is recommended
In terms of nutrition there is still no definitive evidence on timing and route of administration,
enteral feeding has not been shown to be better in ICU patients with septic shock, and on the
contrary it might cause greater risk of gastrointestinal complications.

Other considerations
Corticosteroids still remain controversial, it has been proven to be beneficial only in septic shock
but not in sepsis
A restrictive haemoglobin of 7g/dL is appropriate for non-bleeding patients without active
myocardial ischemia
Hyperoxia should be avoided as it increases mortality rate, an FiO2 of 88 – 95% is targeted
Immunomodulation and mesenchymal stem cells are two of the latest developments in terms of
therapeutic interventions.
Endotoxin removal via polymyxin B haemoperfusion is a novel therapeutic approach that is still
under investigation.
Prophylactic platelet transfusions should be given when
the counts are less than 10x10^9,
less than 20x10^9 if there is a significant risk of bleeding or
if the counts are less than 50x10^9 if there is active bleeding or surgical intervention is planned.

Limitations of Sepsis-3 Definitions

Doubt about whether the exclusion of SIRS and inclusion of new sepsis definitions will expedite
identification of patients with sepsis
qSOFA score is a predictor of mortality risk and not a defining characteristic of sepsis
CONTROVERSIES
Absence of clear definition for sepsis that facilitates early identification and definitive treatment
strategies
Absence of a reliable diagnostic marker
Absence on the clarity as to the most effective guide to resuscitation

Cardiogenic Shock 7
Cardiogenic shock is characterised by inadequate end organ tissue perfusion due to cardiac dysfunction.
It includes the following haemodynamic parameters:
Systolic BP less than 80-90mmHg or 30mmHg below baseline
Reduction in cardiac index (less than 1,8L/min/m2 without support, less than 2,0L/min/m2 with
support)

7
 Adequate or elevated filling pressures
Causes include:
Acute myocardial infarction with left ventricular failure
Severe mitral regurgitation
Coronary air embolism
Cardiac Tamponade (cardiac free wall rupture)
Advanced cardiomyopathies, myocarditis

Multiple Organ Dysfunction Syndrome 5,6

Multiple organ dysfunction syndrome (MODS) refers to progressive organ dysfunction in an acutely ill
patient, such that homeostasis cannot be maintained without intervention.
MODS is not a single event but a continuum of processes characterized by serial and incremental
physiologic assaults on individual organs.
Virtually all organs are involved but damage may vary from hardly detectable or mild to completely
irreversible. MODS is a critical condition with high morbidity and mortality.
MODS can be classified as primary or secondary:
Primary MODS is the result of a well-defined insult in which organ dysfunction occurs early
and can be directly attributable to the insult itself.
Secondary MODS is organ failure that is not in direct response to the insult itself, but is a
consequence of the host's response.

The pathophysiology of sepsis-induced MODS remains an area of continued research and has not been
completely understood. Proposed mechanisms leading to the development of MODS include the
following:
Inflammation and endothelial damage
Microcirculatory dysfunction
Impaired mitochondrial function
Enhanced Apoptosis
Bacterial Translocation

Trauma results in the trigger of simultaneous inflammatory and anti-inflammatory responses, namely
Systemic Inflammatory Response Syndrome (SIRS) and the Compensatory Anti-inflammatory Response
Syndrome (CARS). Organ dysfunction is related to the intensity and balance between these opposing
inflammatory responses.
The immune-inflammatory system response is thought to serve the most important role in the
pathogenesis of MODS. In the early stage of MODS, abundant release of proinflammatory cytokines,
including TNF- - sion of vascular cell adhesion molecule 1 and
endothelial leukocyte adhesion molecule 1, and enhances the adhesion of monocytes and T cells to
endothelial cells.
During later stages of MODS, damage to the endothelium activates innate inflammatory cells in the
interstitial region of affected organs and parenchymal injury occurs.
Mitochondrial dysfunction is implicated in organ injury through accelerated release of reactive oxygen
species and promotion of cell death. Impaired perfusion and tissue hypoxia compromises oxygen supply
at the mitochondrial level. A resultant decrease in ATP generation will potentially trigger necrotic cell
death.
The endothelial glycocalyx plays a crucial role in the microcirculation and initiation of coagulation, as well
as the housing of vascular protective enzymes. Alteration in the composition of the glycocalyx after
exposure to an inflammatory insult is one of the earliest features during sepsis. Destruction of the
glycocalyx leads to capillary leakage, accelerated inflammation, platelet aggregation, coagulation, and
loss of vascular tone

8
Several hypotheses about the role of the gut in sepsis-induced MODS have been proposed. The integrity
of the gut wall in critically ill patients is compromised with a resultant increase in apoptosis and
permeability. Bacteria may consequently cross a weakened intestinal barrier, leading to liberation of
endotoxins.

Conclusion

Shock is a medical emergency that requires prompt medical treatment,if left for a prolonged period of
time it deteriorates to irreversibilityand the mortality rate is high.

9
REFERENCES

1. Sridhar SK. Shock. In: Papadakos PJ, Gestring ML, eds. Encyclopedia of Trauma Care. Berlin,
Heidelberg: Springer Berlin Heidelberg; 2015:1478-1484.
2. American College of Surgeons CoT. ATLS - Advanced trauma life support. Vol Tenth2018.
3. Cecconi M, Evans L, Levy M, Rhodes A. Sepsis and septic shock. Lancet (London, England).
2018;392(10141):75-87.
4. Makic MBF, Bridges E. CE: Managing Sepsis and Septic Shock: Current Guidelines and
Definitions. The American journal of nursing. 2018;118(2):34-39.
5. Spapen HD, Jacobs R, Honoré PM. Sepsis-induced multi-organ dysfunction syndrome—a
mechanistic approach. Journal of Emergency and Critical Care Medicine. 2017;1(10).
6. Kaukonen K-M, Bailey M, Pilcher D, Cooper DJ, Bellomo R. Systemic inflammatory response
syndrome criteria in defining severe sepsis. New England Journal of Medicine.
2015;372(17):1629-1638.

10
 16 March 2019
PRINCIPLES OF SURGICAL IMMUNOLOGY AND ORGAN TRANSPLANTATION
Dr G Bhundoo, Dr N Barakzai, Dr KSB Chiliza
Moderator: Ms S Pillay

Introduction 1, 2
There are approximately 4 300 South African adults and children awaiting life-saving organ and
corneal transplants. In 2016, 361 solid organ transplantations were performed of which 234 were
kidney transplants. Advances in surgical technique and a better understanding of the immunology
are the two main reasons that transplants have evolved from experimental procedures to being
widely accepted as treatment for patients with end-organ failure. However, rejection still constitutes
the major threat to long-term survival of transplanted kidneys, and nearly all transplant recipients
require life-long treatment.

Transplantation terminology
Autograft - transplantation of cells, tissues or organs between sites within the same individual
e.g. skin graft.
Isograft - are organs transplanted between identical twins, are immunologically
indistinguishable, and thus do not reject.
Allograft - transplantation of organs or tissues from a donor to a non-genetically identical
individual of the same species
Xenograft - transplantation of an organ or tissue between two different species

Basic immunology3
Major Histocompatibility Complex (MHC)
Cluster of highly conserved polymorphic genes on short arm of chromosome 6.
In humans the MHC is called the Human Leukocyte Antigen (HLA)- the antigen(Ag) primarily
responsible for human transplant rejection.
Primary role of MHC molecules is to present antigens in the form of fragments of foreign
proteins so it can be recognised by T-lymphocytes through antigen-specific receptors.
Class I MHC- present in all nucleated cells. Responsible for presenting antigenic peptides
from within the cell to CD8+ T-cells.
Class II MHC- expressed only on APCs (antigen-presenting cells) including dendritic cells,
macrophages and B cells. Present extracellular antigens to CD4+ T-cells.
Class III MHC- Encodes for complement and certain cytokines.

ABO Incompatibility
Can result in hyperacute rejection of vascularized grafts as a result of:
1. ABO blood group Ag are highly expressed on kidney & cardiac grafts.
2. Preformed natural antibodies to blood group substances.

Histocompatibility testing 3
HLA Typing- serological and molecular typing
HLA Antibody Screening
-Cytotoxic antibody screening: detects Class I HLA Ab, non-HLA Ab, IgM Ab
-Solid phase Antibody screening: detects Class I & II HLA Ab, IgG
Crossmatching
-Complement-Dependent Cytotoxicity Crossmatch
-Flow Cytometry Crossmatch: detects DSA regardless of the ability for complement
fixation

1
 Immunosuppression4
Comprises of three phases following successful organ transplant:
Induction
Maintenance
Rescue

Induction agents Maintenance agents Rescue agents

Polyclonal and monoclonal antibodies Calcineurin inhibitors Mild to moderate cellular rejection
ATG Cyclosporine Corticosteroids
Alemtuzumab Tacrolimus*
Rituximab
Interleukin-2 (IL-2) receptor Anti-metabolites Moderate to severe cellular
antagonists: Azathioprine rejection
Basiliximab* Mycophenolate mofetil (MMF)* Polyclonal and monoclonal
Daclizumab antibodies
Steroids m-TOR inhibitors Acute antibody mediated rejection
Methylprednisolone* Sirolimus Immunoglobulins
Everolimus Rituximab, Bortezomib, Eculizumab
Newer agents
Co-stimulation blocker: Belatacept
Protein kinase C inhibitor: Sotrastaurin
JAK 3 inhibitor: Tofacitinib
* these drugs are used locally

Corticosteroids: block IL-2 gene expression on the T-cells and antigen presenting cells
(APCs). Induction, maintenance and immunosuppression for acute rejection.
Calcineurin Inhibitors: prevent IL-2 production in T-cells. Tacrolimus is effective as rescue
therapy in cyclosporine-treated patients with steroid-resistant acute rejection episodes.
Mammalian target of rapamycin (mTOR) Inhibitors: bind with FK binding proteins, which
further bind with mTOR and block its action and inhibit T cell proliferation.
Antibodies:
Polyclonal: induction, immunosuppression and treatment of acute rejection
Monoclonal: anti-CD25 monoclonal antibodies which inhibit IL-2 binding e.g. Basiliximab and
Daclizumab.

Organ rejection2
Types of rejection
Hyperacute rejection
Within minutes to hours because vascularization is rapidly destroyed.
High titre of pre-existing donor-specific antibodies (DSA’s).
Ag-Ab complexes activate complement system, causing massive thrombosis in the
capillaries, preventing vascularization of the graft.
Induced by prior blood transfusions, multiple pregnancies, previous transplantation.
Acute rejection
Manifests commonly in the first 6 months after transplantation.
Diagnosis: increase liver enzymes ALT, AST, GGT and alkaline phosphatase. INR mildly
elevated.
Histological diagnosis using the Banff criteria: score of 7-9 suggests severe rejection.
Acute cellular rejection:
Accounts for 90% of early rejection episodes( i.e. occurring within 3 months).
Mediated by lymphocytes activated against donor Ag, primarily in the lymphoid tissues.

2
 Acute humoral rejection:
Form of allograft injury, primarily mediated by antibody and complement,
can occur immediately post transplantation (hyperacute) or during the 1st week.
Proteinuria is associated with donor-specific Ab detection. Important factor in determining
rapid GFR decline and earlier graft failure in patients developing antibodies.
Presence of CD4 in peritubular capillaries is highly suggestive
Chronic rejection:
Develops months to years after transplant.
Appears as fibrosis and scarring in all transplanted organs.
Risk factors: previous episode, inadequate immunosuppression, reperfusion injury to
organ, recipient-related factors (diabetes, hypertension, hyperlipidaemia)

The Organ Donor 5, 6, 7

Types of Donors

Organ Donor

Living Cadaveric

Related Unrelated Non-heart beating Heart beating (brain dead)

Living vs Cadaveric donation

Living donors
Living donation takes place when a living person donates an organ or part of an organ for
transplantation to another person.
Living-related: Donor genetically related to the recipient.
Living-unrelated: -Donor genetically unrelated (requires minister of health approval).
Paired exchange: incompatible paired donors perform an exchange, which allows two
antibody-compatible operations.
Absolute and relative contraindications for living organ donation

Absolute Relative
Age (years) < 18 > 65
Abstinence from substance abuse with
Substance abuse Active substance abuse documented completion of
rehabilitation
Uncontrolled, end stage organ
Borderline or controlled on low dose
Hypertension damage, additional risk factor for
single agent
cardiovascular disease
Diabetes Diabetes Mellitus Impaired glucose tolerance
Morbid obesity BMI > 35 or > 30
Obesity Obesity
with co-morbidity
Significant discrepancy in kidney
Renal anatomical abnormalities Vascular anomalies
size/ split renal function

Cadaveric Donors
The majority of organ donors are patients in ICU who have sustained irreversible brain damage for a
variety of reasons, with the final common pathway being the diagnosis of brainstem death. This is
made according to the Minnesota criteria

3
Diagnosis of brainstem death according to the Minnesota criteria
Known but irreparable intracranial lesion
No spontaneous movement
Apnoea (4 minutes)
Absent brainstem reflexes
*Above findings must remain unchanged for 12 hours*

Exclusions
1. Drug or alcohol intoxication
2. Neuromuscular blocking agents
3. Hypothermia and metabolic disturbances
4. Coma of unknown aetiology

Absent brainstem reflexes Apnoea test

Absent pupil light reflex
No attempt to breathe
Absent corneal reflex
despite a PaCO2>50mmHg.
Absent vestibule-ocular reflex
*Avoid hypoxia by pre-
Absent oculo-cephalic reflex (Doll’s eye at movement)
oxygenation for 10 min at
No motor response to stimulation in cranial nerve distribution
100% oxygen*
No cough/ gag reflex or response to bronchial stimulation by
suction catheter

Steps for referral

Diagnosis of brain death having met the exclusion criteria
Living Will regarding organ donation or family counselling and consent obtained for those
without a Living Will
Contact transplant team
Management of the cadaver while awaiting transfer

Cadaveric Donor management guidelines

Cardiac MAP 70-90mmhg (treat hypertension with short acting B-Blockers, hypotension
with volume followed by vasoactive agents)
HR 60 – 120 beats/min
Hb – 8g/dL
SCVO2 – 70%
Respiratory FiO2 - 0.40
Normal arterial PH
Tidal volumes 8 – 10 mL/kg
Plateau pressure < 35cm H2O
Judicious fluid management to avoid pulmonary oedema
Renal Euvolemia with appropriate end organ perfusion and oxygen delivery (UO 0.5-
3ml/kg/hr)
Early recognition and correction of Diabetes insipidus (UO >4ml/kg/hr)
DDAVP 8ng/kg loading dose followed by 4ng/kg/hr titrated to UO <3ml/kg/hr
Plasma sodium concentration 140 – 150mmol/L
Endocrine Thyroid hormone replacement – thyroxine 20mcg bolus followed by 10mcg/hr
infusion for 10hrs
Insulin therapy to maintain normo-glycaemia
Use of steroids to dampen pro-inflammatory and leucocyte adhesion

4
RENAL TRANSPLANT 5
Kidney transplant improves survival and long-term outcomes in patients with end-stage renal failure
over maintenance on dialysis. It is the currently treatment of choice. The pool of eligible patients is
increasing, but organ supply remains inadequate.

Careful donor selection is crucial with living donor transplant offering a better outcome.
Donor sources: cadaveric; living compatible; kidney paired donors; desensitised non-compatible.
Contraindications: contraindications to surgery; to immunosuppression or active systemic diseases13

Surgical Aspects
Recipient
Approach – Heterotopic pelvic approach (Multiple advantages and hence standard) 14

Implantation site selection 11

Pelvic fossa (avoid sites of previous transplant, surgeries or peritoneal dialysis catheters)
Contralateral side implantation advised – renal pelvis/ureter anterior if future surgery required
Right external iliac vessels are longer and more horizontal – facilitate vascular anastomosis

Incision and exposure 10

Considerations – Good access to iliac fossa and bladder with minimal wound related morbidity
Incision: Modified Rutherford Morrison/Pelvic Gibson. (Curvilinear; above pubic tubercle to ASIS)
Transversalis fascia is divided; peritoneum reflected superiorly to expose the iliac vessels
Lymphatic vessels ligated – to avoid lymphocele

Donor kidney placement and reconstruction

Donor kidney placed in operative bed
Vascular reconstruction:
- Renal artery to external iliac artery – end to side
-Renal vein to external iliac vein – end to side
-Beware of congenital anomalies eg. double renal arteries
Urinary tract reconstruction
-After completion of vascular anastomosis
-Ureteroneocystostomy ( transvesical with antireflux tunnel)

Closure considerations
Meticulous haemostasis – as these patients are prone to uremic bleeding
Re-examination
- tension-free ureteroneocystostomy
- no urine leak
- kinking of vessels
- assess perfusion of ipsilateral limb as external iliac artery used for perfusion of graft
Double J stent
- maintains patency of the transplanted ureter while the anastomosis is healing
- reduces anatomic torsion
- stents increase risk for urinary tract infections
- can result in haematuria and stent migration
- require an additional procedure for stent removal (usually removed 4 – 6 weeks following
transplant)
Transurethral urinary catheter and wound drains
- Foleys catheter maintains non-obstructive flow of urine condition and allows for meticulous
monitoring of urine output.
- Wound drain left in situ for 3- 5 days to prevent peri-graft haematoma formation.
5
Complications 12

Pathological Surgical Others

Rejection Vascular Delayed graft function
Arterial stenosis Main cause of primary
Arterial/venous thrombosis non-function of kidneys up
Infection Bleeding to 1 week
Opportunistic – prophylaxis
TB; P. Carinii; CMV Urological Post-transplant DM 13
Urine leak/urinoma Immunosuppressants
Ureteric obstruction Increase infections and
Cardiovascular events Vesico-ureteric reflux CVS complications
Depends on underlying Devascularisation of ureter
disease; cardiac history, resulting in stricture Post-transplant
level of graft function. formation malignancy
Long term
Lymphocele

Wound infections
* DM- diabetes mellitus

Living Donor Nephrectomy; Surgical Options for Harvest

Open surgical approach Laparoscopic

Flank - +/- rib resection Pure
Mini-incision [retroperitoneal] Hand-assisted (preferred)
Transperitoneal

Should be familiar to all transplant - Advantages of minimally invasive donor

surgeons; but increasingly being nephrectomy are well documented with little or
replaced by minimally invasive adverse effect on graft function
techniques - The hand assisted technique enables rapid
extraction of the graft, shortened warm ischaemia
Relative indications time and thus preserves graft function
- Complicated vascular anatomy - Pure laparoscopic harvest has a steep learning curve
- Prior surgery that pose with increased operative time
laparoscopic challenge

Laparoscopic donor nephrectomy Vs Open16

A recent retrospective study by Massachusetts General Hospital showed that there was no
statistically significant difference between laparoscopic and the open donor nephrectomy with
regard to the following parameters i.e. operating time, donor pre-operative renal function, donor
and recipient post-operative renal function, delayed graft function or the incidence of major
complications.

Renal transplantation between HIV-positive donors and recipients17

HIV infection was previously an absolute contraindication to renal transplantation. However with the
advent of highly active antiretroviral therapy (HAART), renal transplantation using HIV negative
donor kidneys has successfully been employed for HIV-infected patients with end-stage renal failure.
The transplantation of HIV-positive donor kidneys to HIV-infected recipients is now a viable

6
alternative to chronic dialysis or transplantation of HIV-negative donor kidneys. This significantly
increases the pool of donor kidneys to the advantage of HIV-positive patients. Muller et al
transplanted 27 HIV-positive patients from HIV positive donors and demonstrated a 74% patient
survival rate at 5 year follow up therefore renal transplantation from an HIV-positive donor appears
to be an additional treatment option for HIV-infected patients requiring renal replacement therapy.

LIVER TRANSPLANT
Liver transplantation remains the only treatment option for those with end organ failure. In addition
to increased mortality associated with end-stage liver disease, patients with liver cirrhosis and
patients with chronic viral hepatitis are at a 20 fold increased risk of developing primary liver
malignancies. This risks associated with liver transplant can be minimised by fully appreciating the
following:
Anatomic variations
Performing appropriate ABO matching
Size matching of the donor liver to the recipient habitus
Adequate maintenance of donor liver function
Minimisation of cold ischaemia time

Indications15

Chronic hepatitis Hepatitis C,B and D; autoimmune hepatitis; Cryptogenic cirrhosis

Alcoholic cirrhosis Abstinence for 6 months required
Primary hepatic tumours HCC with no extrahepatic metastases – UCSF/Milan Criteria
Fulminant liver failure Viral hepatitis infection/ drug toxicity
Cholestatic diseases Primary biliary cirrhosis; cystic fibrosis; sclerosing cholangitis;
biliary atresia; Caroli’s disease
Metabolic diseases Alpha-1 antitrypsin deficiency; glycogen storage disease, Wilson
disease; hemochromatosis
Other conditions Budd-Chiari syndrome; Polycystic liver disease

Evaluating the liver transplant candidate 15

Hepatology evaluation Define severity & etiology of liver dysfunction and its prognosis
MELD Score >/= 7 ; Child-Pugh Score >/= 10
Laboratory testing Liver and renal function tests; Viral studies [CMV, EBV, HIV, Hepatitis];
Tumour markers
Hepatic imaging Ultrasound + Doppler
Cardiopulmonary ABG; Spirometry; Cardiac ECHO
Psychosocial evaluation Support; addiction and recividism; Mental illness 6
Extrahepatic malignancy Chest xray; CT; Upper/lower scopes as necessary
Anaesthetic risk
assessed

Types of liver transplant 9, 11

Orthoptic graft – the donor organ replaces the liver in its native position
Auxillary – a split graft is transplanted as a bridge till the native liver, which is left in its original
position, recovers its function
Heterotopic auxillary liver transplant – graft is placed in an ectopic site]
Auxillary partial orthoptic liver transplantation – the graft replaces the resected native right or
left hemi-liver

7
Surgical aspects of liver transplant 11, 16
Various techniques
conventional technique – orthotopic [liver replacement]
split liver – obtaining 2 grafts from a single deceased donor
living donor liver transplantation
domino liver transplantation (select group of liver transplant recipients can donate their
explanted native livers for use as liver grafts in other patients e.g. Familial amyloid
polyneuropathy, maple syrup urine disease)

Conventional technique – Principles

Removal of native liver with replacement of the retrohepatic vena cava
Involves skeletonization of hilar structures [bile duct/hepatic artery/portal vein]
Replacement with donor liver containing a vena cava segment including the hepatic veins
Vena cava anastomosis above and below the liver is performed
Portal vein; hepatic artery and biliary tract anastomosis are then performed

Living donor liver transplant (LDLT)16

LDLT has emerged as a solution to the current shortage of allografts for those awaiting liver
transplants.
Current recommendation – Right hepatic lobectomies [vs previously – segments II & VII]
The inflow vessels are isolated followed by parenchymal transection using standard liver
resection principles
Hepatic arterial system is reconstructed using a branch of the hepatic artery
Biliary reconstruction more complex due to small size and multiple ducts – use of
microscopes decrease rates of strictures, leaks and biloma formation.
Optimization of venous drainage is crucial – venous congestion may lead to graft
dysfunction and failure.
Major concern – donor morbidity and mortality; decreased with improved harvest
techniques.

Post operative complications

Primary graft non-function
Bleeding
Hepatic artery and portal vein thrombosis
Venous outflow obstruction causing Budd Chiari syndrome
Biliary anastomosis leak
Graft rejection
Infection ( CMV hepatitis, hepatic abscess formation)

Conclusion
Significant advances in surgical techniques, medical diagnosis, patient selection and
pharmacotherapy has transformed the field of organ transplant from an experimental procedure to
standard of care, life-saving procedures and cost-effective management for a variety of end stage
organ failures. Despite these advances however, there continues to be a mismatch between suitable
candidates and donor suitability.

8
References
1. The Organ Donor Foundation of South Africa. https://www.odf.org.za/info-and-faq-
s/statistics.html ( accessed 19 January 2019)
2. Hricik DE. Transplant immunology and immunosuppression: Core Curriculum 2015. Am J
Kidney Dis. 2015;65(6):956-966
3. Chandraker A , Sayegh MH, Singh AK. Core Concepts in Renal Transplantation: Basic
Histocompatibility testing methods. Springer publications 2012; 05 (08):21-42.
4. Kumar A, Shrestha BM. Evolution of Immunosuppressive Agents in Renal Transplantation: An
Updated Review. Int J Stem Cell Res Transplant 2016; 04(3):158-172.
5. Kumar Lakshmi. Brain death and care of the organ donor. Journal of anaesthesiology clinical
Pharmacology.2016; 32:146-132
6. Golia AK, Pawar M. Indian Journal of Critical Care Medicine. The diagnosis of brain death.
2009;13 (1): 7-11
7. Hassamal R, KN Boolaky KN, LP Mugabi. Principles of immunology and transplantation.
Surgical Seminar 2017.
8. Lung-Yi MTA, MD. Living Kidney Donation: Strategies to increase donor pool. Surgical Clinics
of North America. 2019;99:37-47
9. Rampershad SR. Principles of immunology and solid organ transplants. Surgical Seminar
2015
10. Oritz JZPJ. Understanding the complexities of organ transplantation. INTECH. 2011:461-86.
11. Al FR-Se. Outcomes and Surgical Complications in Kidney Transplantation. International
Journal of Organ Transplantation Medicine 2017; 8(2)
12. Maynard EM. Liver transplantation - Patient selection; perioperative surgical issues and
expected outcomes. Surgical Clinics of North America. 2019;99:65-72.
13. Augustine M. Kidney transplant: New opportunities and challenges. Cleveland Clinic Journal
of Medicine. 2018;85(2):138-44.
14. Tung Wan Song A. Liver transplantation: Fifty years of experiece. World Journal Of
Gastroenterology. 2014;20(18):5363-74.
15. Georgios T, Polyxeni A, Dicken SC, Martin H. Laparoscopic vs open donor nephrectomy:
lessens learnt from a single academic centre experience. World J Nephrology. 2017 Jan 6;
6(1): 45-52.
16. Muller E, Barday Z, Mendelson M. HIV-Postive to HIV-postive Kidney transplantation Results
at 3- 5 years. The New england Journal of Medicine. 2015; 372:613-20.

9
 WOUND HEALING AND BURNS
A Gurunand, A Jooma, N Mabaso
Moderator: Ms S Wall 30 March 2019
_________________________________________________________________________________________

Introduction
The severely burned patient presents a unique challenge to the managing team of healthcare professionals.
The multisystemic and dynamic nature of the injury was once poorly understood and accounted for the
former poor prognosis in a Southern African context. However a better understanding of this potentially
devastating injury and appreciation of the concepts of basic resuscitation have greatly improved outcomes.

Wound Healing (5,6)

Wound healing is a complex process governed by numerous cells and cell signalling and follows a pattern and
divided into 4 phases. These overlap and are characterised by distinct cellular populations and biochemical
signalling, and are as follows:
1. Hemostasis
2. Inflammation
3. Granulation
4. Remodelling

Hemostasis
This first phase is characterised by exposure of subendothelial collagen to platelet aggregation and the
coagulation cascade. Alpha-granules of the platelets release chemotactic factors from the wound bed
including ADP, PDGF, PAF, serotonin and fibronectin. Vasoconstriction also occurs with a fibrin clot and forms
the scaffolding for inflammatory cells migration.
Inflammation
Neutrophils first migrate into the wound bed with the function of phagocytosis of bacteria, cytokine release
and angiogenesis. Macrophages are also involved in debridement and NO/ free radical production. They also
play a role in angiogenesis and matrix deposition through cytokines/ growth factor release and are present
during the other phases. T-lymphocytes are the last line of cells to enter the wound with an incompletely
understood role and bridge the role between the inflammatory and granulation phases.
Granulation
Occasionally known as the proliferative phase, this starts from 4 days post injury up to 4 weeks and involved
cell types fibroblasts and endothelial cells. Fibroblasts synthesise collagen, which is initially secreted as a type
III form and later then converted to a type I, responsible for wound strength. Collagen synthesis is also
dependent on systemic factors like oxygen supply, nutrition and wound environment. Fibroblasts synthesize
the wound matrix and is made up of glycosaminoglycans and fibronectin, which are gradually incorporated
into collagen fibrils during maturation. Endothelial cells enter the wound and allow angiogenesis which starts
the process of epithelialization; a process which occurs from the wound periphery.
Remodelling
This is the re-organisation of previously laid down collagen. This phase can last for 6-12 months post injury
and leads to the formation of a collagen rich, mature and avascular scar.

Pathophysiological response to burns (1,4,6)

The systemic response to a burn injury is profound ranging from a mild local response to an acute
widespread inflammatory response effecting all organs systems. The systemic response that follows is a
sustained hypermetabolic state. Understanding this response and the attenuation thereof is key in
understanding the management of a severe thermal injury.
Local response
Burn zones
Understanding Jackson’s burn zones plays an imperative role in early burn wound management and the
concept of burn wound conversion. 3 zones are described:
1. Zone of coagulation – This is the most severely burned area and is typically at the centre of the
wound. Protein coagulation results in irreversible tissue loss.

1
 2. Zone of stasis – This is a zone of varying degrees of vasoconstriction and ischemia. This is of clinical
relevance as this is potentially salvageable tissue. Sepsis or inappropriate fluid administration can
cause a deeper and larger burn, and occurs from impaired dermal microcirculation, free radical
generation, local oedema and vessel thrombosis.
3. Zone of hyperemia – This is often the outermost area of the burn and is characterised by increased
blood flow, tissue oedema and capillary leakage secondary to the influx of inflammatory mediators.
In the absence of severely impaired perfusion or sepsis this zone heals with conservative
management with little or no scarring.

Zone of coagulation

Zone of stasis

Zone of hyperaemia

Systemic response: The Hypermetabolic Response to Burns

The systemic response to large area burns (>15%) is profound with studies showing that this response
persists until the wound is closed with the effects felt for period of up to 2 years. This response is multi-
systemic with the understanding of such forming the foundation of care.
1. Cardiovascular changes – Cardiac changes include initial myocardial depression from circulating
cytokines as well as elevated heart rate and later an increased cardiac output. Vascular changes
include increased capillary permeability with subsequent interstitial fluid loss and loss of
intravascular volume.
2. Respiratory changes – An increased respiratory rate with bronchoconstriction
3. Metabolic changes – A raised basal metabolic rate with an overall catabolic state result with BMR
raised as high as 180% of normal. This state peaks at about 2 weeks post injury however can be
sustained for as long as 2 years. Severe protein catabolism results with decrease in lean body mass
and muscle bulk with overall weight loss. Hepatic synthesis of albumin and pre-albumin are
significantly decreased which have significant effects on drug dosing and metabolism as well as
immune function.
4. Immune system - Dysregulation results from impaired function of acute phase reactants rendering
severely burned patients more susceptible to sepsis. In addition they do not exhibit classical signs of
sepsis due to a heightened inflammatory state.
Burn shock is a phenomenon seen in patients with large TBSA burns. It is multifactorial in its causation and
occurs as a result of the following:
Vasodilation/ relative hypovolemia – Due to systemic release of inflammatory mediators
Absolute hypovolemia
Due to increased losses from burn wounds
Ongoing capillary leak from release of inflammatory mediators
Myocardial depression – Due to the effects of inflammatory mediators
This underlying mechanism occurs over time and not acutely necessitating this process to be reversed over a
longer period and not through fluid boluses or vasopressors.

Acute burn management (2,3,4,6)

Effective initial management of severely burned patient can drastically alter outcomes. Patients are managed
according to ATLS principles with attention being paid to airway and circulatory support.
1. Airway – Careful assessment of the airway and the need to intubate is of prime importance. This
decision is made on history regarding mechanism of injury and length of exposure as well as clinical
2
 features. Patients entrapped in enclosed spaces for prolonged periods are at risk for inhalational
injuries. Clinical findings such as a depressed LOC, respiratory distress, stridor, singed facial hair/
nasal hair or facial burns raise the suspicion of an inhalational injury with early intubation often being
the prudent choice; bearing in mind in that intubation may become difficult later due to swelling
after fluid resuscitation. Intubation in this case serves to stent the larynx and prevent airway
collapse. This represents a supraglottic or upper airway injury and results from direct thermal injury
to the vocal cord structures causing oedema.
2. Breathing – Oxygen should be administered to maintain normal saturations. Burn patients have
many factors which may impair respiration and oxygenation. Lower airway or subglottic injury results
from inhalation of gases, carbonaceous deposits and thermal trauma and results in parenchymal
damage. These injuries can confirmed on bronchoscopy and in severe forms require treatment with
invasive ventilation. CO or CN3 poisoning also pose significant impairments to ventilation and are
treated with or 100% inhaled oxygen. Secondary injury from ARDS is also a possibility and is also
treated with invasive ventilation. Full thickness circumferential chest wall burns alter compliance by
altering dynamics of respiration requiring urgent bedside escharotomy.
3. Circulation – Assessment of patient fluid status and early establishment of IV fluid therapy is of
paramount importance in those with a TBSA of over 15%. Other injuries may also require additional
fluid therapy.
4. Disability – Patients GCS must be evaluated and managed regarding investigation and airway
management with investigation of this via a CTB considered in those with features suggesting head
trauma.
5. Exposure – Patients must be exposed to search for other sources of trauma however should be done
in a way not to cause hypothermia. Several studies have linked hypothermia and poor outcomes and
every effort should be maintain core temperature. Minimising delay between immediate exposure
and definitive dressing, with the use of forced air warming devices, warm fluids and maintaining an
acceptable ambient temperature is indicated to prevent hypothermia.
6. First Aid - First aid is effective up to 3 hours post burn. If a patient presents in that window, first aid
should be performed. The only proven effective first aid is cool running water for 20 mins. The aim of
first aid is to holt the burning process thus limit the size and depth of the burn.

Fluid management (2,4)

Burns with a TBSA of over 15% require intravenous fluid resuscitation in the acute phase due to the
increased capillary permeability present from the systemic inflammatory response. Fluid therapy is aimed at
addressing this loss of fluid and ensuring tissue perfusion to attenuate “Burn Shock.”
Numerous formulas have been used in the calculation of fluid requirement and depend on TBSA % and
patients weight. Isotonic crystalloid such as MRL remains the fluid of choice. Traditionally the Parklands
formula has been used. Total fluid is calculated at 4ml/kg/ TBSA% with half of this fluid given in the first 8
hours with the remainder given over the remaining 16 hours. An alternative formula used is the Modified
Brooks’ Formula where total fluid is calculated at 2ml/kg/TBSA% and administered in a similar fashion.
In accordance with ISBI Guidelines of 2016 the following principles should be adhered to:
Crystalloids remain the first choice of fluids. While colloids offer the advantage of superior expansion
of the intravascular compartment, studies have shown no survival benefit; except in large TBSA
burns (>60%). Locally the majority of these patients are palliated leaving little role for colloids.
Fluid boluses are associated with increased incidence of oedema and pulmonary oedema and are
only indicated in cases of hypotension.
Fluid rate should be titrated to urine output:
Adults – Aim for 0,5-1ml/kg/hr
Children – Aim for 1-1,5ml/kg/hr
Paediatric patients require maintenance fluids containing glucose in addition to resuscitation fluids.
5% Dextrose Ringers Lactate administered according to the 4:2:1 rule is indicated until full feeds are
established. This is due to the relative paucity of hepatic glucose stores.

Calculation of TBSA (4,6)

TBSA of a burn is required to calculate fluid requirement however is a deceptively difficult task to achieve.
The Lund and Browder chart encompasses all ages in terms of calculation of burn area. An alternative (albeit
3
slightly less accurate) is the Rule of Nines or calculating area using the surface area of the patients palm and
fingers as 1%.
Prior to calculating area all blisters must be removed and all burn wounds must be scrubbed which tends
toward a more accurate calculation. Leaving behind blisters has several problems including inability to assess
underlying burn wound depth, burn wound sepsis and pain.

Burn wound depth assessment (4,6)

Burn wound are classified as follows:
Superficial – Usually involves epidermis only and heals with minimal scarring.
Partial – These are further sub-classified into superficial partial and deep partial burns with the
difference being the amount of dermis involved.
Superficial partial – Involves superficial aspect of dermis and form blisters and blanches on
depression.
Deep partial – Involves deeper layers of dermis, are with involvement of vessels. Are exquisitely
painful and do not blanch on depression.
Full thickness – These extend beyond the dermis and can involve subcutaneous tissues and have a
hard leathery consistency, are insensate and are often cool to touch.
Burn depth does not play a role in calculation of initial fluid requirement but rather predicts the need for
operative intervention with deep partial thickness and full thickness burns often requiring excision and
grafting to effect healing.
The main principles of successful management of postburn hypermetabolic response are:
Provision of energy and aggressive nutritional support throughout the postburn period; this reduces
mortality and complications.
Controlling external environment by warming the patient
Preventing sepsis
Achieving early wound closure

Early Excision and Grafting (6,7,8,9)

The sub-acute treatment of deep dermal burns and full thickness burns is early excision and grafting. This
approach removes necrotic and inflammatory tissues and promotes rapid wound closure. Excision of burn
eschar removes a focus for bacterial infection and adequate debridement a viable bed for skin grafting. Early
grafting minimizes fluid loss, reduces metabolic demand, and protects the wound from exposure to
infectious organisms (i.e. closely mimics the function of normal skin)
Early excision and grafting within 24 – 48 hours of burn has been shown to reduce inflammation, as well as
the risks of infection and systemic complications such as Burn shock. Early excision and grafting has improved
mortality and morbidity& also reduces hospital stay.
The most physiological form of coverage post excision is an autograft. In extensive burns, patients require
temporary coverage with the use of allografts; xenografts; skin substitutes or dermal analogue due to
insufficient donor sites.

Skin Grafts
1) Graft Selection
Skin transplanted from one location to another on the same individual is termed an autograft. These
grafts consist of the entire epidermis and a dermal component of variable thickness. If the entire
thickness of the dermis is included, the appropriate term is full-thickness skin graft (FSG). If less than the
entire thickness of the dermis is included, this graft is a split-thickness skin graft (SSG). SSGs require less
ideal conditions for survival & have a broader range of applications (e.g. resurfacing large wounds, line
cavities, resurface mucosal deficits, close flap donor sites, and resurface muscle flaps.)

4
STSG’s disadvantages

SPLIT-THICKNESS SKIN GRAFT FULL-THICKNESS SKIN GRAFT

Advantages - Broader spectrum of uses - Higher collagen content, dermal vascular

- Less ideal conditions for survival complexes & epithelial appendages
- Better cosmesis
- Less wound contraction

Disadvantages - More fragile - Require optimum conditions for survival

- Unable to withstand radiotherapy - Higher likelihood of graft failure
- Wound contraction
- Poor cosmetic outcome
- Wound care for donor site

2) Donor Site Selection

Can be harvested from any surface of the body. Usually selected from areas that can be concealed easily in
recreational clothing & minimize discomfort during healing.
Common sites are the anterior and lateral thighs. The scalp may be used for resurfacing areas of the face that
are too large for FSG’s or in severe burns in which donor-site availability is limited. Because of its thickness,
scalp skin may be harvested repeatedly with minor risk of alopecia.

3) Wound Preparation
Skin grafts will not survive on tissue with limited blood supply (cartilage, tendon, nerve). Skin grafts will
survive on periosteum, perichondrium, peritendon, perineurium, dermis, fascia, muscle, and granulation
tissue. Bacterial counts greater than 100,000 per square centimeter are associated with a high likelihood of
graft failure. Debridement, dressing changes, and topical or systemic antibiotics may be indicated prior to
grafting to achieve an adequate wound bed. Vacuum assisted wound closure devices are most effective in
stimulating granulation of wounds while simultaneously decreasing bacterial loads in wound beds.

Wound preparation involves cleansing with saline, judicious debridement, and meticulous hemostasis.
Minimal use of electrocautery is recommended as it creates devitalized tissue. Use of epinephrine at the
donor or recipient site does not compromise graft survival.

4) Operative Technique
i) Harvesting
The commonest technique involves a dermatome, which provides rapid, consistent harvest of large
uniform-thickness grafts. Thickness is adjusted on the instrument. Surgeons must be familiar with the
installation of the blade and depth settings. The dermatome is held in the dominant hand of the
operator at a 30-45° angle from the donor skin surface. Greater angulation of the dermatome leads
to gouging or trenching of the skin. Traction is applied with non-operating hand and by the assistant
in the proximal and distal edges of the skin area. The dermatome is running when it engages the skin
surface & then advanced in a smooth motion over the skin with gentle downward pressure. After an
appropriate length has been harvested, the dermatome is tilted lifted off of the skin. If fat is exposed
the dermatome has gone too deep and the angle should be shallowed.
ii) Placement
A SSG may be meshed by placing the graft on a carrier and passing it through a meshing device. The
carrier has a grooved side that must be directed superiorly and upon which the graft should be laid
out. Meshing allows expansion of the graft surface area up to 9 times the donor site area & the gaps
in meshed skin prevent underlying fluid collection. This technique is indicated for large wounds. Once
the recipient site has been prepared, the graft is placed over the wound bed. Placing the dermal,
typically white, side down is important. Take care to prevent wrinkling or excessive stretching. The
Graft can be secured with sutures or staples

5
 Wound care
The dressing should provide uniform pressure over the grafted area and be non-adherent, semi-
occlusive and absorbent. Dressings should immobilize the graft, prevent shearing & prevent
seroma/hematoma formation beneath the graft. “Tie-over” bolster dressings are useful over joints or
other areas where motion is difficult to avoid, in wounds with irregular contours & locations where
securing a dressing is difficult (oral/nasal cavities/nasal tip).
The donor site must also be dressed appropriately at the conclusion of the operation. After skin has
been harvested, spray an epinephrine solution over the donor site to limit bleeding and wrap in
plastic until you are ready to dress. The ideal donor site dressing is one that promotes rapid re-
epithelialization, causes little pain, is low maintenance, cheap, and has a low rate of infection.
iii) Graft Survival
Graft adherence is maximal during the first 8 hours post-grafting, but the initial dressing should be
left in place for 3-7 days unless pain, odor, discharge, or other signs of complications exist. The
period of time between grafting and revascularization of the graft is referred to as the phase of
plasmatic imbibition. This process is entirely responsible for graft survival for 2-3 days until
circulation is re-established. During this time, the graft typically becomes edematous and increases in
weight by 30-50%

Sub- Acute Complications of Burns (6,10,11)

Primary hyperalgesia
An acute burn induces a potent inflammatory response. The release of inflammatory mediators sensitizes
the active nociceptors at the site of injury. This causes the wound and surrounding skin to become especially
sensitive to mechanical stimuli.

Toxic shock syndrome

This is a toxin-mediated syndrome caused by staphylococcal/streptococcal infection and is the commonest
cause of unexpected mortality in children with small burns. The diagnosis is often missed as signs are non-
specific and mimic other childhood illnesses. Patients (especially kids) may develop pyrexia, new rash, acute
diarrhoea or sudden change in clinical condition a few days after a burn indicates a diagnosis of toxic shock
syndrome. It usually occurs in children under 2 years with burns less than 10% TBSA, 48 hours post injury.
Management is aggressive resuscitation, appropriate antibiotics & management in a high care/ICU setting.

Compartment Syndromes
Usually due to Compartmental restriction (e.g. circumferential burns) or increased intra-compartmental
pressure due to massive fluids shift due to large fluid resuscitation. Treatment is escharotomy for a
peripheral region or decompressive laparotomy for abdominal compartment syndrome.

Line Sepsis
Burns patients are more prone to developing intravenous catheter related-blood stream infections. All lines
should be removed as soon as possible, checked every day & kept only for appropriate time periods.

Chronic Complications of Burns (12,13,14,15,16)

Chronic pain - In severe burns pain does not decrease with time due to secondary hyperalgesia and drug
tolerance. These may develop into chronic pain syndromes such as hyperalgesia and allodynia & can persist
for years. Chronic pain also manifests as severe depression/other mental illness requiring appropriate
psychological care (e.g. SSRI’s, CBT, support groups, counselling). Neuropathic pain is a common long term
phenomenon. Gabapentin has been shown to be most effective in reducing chronic pain syndromes.

Scarring & Wound contraction – Any deep dermal and full thickness burn is at risk of contracture as well as
hypertrophic scar development. This hinders mobility if the burn is near or involving a joint as well as
significant psychological consequences if scarring occurs in exposed areas (especially the face). Risk factors
for wound contractures and hypertrophic scarring include complicated or delayed wound healing and
massive tissue loss. Early excision and grafting as well as early rehabilitation therapy such as splinting and
mobilisation is essential. In severe cases plastic surgery referral for surgical correction may be indicated.
6
Pruritis - Itching is a common problem. Scratching causes breaks in the skin & prolongs healing. It may serve
as a portal for infection or compromise graft healing. Sleep disturbances are common. Pruritis occurs at all
phases of recovery such as healing skin, wound contraction & collagen accumulation. It can also occur due to
opioid use, local skin reaction to topical agents & infections (especially fungal). Treatment is with a
combination of gabapentin, antihistamines, and hydroxyzine. Cold compresses, massage therapy & aqueous
cream can provide relief.
Psychological – Psychological distress is a common problem. Between 25-33% patients initially experience
acute stress disorder (ASD) & Posttraumatic stress disorder (PTSD). In the long term, patients manifest sleep
disturbances, body image dissatisfaction and depression. These are commonly misdiagnosed/ overlooked.

Sepsis In The Burn Patient (17, 19, 20)

Many factors predispose burn patients to increased infections. These include disruption of skin integrity,
presence of damaged and dead tissue, impaired blood supply to and from both damaged and penumbral
tissue, and impaired systemic immune defences. This decrease in humoral and cell-mediated immunity with
altered phagocytic and lymphocytic function predisposes these patients to infections by many micro-
organisms. The commonest of these are Gram-positive bacteria initially (exogenous sources). The Gram-
negative organisms are usually translocations from the gut (endogenous infections). Staphylococcus aureus
and Pseudomonas aeruginosa together make up 70% of infections in these patients. Common infections in
burn patients include burn wound infections, pneumonia, catheter related infections, blood stream
infections, and urinary tract infections. Even when infection has been eliminated, systemic inflammation—
induced by tissue injury and multiple infectious episodes—may cause death by multisystem organ failure.

Risk Factors for Infection in Burn Patients 18

Thermal Injuries themselves
Intubation
Smoke inhalation injuries
Invasive indwelling devices such as urinary catheters or central lines
Type of burn, percent total body surface area and depth involved
The treatment of burns requires continuous vigilance to watch for subtle early signs of sepsis and the
expeditious initiation of aggressive therapy.
The definition of sepsis in burns is the presence of three or more of the following criteria: 17

It is difficult to determine sepsis from SIRS in burns patients due to the hypermetabolic syndrome. The
standard diagnostic criteria for infection and sepsis do not apply to acute burn injury patients as they have an
elevated normal body temperature (reset to about 38.5 degrees), tachycardia and tachypnoea all of which
can persist for months, along with significant changes in their WCC resulting from continuous exposure of
healing skin to the environment. However they are neither specific nor sensitive for sepsis, and can be
misleading because critically ill burn patients often manifest a systemic inflammatory response syndrome
without infection.
Diarrhoea in burns patient is sepsis not gastro-enteritis and must be treated as sepsis until proven
otherwise.

7
Severe sepsis is sepsis with evidence of organ hypoperfusion as evidenced by:
Oliguria
Lactic acidosis
Confusion
Septic shock is sepsis with systolic blood pressure < 90 mmHg despite adequate fluid resuscitation or
requirement of vasopressors and/or inotropes to maintain the blood pressure.
We only treat with systemic antibiotic if the patient is systemically septic, we do not treat pus swab results
and there is no place for prophylactic antibiotics in burns. 2

Local evidence of invasive wound infection includes: (18, 21)

Black or brown patches of wound discoloration
Rapid eschar separation
Conversion of wounds to full thickness
Spreading peri wound erythema
Punctuate haemorrhagic sub-eschar lesions
Violaceous or black lesions in unburned tissues (ecthyma gangrenosum)
As sepsis remain an important cause of morbidity and mortality in burn patients, rapid diagnosis and
treatment of septic complications is essential. Early wound closure and good nutrition are vital to reduce the
chances of sepsis and improve outcome.

Surviving Sepsis Campaign And The Burn Patient

Initial resuscitation should begin with giving 30ml/kg of intravenous crystalloid fluids within 3 hours
of diagnosis of septic shock.
Target MAP > 65mmHg
Aim to lower lactate levels to normal levels
Cultures should be obtained prior to starting any antibiotics
Empiric broad-spectrum antibiotics should be started within one hour of diagnosis
De-escalate antibiotics as soon as possible
Antibiotics should be narrowed to cover that organism
Source control e.g. drainage of abscesses and removal of infected tissue or devices
First choice of vasopressors is adrenaline.

8
References
1. Marc G Jeschke, David L Chinkes et al. The pathophysiological response to a severe burn injury. Ann
Surg. 2008 September ; 248(3): 387–401
2. ISBI Practice Guidelines Committee. ISBI Practice Guidelines for Burn Care.
3. Sabri A., Dabbous H., Dowli A., Barazi R. The airway in inhalational injury: diagnosis and
management. Annals of Burns and Fire Disasters - vol. XXX - n. 1 - March 2017
4. Helen E. Douglas, Jonathan A Dunne, Jeremy M. Rawlins. Management of Burns. Oxford Handbook of
Surgery. 2017.
5. Peng-Hui Wang, Ben-Shian Huang, Huann-Cheng Horng, Chang-Ching Yeh Yi-Jen Chen. Wound
healing. Journal of the Chinese Medical Association 81 (2018) 94e101
6. F. Charles Brunicardi et al. Schwartz Principles of Surgery. 10th Edition. 2010. References
7. Brölmann F, et al. Evidence-based decisions for local and systemic wound care. British Journal of
Surgery. 2012. 99(9): 1172-83.
8. Mimoun M et al. The scalp is an advantageous donor site for thin-skin grafts: a report on 945
harvested samples. Plast Reconstr Surg. 2006; 118(2):369-73
9. White N et al. The choice of split-thickness skin graft donor site: patients' and surgeons' preferences.
Plast Reconstr Surg. 2003; 112(3):933-4 (ISSN: 0032-1052)
10. Young AE, et al. Toxic shock syndrome in burns: diagnosis and management. Arch Dis Child Educ Pract
Ed. 2007. 92(4): 97-100.
11. Yizhi P, et al. Diagnostic criteria and treatment protocol for post-burn sepsis. Critical Care. 2013.
17:406.
12. Beushausen T, et al. Anaesthesia and pain management in paediatric burn patients. Paediatr Surg Int.
1997. 12: 327-333.
13. Latarjet J, et al. Pain in burn patients. Burns. 1995. 21(5): 344-346.
14. Young AE, et al. Toxic shock syndrome in burns: diagnosis and management. Arch Dis Child Educ Pract
Ed. 2007. 92(4): 97-100.
15. Yizhi P, et al. Diagnostic criteria and treatment protocol for post-burn sepsis. Critical Care. 2013.
17:406.
16. Fauerbach et al. Psychological Distress After Major Burn Injury. Psychosom Med. 2007 Jun; 69(5):
473–482.
17. David G. Greenhalgh. Burns Trauma. 2017; 5:23.
18. J Thomas and H Rode A practical guide to paediatric burns.
19. L Schultz et al. Identification of predictors of early infection in acute burn patients. Burns 39 (2013)
1355-136
20. A Lavrentieva et al. Inflammatory markers in patients with severe burn injury. Burns 33 (2007-03-01),
189-19.
21. A Modiba. Burns Seminar. 2009.

9
 MEDICAL OPTIMISATION OF THE HIGH RISK SURGICAL PATIENT
C. Anauth, AR Rampershad, CM Kithuka
Moderator: Dr Kim De Vasconcellos 06 April 2019

Despite significant advances in perioperative medicine there is still a risk of perioperative death and
morbidity after a surgical procedure. Perioperative risk may arise from the surgical procedure or from
patient-specific risk factors. The latter are generally medical comorbidities and it is the assessment and
management of these that will be the focus of this review.

The nature of risk and risk stratification

The goal of risk stratification is to separate patients into clearly defined subgroups that have clinically
meaningful differences in the outcome of interest (often mortality). The risk assessment may then be
used to:
Communicate perioperative risk to the patient to allow for informed decision making
Recommend needed specialty consultation or further testing
Decide on nature or timing of surgical procedure
Guide pre-, intra- or postoperative optimization
Guide the appropriate level of perioperative care for the patient
There are number of concerns with current methods of risk stratification. The first is that there is no
consensus on what makes a patient “high risk” and both physicians’ and patients’ views of risk often
differ significantly. A risk of >10% for an outcome is often viewed as high risk, however this still means
that the majority of patients will still not have the event. This highlights a further problem with risk
stratification for relatively rare outcomes (e.g. perioperative mortality).
In this scenario risk stratification tools are better in identifying low-risk patient groups that are unlikely
to require specific intervention, and do not perform well in identifying truly high-risk patients. This
means that many patients labelled as high risk will receive unnecessary interventions. Risk stratification
tools are also often eithercomplex and time consuming or too simple to offer much clinical utility.

Global risk assessment

1. ASA: The American Society of Anaesthesiologists (ASA) classification gives a global impression of the
clinical state of the patient that correlates with post-operative outcomes. Provides risk assessment
of anaesthesia and surgery. The ASA classes are subjective and provide limited outcome-specific
information.1
2. NSQIP: The NSQIP Surgical Risk Calculator (found at http://riskcalculator.facs.org ) calculates
risk based on 21 patient -specific variables (eg age, sex, previous MI, functional status) and the
actual operation and gives patient-specific risks for a number of perioperative complications.2,3
3. POSSUM: The POSSUM (Physiological and Operative Severity Score for the enumeration of
Mortality and Morbidity) approach to measuring risk in surgery has been applied to a number of
surgical specialties. Based on 12 physiological and 6 operative variables.4 Useful tool for surgeons –
more objective than the ASA Score, but not as complex as the APACHE II Score.

PREOPERATIVE ASSESSMENT
Cardiac
Approach to pre-operative cardiac risk assessment
Surgeries are divided into 3 categories on the basis of the timing of surgery. This influences preoperative
cardiac risk assessment.
1. Emergency: Do not delay surgery
2. Urgent or semiurgent surgery: Undertake preoperative cardiac risk assessment only if history
or physical examination suggests there is a potential undiagnosed severe obstructive
intracardiac abnormality, severe pulmonary hypertension, or an unstable cardiovascular
condition.
1
 3. Elective noncardiac surgery: with age >45 or 18-44 with known significant cardiovascular
disease: Undergo preoperative cardiac risk assessment.

Methods of preoperative cardiac risk assessment

Revised Cardiac Risk Index (RCRI)
The most commonly used clinical risk stratification tool to assess cardiac risk.6 Developed by Lee et al.
in 1999, it identifies 6 predictors of major cardiac complications (listed below), and has been widely
validated. Increasing scores are associated with increasing risk of perioperative major adverse cardiac
events (MACE).

Variables Points
Hx of IHD 1
Hx of CHF 1 Points Risk Estimate 95% CI
Hx of CVD 1 0 3.9% 2.8%-5.4%
Insulin for Diabetes 1 1 6.0% 4.9%-7.4%
Crt > 177uMol/L 1 2 10.1% 8.1-12.6%
High – risk surgery 1 15.0% 11.1%-20.0%

Functional capacity
Patients’ self-reported functional capacity is used to determine their metabolic equivalents (METs). This
has been used by the AHA/ACC and ESC to guide perioperative cardiac risk assessment. Studies however
showed METs were not independently predictive of major perioperative cardiac complications and the
latest Canan]dian Cardiovascular Society (CCS) guidelines no longer recommend the use of functional
capacity in risk-stratifying patients.
Cardiac biomarkers
Preoperative NT-proBNP/BNP measurement before noncardiac surgery improved risk prediction among
patients who did and did not suffer adverse cardiac events. Values > 300 ng/L for NT-proBNP and > 92
mg/L for BNP have been identified as significant thresholds associated with an increased risk.
Resting echocardiography
LVEF< 50% is an independent predictor of cardiovascular complications. However, preoperative NT-
proBNP is a stronger independent predictor.Therefore, evidence does not support the use of routine
preoperative echocardiography for risk assessment in patients who undergo noncardiac surgery.
Coronary computed tomographic angiography (CCTA)
Of the preoperative CCTA studies, VISION CCTA study is the highest-quality study.Preoperative CCTA
overestimated cardiac risk and this may result in delays and cancellations of beneficial surgery or
inappropriate use of postoperative high intensity beds, precluding access for patients at greater risk.
Exercise stress testing and cardiopulmonary exercise testing (CPET)
Risk stratification with exercise testing is not suitable for patients with limited exercise capacity. There
is limited value in preoperative exercise testing to stratify perioperative cardiac risk, as it is inconvenient
for patients and cost more than BNP. CPET is a weak independent predictor of longterm postoperative
mortality and is thus not recommended by the CCS for cardiac risk stratification.
Pharmacological stress echocardiography and radionuclide imaging
No study has adequately assessed the incremental value of these stress tests to well-established
perioperative cardiac risk factors (eg. RCRI) and as such their use is not recommended.
Recommended algorithm for cardiac risk assessment: see flowchart at the end of booklet

Respiratory
Pulmonary function is greatly affected in patients undergoing surgery. Pulmonary complications are
common after surgery and result in significant morbidity post-operatively.9 Unlike cardiac risk
prediction, there are currently no validated models of pulmonary risk stratification. However, the
American College of Physicians have adopted several scales for assessing the risk of developing specific

2
respiratory complications such as acute respiratory failure and pneumonia. The type of surgery was the
most significant predictor in both developing both postoperative respiratory failure and pneumonia.
Most of the factors identified as predictors for developing pneumonia were also significant in predicting
development of respiratory failure.

Risk Factors for Acute Resp. Failure in post - operative

period of general non cardiac surgery
Risk Factor Score
Abdominal aortic aneurysm repair 27
Thoracic 14 Class Score %Risk
Upper abd, peripheral vascular or neurosurgery 21 1 0.5
Neck 11 2 11-19 1.8
Emergency Surgery 11 3 20-27 4.2
Albumin <3.0 mg/dl 9 4 28-40 10.1
Plasma urea > 30 mg/dl 8 5 26.6
Totall or partly dependent functional status 7
COPD 6
6
Age 60 – 69 4

Renal
Acute kidney injury is associated with increased length of stay, cost, morbidity and mortality. Studies
identified 7 independent risk factors: 10
I. Age > 59
II. Emergency surgery
III. CKD
IV. BMI >32
V. High risk surgery
VI. PVD and COPD
VII. Intra-operative factors:
use of vasopressor infusion
total vasopressor dose
diuretic administration

ACS NSQIP identified other risk factors and created the General Surgery Acute Kidney Injury Risk Index
Classification System. Intra-operative risk factors were not investigated, and this system has not been
validated in other populations or countries.

Risk factors
Age > 56 yrs Risk class No. of Risk of major
Male sex Risk complications
Active CHF Factors
Ascites I 0-2 0.2%
HPT II 3 0.8%
Emergency surgery III 4 2.0%
Intraperitoneal surgery IV 5 3.6%
Renal insufficiency – mild or moderate V 6 9.5%
Diabetes mellitus – oral or insulin
therapy

3
Hepatic
Main tool for assessing the perioperative morbidity and mortality in patient with liver cirrhosis is the
Child-Turcotte-Pugh (CTP) score - based on patient’s levels of bilirubin, albumin, the INR and the severity
of encephalopathy and ascites. Studies have consistently reported similar perioperative outcomes e.g.
mortality rates for patients undergoing surgery were 10% for those with Child class A, 30% for those
with Child class B, and 76–82% for those with Child class C cirrhosis.
MELD (Model for End-Stage Liver Disease) is now used to risk stratify patients awaiting liver
transplantation and more recently used to predict perioperative mortality. The MELD score is a linear
regression model based on serum bilirubin, creatinine, and INR. It has several advantages over the CTP
score: it weights the variables; it does not rely on arbitrary cut off values and appears to be more
objective. Each point increase in the MELD score makes an incremental contribution to the risk and thus
appears to be more precise in predicting perioperative mortality. The use of the MELD score and Child
class are not mutually exclusive and can complement each other.

PERIOPERATIVE RISK MANAGEMENT/ OPTIMISATION

Cardiac
Pharmacological 8,9
1. Aspirin – The POISE 2 trial showed no benefit from perioperative initiation and continuation of aspirin.
It is recommended by the CCS guidelines that aspirin be stopped 3 days prior to non-cardiac surgery and
restarted 8-10 days after major surgery to minimize bleeding risks. However high-risk patients taking
lifelong aspirin for a guideline-based primary or secondary indication likely warrant continuation of their
aspirin throughout the perioperative period except when undergoing a closed- space procedure,
intramedullary spine, or prostate surgery.
2. Antihypertensives:
a. -blockers should not be initiated in the perioperative period due to risks of hypotension and
stroke which outweigh the benefits. Those patients already on -blockers should continue with
therapy however hypotensive risk is still present and should be carefully monitored. Dose adjustment
might be required.
b. -2 agonists (clonidine) have shown no benefits when initiated in the perioperative phase due to
increased adverse cardiac events.
c. Calcium channel blockers should not be initiated in the perioperative period.
d. ARB/ ACE-I should be discontinued 24 hours before surgery and reinitiated on the 2nd post-
operative day due to increased hypotensive risk.
3. Statins: There is insufficient evidence to support initiation of statins in the perioperative period. NB:
Patients on chronic statin therapy should continue with their medication.

Coronary Revascularisation 8,9

Routine prophylactic coronary revascularization is not recommended for patients with stable cardiac
disease undergoing non-cardiac surgery.
Patients with unstable coronary artery disease (CCS III-IV/unstable angina) may benefit from
revascularization, either PCI or CABG, before non-cardiac surgery. The decision will need to balance the
risk of untreated coronary artery disease, against the risk of delaying surgery and the risk of bleeding
from antithrombotic drugs that maybe required after revascularization.
The choice of revascularization procedure may be influenced by the urgency of surgery and the duration
of antiplatelet therapy required for different revascularisation techniques.
Elective surgery should be delayed for at least 14 days post balloon angioplasty. Patients with bare metal
stents require at least 4-6 weeks of dual antiplatelet therapy. The recommendation for drug eluting
stents is 6-12 months. If surgery is required during this period at least aspirin should be continued. These
patients usually require lifelong ASA after dual antiplatelet therapy.

4
Perioperative Haemodynamic monitoring and optimization 11
High risk patients should be monitored in a high-care setting using standard blood pressure, pulse, ECG,
and saturation monitoring. Even brief periods of hypotension may increase adverse outcomes and
should be treated aggressively with judicious fluid therapy and early initiation of
inotropes/vasopressors. Tachycardia may be harmful in patients with ischaemic heart disease and the
cause of a tachycardia should be investigated and treated wherever possible. Hypoxia should be
prevented/treated with supplemental oxygen.

Major surgery triggers an inflammatory reaction which is associated with increased oxygen demand.
Healthy patients respond by increasing cardiac output (CO) and oxygen extraction. High risk surgical
patients, however, lack the physiological reserve to mount an adequate response. This results in tissue
hypoxia and ultimately organ failure. Perioperative haemodynamic optimization (aka perioperative
goal-directed therapy) is a strategy that aims to maximise a patient’s oxygen delivery to prevent
postoperative morbidity and mortality. While specific strategies differ, they all include the following
elements:
Advanced haemodynamic monitoring using some form of “cardiac output” monitoring e.g.
oesophageal doppler or arterial waveform-based devices (Vigileo, LidCO, PiCCO)
A protocolized approach to achieving predetermined oxygen delivery goals using
Fluids boluses: as guided by markers of fluid-responsiveness
Inotropes/vasopressors
Strategies for haemodynamic optimization are still widely debated and are often the domain of the
anesthetist, however the most successful strategies begin pre- or intraoperatively and are continued
into the postoperative period.
Goal-directed fluid therapy is recommended as part of enhanced recovery protocols. There is no clear
consensus on which parameters are best. Studies which have used cardiac index and oxygen delivery
index as targets, and fluids and inotropes as interventions, have shown some benefit regarding
postoperative complications.
Multiple studies have compared liberal against restrictive fluid strategies. The current trend seems to
be fluid restrictive goal-directed haemodynamic optimization, however this needs further validation.

Respiratory: Preventing post-operative pulmonary complications (PPCs): 13,14

Good evidence suggests that lung expansion therapy (for example, incentive spirometry, deep
breathing exercises, and continuous positive airway pressure) reduces postoperative pulmonary
risk after abdominal surgery.
Smoking cessation, at least 6- 8 weeks prior to surgery, should be provided to all smokers.
Preoperative pulmonary rehabilitation (including respiratory muscle training and abdominal
breathing) for patients with severe COPD undergoing elective surgery.
If bronchospasm is present, inhaled 2-agonists are the drugs of choice
Patients at risk for developing complications or who have a pre-operative FEV1 <80% to
receive oral corticosteroids.
Hydration and fluid deficits to be corrected before surgery. Hydration helps in easier
mobilisation and removal of sputum.
Chest physiotherapy and postural drainage should be used to improve sputum clearance.

Nutrition 13-15
For all preoperative patients, a properly balanced diet of key nutrients, including carbohydrates,
fats, protein, vitamins, and minerals, as well as nutrition education, should be part of the
preoperative process. Fasting should be kept to an absolute minimum.
Patients who screen positive on the risk scoring warrant a full assessment by a dietician and
should initiate immediate nutritional support.

5
 Physicians and dieticians should consider disease-specific formulas when recommending
nutritional supplementation if available for the clinical condition.
Supplemental or total parenteral nutrition (PN) may be indicated if enteral intake is inadequate,
and a decision to initiate PN should be taken early in nutritionally at-risk patients.
Low albumin levels in a setting of poor nutrition may have an increased incidence of PPCs,
however supplementation of albumin does not improve patient outcomes.
Obesity with a body mass index >27 kg/m2 is associated with increased incidence of atelectasis
and pneumonia following abdominal surgery. Weight-loss strategies may be considered prior
to elective surgery.

Renal 15
The most practical approach to prevention of perioperative AKI is the KDIGO bundle:
discontinue all nephrotoxic agents when possible
ensure adequate volume status and perfusion pressure
consider functional haemodynamic monitoring
monitor serum creatinine and urine output
avoid hyperglycemia
consider alternatives to radiocontrast procedures

Hepatic 12
Ascites should be controlled, variceal bleeding risk reduced, and acute hepatic encephalopathy treated
preoperatively, with continuation of medical therapy to prevent recurrent hepatic encephalopathy. AGA
recommends in patients with symptomatic ascites, large-volume total abdominal paracentesis should
be performed preoperatively, with intravenous administrative of albumin in a dose of 6–8 g for each
liter of ascitic fluid removed. Elective operations in patients with cirrhosis should generally be avoided
until the liver disease can be optimised.
Protocolised transfusion strategies based on preoperative platelet counts and the INR are generally
ineffective in reducing intra- and postoperative bleeding. Patients with cirrhosis are known to be in a
state of “rebalance” in that deficits in procoagulant factors are offset by deficits in anticoagulant
proteins synthesized by the liver. Viscoelastic testing (thromboelastography and rotational
thromboelastometry) to guide intraoperative transfusions has been shown to decrease the need for red
blood cell and plasma transfusions.

POSTOPERATIVE STRATEGIES
Cardiac
The CCS guidelines on perioperative cardiac risk assessment give the following recommendations for
the postoperative management of the cardiac patient undergoing surgery 8
1. Troponins: Perioperative myocardial ischaemia will result in elevated cardiac troponins. Daily
troponin levels are required for patients with preoperative risk of adverse cardiac events of >5%
for up to 72 hours.
2. Postoperative ECG: Recommended for patients with elevated NTproBNP/BNP preop, RCRI>1,
>45 with cardiovascular disease and all patients above 65yrs.
3. Postoperative telemetry and pulmonary artery catheter monitoring: Latest guidelines
recommend against the use of these.
4. Statin and Aspirin: Initiate long-term therapy in patients who suffer myocardial injury or
myocardial infarction after non-cardiac surgery.
5. Continued follow up: High risk patients need continued follow up from multidisciplinary teams
to optimise postoperative care.

6
Myocardial Injury after non-cardiac surgery (MINS) 8,18, 9
Patients who do not fulfil the clinical criteria for myocardial injury might still sustain a myocardial injury
during the postoperative period without exhibiting ischaemic symptoms or hallmark ECG changes. MINS
is a relatively new clinical concept, which is a prognostically relevant myocardial injury due to ischaemia
that occurs during, or within 30 days of noncardiac surgery. MINS is defined as a peak 4th generation
TropT >0.03mg/ml believed to be due to myocardial ischaemia within 30 days of surgery. It results in
an increase of almost 10% in 30-day mortality. The most likely pathophysiology is that of delayed plaque
rupture. Due to post-operative analgesia, symptoms of a classical myocardial ischaemic episode are
masked, and a high degree of suspicion is required along with raised biomarkers and abnormal ECG
findings. Although no randomized, controlled trial has established an effective treatment for patients
suffering from MINS, the prognosis of these patients may be modifiable. The POISE trial suggest that
ASA and statin therapy may benefit patients who suffer from MINS 7, 8
The MANAGE trial 19 is a randomised placebo-controlled trial that showed dabigatran (in a dose of
100mg twice daily) reduced the risk of major vascular complications, both arterial and venous, with
minimal risk of major bleeding, following an episode of MINS. Data from the trial also illustrated the
high risk of vascular complications following MINS as 1 in 7 patients in the placebo group had a major
vascular complication.

Respiratory 13,14
1. Analgesia: Addition of epidural analgesia to general anaesthesia significantly reduces the risk of
postoperative pneumonia, post-operative ventilation and unplanned re-intubation compared with
systemic opioids alone. It is especially beneficial for patients with severe COPD having major abdominal
surgery as a result of improved analgesia and reduced opioid consumption. Obese patients are more
likely to have obstructive sleep apnea (OSA). Those with OSA are at risk of respiratory depression after
surgery because of increased sensitivity to opioids and sedatives, and therefore, reduced doses of
opioids should be administered in these patients.
2. NGT: Patients undergoing abdominal surgery are five to eight times more likely to have increased
rates of atelectasis and pneumonia if an NGT is used in the perioperative period.
3. Supplemental oxygen and non-invasive ventilation (NIV): Postoperatively, evaluate the need for
supplemental oxygen by facemask or catheter through pulse oximetry or blood gas analysis. In patients
with COPD, OSA and/or heart failure, the use of NIV if respiratory distress occurs may avoid reintubation.
Patients with OSA have a higher risk of developing hypoxaemia and hypercapnia postoperatively and
should be considered for CPAP routinely in the postoperative period. Prophylactic nasal high-flow
oxygen may benefit high-risk cardiac patients with respiratory co-morbidity.
4. Postoperative early physiotherapy, mobilisation and oral hygiene: These strategies seem to be
beneficial in reducing PPCs. Lung expansion exercises such as incentive spirometry and deep breathing
exercises should be encouraged.

Renal 15,16
Early diagnosis is the first step in managing AKI. The use of KDIGO criteria to diagnose AKI early may
allow for interventions to prevent worsening of AKI. The use of novel biomarkers (e.g. neutrophil
gelatinase-associated lipocalin (NGAL), or cystatin C) may allow for even earlier detection of kidney
injury and thus earlier intervention.
Protecting Renal Function:
1. Fluid management: Both hypovolemia and excessive fluid resuscitation can increase the risk of AKI in
noncardiac surgery patients. Postoperative positive fluid balance has been associated with increased
incidence of AKI compared with zero fluid balance. Monitoring of urine output is imperative during
the perioperative period. Features of hypovolemia can be masked by anaesthesia and surgery.
2. N-acetylcysteine in high doses reduced the incidence of AKI in patients with CKD stage 3 and 4
undergoing CABG.
3. Dexmedetomidine a highly-selective alpha-2-adrenoreceptor agonist may reduce the risk of

7
 perioperative AKI 16.
4. Analgesia: NSAIDs are not recommended for patients with CKD or AKI.
5. Aspirin: In the POISE trial, in non-cardiac surgery patients, neither aspirin nor clonidine started 2-4
hours preoperatively and continued up to 30 days after surgery altered the risk of AKI significantly
more than placebo.
6. Statins and Erythropoietin - ineffective in reducing the incidence of AKI in cardiac surgery patients.

Hepatic(17)
1. Nutrition
Intravenous albumin infusion for correction of hypoalbuminemia has no effect on mortality and
routine use is not justified. Nutritional supplementation should be continued in the postoperative
period. Branched-chain amino acid formulae may also be used as a source of protein in patients with
hepatic encephalopathy (HE).
2. Fluid and electrolytes
Hyponatremia in liver cirrhosis can lead to severe ascites, HE, renal impairment, and increased hospital
stay. Oral fluid restriction is required when the serum Na is less than 125mmol/L. Postoperative ascites
can be prevented from accumulating by restricting sodium and minimising intravenous fluid
administration. Correction of hypokalemia also helps to restore the sodium level.
3. Hepatic encephalopathy
Careful assessment of the mental status should be performed to identify subtle signs of low-grade HE.
Dietary modification should include protein intake of 1.0 to 1.5 g/kg daily, zinc replacement and
sodium restriction to 2 g in those with ascites. Benzodiazepines, opiates, antidepressants and
antipsychotics should be avoided. Lactulose can be used to treat HE.
4. Ascites
Low sodium diet should be continued to prevent re-accumulation of ascites. Diuretics at appropriate
doses can be started. If therapeutic ascitic tap is performed, then albumin infusion at a rate of 6-8 g
for every litre in excess of 4 L of ascitic fluid should be given.
5. Infections
Prophylactic antibiotics recommended in setting of low-protein ascites (<15 g/l) with advanced
cirrhosis, prior history of spontaneous bacterial peritonitis and gastrointestinal haemorrhage.
6. Oesophageal varices
Fluid overload worsens portal hypertension hence should be avoided. Patients with small
oesophageal varices, in conjunction with CTP class B or C cirrhosis or large varices irrespective of CTP
class, may benefit from -blockers.
7. Analgesia
Opioid dose and frequency should be reduced due to their increased half-life and bioavailability in
patients with cirrhosis. Epidural analgesia should be considered only6 due to their potential
nephrotoxicity, gastrointestinal bleeding, and platelet dysfunction.

Multi-disciplinary teams and the Perioperative Surgical Home concept 20-22

The pre- and postoperative care of high-risk patients is no longer the sole domain of anaesthetists and
surgeons. Chronic non-communicable diseases like IHD, cerebrovascular disease, and pulmonary
disease are now so common as “the main causes of both disability and death worldwide” that risk
stratification and development of a clear surgical plan requires input from multiple specialised
personnel depending on the risk factors of the patients. This has led to the development of specialist
preoperative assessment clinics.
A concept that has come to the fore is the Perioperative Surgical Home (PSH). The PSH is defined by
the American Society of Anaesthesiologists as “a patient-centered and physician-led” multidisciplinary
and team-based system of coordinated care that guides the patient throughout the entire surgical
experience and aims to reduce variability in perioperative care, therefore decreasing the likelihood of
errors and complications.

8
Continuity of care in this model is achieved by treating the entire perioperative episode as one
continuum rather than discrete preoperative, intraoperative, postoperative, and post-discharge
episodes. This is achieved by having one team to manage all aspects of this continuum from the time
the patient and surgeon make the decision for surgery until 30 days after discharge. The PSH emphasises
"pre-rehabilitation" of the patient before surgery, intraoperative optimisation, improved return to
function through follow-up, and effective transitions to home or post-acute care guided by the best
evidence and best practices applied in a consistent and standardised way to every patient undergoing
surgery
The Surgical Home is not intended to replace the surgeon’s patient care responsibility, but rather
leverages the talents and abilities of the entire perioperative care team in the service of the patient. By
applying these concepts, the team have a unique opportunity to improve outcomes, decrease length of
stay and other metrics, and improve patient satisfaction.

References:
1. Tomoaki H, Yoshihisa K. Modified ASA physical status (7 grades) may be more practical in recent
use for preoperative risk assessment. Internet J Anesthesiol. 2007
2. Gupta PK, Gupta H, Sundaram A, et al. Development and validation of a risk calculator for
prediction of cardiac risk after surgery. Circulation 2011;124:381-7.
3. Bilimoria KY, Liu Y, Paruch JL, et al. Development and evaluation of the universal ACS NSQIP surgical
risk calculator: a decision aid and informed consent tool for patients and surgeons. J Am Coll Surg
2013;217:833-42.
4. Copeland GP, Jones D, Walters M. POSSUM: a scoring system for surgical audit. Br J Surg 1991; 78:
366-60.
5. Weiser TG, Regenbogen SE, Thompson KD, et al. An estimation of the global volume of surgery: a
modelling strategy based on available data Lancet 2008;372:139-44.
Lee TH, Marcantonio ER, Mangione CM, et al. Derivation and prospective validation of a simple
index for prediction of cardiac risk of major noncardiac surgery. Circulation 1999;100:1043-9.
6. The post-operative electrocardiogram and creatine kinase: implications for diagnosis of myocardial
infarction after non-cardiac surgery Charlson ME1, MacKenzie CR, Ales KL, Gold JP, Fairclough GF
Jr, Shires GT.
7. Association of Postoperative High-Sensitivity Troponin Levels With Myocardial Injury and 30-Day
Mortality Among Patients Undergoing Noncardiac Surgery P. J. Devereaux, MD, PhD, Population
Health Research Institute, David Braley Cardiac, Vascular, and Stroke Research Institute,
8. Duceppe E, Parlow J, MacDonald P, Lyons K, McMullen M, Srinathan S, et al. Canadian
Cardiovascular Society Guidelines on Perioperative Cardiac Risk Assessment and Management for
Patients Who Undergo Noncardiac Surgery. Canadian Journal of Cardiology. 2017;33(1):17-32.
9. Devereaux PJ, Sessler DI, Leslie K, et al. Clonidine in patients undergoing noncardiac surgery. N Engl
J Med 2014; DOI:10.1056/NEJMoa1401106.
10. Grounds RM, Tote SP. Performing perioperative optimization of the high-risk surgical patient. BJA:
British Journal of Anaesthesia. 2006;97(1):4-11.
11. Pearse RM, Harrison DA, MacDonald N, Gillies MA, Blunt M, Ackland G, et al. Effect of a
Perioperative, Cardiac Output–Guided Hemodynamic Therapy Algorithm on Outcomes Following
Major Gastrointestinal Surgery: A Randomized Clinical Trial and Systematic Review. JAMA.
2014;311(21):2181-90.
12. Northup PG, Friedman LS, Kamath PS. AGA Clinical Practice Update on Surgical Risk
Assessment&#xa0;and Perioperative Management in Cirrhosis: Expert Review. Clinical
Gastroenterology and Hepatology. 2019;17(4):595-606
13. Degani-Costa LH, Faresin SM, dos Reis Falcao LF. Preoperative evaluation of the patient with
pulmonary disease. Brazilian journal of anesthesiology (Elsevier). 2014;64(1):22-34.

9
14. Miskovic A, Lumb AB. Postoperative pulmonary complications. BJA: British Journal of Anaesthesia.
2017;118(3):317-34
15. Sharma K, Slawski B. Renal disease and the surgical patient: Minimizing the impact. Cleve Clin J
Med. 2018;85(7):559-67
16. Liu Y, Sheng B, Wang S, Lu F, Zhen J, Chen W. Dexmedetomidine prevents acute kidney injury after
adult cardiac surgery: a meta-analysis of randomized controlled trials. 2018;18(1):7
17. Abbas N, Makker J, Abbas H, Balar B. Perioperative Care of Patients With Liver Cirrhosis: A Review.
Health services insights. 2017;10:1178632917691270
18. Botto F, Alonso-Coello P, Chan MT, Villar JC, Xavier D, Srinathan S, et al. Myocardial injury after
noncardiac surgery: a large, international, prospective cohort study establishing diagnostic criteria,
characteristics, predictors, and 30-day outcomes. Anesthesiology. 2014;120(3):564-78
19. Devereaux PJ, Duceppe E, Guyatt G, Tandon V, Rodseth R, Biccard BM, et al. Dabigatran in patients
with myocardial injury after non-cardiac surgery (MANAGE): an international, randomised,
placebo-controlled trial. Lancet (London, England). 2018;391(10137):2325-34
20. Kain ZN, Vakharia S, Garson L, Engwall S, Schwarzkopf R, Gupta R, et al. The Perioperative Surgical
Home as a Future Perioperative Practice Model. Anesthesia & Analgesia. 2014;118(5):1126-30
21. Kwon MA. Perioperative surgical home: a new scope for future anesthesiology. Korean journal of
anesthesiology. 2018;71(3):175-81
22. Vetter TR, Goeddel LA, Boudreaux AM, Hunt TR, Jones KA, Pittet J-F. The Perioperative Surgical
Home: how can it make the case so everyone wins? BMC Anesthesiology. 2013;13(1):6

Fig: Algorithm for cardiac risk assessment

10
 ACUTE UROLOGICAL CONDITIONS
Dr K Kabongo, Dr S Thaver, Dr S Mbatha
Moderator: Dr V Ramloutan 13th April 2019

Acute urological conditions are not uncommon, they range from trauma to the urogenital tract to
acute infections as well as a number of other acute conditions in between. Most of these conditions
represent General Surgical emergencies and the identification and acute management is of
paramount importance for any General Surgeon to know.

UROLOGICAL TRAUMA
The importance of recognizing and appropriately managing urogenital injuries has been appreciated
for centuries. Timely identification and management of these injuries is often organ saving, and at
times lifesaving3.
Renal trauma1,2,3
Renal trauma occurs in approximately 1-5% of all trauma cases1. Unlike developed countries where
blunt trauma is the most common cause, penetrating injuries have been reported to be the leading
cause in South Africa3. Patients usually present with multiple injuries. Haematuria is usually present.
During the assessment, special consideration should be given to pre-existing renal conditions as they
can complicate minor injuries.
Enhanced CT with intravenous contrast and delayed images is the preferred method for diagnosing
and staging renal injuries in haemodynamically stable patient. The AAST grading scale, which is based
on CT scan findings, is used to grade the severity of the injuries and guide the management. Most
injuries can be managed conservatively.

1
Ureteral injury1,3
These injuries are relatively rare, 1-2.5% of urological trauma, about 80% are iatrogenic and usually
missed intra operatively. Gynaecological procedures are the most common cause.
Risk factors are; Altered normal anatomy, major bleeding, malignancy, diverticulitis, endometriosis.
The diagnosis is very challenging and usually delayed in blunt trauma or when the cause is iatrogenic.
The diagnosis is made by a contrasted CT scan which can reveal:
- Extravasation of contrast medium - Urinoma
- Hydronephrosis - Mild ureteric dilatation
- Ascites
Urethral stenting to allow intra operative identification has not shown any benefit in reducing the
incident, whereas intra-operative cystoscopy after intravenous contrast injection increases the
detection rate of iatrogenic injuries.

Treatment options in early presentation are:

- Stable patients: Primary repair with stenting. Wide debridement is highly recommended for
gunshot injuries due to ‘blast effect’ of the injury.
- Unstable patients (Damage control surgery):
Ligation.
Diversion. (Nephrostomy)

Delayed presentation injuries are better managed initially by diversion (Tube nephrostomy).

Bladder Injury1,3
Injury to the bladder is usually associated with pelvic fracture in blunt trauma, with motor vehicle
accident being the most common cause. It can be isolated in penetrating trauma. Iatrogenic cause has
also been described.
Direct inspection is the most reliable method to assess bladder integrity, methylene blue injection
maybe helpful in detecting smaller injuries. Ureteric orifices should be inspected when the injury is
close to the trigone.

Cystography (Plain or CT) is the preferred diagnosis modality for non-iatrogenic injuries and for
suspected iatrogenic injuries in the post-operative period. Cystoscopy has shown to be useful in
diagnosing intra - operative bladder injuries.

Catheterization has proven to be an important preventive measure for iatrogenic bladder injury.

Conservative management is advocated for uncomplicated extraperitoneal bladder injuries due to

blunt trauma. Bladder drainage and prophylactic antibiotics should be offered. A bladder neck
involvement, bone fragments in the bladder wall, concomitant rectal or vaginal injuries or entrapment
of the bladder wall will warrant surgical intervention in blunt trauma injuries. Surgical repair should
also be undertaken if the patient is undergoing pelvic fracture fixation or pelvic exploration for another
indication.

All intra – abdominal injuries should be repaired, open surgery is preferred when associated with other
intra-abdominal injuries, laparoscopic repair can be performed for isolated intraperitoneal bladder
injury.

Urethral trauma1,3
Iatrogenic injuries are the most common in urethral trauma, the male urethra is the most affected and
the most common site, in blunt trauma, is the bulbar urethra.
In non-iatrogenic injuries the cause depends on the location of the injury:

2
 - Anterior (Blunt trauma, sexual intercourse, penetrating trauma.)
- Posterior urethra (Pelvic fractures).
Delayed morbidity associated with posterior urethral injuries include: stricture, incontinence and
erectile dysfunction which can significantly affect patient’s quality of life.

Types
- Incomplete.
- Complete.
Imaging
1. Retrograde urethrography is standard for evaluation of male urethral injuries. But it does not
always distinguish partial from complete injuries.
2. Flexible cysto-urethroscopy can differentiate partial from complete injuries.
3. Ultra-sound and MRI can, respectively, assist with placement of supra pubic catheter and
evaluation of the extent of the injuries for treatment strategy decision.

Management options:
- Emergency room management:
Urinary diversion by a suprapubic catheter insertion.
Gentle transurethral catheterisation.
- Urethroplasty (Early vs deferred)
- Re-alignment

FOURNIER’S GANGRENE (FG)

It is defined as a polymicrobial/type 1 necrotising fasciitis of the perineal, perianal or genital areas7.
Initially described in 1883 by Fournier as an idiopathic, rapidly progressive gangrene of the penis and
scrotum without apparent cause in young males; it is now known that the disease affects people of all
ages, affects both males and females, and the cause is usually identified. It is a surgical emergency
with a high mortality rate despite advances in therapy.
Aetiology 6
Causes may be classified anatomically:
Urogenital: infection in the bulbourethral glands, urethral injury, iatrogenic injury secondary
to urethral stricture manipulation, epididymitis, orchitis, or lower urinary tract infection.
Anorectal: perianal, perirectal, and ischiorectal abscesses; anal fissures; anal fistula; colonic
perforations; appendicitis, rectosigmoid malignancy; diverticulitis.
Dermatological: hidradenitis suppurativa, ulceration due to scrotal pressure, and trauma.
Gynaecological: Infected Bartholin’s gland, septic abortion, episiotomy wound, coital injury,
genital mutilation.
Accidental, intentional, or surgical trauma may also lead to the disease.

Clinical Presentation6,7
History: - Painful swelling of the scrotum or perineum.
- May be out of proportion to physical findings and in late presentation may even be absent
due to necrosis of nerve tissue.
- Systemic features: Fever, rigor and tachycardia.
- Evaluation of risk factors: Diabetes mellitus (present in as many as 60% of cases), HIV 5,
alcoholism, cirrhosis, malignancy, SLE, Inflammatory bowel disease, malnutrition, steroid use, morbid
obesity, vascular disease of the pelvis, or recent urethral or perineal surgery.

3
Examination: A thorough examination and high index of suspicion, especially of the obese patient, is
required of the genitalia, perineum, and anorectal areas.

Investigation6: Diagnosis is based primarily on clinical findings - only made certain after surgical
exploration.
Laboratory studies and radiological evaluation: helpful in cases of diagnostic uncertainty, risk
assessment and in planning surgery.
Lab studies: FBC, U&E, ABG, coagulation profile, early urine and blood cultures, pus swabs.
Imaging: presence of soft tissue gas, fluid along fascial planes on X-rays, ultrasound, CT, MRI.

The Fournier’s Gangrene Severity Index Score (FGSI)8:

FGSI > 9 predicted 44.4% mortality, FGSI < 9 predicted 95.5% survival6.

Management 4,6,7,9:
The EUA 2018 recommendations on management of FG:
Broad spectrum antibiotics on presentation, refine according to culture and clinical response.
Suggested regimen: Broad spectrum penicillin/ 3rd gen cephalosporin + gentamycin +
metronidazole/ clindamycin
Surgical debridement for FG within 24hrs of presentation
Do not use adjunctive treatments for FG except in the context of clinical trials.
Reconstruction: Options include; primary closure of the skin, local skin flap coverage, split-
thickness skin grafts, or muscular flaps.

EMPHYSEMATOUS PYELONEPHRITIS (EPN)10

It is an acute severe necrotizing infection of the renal parenchyma and its surrounding tissues that
results in the presence of gas in the renal parenchyma, collecting system, or perinephric tissue. The
clinical course can be severe and life-threatening if not recognized and treated promptly due to septic
complications. Most patients present in the fourth or fifth decade and risk factors include uncontrolled
diabetes mellitus & urinary tract obstruction.
Presentation: Mimics pyelonephritis: dysuria, fever/rigours, nausea, vomiting, and flank pain.
Loin tenderness: most common physical sign; crepitus around the renal area and the scrotum.
Acute renal dysfunction, acid-base disturbances on blood gases, hyperglycaemia, thrombocytopenia
and impaired consciousness with rapid progression to septic shock in severe cases.

4
Diagnosis: Emphysematous pyelonephritis is a radiological diagnosis.
Clinical and the laboratory findings will only indicate sepsis of renal origin.
A plain radiograph shows an abnormal gas shadow in the renal bed raising suspicion.
Ultrasonography or CT will confirm the presence of intra renal gas; CT is preferred as it is more
sensitive and defines the extent of EPN by identifying features of parenchymal destruction.

Management: based on the Huang and Tseng grading:

RENAL COLIC11
It is a common presentation, it has a lifetime risk of 12% in men and 6% in women, causing pain and
morbidity. The pain may mimic surgical and gynaecological conditions. Non-contrast computed
tomography is the imaging method of choice: high sensitivity and specificity.

Non-steroidal anti-inflammatory drugs offer the best initial analgesia, with opiates as a second line
treatment.

ACUTE SCROTUM

Acute
scrotum

Infectious Non-infectious Trauma

Epididymitis Testicular torsion Haematocele
Orchitis Torsion of appendages of testis Testicular rupture
Scrotal abscess Hernia: incarcerated Haematoma
Referred pain

1. Epididymitis12
It is an inflammatory reaction or infection of epididymis.
Ascending infection: lower genital tract/ STI related.
Descending infection: upper obstructive urogenital tract/ non-STI related.
Can occur as an inflammatory post-infectious reaction to bacterial and viral pathogens.
Occasionally may be related to trauma, systemic disease (Henoch-schonlein purpura,
Kawasaki disease), medication (amiodarone).

5
Causes
Predisposing Factors Etiology Incidence

Underlying Enterobacteriaceae
genitourinary Pseudomonas Common
tract disorder Aeruginosa

Haematogenous Streptococcus pneumoniae

spread from Neisseria meningitidis Rare
primary focus Mycobacterium tuberculosis

Post-infectious Adenovirus,
Factors enterovirus Uncommon
Mycoplasma pneumoniae

Urethritis (STI related) Chlamydia trachomatis, Neisseria Related to frequency

gonorrhoeae of sexual activity

Symptoms
Typically has an acute onset
With unilateral scrotal pain and swelling that increases over 1 or 2 days.
Associated symptoms dysuria and other lower urinary tract symptoms.
Accompanied by urethritis - STI symptom complex.
Fever if there is systemic involvement.

Diagnostic Evaluation
Largely on clinical examination with supporting adjuncts
Urine dipstick and urinalysis: positive for leucocyte and nitrate.
Urine – midstream specimen for MC&S.
Nuclei acid amplification test for STI related bacteria if gram stain equivocal.
If tuberculous epididymitis is suspected, three sequential early morning urine samples for
acid-fast bacilli (AFB) and sent for screening by NAAT for M. tuberculosis DNA.
Treatment
Analgesia, bed rest and scrotal support.
Ceftriaxone 500 mg imi single dose plus Doxycycline 200 mg initial dose p.o. and then 100
mg twice daily 10-14 days.
Quinolones for 10-14 days.

2. Torsion14
Testicular torsion refers to the torsion of the spermatic cord structures and subsequent loss
of the blood supply to the ipsilateral testicle. This is a surgical emergency; early diagnosis and
treatment are vital to saving the testicle and preserving future fertility. The rate of testicular
viability decreases significantly after 6 hours from onset of symptoms.
It’s primarily a disease of adolescents and neonates. It is the most common cause of testicular
loss in these age groups. However, torsion may occasionally occur in men 40-50 years old.

Pathophysiology
- Intravaginal testicular torsion accounts for 90% of torsion occurring in 13-30yr old males, it’s due
to inappropriately high attachment of the tunica vaginalis and abnormal fixation to the muscle
and fascial coverings of the spermatic cord causing the testicle to rotate freely on the spermatic
cord within the tunica vaginalis. This congenital anomaly, called the bell clapper deformity present
in approximately 12% of males and is bilateral in 40% of cases.

6
- Extravaginal testicular torsion occurs in neonates, the testicle frequently has not yet descended
into the scrotum, where it becomes attached within the tunica vaginalis. This mobility of the
testicle predisposes it to torsion.

Presentation
Sudden onset of severe unilateral scrotal pain.
May be associated with nausea and vomiting.
Can be related to trauma in 4-8% of cases.
Some patients may report previous episodes
of recurrent acute scrotal pain with spontaneous resolution.
Examination
Severely tender, erythematous enlarged hemiscrotum.
High riding compared to contralateral testis with abnormal lie (transverse).
Absent ipsilateral cremasteric reflex with negative Prehn test.
Investigation
- Torsion is diagnosed clinically and requires immediate surgical exploration
- There is no laboratory test with high sensitivity/specificity in diagnosing testicular torsion
- Imaging studies (ultrasound, radio-isotope scan) are usually not necessary. because they waste
valuable time for emergent surgical exploration, as negative finding upon exploration of the
scrotum is more acceptable than the loss of a salvageable testis.13
Management
Immediate surgical exploration is indicated for testicular torsion. For reliable salvage of the testicle,
surgical repair must occur within 6 hours of symptom onset orchidopexy +/- orchidectomy +
contralateral orchidopexy. Manual detorsion is not a substitute for surgical exploration, but it may
improve rates of surgical salvage by ensuring testicular viability in cases of surgical delay, and also
provides significant pain relief.13

ACUTE URINARY RETENTION 15

7
Urinary retention is an inability to completely empty the bladder, it can be vesical (bladder
dysfunction-atonic) or infravesical (obstructive).
Causes
Infravesical/obstructive: Prostate disease (BPH, Cancer), urethral strictures (2nd to iatrogenic
causes from catheterization or endo-urological procedures, trauma, STI, penile fracture), pelvic
organ prolapse (cystocele, rectocele), drugs (opioids and anticholinergic)
Vesical: Neurologic disorder responsible for retention via inability of bladder to sufficiently
contract (spinal cord injuries, compression, multiple sclerosis, Parkinson’s disease)
Management prompt bladder decompression

PRIAPISM16
Priapism is a pathological condition representing a true disorder of penile erection caused by
disturbances in the mechanism controlling penile detumescence and the maintenance of penile
flaccidity, persisting for more than 4 hours and is unrelated to, sexual interest or stimulation.
Classification
Low-flow (ischaemic) priapism: due to veno-occlusion (intracavernosal pressures of 80-
120mmHg). Most common form which manifests as painful, rigid erection, with absent or low
cavernosal blood flow. Ischaemic priapism > 4 hours requires emergency intervention. Blood
gas analysis shows hypoxia and acidosis.
High-flow (non-ischaemic) priapism: due to unregulated arterial blood flow, presenting with a
semi-rigid, painless erection. Usually due to trauma and subsequent fistula development and
usually self-limiting. Blood gas analysis shows similar results to arterial blood.
Recurrent (or stuttering) priapism: most commonly seen in sickle cell disease. Usually high flow,
but may change to low flow with anoxia.
Typical blood gas values (adapted from Broderick et al)

pO2 (mmHg) pCO2 (mmHg) pH

Normal arterial blood (room air) [similar > 90 <40 7.40

values are found in arterial priapism

Normal mixed venous blood (room air) 40 50 7.35

Ischaemic priapism (first corporal aspirate) < 30 >60 < 7.25

8
Management

9
REFERENCES

1. 2019 urological trauma guidelines taken from https://uroweb.org/guideline/urological-

trauma/#4
2. Erlich T, Kitrey ND. Renal trauma: the current best practice. Therapeutic advances in urology.
2018;10(10):295-303.
3. McGeady JB, Breyer BN. Current epidemiology of genitourinary trauma. Urol Clin North Am.
2013;40(3):323-34.
4. BG Singh, S Chawla; Aggressiveness – the key to a successful outcome in Fournier’s
Gangrene; MJAFI 2004; 60: 142-145.
5. Ngugi, Magoba et al, Fournier’s Gangrene in the HIV era, African Health sciences 2014; Vol
14: 1063-1068.
6. Pais, Schwartz et al; Fournier’s Gangrene;
https://emedicine.medscape.com/article/2028899-overview
7. EUA Guidelines on Urological Infections 2018
8. Elsakat, Maharaj et al, The presentation, management and outcomes of Fournier’s gangrene
at a tertiary urology referral centre in South Africa, S Afr Med J 2018; 108(8): 671-676.
9. Steyn et al, Fournier’s gangrene: challenges and pitfalls for genital reconstruction from a
tertiary hospital in South Africa; Wound Healing Southern Africa 2017; 10(1); 29-34
10. Ubee et al; Emphysematous pyelonephritis; BJU International 2010; 107: 1474-1478.
11. Bultitude et al; Management of Renal Colic; BMJ 2012;345: e5499
12. Noni E. MacDonald and William R. Bowie. Epididymitis, Orchitis, and Prostatitis, Principles
and practice of pediatric infectious diseases, 5th Edition, 2018, pages 371-373.
13. Michael Wang et al. Testicular Torsion Post orchiopexy: A Case of Twisted Hammock.

14. G. Bonkat et al. European Association Guideline. 2017, urological infection

15. Adarsh et al Urologic Emergencies. Volume 102, Issue 2, March 2018, Pages 373-385
16. K. Hatzimouratidis et al. EUA Guideline. 2017, Erectile Dysfunction,
Premature Ejaculation Penile Curvature and Priapism

10
 TRAUMATIC BRAIN INJURIES AND SPINAL CORD INJURIES
Drs R. Bux, J. Khan, M. Ramaphoko
Moderator: Dr R. Harrichandparsad 4th May 2019

Introduction1, 2
Traumatic brain injury (TBI) is an important cause of morbidity and mortality in the developed and developing
worlds. In the western hemisphere, TBI is the leading cause of mortality in those <45 years1. Population-based
studies in SA, Taiwan and India suggest even higher rates in developing countries. Injury-related mortality
rates in SA are 6 times higher, and the incidence of road traffic injuries to be double the global rate2.

Classification of head injuries 4

Mechanism of Injury Severity (Based on GCS)
Blunt Minor – 13 to 15
Penetrating Moderate – 9 to 12
Severe – 3 to 8
Morphology (Skull Fractures) Intracranial Lesion
Base of skull – With or without CSF leakage and Focal: Epidural, Subdural (SDH), Subarachnoid (SAH),
cranial nerve palsy Intracerebral (ICH), intraventricular (IVH)
Vault – Linear, Stellate, Depressed, Open or Closed Diffuse: Concussion, Contusion, Hypoxic and ischaemic injury

Definitions3
Traumatic brain injury: Presence of neurological symptoms or demonstration of intracranial pathology is
needed to establish the diagnosis of TBI; maybe suggested by a skull fracture and may not always be caused by
direct trauma to the head. TBI is divided into 10 into and 20 injuries.
Primary brain injury: It occurs at the time of impact and is currently believed to be irreversible. Energy
transfer to the brain causes irreversible neuronal and mechanical disruption, as well as disruption of brain
vasculature. 10 injury prompts a cascade of 20 inflammatory, oxidative stress, mitochondrial, metabolic and
vascular mechanisms that further initiate and perpetuate cellular injury.

Secondary brain injury: Maintained and worsened by intracranial and extracranial insults, the combined
effects of which are multiplicative rather than additive. Greatest insult thought to occur within 12-24 hours
post trauma. These insults include: raised ICP, hypotension and hypoxia, anaemia, fever and infection,
metabolic (hypo- and hyperglycaemia), electrolyte abnormalities, hypo/hypercarbia and convulsions. Thus,
primary aim of management of head injury is prevention and/or limitation of secondary brain injury.

Types of primary injury3

Concussion: Trauma induced alteration in mental status lasting <24hrs, no parenchymal abnormality on CT.
Coup: A contusion is an area of inflamed brain tissue, with bleeding. Damage at the site of blow.
Contrecoup: similar to coup contusions but are situated on the opposite side of the direct insult.
Diffuse axonal injury: Broad spectrum of injury following rotational forces causing shearing of axons and
blood vessel; CT scan may initially be normal.
Intracranial haematomas: See table below*

Pathophysiology3
TBI results from a violent collision, acceleration – deceleration and rotational movement of the brain. The
cerebral injury is manifested by extreme tissue harm and diminished metabolism and CBF regulation. These
produce an ischemia-like condition that results in anaerobic glycolysis; gathering of lactic acid and elevated
membrane permeability results in oedema formation. Insufficiency of anaerobic metabolism to sustain cellular
energy levels causes depletion of ATP-stores and energy-dependent membrane ion pumps stoppage.
1
These processes increase the intracellular accumulation of oxygen radicals and free fatty acids. All these result
in membrane cellular and vascular system destruction and ultimately apoptosis or necrosis. 4

SPECIFIC PATHOPHYSIOLOGY OF TRAUMATIC BRAIN INJURY4

Oedema
Brain oedema is of two types: vasogenic (interstitial) and cytotoxic (intracellular). Both these types take place
promptly after TBI and both may result in 20 impairments.
Oedema is normally worse 24-48 hours post-injury. Both these types result in elevated ICP and 20 ischaema.
Vasogenic oedema follows autodigestive disturbance or mechanical/functional disintegration of the blood–
brain barrier or from reflex dilatation of vessels.
The cerebral vascular endothelial wall breakdown promotes ion and protein removal from the intravascular to
the interstitial space with water gathering. This results in accumulation of volume in the extracellular space.
Cytotoxic oedema follows intracellular water gathering of astrocytes, microglia, and neurons, regardless of the
reliability of the vascular endothelial wall. The oedema follows modifications in cellular osmolality with the
subsequent failure of cellular capability to manage its ionic gradients.

Increased Intracranial Pressure

ICP is normally 7–15 mmHg (supine adult), and is influenced by abrupt changes in intra-thoracic or intra-
abdominal pressure, valsalva manouvre, and communication with the vasculature (venous and arterial
systems). ICP is elevation of the pressure in the cranium.
At ICP 20–25 mm Hg (upper limit normal), treatment to reduce ICP may be needed. TBI worsens because of
raised ICP, specifically >40 mm Hg.
Cerebral perfusion pressure (CPP) is commonly invariable because of autoregulation. Increase or decrease
change in CPP leads to cerebrovascular constriction or dilation, a process termed as CBF auto regulation.
CPP = Mean Arterial Pressure (MAP) – ICP. As ICP increases, the CPP decreases.
The response to drop in CPP causes an increase in systemic BP and dilation of cerebral blood vessels. All these
processes enlarge the cerebral blood volume that raises ICP, reducing CPP additionally - which further leads to
an extensive decrease in cerebral perfusion and flow, ultimately resulting in brain infarction and ischemia.

2
Mitochondrial Dysfunction
After TBI, mitochondrial dysfunction results in free radical generation following apoptosis; thus, treatment is
required which particularly limits the 20 injury damage.

Excitotoxicity and Oxidative Stress

An increase in the levels of glutamate follows minutes post TBI. This increased glutamate produces elevated
Na+ and Ca2+ influx to the cell and leads to cell damage. Cell damage mechanisms result in apoptosis.

Oxidative stress is described as the imbalance between the production of free radical and the ability of the
body to detoxify their damaging effect through neutralization by antioxidants. Oxidative stress involves
reactive oxygen species production (generation of oxygen free radicals and related species such as nitric oxide,
superoxide, hydrogen peroxide, peroxynitrite in response to TBI.

CO2-reactivity
CBF is maintained by autoregulation and CO2 reactivity. CO2 reactivity refers to cerebrovascular constriction or
dilation in response to hypo or hypercapnia. In patients having severe brain injury and poor outcome, the CO2-
reactivity is diminished at early stages after trauma.

Cerebral metabolic dysfunction

Cerebral metabolism is indicated by cerebral oxygen and glucose consumption whereas cerebral energy state
is indicated by the concentrations of ATP and phosphocreatine in tissue or indirectly by the ratio of
lactate/pyruvate. These factors are significantly reduced post TBI (10 insult)

Excitatory Amino Acids (EAAs)

EAAs) such as glutamate and aspartate are considerably increased following TBI; this results in neuronal death,
cell vacuolization, and swelling (secondary to an influx of chloride, sodium, and calcium).

Cerebral oxygenation and Glucose Metabolism

TBI leads to an imbalance between cerebral oxygen delivery and consumption with the end result being tissue
hypoxia. The brain tissue oxygen pressure in patients with TBI has a critical threshold of 15-10 mm Hg.
When partial pressure of oxygen decreases below 10–15 mmHg, infarction ensues. Brain tissue hypoxia may
occur even in the presence of normal ICP and CPP.
Thus, for treatment of head trauma, balance between oxygen delivery and cerebral oxygen consumption
should also be taken into consideration, in addition to ICP and CPP.
Hyperglycaemia is present in about 50% of patients with TBI. It is associated with severity of injury and poor
outcome. TBI causes considerable enhancement of glucose utilization following the initial 30 minutes post-
injury, followed by a decline in glucose uptake and then is maintained in a low state for around 5-10 days.
Reduced cerebral glucose metabolism is noted in both severe and mild TBI patients, indicating that
neurometabolic abnormalities may be present in patients with or without symptoms.

Cerebral blood flow (CBF)

Normal CBF in the human brain is approximately 50 ml/100 g/min, with blood flow to the gray matter higher
(80 ml/100 g/min) than the white matter (20 ml/100 g/min). The brain consumes 20%of oxygen and 25% of
glucose used by the whole body, and is dependent on a constant supply of 15% of the cardiac output.
However, with head trauma, auto regulation of cerebral blood flow deteriorates and cerebral ischemia can
develop in association with inadequate blood flow at the level of 50 mL/100g because of increased cerebral
oxygen consumption.
Three distinct phases of blood flow following traumatic brain injury have been described:
Phase I – Hypo-perfusion (day 0)

3
 Cerebral blood flow decreases during the first 24 hours after the injury, and is thought to be due to
narrowing of the cerebral microcirculation.
Phase II – Hyperaemia (days 1-3)
Hyperaemia occurs maximally between 48 and 72hour post injury, and may continue to 96 hours.
There has been suggestion that this increased CBF is the primary cause of increased ICP.
Phase III: vasospasm (days 4-14)
Vasospasm occurs in > one-third of patients with TBI and indicates severe brain damage. Onset varies
from post-traumatic day 2 to 15, with hypoperfusion occurring in 50% of all patients with vasospasm.

Inflammation
Trauma induces a complex immunological and inflammatory tissue response (release of cytokines,
prostaglandins, and leucocytes). This inflammatory response forms scar tissue within days and even months.

Endogenous Opioid Peptides3

By regulating the presynaptic release of neurotransmitters, endogenous opioid peptides may exacerbate
neurologic damage.

COMPARISON OF FOCAL INTRA CRANIAL HAEMORRHAGE

Types Aetiology Epidemiology Clinical CT features Treatment Prognosis

features

Epidural Skull fracture M>F 4:1 Lucid interval Hyperdense Craniotomy Good with
under cranium, causing Associated before LOC lenticular mass; prompt
outside the middle trauma sharp margin intervention
dural space meningeal usually limited by
arterial bleed suture line
Acute SDH Ruptured <50 yrs with No lucid Hyperdense Craniotomy if Poor due to
- intra-dural subarachnoid associated interval, focal crescentic mass bleed >1cm underlying
- extra-axial bridging trauma neurology, crossing suture line thick, midline cerebral
veins pupil changes shift > 5mm injury
Chronic SDH Ruptured >50yrs, ETOH Symptomatic Hypodense Burr hole to Good
- intra-dural subarachnoid abuser, on with minor crescentic mass drain,
- extra-axial bridging anti- H/A, crossing suture line craniotomy if
veins coagulation confusion, recurrs
signs of ICP
SAH Traumatic or Age 55-60, Sudden onset Hyperdense blood Conservative, Poor 50%
within the spontaneous: 20% of cases of in cistern/fissure, operative mortality
subarachnoid - aneurysm are usually thunderclap sensitivity (open or endo
space - AVM under 45 headache, decreases overtime vascular)
- idiopathic signs of ICP
ICH HPT, vascular Age >55yrs, TIA Hyperdense intra May be Poor
within brain abnormality, male drug symptoms, parenchyma medical or
parenchyma tumour, users such as ICP collection surgical
infection, cocaine, ETOH
coagulopathy
IVH Traumatic or Neonatal IVH ICP Hyperdense Temporary Variable
within the spontaneous. or age> 55 At risk of collection within (External Depends on
ventricular HPT, with HPT hydrocephalus ventricular system ventricular underlying
system aneurysms, ± hydrocephalus drain) or cause
coagulopathy permanent (VP
shunt) CSF
diversion
4
EVALUATION OF THE HEAD INJURED PATIENT 5,6
History
Mechanism of Injury – high vs low velocity, blunt vs penetrating
Pre-hospital condition of patient
Any symptoms associated with an injured brain – seizures, vomiting, amnesia, loss of consciousness
Physical Examination
Assessment as per ATLS principles
Assume all head injuries have an associated cervical spine injury until ruled out – head blocks provide
better cervical spine immobilization than a hard collar
Assessment of vital signs
Features of shock are not likely due to an isolated head injury and another cause must be
sought in a polytrauma patient
Be cognizant of the Cushing response to raised ICP (hypertension, bradycardia, irregular
respiratory pattern)
Examination of the head to determine the type of head injury with regard to associated skull fractures
Evaluation of the neurological status of the patient
Level of consciousness (Intubation required if GCS
Pupillary size and light response
Localizing signs (unreliable in sedated patients or those with a moderate to severe head
injury)
Investigations
Skull and c-spine radiographs
Laboratory investigations: U&E, FBC, glucose, coagulation profile and toxicology screen
Unenhanced CT Brain

Indications for Urgent Unenhanced CT Brain

Adults
GCS <13 on initial assessment in the emergency department or less than <2 hours post injury
Post-traumatic seizure
More than one episode of vomiting
Amnesia of more than 30 minutes before impact
Any sign of base of skull fracture (haemotympanum, periorbital echymosis, cerebrospinal fluid leakage
from the ear or nose, Battle’s sign)
Open or depressed skull fracture.
Focal neurological deficit.

Children
GCS < 14, or <15 in babies under 1 year of
Loss of consciousness lasting more than 5 minutes (witnessed)
Abnormal drowsiness
Post-traumatic seizure
Three or more episodes of vomiting
Amnesia (antegrade or retrograde) lasting more than 5 minutes.
Clinical suspicion of non-accidental injury.
Open or depressed skull injury or tense fontanelle.
If under 1 year, presence of bruise, swelling or laceration of more than 5 cm on the head.
High risk mechanism of injury (high speed road traffic accident, ejection from vehicle, fall from a
height of greater than 3 m, high speed injury from a projectile or an object).

5
MANAGEMENT PRINCIPLES5,6,7
The primary goal of management is to prevent secondary injury to the brain. Interventions should be aimed at
optimizing cerebral perfusion and oxygenation.

Prehospital Management
In the prehospital setting, the aim main should be to stabilize the patient for transfer to an emergency unit.
This means providing supplemental oxygen, attempting to achieve haemostasis, and instituting appropriate
volume resuscitation.
Patients who have sustained TBI and are classified as severe according to their GCS may be unable to protect
their airways. This puts them at increased risk of airway obstruction, aspiration, and subsequently hypoxia. It
may seem intuitive to intubate these patients on scene, but a number of studies have noted an increased
morbidity with prehospital intubation as opposed to basic airway management. The outcomes of 124 patient
presenting to 2 trauma centres in the Western Cape showed that those patients who were intubated on scene
via Rapid Sequence Induction had the poorest outcomes compared to other methods of airway management.

Management in the Emergency Unit

Primary goals on arrival at an emergency unit should be the prevention of hypoxia and hypotension.
Maintaining a low systolic BP (SBP) in an attempt to prevent intracranial hypertension is no longer advocated.
More emphasis is now placed on maintaining an adequate cerebral perfusion pressure (CPP).
Cerebral Perfusion Pressure (CPP) = Mean Arterial Pressure (MAP) – Intracranial Pressure (ICP),should be
maintained between 50-70mmHg.
The following should be instituted in order to prevent secondary brain injury:
Maintain SBP>90 or MAP>60
Supplemental oxygen therapy
Maintenance of euthermia
Aim for normoglycaemia

Indications for ICP Monitoring

The normal ICP is <15. Raised ICP can be classified as mild (15-20mmHg), moderate (20-40mmHg) and severe
(>40mmHg). ICP monitoring is indicated in the following:

GCS 3-8 GCS 9-12 GCS 13-15

Abnormal CT scan Abnormal CT scan ICP monitoring rarely
Normal CT scan with: Unable to assess pupils due to brain indicated
Age> 40 stem or midface injuries
Motor posturing Requiring anaesthesia
SBP<90mmHg Requires ventilation for other injuries

ICP monitors can be either intraventricular (gold standard), subarachnoid via a bolt or Richmond screw,
intraparenchymal or epidural. Complications of insertion include infection and haemorrhage.
Decompressive Craniectomy 8
Decompressive craniectomy aims to remedy the deleterious effects of sustainedICP. Clear cut indications for
craniectomy have not yet been defined. Two large trials have evaluated the outcome of patients following
craniectomy at 6 months. These are the DECRA and RESCUE-ICP trial. The DECRA showed similar mortality
rates between the surgical and medical intervention arm, but the RESCUE-ICP trial showed an improved
mortality rate in the surgical arm. Both trials, however showed an increase in morbidity and lower functional
scores at 6 months in the surgical arm. More research into long term quality of life outcomes following
decompressive craniectomy following head trauma are required.

6
Inpatient Management
Ongoing care of patients in hospital should focus on limiting secondary insults as well as creating an
environment for the injured brain to recover. Patients who have suffered a severe head injury, those who
have had an ICP monitor placed, and those who have undergone decompressive craniectomy should ideally be
housed in an intensive care unit. Inpatient management of head injured patients should include:
Optimization of oxygenation
Maintenance of normocarbia (PaCO2 35-40mmHg)
Maintaining normotension
Maintaining CPP > 50mmHg and ICP<20mmHg (when an ICP monitor is in place)
Maintaining euglycaemia
Adequate sedation
Nutritional support whether by enteral, nasogastric or parenteral route. Enteral feeding is preferred in
patients who can take in orally and are able to protect their own airway
Thromboprophylaxis starting 48 hours post injury
Seizure prophylaxis for 7 days
Early initiation of beta antagonists to blunt the sympathetic response has been described in the literature
but no well controlled trials exist in order to formulate recommendations

Outcomes
A number of factors can aid in predicting outcome in head injured patients.
The first is the age of the patient. Younger patients have a better chance of recovery than the elderly, with a
100% mortality noted in patients >75 years with a GCS<5 on arrival. Across all age groups, outcomes are poor
in those with GCS <6 after resuscitation and who are not amenable to a decompressive procedure.
Hypotension and hypoxia are also predictors of poor outcome.
Other factors to consider are mechanism of injury, pupillary response on arrival and time from loss of pupillary
response to decompressive surgery. The Glasgow outcome scale is used to stratify patients according to their
disability:
5= Dead 4= Vegetative State 3= Severe Disability 2= Moderate Disability 1 = Mild Disability

SPINAL CORD INJURIES (SCI)

Cause of a major morbidity and mortality with devastation impact on financial, psychological and social well-
being. SCIs are a burden to the economy; most involved are young and working group, with mean age 40 yrs.1
Epidemiology 9,11
MVAs account for 42%, with falls (about 26.7%), followed by violence (15.1%) and sporting activities (7.6%).
Males are more affected than females
Of all spinal injuries 55% involve cervical spine, 15% the thoracic spine, 15% involve lumbar spine, and 15%
lumbosacral spine.
C6 and C7 are most frequently fractured vertebrae (50%), followed by C2 (33%) with odontoid process
fracture occurring in 15% of all the cervical spine fractures.
The overall incidence of cervical spine fracture without SCI is 3%
Presentation 9,10,11
Either complete or incomplete, according to American Spinal Injury Association (ASIA) Impairment scale.
Depending on the level of injury can be classified as either tetraplegia or paraplegia
American Spinal Injury Association (ASIA) Impairment Scale
A - complete (no motor or sensory function down to S4 and S5)
B - incomplete (preserved sensory, but not motor)
C - incomplete (persevered motor function with power less than 3)
D - incomplete (persevered motor function with power of 3 or greater)
E - normal

7
Incomplete Spinal dysfunction syndromes
Brown-Sequard syndrome
Hemisection of the cord with disruption of the descending lateral corticospinal tracts - contralateral loss of
pain and temperature, ipsilateral loss of proprioception and fine touch below the level of the lesion
Anterior spinal cord syndrome
Due to occlusion of the anterior spinal artery or anterior cord compression- bilateral pain and temperature.
Intact proprioception and touch
Posterior cord syndrome
Injury of the posterior spinal cord affecting the posterior column - ipsilateral loss of vibration and
proprioceptive sensation below the lesion
Central cord syndrome
Bilateral central corticospinal tracts and lateral spinothalamic tracts - Bilateral paresis: upper >
lower extremities.

Neurogenic shock
Haemodynamic sequelae of SCI: (hypotension resulting from loss of peripheral vascular resistance)
Results from disruption of descending sympathetic pathways in the spinal cord; thus unopposed vagal
parasympathetic tone having 2 effects:
Loss of vasomotor tone, results in vasodilatation of visceral and lower extremity blood vessels
(warm skin) pooling of blood hypotension.
Loss of sympathetic innervation to the heart bradycardia or failure to develop tachycardia in
response to hypovolaemia. Blood pressure may not be restored by fluid infusion alone (massive
fluids can result in fluid overload and pulmonary oedema). Restore BP with vasopressors after
moderate volume replacement. Atropine can be used to counteract significant bradycardia.

Spinal shock
Spinal cord dysfunction based on physiological rather than structural disruption.
Refers to the flaccidity paralysis, loss of reflexes, hypotonia, absent sensation seen after SCI. May appear
to be completely functionless although all areas are not necessarily anatomically destroyed.
Duration is variable. Usually resolves in 48 hours. First to return is bulbocavenosus reflex (S3-S4)

Special considerations 9
Elderly
C2 fractures are much more common in the elderly. This is due to a combination of osteopenia,
degenerative changes
Spinal cord injury can occur as a result of otherwise trivial fall
central cord syndrome common in this age group
Children
spine fracture uncommon in this age group
cord injury without spine fracture should always be suspected

SCIWORA - Spinal cord injury without radiographic abnormality

most common in kids
Adults - due to hyperextension on the background of pre-existing cervical spondylosis and critical
canal stenosis

8
Cervical Spine 11
Occipital condyle fractures
Rare; using Anderson-Montesano system:
Type I comminuted fracture due to axial loading
Type II base of skull fracture that propagates into one or both occipital condyles;
Type III inferomedial avulsion fracture
Atlanto-occipital dislocation
Between occiput and C1, most frequent in children due to size of the head
Mostly fatal, no traction should be applied. Mortality decreased with c-spine protection at the scene
Acute atlantoaxial dissociation (AAD)
Characterized by excessive motion between C1 and C2 caused by a bony or a ligamentous injury
Common in Down syndrome, osteogenesis imperfecta, neurofibromatosis, Morquio syndrome,
spondyloepiphyseal dysplasia congenital, and chondrodysplasia punctata
Fractures of the atlas (C1)
Posterior and anterior arch fractures, as well as Lateral mass fracture – can be treated with hard collar
or halo vest
Jefferson fracture – axial compression with fracture of both ant and posterior aches
Fractures of the axis (C2)
Odontoid – type 1 avulsion of the tip, type 2 fracture of the base (most common), type 3 extending to
body of C2
Hangman’s fracture (traumatic spondylolisthesis of C2)- bilateral pars interarticularis fractures
Fractures of lateral mass – secondary to axial loading mechanism

Thoracic Spine 10,11

Denis’s three column model
Divides the spine into anterior posterior and middle column to assess stability of the injury
therefore involvement of the middle column along with the posterior or anterior column equates to
instability and requires internal fixation
Four major injuries : wedge compression fracture(stable); Burst fracture (unstable); Seat belt-type
injuries or Chance fracture (unstable); Fracture-dislocations (traumatic spondylolisthesis- unstable)

Management 9
Prehospital - according to ATLS principles
Clearing cervical Spine
National Emergency X-Radiography Use Study (NEXUS) – with 99,6% sensitivity, no imaging if:
no midline cervical spine tenderness
no focal neurologic deficit
normal level of alertness
no intoxication and no painful distracting stimuli
Imaging
Multidetector CT is a preferred initial imaging technique in suspected C-spine injury
X-ray used as a screening tool – high negative predictive value of 99.5% . more sensitive in odontoid
fractures
MRI reserved for:
Primary imaging modality in assessing for epidural hematoma, ligamentous injury, traumatic disc
herniation, and spinal cord compression
SCIWORA - Spinal cord injury without radiographic abnormality
Prognosticate the injury

9
Steroids in Acute Spinal Cord Injury 11
Rationale is to improve neurological outcome in acute SCI by minimizing the effect of inflammatory mediated
secondary spinal cord injury.
Evidence: conflicting and inconsistent, definite benefit not proven and studies claiming benefit not
reproducible (NASCIS I, II III)
Definite risks associated with steroid therapy: pneumonia, sepsis, hyperglycemia
Medico-legal aspects
American Association of Neurologic Surgeons (2013): Advises against routine use of methylprednisolone in
acute spinal cord injury. It is widely held that steroid therapy in acute SCI is not the standard of care and
should not be administered routinely, but remains a treatment option in patients with incomplete
neurological deficit, if treatment is initiated within 8 hours of the injury (bolus Methylprednisolone 30mg per
kg, 5.4mg /kg/hr for 24)hours.

References :
1. Naidoo D. Traumatic Brain Injury: The South African Landscape - South African Medical Journal. 2013;
103(9):613-614.
2. Nell V, Brown DS. Epidemiology of traumatic brain injury in Johannesburg--II. Morbidity, mortality and
aetiology. Social Science & Medicine 1991; 33(3):289-96
3. Werner C and Engelhard K. Pathophysiology of traumatic brain injury. British Journal of Anaesthesia.
2007; 99 (1):4–9.
4. Kaur P and Sharma S. Recent Advances in Pathophysiology of Traumatic Brain Injury. Current
Neuropharmacology. 2018; 16(8):1224–1238.
5. ATLS Advanced Trauma Life Support for Doctors Student Course Manual, 10th Edition
6. Brain trauma foundation TBI guidelines 4th edition
7. Sobuwa S, Hartzenberg HB, Geduld H, Uys C. Outcomes following prehospital airway management in
sever traumatic brain injury. SAMJ 2013;103:644-646
8. Hutchinson PJ, Kolias AG, Timofeev IS. Trail of decompressive craniectomy for traumatic intracranial
hypertension. N Engl J Med 2016;375:1119-1130
9. Looby S and Flanders A. Spinal Injury. Radiol Clin N Am. 2011;49:129-163, 2011
10. Kiratu ME. Head injuries and spinal cord injuries. 2013:1-20
11. Bracken MB. Steroids for acute spinal injury. Cochrane Database Review, 2012
12. John AMT, Tudor HH, Donald R, Spinal imaging: 2nd edition. 2011:1068-1104

10
 PANCREATICO-DUODENAL AND HOLLOW VISCERAL INJURIES
ML Kashasha, A Gurunand, R Lukusa

Moderator: Dr W Bekker 18 May 2019

Gastric Trauma5,6
The position of the stomach in the abdomen depends upon the degree of distension, the movement of
the diaphragm and the positioning of the individual at the time of the injury. The blood supply arises from
the 3 branches of the coeliac truck, and its well vascularised nature confers with it significant surgical
advantages. Venous drainage follows the arterial supply.
The stomach is relatively free of bacteria and other micro-organisms due to the low pH but some
lactobacilli, streptococci, anaerobes and candida can be isolated. Stat dose fluconazole intra-operatively is
recommended to prevent fungal peritonitis in following gastric perforation.
Gastric injuries usually result from penetrating trauma and occur in approximately 20% of gunshot
wounds and 10% of stab wounds and often involve the anterior and posterior wall and it is imperative to
search for a second injury if one perforation is found. Missed injuries of the OG Junction and the posterior
wall are common. Blunt gastric trauma is much less common (+/- 1%), and is associated with severe
adjacent organ injuries. It requires excessive force to cause a blowout injury (i.e high speed MVA, PVA).
The injuries encountered includes: contusions, intramural hematomas, lacerations, full thickness
perforation and mesenteric avulsions.

Severity Grading. AAST Stomach Injury Grading

The presence of a bloody gastric aspirate on the NGT, and free air under the diaphragm on CXR is highly
suspicious of gastric injury.
After initial evaluation and resuscitation (ATLS principles), for damage control, the unstable patient’s
lacerations can be over sewn or stapled regardless of the injury grading. Bleeding require precise
haemostasis.

Surgical management is based on the grading system. The stomach should be decompressed first by a
NGT followed by mobilisation via opening of the gastro-hepatic ligament and the triangular ligament,
allowing exploration of the OG junction. The gastro colic ligament must be divided to inspect the posterior
wall. Inspect the lesser and greater curvature. All hematomas should be explored to rule out underlying
perforations.
Grade 1 and 2 lacerations are repaired primarily after wound edges have been debrided to healthy tissue.
Grade 3 can also be closed in a similar. Injury involving the pylorus will need pyloroplasty. Partial thickness
injuries need to be closed as they could progress to full thickness perforation. Destructive injuries like
Grade IV and grade V may require a proximal or distal gastrectomy and reconstruction by Bilroth I or II
depending of the presence of associated duodenal injuries. In rare cases, a total gastrectomy and a
Roux-en-Y esophagojejunostomy for grade V is done.

1
Gallbladder Trauma4,5,6
Injury to the GB is extremely rare (< 1%). The GB is more frequently affected by penetrating injury. Blunt
injury to the right upper quadrant can cause transection, and biliary disruption. If isolated, it is often
discovered late due to the non-specific clinical presentation, with missed injuries being associated with
high mortality and morbidity.
Management is completely surgical. Cholecystectomy is the best treatment of most injuries regardless of
the mechanism of injury. Primary suture repair of the GB is not recommended because of the high risk of
bile leakage. Almost all GB injuries following blunt trauma are associated with other significant intra-
abdominal injuries and it is imperative to use an open procedure to facilitate a detailed exploration of the
peritoneal cavity.

Pyloric exclusion 1,2

Used as adjunct in intermediate and high grade duodenal injuries. It consists of closing the pylorus
through a gastrostomy (thus reduce the risk of leak at the duodenum repair) with a purse string, and
thereafter perform a loop gastrojejunostomy. Within 3 to 6 weeks the pylorus will reopen regardless of
the suture used. However there are controversies on whether this technique makes a difference. Two
retrospective studies, did not show any difference comparing primary repair (PR) and pyloric exclusion PE.
Although PE complicates with gastro-jejunostomy marginal ulcer, an extra anastomosis and its
complications, there is currently not enough evidence to forsake this procedure. PE must be
individualized. PR is enough for most of the cases “less is better”.

Isolated Free fluid 3,7

CT scanning of the abdomen and pelvis is the procedure of choice for hemodynamically stable injured
patient following blunt abdominal trauma. It is capable of revealing the presence of intra-abdominal or
intra-thoracic haemorrhage and extent to identify the organ involved. Patients with isolated free fluid on
CT or patients with suspected hollow viscous injury do not profit from this diagnostic strategy and present
a management dilemma.
The new studies use Multi Detector CT scanners (MDCT) in which oral contrast is omitted. MDCT
unfortunately misses up to 15% of small bowel injuries, mesenteric injuries as well as some acute
pancreatic injuries. What should we do if a CT scan does not provide us with the answers?
Current studies propose that; these patients should be admitted and managed conservatively with serial
abdominal examination and laboratory tests. Assuming that, only a minority will need surgical
intervention. The amount of free fluid and the presence of abdominal tenderness are considered
indicators for surgical intervention. Patients without these findings should be carefully observed.
To date, there is still no consensus reached on the finding of isolated free fluid.

Pancreaticoduodenal Trauma
Anatomy 15
The duodenum and pancreas are closely related with complex loco-regional vascular and visceral anatomy
accounting for the often devastating associated injuries. The duodenum forms the first part of the small
bowel extending from the pylorus for 30cm to the Ligament of Treitz and is divided into 4 parts:
1st part – pylorus to CBD/ gastroduodenal artery
2nd part – gastroduodenal artery to ampulla of Vater
3rd part – Ampulla to SMA/SMV
4th part – SMA/SMV to DJ flexure
The duodenum is entirely retroperitoneal except for the anterior half of the first part and the distal fourth
part. The duodenum is related to the vertebral column posteriorly as well as the aorta/ IVC and right
kidney. Anteriorly the liver and gallbladder are closely related as well as the transverse and hepatic
flexure of the colon and stomach. The head of the pancreas lies within the C-loop and share a blood
supply.
The pancreas is divided into the following parts:
Head – lies within the C-loop of the duodenum
Neck – overlies the SMA/ SMV
Body – extends across vertebral column
Tail – extends to splenic hilum
2
Important relations include the transverse mesocolon anteriorly, the aorta, SMV/SMA and vertebral
column posteriorly, the splenic artery superiorly with the kidney and spleen abutting the tail.
Considering the combined anatomy the following conclusions can be drawn:
Combined pancreaticoduodenal trauma is common – especially near the head of the pancreas.
Associated major vascular and visceral trauma is common.
The vertebral column acts as a rigid structure against which blunt trauma can occur.
Severe trauma to the head of the pancreas can result in major bleeding and devascularisation of
the duodenum as well as biliary tract trauma.
Mechanism of trauma 11 ,12, 14
Penetrating
Stab – low energy
GSW – high energy – high % of associated injuries
Blunt
Blow-out, rupture of hollow viscera
Fracture of pancreas against vertebral column

Duodenal trauma 9,10

Duodenal trauma is uncommon and accounts for only 3-5% of all intra-abdominal injuries.. Associated
injuries are more common (70%) in those suffering penetrating trauma and higher grade injuries; with the
most common organ injured being the liver, followed by the colon, stomach, pancreas, small bowel and
great vessels.
Classification of Injury 9
Duodenal injuries are graded based on the AAST classification which directly impacts on management. es.

Assessment/Investigations 9,11
All patients are assessed in an emergent setting according to ATLS principles and stabilised accordingly.
Penetrating trauma
Patients is assessed according to principles of penetrating abdominal trauma with many warranting
exploration on clinical grounds alone with duodenal injuries found at exploration with routine specialised
imaging discouraged.
Blunt trauma
In this group of patients findings do not correlate to injury type or severity. Imaging/ serial examinations
are often used to diagnose injuries however can bring delay treatment. The retroperitoneal nature of the
duodenum can mask clinical signs of injury, leading to significant delays in management and a high index
of suspicion must be kept in blunt abdominal trauma.
Investigations
1. Plain chest/ abdominal radiographs
Mild scoliosis/ obliteration of right psoas muscles shadow
Air in retroperitoneum
2. CT abdomen
Currently most reliable modality however 27% of injuries will be missed (Ballard et al, 1997),
with subsequent re-scan showing injuries
Unreliable in diagnosing hollow viscus injuries
False positives can also occur
3
 Features:
Free retroperitoneal air
Unexplained free fluid
3. Upper GI contrast study
Using water soluble contrast
54% sensitivity with 98% specificity
More cumbersome to perform and often difficult to interpret
4. FAST/ DPL
No role in diagnosis of duodenal trauma
Useful in unstable patients with uncertainty of origin of haemorrhage
Diagnosis of duodenal trauma remains challenging despite the many modalities available, and these need
to be interpreted by experienced surgeons and radiologists bearing the history and examination.
Inconclusive studies often prompt exploration to avoid the sequalae of missed injuries.
Management/ operative principles 8,9,11,14

Patients are resuscitated and assessed via ATLS principles. Non-responders/ transient responders undergo
surgical exploration. Stable patients are then further assessed and explored based on clinical findings/
investigations.
Surgical options/ principles
Surgical exploration in this group of patients is technically challenging considering the high likelihood of
associated major vascular and visceral injuries. The operating surgeon should be comfortable with
damage control surgery ie the arrest of haemorrhage and limiting contamination. Stable patients should
have full exposure of the injury with definitive repair based on the AAST grading.
Findings suggestive of a duodenal injury intra-operatively include a central supra-mesocolic hematoma,
blood, bile or bubbles visible in the retroperitoneum or an obvious missile or stab tract in the region.
Exposure of the duodenum is performed by mobilisation of the hepatic flexure of the colon with medial
rotation up until the visualisation of the right renal vein. A Kocher maneuver is performed via mobilisation
of the duodenum medially up to the pancreas. This allows complete visualisation of both anterior and
posterior aspects of the duodenum.

Morbidity and Mortality 10,11

These patients have a significant trauma burden and are particularly prone to morbidity with local studies
revealing a 58% morbidity rate including duodenal fistula and abscess collection as well as extra-
abdominal complications associated with prolonged hospitalisation
4
Morbidity
Factors associated with duodenal leak include:
Physiology at presentation: Low pH and raised lactate
Delay in definitive surgery
Mechanism
Penetrating > blunt injuries
GSWs > stab wounds
Type of injury
Greatest in grades 3-5
Loss of tissue
D2 injuries
Mortality
Early mortality (within 24 hours) occurs secondary to associated trauma and not as a direct result of the
duodenal injury and is usually secondary to irreversible shock secondary to haemorrhage. Late mortality is
secondary to duodenal wound dehiscence, intrabdominal sepsis and multiorgan dysfunction.

Pancreatic Trauma 14,15

Traumatic pancreatic injuries account for 0.2% of those suffering blunt trauma and 1-12% of those
sustaining penetrating trauma, however are often the cause of significant mortality and morbidity due to
lack of specific diagnostic and clinical tests. The associated injury rate to other viscera and major vascular
structures is high due to related anatomy and are often the cause of short-term mortality.
Classification 14
Grading is by the AAST system which classifies injuries according to extent of trauma, part of the pancreas
injured and presence of ductal involvement. These directly impact management strategies.

Assessment and investigations 12,13,15

Patients are assessed and stabilised according to ATLS principles. Patients with penetrating trauma are
assessed clinically and explored accordingly. Those sustaining blunt trauma and are stable are further
investigated.
Investigations
1. Serum amylase/ lipase
Poor sensitivity/ specificity for pancreatic trauma
Persistent raised serum pancreatic enzymes can indicate an injury and prompt further
investigation
2. Plain chest/ abdominal radiographs
Retroperitoneal gas, associated lumbar spine fractures can indicate loco-regional trauma
Little use in pancreatic trauma
3. CT Abdomen
85% sensitivity and 90% specificity for injuries
Can miss ductal injuries and contusions without fracture
Features include fractures/ lacerations, active haemorrhage from peri-pancreatic vessels, oedema
or hematoma
4. ERCP/ MRCP
5
 Both useful in patients with equivocal CT findings in which exploration is not performed
Greater accuracy in identifying ductal injuries and guiding further management
ERCP – invasive however is also therapeutic
MRCP – non-invasive but purely diagnostic

Management/ operative principles 13,14,15

As per ATLS principles, non-responders or transient responders should be explored while stable patients
having sustained blunt trauma should be investigated.
Surgical options
the operating surgeon must be prepared for the high incidence of associated trauma. Patients imaged
may well have their injury underestimated, highlighting the importance of a full operative pancreatic
exposure.
Exposure is gained to the head and uncinate process via a full Kocherisation of the duodenum. The body
and tail of the pancreas is exposed by division of the gastrocolic ligament and superior retraction of the
stomach. Posterior exposure of the pancreas is gained by dividing retroperitoneal attachments and
reflection of the body superiorly. Features suspicious of pancreatic injury intraoperatively include lesser
sac fluid collection, retroperitoneal bile staining, crepitus/hematoma over the pancreas or fat necrosis/
saponification in the region. Features suggestive of a major duct injury include a transected pancreas,
large laceration or a large central perforation.

Morbidity and Mortality 12,14

Morbidity
Due to the often significant trauma burden these patients are prone to systemic post-operative
complications such as LRTI, DVT and renal dysfunction. Local observational studies reveal up to 75% of
patients having undergone resection will complicate in the post-operative period with up to 44% requiring
relaparotomy with the most common indication being intraabdominal sepsis.
Pancreas-specific complications were less common and include:
Pancreatic fistula – 15% incidence – usually close spontaneously, high output fistulae require
ERCP and stenting
Pancreatic necrosis – addressed with debridement – open or minimally invasive
Abscess – percutaneous drainage
6
 Pseudocyst – endoscopic drainage with cystgastrostomy/ open drainage
Pancreatic insuffiency – endocrine/ exocrine dysfunction

Small Bowel Trauma 16,17,18,19

Small bowel sustains mostly penetrating injury due to its central position. Injury due to blunt injury is
explained by 2 mechanisms: increased intraluminal pressure when a knuckle of small bowel is caught
between 2 hard surfaces (blunt object and vertebral body) and ischaemia secondary to mesenteric injury
due to rapid acceleration and deceleration of small bowel.
Presentation
Abdominal pain, sepsis/peritonitis if delayed presentation, ileus, bowel obstruction if internal hernia
through mesenteric defect.
Imaging
Chest X-Ray may show free air under diaphragm (uncommon); FAST will show free fluid in abdomen and
CT abdomen free intraabdominal air and/or only free fluid.
Management depends on presentation picture;
Blunt abdominal trauma
Observation with serial abdominal examination for stable patients non-peritonitic with CT abdomen non-
suggestive of free air and no other injury requiring laparotomy; Patient should be clinically assessable;
Otherwise laparotomy.
Penetrating injury
Selective conservative management (serial abdominal examination) for stable non-peritonitic patient with
tenderness limited at the stab area, GCS 15 and patient assessable. Laparotomy if unstable, diffusely
tender, peritonitic, bowel evisceration or free air under diaphragm on chest X-ray.
For gunshot abdomen, exploratory laparotomy is usually required unless it is suspected to be tangential
or single gunshot in right upper quadrant through liver, with patient stable, non-peritonitic and without
other indication for laparotomy. CT abdomen is required to confirm the trajectory of the bullet and
exclude other injuries.
At laparotomy, the management depend on AAST grading

Grade Description of injury Management

I Contusion or hematoma without devascularization Observe
Partial thickness laceration with no perforation Repair
II Laceration < 50% circumference Debridement + Repair
III Laceration > 50% circumference without transection Resection + anastomosis
IV Transection of small bowel Debridement + anastomosis
V Transection of small bowel + segmental tissue loss Debridement + anastomosis
Devascularized segment

Careful bowel inspection and look for contralateral injury; Sero-muscular repairs and anastomosis with an
absorbable suture. Consider exteriorization when there is high risk for anastomotic breakdown (shock,
inotrope requirement, delayed presentation, gross contamination), except for proximal injuries. No
difference in outcome and leak rate between handsewn and stapled anastomosis.

Colonic Trauma 20, 21

Often secondary to penetrating injuries; infrequent in blunt. The mechanism of injury is similar to small
bowel.
Anatomic relevance
The posterior wall of ascending and descending colon are extraperitoneal and injury will not lead to
peritonitis; Colon watershed areas include the splenic flexure (Griffith’s point) and the rectosigmoid
junction (Sudek’s point).
Presentation
Similar to small bowel; However, delayed retroperitoneal injury will present with necrotizing fasciitis.

7
Imaging
Free air under diaphragm tends to be more evident compared to small bowel injury. Triple contrast CT is
97% sensitive and 98% specific.
Management
Selective conservative management as for small bowel
At laparotomy, management depends on AAST grading (below)

Grade Description of injury Management

I Contusion or hematoma without devascularization Explore
Partial thickness laceration, no perforation Repair
II Laceration < 50% circumference Debridement + Repair
III Laceration > 50% circumference without transection Resection + Anastomosis

IV Transection of the colon Debridement + Anastomosis vs

Defunctioning
VI Transection of the colon with segmental tissue loss Debridement + Anastomosis vs
Devascularized segment Defunctioning

Contrary to old practice (exteriorization), there is a shift toward repair and anastomosis of colonic injuries.
Good debridement is necessary and no drain required.
In selective cases, diversion may be an option, considering risk factors such as severity of colon injury
(destructive), general condition of patient, delay to surgery, faecal contamination, hemodynamic stability
and massive transfusion

Rectal Trauma 21
Usually occurs after penetrating abdominopelvic trauma, particularly gunshot wound. In blunt trauma,
rectal injury is often associated with pelvic fracture.
Absence of blood on PR examination does not exclude injury; Rigid proctosigmoidoscopy should be done
for all patients with suspected rectal injury.
Management depends on the type of injury:
Intra-peritoneal rectal injury should be repaired, covering stoma only if high risk of
breakdown.
Extraperitoneal injury, often detected or suspected at sigmoidoscopy, are managed with
defunctioning loop sigmoid colostomy; injury is repaired only if exposed by trauma or during
exploration of another pelvic injury; Distal washout and pre-sacral drainage are no more
advocated due to increased morbidity
Combined intra and extra-peritoneal injuries are managed by repair of intraperitoneal injury
and extraperitoneal injury if exposed and covering stoma.

Role of Laparoscopy 23
There is a well-established role of laparoscopy in the diagnosis and repair of diaphragmatic injury in
penetrating thoraco-abdominal trauma on a stable patient.
It is also used for diagnosis of peritoneal breach in penetrating abdominal injury on a stable patient,
especially if patient cannot be clinically assessed.
Some centres use laparoscopy for diagnosis and management of intraabdominal visceral injuries on a
stable patient; However, this practice is not fully supported by all in the literature.
Contraindications include: unstable patient, traumatic brain injury, previous abdominal surgery, lack of
surgical expertise or unavailable equipment.

8
References

1. 10 year retrospective review: Does pyloric exclusion improves clinical outcome after penetrating
duodenal and combined pancreaticoduodenal injuries? J Trauma. 2007;62(4):829
2. Cruvinel Neto J, Pereira BM, Ribeiro MA Jr, Rizoli S, Fraga GP, Rezende-Neto JB. is there a role for
pyloric exclusion after severe duodenal trauma? Rev Col Bras Cir. 2014 May-Jun;41(3):228-31
3. Laura N. Gonser-Hafertepen, DO, James W Davis. Isolated Free Fluid on Abdominal Computed
Tomography in Blunt Trauma: Watch and Wait or Operate? J Am Coll Surg 2014, 219: 599-605.
4. Asensio, Juan A. Trunkey, Donald D. Current therapy series. Current therapy of trauma and surgical
critical care. Elsevier Saunders (2016)
5. www.up-to-date.com
6. www.emedecine.com
7. Kong VY, Clark DL. G Oostuizen G. Isolated free intra-abdominal fluid on CT in blunt trauma: The
continued diagnostic dilemma.
8. Weale RD, Kong VY, W. Bekker W, Bruce JL, Oosthuizen GV, Laing GL, Clarke DL. Primary repair of
duodenal injuries: A retrospective cohort study from a major trauma centre in South Africa.
Scandinavian Journal of Surgery (2019).
9. Ferrada PA et al. Management of Duodenal Trauma: A retrospective review from the Pan-American
Trauma Society. Journal of Acute Care Surgery (2018).
10. Talving P, Nicol AJ, Navsaria PH. Civilian Duodenal Gunshot Wounds: Surgical Management Made
Simple. World J Surg (2006) 30: 1–8.
11. Phillips B, Turco L, McDonald D, Mause A, Ryan W. Walters RW. Penetrating injuries to the
duodenum: An analysis of 879 patients from the National Trauma Data Bank, 2010 to 2014. J Trauma
Acute Care Surg.
12. Krige JEJ, U.K. Kotze UK, Nicol AJ, Navsaria PH. Morbidity and mortality after distal pancreatectomy
for trauma: A critical appraisal of 107 consecutive patients undergoing resection at a Level 1 Trauma
Centre. Injury (2014).
13. Chinner, GE,Krige JEJ, Kotze UK, Navsaria P and Nicol A. Surgical management and outcome of
civilian gunshot injuries to the pancreas. British Journal of Surgery. 1.140–148 (2012).
14. Iurcotta T, Addison P, Amodu LI, Fatakhova K, Akerman M, Galvin D and Rilo HLR. Patterns and
outcomes of traumatic pancreatic injuries: A retrospective review from a large multi-institutional
healthcare system. Trauma (2018). Vol. 20(1) 11–19.
15. Mattox KL, Moore EE, Feliciano DV. Trauma. 7th Edition. 2013
16. Coleman et al. Surgical Management of Abdominal Trauma. Surgical Clinics of North America. 2017,
Volume 97, Issue 5, Pages 1107-1117
17. Bekker et al. The spectrum and outcome of blunt trauma related enteric hollow visceral injury.
Annual of Royal College of Surgeons. England. 2018; 00:1-6
18. Chmielewski GW, et al. The American Surgeon. 1995, Aug;61 (8): 665 L8
19. Como JJ, et al. Practice management guidelines for selective non operative management of
penetrating abdominal trauma. Journal of Trauma. 2010
20. Yamamoto R., Logue A.J. Logue, Muir M.T. Colon Trauma: Evidence-Based Practices. Clinics in Colon
and Rectal Surgery 2018; 31:11-16
21. Choi WJ. Management of colorectal trauma. Journal of the Korean Society of Coloproctology
2011;27(4):166-173
22. Steenkamp CJ, Khan MZ, Mbambo T. Seminar on Pancreaticoduodenal and hollow viscus trauma,
May 2017
23. Coleman et al. Trauma laparoscopy from 1925-2017: Publication History and Study Demographics of
an Evolving Modality. Journal of Trauma and Acute Care Surgery. 2017

9
 INJURY TO ABDOMINAL SOLID ORGANS
MZ Khan, ML Kashasha, R Lukusa
Moderator: Mr VN Manchev 25th May 2019

Historically injury to abdominal solid organs injuries were managed by open operative intervention;
however there has been a paradigm shift in recent decades with a move towards conservative management
and organ preservation or salvage. This has been attributed to superior imaging modalities,
angioembolization and other minimally invasive tools.
Notwithstanding this, open operative surgery remains a powerful tool in the management of the critically
ill trauma patient 1,3,10.

Special investigations 1,2,5,6,7

Currently, ultrasound and Contrasted CT abdomen (CECT) are the most commonly used modalities in the
diagnosis of solid visceral in juries.
Diagnostic Peritoneal Lavage (DPL) is now limited to where there is diagnostic uncertainty in an
unstable patient, where other investigative tools are not readily available.

Focused Abdominal Sonography of Trauma (FAST) has largely been replaced DP. Readily available in
most emergency departments. Neither delineate specific injuries but assist in making a decision to
operate in an unstable patient.
The success of FAST follows its noninvasive nature and its availability over CT scan. In the emergency
setting, a FAST scan is often performed.
FAST is operator dependent: sensitivity and specificity range 63-100% and 95-100%, respectively.
The presence or absence of free fluid translates to the presence of blood, urine or bowel content;
unfortunately FAST is not specific enough to adequately grade injuries.
Other limitations include its limited reproducibility and its operator dependent nature.

CECT abdomen is currently considered the gold standard for both diagnosing and grading solid visceral
trauma, with sensitivity and specificity often stated in excess of 95%. CECT scan offers one major
advantage over other imaging tools in that it allows one to accurately quantify and grade injuries.
Currently the AAST grading scale is the most accepted and universally used scale.
Other advantages include the ability to identify and quantify associated injuries to hollow viscera or
other systems. This leads to better holistic management of the polytrauma patient.
It has to be emphasized that the role of a contrasted CT scan is strictly for haemodynamically stable
patient, as unstable patients belong in the operating theatre.
Other limitations and disadvantages include cost and access factors, radiation exposure, as well as
contrast related issues such as anaphylaxis and contrast induced nephropathy.

Grading of Injuries- See Appendix A for AAST Grading (Page 9)

1
Management principles
Solid organ injuries are often associated with high energy trauma. The initial evaluation and resuscitation
should be aligned with or guided by current ATLS principles. Hemodynamic stability remains the
determinant factor in management algorithms.
A non-responder belongs in the operating theatre.
Transient responders may require open surgical intervention or other minimally invasive tools such as
angioembolization.
For the haemodynamically stable patient, non-operative or selective conservatism has become the
standard, particularly for hepatic, splenic or renal injuries detected on CT scan with no other indication
for laparotomy. Angioembolization is emerging as an effective adjunct to non-operative management,
providing control of bleeding and reducing needs for surgery. ERCP may be useful for biliary
complications.

SPLENIC INJURY 1,3 ,10

The spleen is one of the most commonly injured intra-abdominal organs. It is a major lymphopoietic organ
and plays an important role in opsonization of encapsulated organisms (Haemophilus influenzae,
Streptococcus pneumonia, Neisseria meningitidis). Splenic injury is commonly secondary to blunt thoraco-
abdominal trauma, although penetrating and iatrogenic injury (from excessive traction during surgery) do
contribute to the spectrum.
Presentation
Following trauma, patients may present with left upper quadrant or left sided chest pain. Left shoulder pain
(Kehr’s sign), is secondary to phrenic nerve irritation from blood adjacent to the left hemidiaphragm.
Clinical examination may reveal a tender left upper quadrant, abdominal wall contusion or hematoma or
left chest wall tenderness. Haemodynamic stability is a critical component of examination and dictates
management.
Special investigations
1. FAST scan may show peri-splenic or free intra-abdominal fluid
2. Plain X-rays are not specific but may show ribs fractures, medial displacement of the gastric air bubble
(Balance sign), elevation of the left hemidiaphragm or a left pleural effusion.
3. CT scan is the modality of choice in a stable patient. It may demonstrate free fluid in the abdomen,
contrast extravasation or blush and other associated injuries. CT allows grading of splenic injuries (AAST
grading). Both arterial and venous phases are required; blush will be seen on arterial phase and
lacerations on venous phase.
Management approach
Management is dependent on haemodynamic state, grading of injury, the presence of associated injuries
and patient co-morbidities. Management options may be divided into operative or conservative. Unstable
patient with positive FAST or DPL requires an emergency laparotomy. Stable patients with low grade
injuries (AAST I to III) and no contrast extravasation or blush on CT can be observed. Patients with contrast
blush or extravasation can be embolized.

Non-operative Management
This is the standard of care for hemodynamically stable patients, provided they have no other injuries that
require a laparotomy. Its success relies on correct patient selection. Its advantages include preservation of
functional splenic tissue, avoidance of post splenectomy sepsis as well as complications due to surgery and
anesthesia. Conservative management must occur in a center where surgery can take place.
Observation requires close monitoring, preferably in a high care setting. The duration of observation
should be individualized based on the grade of injury, nature and severity of other injuries and patient
clinical status.

2
 60% of failures occur within first 24 hours with the majority occurring within 5 days. However, delayed
splenic rupture has been described at up to 2 weeks. Failure of observation occurs if the patient
becomes hemodynamically unstable, develops peritonitis or has a decreasing hemoglobin trend.
Splenic embolization is an effective adjunct to non-operative management and reduces the need for
surgery. It is indicated in stable patients with contrast extravasation on CT or a splenic pseudo-
aneurysm. Its complications include abscess formation, infarction, coil migration, pseudo-aneurysm at
arterial puncture site, allergic reaction to contrast or contrast induced nephropathy.
Although re-imaging is not routinely advocated, it may be considered at 48-72 hours in high risk
patients to detect a late vascular injury or pseudo-aneurysm.

Operative Management
Operative management includes splenic preservation surgery and splenectomy. Overwhelming post-
splenectomy infection (OPSI) has driven a prompt shift toward splenic preservation. Splenectomy is the
procedure of choice for an unstable patient. Ideally patients should receive a pneumococcal vaccine 2
weeks prior to or after surgery. However due to the nature of trauma and difficult follow ups, many
institutions immunize patients on discharge if they are well. Annual influenza vaccination is also
recommended.
Spleen preservation techniques include:
1. Partial splenectomy is based on segmental splenic arterial supply. It leaves behind a raw cut surface
that is at risk of recurrent bleeding, particularly in the coagulopathic patient. Hemostasis is achieved
with electrocautery and hemostatic agents prior to splenorrhaphy.
2. Mesh wrapping is performed with an absorbable (+/- hemostatic) mesh.
3. Splenorrhaphy is used to achieve hemostasis. Topical hemostatic agents, electrocautery or argon beam
coagulation can be used. Mass closure technique with absorbable sutures with or without pledgets is
used.

LIVER TRAUMA
The liver is the most commonly injured organ in blunt abdominal trauma. Given its large size in the
abdominal cavity, it can also be frequently injured with penetrating abdominal injuries. The liver’s anterior
location in the abdomen, its fragile parenchyma, and the relative ease in which Glisson’s capsule is violated,
makes it susceptible to injury from blunt forces. The right lobe of the liver is the most commonly injured
portion in both blunt and penetrating injuries. 2-4,7
Most hepatic injuries are minor and can be graded with the AAST Hepatic Injury Scale.
Most injuries are AAST Grades I to III and are successfully managed non-operatively or by means of
interventional radiological procedures such as angio-embolization.
AAST Grade IV and V injuries may necessitate massive resuscitation efforts, operative interventions, and
damage control laparotomy in approximately 60% of cases.
Management may be divided into three categories: conservative or selective non-operative management
(SNOM), angiography with embolization and surgical/operative.
Epidemiology 3,4,7
Liver injuries make up approximately 5% of all trauma admissions. Mortality increases with grade of injury,
and grade VI liver injuries are often fatal. Liver injury is the primary cause of death in severe abdominal
trauma and has a 10% to 15% mortality rate.
Assessment 3,4,8,10
Physical Examination
Trauma to the right thoraco-abdominal region may raise the suspicion of a possible hepatic injury.
Evaluation must be guided by ATLS principles.

3
 For patients with hepatic injury, the primary survey should identify the presence of hypovolemic
shock from liver bleeding. The secondary survey may reveal right upper quadrant tenderness, or
abdominal distention that may suggest hemoperitoneum.
These signs may be absent in blunt abdominal trauma with no obvious signs in up to 40% of patients
with significant haemoperitoneum.
Imaging modalities include FAST and CT scan as highlighted above.
CT still remains the gold standard in stable patients.
AAST grades injuries from 1-6, which then helps guide further management.

Selective Non-Operative Management (SNOM) 2,3,9,10

SNOM is the treatment of choice for blunt or penetrating injury, provided hemodynamic stability is
present. High success rates have been noted, especially in patients with grades I to III injuries.
SNOM is only appropriate at a facility capable of hemodynamic monitoring, serial abdominal
examinations, and an operating room that is immediately available for emergency laparotomy.
Patients with higher injury grade are more likely to fail non-operative management with hemodynamic
instability being the leading cause of failure in 75% of patients.

Blunt Trauma
Blunt liver trauma may be managed conservatively in up to 80% of cases. Angio-embolization may be used
to complement care in patients demonstrating a contrast blush on CT scan. The World Society of Emergency
Surgery (WSES) recommendations for SNOM in blunt trauma include:
Haemodynamic stability (irrespective of injury grade)
Absence of other intra-abdominal injuries requiring operative management (irrespective of injury
grade)
Absence of peritonitis
For AAST grades III-V, in an environment with intensive monitoring, angiography, immediate availability
of an operating theatre and of blood and blood products.
Contrast-enhanced CT scan to define liver injury grade and identify associated injuries

Penetrating Trauma
SNOM is commonly practiced for stab or low-velocity gunshot wounds to the right upper quadrant. It fails
in up to 33% of patients due to continued bleeding, abdominal compartment syndrome or a missed
gastrointestinal tract injury. The WSES recommendations for SNOM in penetrating trauma include:
Haemodynamic stability
Absence of peritonitis, free air, thickened bowel wall, impalement or evisceration
The availability of intensive monitoring, angiography, immediately available operating theatre, blood
and blood products
CT scan to evaluate the liver injury’s suitability for non-operative management
Serial physical exams and laboratory testing

Angiography and Embolization 2,3,9,11,12

Angiography with selective embolization is effective for patients undergoing non-operative therapy of
bleeding liver injuries, especially those with blunt hepatic injuries.
Success rates for angiography and embolization are as high as 83%; success rates highest in
haemodynamically stable patients with extravasation of contrast noted on CT scan.
Angio-embolization can be used in those who fail SNOM or even in patients who have been operated
upon yet still have ongoing hemorrhage or are re-bleeding.

4
Operative Management 2,3,11-12
Surgery is indicated in patients who are unstable, have peritonitis or who fail SNOM. Damage control
laparotomy principles should be followed in the unstable patient undergoing laparotomy. The liver may
need to be mobilized off the diaphragm and retroperitoneum to fully assess injuries. A list of operative
techniques for managing liver injuries is listed below.

Operative Techniques
Peri-hepatic Packing: aims to restore liver anatomy and provide direct manual compression. The first
pack is placed directly across the injury to stabilize the damaged tissue.
Final Packing: Dry, folded swabs with radio-opaque markers are used. Packs should be removed in 24
to 72 hours. Complications of packs include respiratory compromise from diaphragmatic compression
and impaired venous return from IVC compression.
The Pringle manouvre: This technique provides hepatic inflow control and is defined as temporary
compression of the hepatic pedicle across the hepatoduodenal ligament. The lesser omentum is
dissected, followed by placement of a non-crushing clamp over the pedicle. Alternatively a vascular
sling loop may be placed and tightened down until no pulse is felt. Care must be taken to protect the
common bile duct.
Hepatic Isolation: This entails hepatic vascular exclusion. It is achieved by performing a Pringle
manoeuvre, clamping the aorta at the diaphragm and the inferior vena cava above and below the liver.
This may be an extremely challenging feat in the trauma setting, with intrathoracic control of the IVC
being an alternative option. Isolation time should be limited to 30 minutes.
Finger Fracture: This is used to access deeper bleeding sites. The normal parenchyma is rubbed away
and the blood vessels are left intact for ligation or clipping. One must avoid being too aggressive as this
may aggravate bleeding
Hepatic Resection: This is associated with a high mortality rate and should not be performed in a
damage control setting.
Hepatic Suture: This is advocated for deep lacerations with a need to restore liver architecture and
control bleeding. Use a large, curved, blunt-nose needle with an absorbable suture.
Hepatic Tourniquet: For cases of ongoing bleeding from the left lobe, mobilize the lobe and apply a
Penrose drain at the division of the right and left lobes. The tube is stretched until the bleeding stops,
followed by application of a clamp. Definitive control is then achieved by resection using stapling
devices.
Stapling Devices: The best devices are crushing staples with vascular load
Balloon Tamponade: This is useful to obtain haemorrhage control along a gunshot or stab tract.
Perihepatic Drainage: Drains should not be placed during damage control surgery. Non-suction or open
drain systems carry a higher infection risk than closed suctions drains.

Complications 2,3,6,11-12
Complications following liver trauma include bile leak, hepatic abscess, hepatic necrosis and hepato-biliary
fistulae.

RENAL TRAUMA 1, 2,9-12

The kidney is the most commonly affected organ in urogenital trauma, making up 43% of injuries.
Renal Trauma may involve the parenchyma, renal pedicle and vessels or the collecting system.
Bleeding may be contained within Gerota’s fascia and present as a haematoma, or may drain into the
collecting system and present as a haematuria.
Collecting system injuries may present with haematuria, urinoma or contrast extravasation on delayed
CT films.

5
 Renal injuries are often successfully managed conservatively. This is due to the nature of Gerota’s fascia
that has a tamponading effect, the improvement in imaging modalities and the evolution of minimally
invasive procedures and angioembolization.

While blunt renal trauma has often been cited as the most common cause (80%), this is dependent of
incidence patterns, regional factors and age.
In paediatric populations, injuries from falls and pedestrian vehicle accidents are often leading causes.
Renal injury is often associated with other organ injuries in 80-95% of cases. Penetrating trauma is
associated with significant injury and higher rates of operative management.

Presentation
Clinically patients may present with flank pain or haematuria following injury. Physical examination
may include ecchymosis, flank tenderness or lower rib fractures.
While haematuria remains the hallmark sign of renal injury, its degree nor its duration correlates with
severity of injury. Furthermore its absence does not exclude an injury, particularly in the setting of
penetrating trauma where between 9 and 12% are noted in patients having significant injuries with
normal urinalysis.

Imaging
1. Contrast enhanced CT: Is the gold standard. For renal injuries, multiple phases should be obtained,
including delayed films at 7-10 minutes. While arterial and venous phases help detect vascular and
parenchymal injury, the delayed phase provides information on the collecting system and ureters and
may point towards contained or free leaks.
2. Catheter Directed Angiogram: While this tool is superior to CT in terms of sensitivity, it is still an
invasive procedure. Its current use is as an adjunct in angioembolization or for cases where CT imaging
is inadequate to define injuries.
3. Ultrasound: This may be used in follow-up to assess for resolution of haematoma or urinoma.
4. Intra Venous Pyelogram: This may be used in the acute setting to evaluate injuries, although this has
largely been replaced by CT scan. Its current use in practice lies in single shot on table pyelogram, to
assess functionality of a contralateral kidney prior to emergency nephrectomy.

Conservative Management
Currently, conservative management is advocated for most Grade I-III injuries, with some role in Grade
IV-V injuries.
Principles include bedrest, monitoring of vitals, serial abdominal examinations, serial haemoglobin
levels, analgesia, bladder irrigation to prevent clot build-up and obstruction.
Grade I-II injuries are widely managed conservatively.
Grade III injuries are quoted to have nephrectomy rates of 3-9%, with angioembolization being
cited as a useful adjunct to reduce this figure.
Grade IV-V injuries may undergo a trial of conservative management, provided haemodynamic
stability.
Angioembolization has been shown to reduce nephrectomy rates in this group from 89% to 52%.
Additional tools involve ureteric stenting as indicated.

Operative Management
Surgery is reserved for patients who do not respond to resuscitation, failed conservative management,
Grade V renovascular injuries or uncontained collecting system leaks.

6
 Principles of operative intervention include control of haemorrhage, repair of the kidney with
functional conservation and the establishment of peri-renal drainage.
Exploration of renal haematoms at laparotomy should only occur if expansile, pulsatile or if critically ill.
Vascular control may be obtained either centrally at the origin of the renal vessels or by posterolateral
access from medial visceral rotation.
It is important to consider the anatomical differences between the right and left kidney as these will
affect surgical exploration as well as patterns of trauma. At the level of the renal pedicles there are
most commonly single arteries and veins present. On the right, the gonadal, adrenal and lumbar veins
drain directly into the IVC. On the left side, branches of the renal vein include the left gonadal, adrenal,
and one or more lumbar veins. Thus the left renal vein may be ligated close to the IVC with successful
left renal salvage.

Operative techniques
1. Nephrectomy. Access is often via a standard trauma laparotomy with control of renal vasculature being
the first priority.
2. Partial nephrectomy. This is useful for damage localized to the renal poles. Non-viable tissue is
debrided with vessels ligated and collecting system closed with a continuous absorbable suture. The
capsule is then closed primarily or with the help of an omental patch. The placement of a drain is
advised.
3. Renorrhaphy. This is indicated in injuries to the middle of the kidney. Following debridement and
haemostasis, water tight repair of collecting system is done then parenchymal edges are opposed with
capsular closure. A drain is then left.
4. Vascular repair. This can be attempted for small isolated injuries to vessels, however outcomes are
variable. This should only be attempted in the absence of a contralateral kidney or a non-functioning
contralateral kidney.

Complications
Complications after renal trauma include delayed onset bleeding, pseudoaneurysm, renal abscess
formation, urinoma and hydronephrosis.
Renal vascular hypertension following renal trauma is uncommon (5%) and is almost always transient. It is
more common with higher grades of injuries and occurs from renal artery injury or direct compression of
the kidney itself. Blood pressure is medically managed initially with delayed nephrectomy indicated in
severely resistant cases.

Appendix A- AAST Grading of Solid Organ Injuries

Splenic Injury
Grade Injury Description
I Haematoma: Subcapsular <10%
Laceration: Capsular tear <1cm depth
II Haematoma: Subcapsular 10-50%, intraparenchymal <5cm
Laceration: Capsular tear, intraparenchymal 1-3cm without trabecular vessel involvement
III Haematoma: Subcapsular >50%, expanding or ruptured, intraparenchymal >5cm
Laceration: >3cm parenchymal depth or trabecular vessels
IV Laceration: Segmental or hilar vessels, devascularization of >25%
V Shattered spleen
Hilar injury with devascularization

7
Liver Injury
Grade Injury Description
I Haematoma: Subcapsular < 10% surface
Laceration: Capsular tear <1cm parenchymal depth
II Haematoma: Subcapsular 10-50% surface or intraparenchymal <10cm
Laceration: 1-3cm parenchymal depth, <10cm in length
III Haematoma: Subcapsular >50% surface or expanding, ruptured or intraparenchymal >10cm
Laceration >3cm parenchymal depth
IV Laceration: 25-75% Parenchymal disruption
V Vascular: Juxtavenous hepatic injury- Retrohepatic IVC, major hepatic veins
VI Hepatic avulsion

Renal Injury (see below)

Grade Injury Description
I Contusion: Microscopic or gross haematuria, normal urologic studies
Haematoma: Subcapsular, non-expanding
II Haematoma: Non-expanding peri-renal haematoma confined to renal retroperitoneum
Laceration: <1cm into renal cortex without urinary extravasation
III Laceration: >1cm into renal cortex without rupture of collecting system or urinary extravasation.
Laceration: extending beyond cortex into medulla and collecting system.
IV Vascular: Main renal artery or vein injury with contained haemorrhage
V Shattered kidney
Avulsion of renal hilum with Devascularized kidney

8
References
1. Clarke DL et al. Selective Conservatism in Trauma Management: A South African Contribution.
World J Surg, 29, 962-965 (2005)
2. Boffard KD et al. Manual of Definitive Surgical Trauma Care. 4th Edition; 2016.
3. Cimbanassi et al. Nonoperative management of abdominal solid organ injuries following blunt
trauma in adults: results from an international consensus conference. Journal of Trauma and
Acute Care Surgery.2017
4. Ahmed N, Vernick JJ. Management of Liver Trauma in Adults. J. Emerg. Trauma Shock, 2011 Jan-
Mar, 4(1): 114-119
5. Bala M et al. Complications of High Grade Liver Injuries: Management and Outcome with Focus on
Bile Leaks. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine. 2012, 20:2
6. Coccolini F et al. Liver Trauma: WSES Position Paper. World Journal of Emergency Surgery (2015)
10:39
7. Coccolini F et al. WSES Classification and Guidelines for Liver Trauma. World Journal of Emergency
Surgery (2016) 11:50
8. Christmas AB et al. Management of Hepatic Trauma in Adults. UTD March 2018
9. Yu W et al. Treatment Strategy for Hepatic Trauma. Chinese Journal of Traumatology 19(2016) 168-
171
10. Tomer Erlich T, Kitrey ND. Renal trauma: the current best practice. Ther Adv Urol 2018, Vol.10(10)
295-303
11. Steve P. McCombie. The conservative management of renal trauma: a literature review and
practical guideline from Australia and New Zealand. 2014. BJU International/
doi:10.1111/bju.12902
12. Wain HR, Gurunand A, Ngcobo QN. Seminar on Injuries to abdominal solid organs, 2017.

9
 DAMAGE CONTROL SURGERY AND ABDOMINAL COMPARTMENT SYNDROME
Dr A Jooma, Dr P Pillay, Dr H Wain
Moderator: Mr J Bruce 1 June 2019

Damage Control Surgery

Introduction1,2
Historically, surgical practice has prioritized the restoration of anatomy over the physiological condition of
the patient. Literature of the past 40 years has caused a paradigm shift towards staged operations with the
initial operation focusing on preserving life (i.e. physiology) rather than anatomical continuity.

Damage Control Surgery (DCS) emerged as a concept in the 1970’s after clinical observations in patients with
major hepatic trauma. The original description of the ‘staged laparotomy’ was first described by Stone et al
in 1983, the principles being the establishment of intra-abdominal pack tamponade and definitive procedure
once “coagulation returned to an acceptable level.” A large body of evidence in the 1990’s showed improved
outcomes in patients receiving staged operations after major abdominal trauma; with further recognition of
the contributing factors (ie. hypothermia acidosis and coagulopathy) and hence DCS is now a standard in
trauma care.

The Role of Damage Control3, 4

The goal of the Damage Control approach is to minimize mortality & morbidity. Uncontrolled haemorrhage
and prolonged iatrogenic interventions leads to a
Decrease in core body temperature (Hypothermia)
Depletion of clotting factors (Coagulopathy)
Metabolic derangements leading to acidosis

This is known as the “triad of death.” Ferrara et al. reported a 90% mortality in polytrauma patients with
hypothermia, acidosis, and coagulopathy; these patients often required massive transfusion. The
development of these can be countered by active warming, replacement of clotting factors and adequate
and appropriate fluid resuscitation.
The “Damage Control” approach encourages recognition of this potentially fatal triad by advocating the
following operative principles:
Rapid, definitive haemorrhage control
Control of contamination by either closure or performing essential resections
Delay of complex, time consuming repairs or reconstructions to a time when the patient has been
stabilized and physiologic derangements have been corrected
The purpose of these principles is to prevent/limit morbidity.

Damage Control Resuscitation5

With the implementation of DCS, severely injured patients were able to survive the initial operation.
However, a different set of problems were encountered. The combination of shock, large volume
resuscitation, intestinal oedema and tightly packed, closed abdomen led to abdominal compartment
syndrome (ACS).

Damage Control Resuscitation (DCR) differs from other approaches in that it advocates early, aggressive
correction of coagulopathy as well as metabolic derangements. This is achieved by permissive hypotension

1
(in selective cases), the restriction of isotonic fluid for plasma volume expansion and the early, rapid
administration of blood products to replace what is lost. This strategy begins in the emergency room and
continues through the operating room and into ICU. The DCR consists of 4 phases
- DC0: emphasizes injury pattern recognition for potential damage control. Key elements include
RSI, early rewarming & expedient transport to OT.
- DC I: Operative phase. Key elements include rapid control of bleeding & contamination, Abdominal
packing and temporary closure.
- DC II: Resuscitation in ICU & biochemical stabilization.
- DCIII: occurs once physiology has normalized. Consists of re-exploration and definitive repair of all
injuries (this may require multiple visits to the OT if multiple organ systems are affected).

The “Triad of Death”3

Hypothermia
Loss of heat begins with injury and is exacerbated by factors such as hypovolaemia, poor perfusion,
prolonged exposure to the elements, and immobility. Heat loss is not commonly addressed at the place of
injury and hence continues into the emergency department where the patient is completely exposed to allow
for proper assessment. Clinically significant hypothermia is present when core temperature drops below
35°C and mortality approached 100% with a core temperature of less than 32°C.
Acidosis
Acidosis in trauma patients is attributed to lactic acid production secondary to anaerobic metabolism. It
worsens coagulopathy, causes myocardial depression and causes diminished response to inotropic agents.
Elements of the DCR aim to counteract this by prescribing early initiation of transfusion therapy and limiting
the amount of isotonic IV fluids.
Coagulopathy
The development of coagulopathy in the setting of trauma is multi-factorial. All resuscitation fluids usually
administered to acutely injured patients are devoid of clotting factors. As a result, dilution of clotting factors
and platelets occurs, which compounds the significant consumption of these factors that results from the
initial trauma. Other contributing factors include hypothermia, acidosis and a deficiency in ionized calcium.

Hypothermia has been directly linked to platelet dysfunction by decreasing thromboxane A2 production,
promotes platelet margination by increasing haematocrit, increases the expression of adhesion molecules
and is associated with increased fibrinolytic activity (stimulates intrinsic catecholamine release).

Thromboelastography (TEG) is a simple, point of care test that can guide resuscitative efforts. It provides
information on the duration of clot formation, clot strength, fibrin activity and clot lysis. This allows the
clinician to decide on further component therapy administration.

Indications for Damage Control Surgery3,5

Many authors have attempted to suggest guidelines for establishing which patients would benefit from a
“Damage Control” approach. One has to appreciate that the physiology of the patient is dynamic and a
decision needs to be made based on the objective parameters such as hemodynamic status, temperature,
blood loss, metabolic status, number of units transfused, injury patterns and coagulation parameters.

2
Absolute Indications:
Hypothermia < 34°C
Severe Metabolic Acidosis
pH <7,2
Lactate > 5 mmol/l
Coagulopathy
Massive transfusion
Secondary Factors
Severe Injury
Operating time > 90 min

Damage Control Techniques6-11

General considerations
Planning and preparation are key elements for a trauma laparotomy. It is vital to establish good
communication with the nursing and anaesthetic teams. Warmed fluids, blood and cell saving equipment
should be prepared. Abdominal swabs, appropriate surgical sets and instruments are a must.
Entry
Rapid entry via midline incision is advised. Wide exposure from the xiphisternum to the pubic symphysis is
necessary. Small bowel is eviscerated and all 4 quadrants are packed with swabs. The packs are then
sequentially removed starting with the least likely source of bleeding. Vascular injuries are addressed as a
priority, then control of contamination is achieved. Temporary abdominal closure is then performed and the
entire operation should be performed in less than 45 minutes. The patient should be transferred to ICU. The
definitive procedure is then planned once the patients physiology has improved.

Damage control of Specific Organs

This has been covered in previous seminars and readers are directed to them for further reference.

Abdominal Compartment Syndrome

Definitions12
Intra abdominal pressure (IAP) refers to the steady state pressure that is concealed within the
abdominal cavity.
Abdominal perfusion pressure (APP) is calculated by subtracting the IAP from the mean arterial
pressure (MAP).
In critically ill adult patients, IAP is approximately 5-7mm Hg.
Intra-abdominal hypertension (IAH) is defined as a sustained or repeated pathological elevation in
IAP more or equal to 12mm Hg.
Abdominal Compartment Syndrome (ACS) is defined as a sustained IAP>20mm Hg, with or without
an APP<60, that is associated with new organ dysfunction.
Measurement12
The reference standard for measuring IAP is via the bladder. Alternatively, the IAP can be measured
via the stomach. This is useful in cases of pelvic packing and bladder injury.
25ml of sterile saline is instilled into the catheter.
The patient needs to be fully relaxed.
Measure at the end of expiration in the supine position.
The transducer is zeroed along the mid-axillary line at the level of the anterior superior iliac spine.
Measurements are expressed in mm Hg.

3
Grading of IAH12
Grade I- IAP 12-15mm Hg
Grade II- IAP 16-20mm Hg
Grade III- IAP 21-25mm Hg
Grade IV- IAP >25mm Hg

Types of IAH/ACS12
Primary IAH/ACS:
Condition that is associated with disease or injury in the abdominopelvic region that frequently requires
early surgical or interventional radiology intervention.
Secondary IAH/ACS:
Condition that does not arise primarily from the abdominopelvic region.
Recurrent IAH/ACS:
ACS/IAH that redevelops following previous surgical or medical treatment of primary or secondary ACS.

Risk factors12
Risk factors can be divided into five main categories:
Diminished abdominal wall compliance:
Abdominal surgery, major trauma, major burns, prone positioning
Increased intra luminal contents:
Gastroparesis, ileus, colonic pseudo-obstruction, volvulus
Increased intra-abdominal contents:
Acute pancreatitis, haemo-/pneumoperitonuem, intra-abdominal fluid collections, intra-
abdominal tumours, laparoscopy with high insufflation pressures, ascites
Capillary leak/fluid resuscitation:
Acidosis, damage control laparotomy, hypothermia, massive fluid resuscitation
Miscellaneous:
Age, bacteraemia, coagulopathy, massive incisional hernia repair, mechanical ventilation with
high PEEP, obesity
Three groups of patients are at risk of ACS; the post-operative trauma patient who was near exsanguination,
the septic medical patient who required large volumes of fluid, and the general surgery patient who required
large volume resuscitation for intra-abdominal catastrophe regardless of ethology.3

Pathophysiology12-14
Intra-abdominal pressure is affected by abdominal volume and abdominal wall compliance. Small changes
are usually well tolerated but as IAH worsens, it leads to organ dysfunction. This occurs by compromising
arterial inflow, obstructing venous outflow and an impaired microcirculation.

Effect on organ systems

CVS: Increased intra thoracic pressure (ITP) leads to reduction in preload through compression of the
inferior vena cava. Cardiac contractility is reduced through right ventricular compression against raised
pulmonary pressures. This leads to reduced cardiac output.
Renal: Renal artery blood flow is reduced due to reduced cardiac output. Renal vein pressure and renal
vascular resistance increases. Blood is shunted away from the glomeruli, leading to reduced GFR and
oliguria.

4
 GIT: There is reduction in mesenteric blood flow and compression of mesenteric veins leading to
intestinal oedema. This leads to bacterial translocation. Intestinal perforation may also occur.
Brain: Increased IAP leads to increased ICP via global vasoconstriction. This causes a reduction in CPP.
Lung: Increased ITP causes compression of the lung parenchyma which in turn leads to alveolar
atelectasis. There is reduced lung compliance and high pressures are required for ventilation.

Management of ACS/IAH12,13
Operating surgeons need to consider IAH/ACS when operating on at risk patients. Patients at risk should have
4 hourly IAP monitoring in an intensive care setting. Early recognition is important to allow medical
intervention to prevent the development of ACS. Trauma patients should receive damage control
resuscitation which includes permissive hypotension, limited use of crystalloid and higher use of colloid and
blood products. These patients should also have a temporary abdominal closure. Non-trauma cases with
devastating intra-abdominal pathology should not routinely have a temporary abdominal closure. Other
preventative strategies follow similar principles to the medical management of IAH listed below.

Medical management follows three principles

1. Evacuate intraluminal and extraluminal contents
Insert NG and flatus tubes
Drain intra-abdominal collections percutaneously
2. Improve abdominal wall compliance
Use of muscle relaxants- temporary measure. Consider long term issues of critical illness weakness
Adequate analgesia and sedation
3. Optimise fluids
Consider haemodialysis (if indicated)
Maintain an overall negative fluid balance- use of diuretics, also reduces bowel oedema
Avoid crystalloid resuscitation
Consider use of fluids combined with inotropic support to maintain MAPs

If medical management fails; or if ACS is present, patients require a decompressive laparotomy which may
occur in ICU as an emergency procedure or in theatre. The sheath needs to be released followed by a method
of temporary abdominal closure.

Damage Control Surgery in Non-Trauma Patients 22

Damage control surgery has been widely accepted as part of the management of a severely traumatised
patient. In most centers the same surgeon operates on both traumatic and non-traumatic abdominal
emergencies, and thus the damage control concept has crept into general surgical practice. Whilst the ‘lethal
triad’ guides the decision for damage control surgery in trauma, the physiological derangements in
emergency general surgery are often less acute, and are usually not able to be corrected within as short a
time frame; this brings into question the utility of trauma damage control indications in the general surgery.
Severe intra-abdominal sepsis with septic shock, mesenteric ischaemia, and severe pancreatitis are the most
common indications given in literature for abbreviated surgery in non-trauma patients. Acidosis (pH <7.25),
lactate >3, age >70, male gender, and multiple co-morbidities (>3) have been shown to be predictors of
mortality from general surgery emergencies, and some authors postulate these as reasonable indications for
abbreviated laparotomy in non-injured patients.

5
Randomised prospective trials on the topic are lacking, meaning that the best available evidence comes from
meta-analyses of retrospective reviews of small cohorts. The available data suggest survival advantage in
patients with septic shock who undergo damage control surgery vs matched patients undergoing definitive
surgery. Additionally, several studies have demonstrated better than expected survival based on
physiological scoring (APACHE II) in patients who have undergone damage control laparotomies. The
heterogeneity between compared population groups limits the utility of reported findings, which makes
interpreting such data challenging. There appears to be a role for damage control surgery in non-traumatic
abdominal emergencies, in particular those that present with septic shock; however more research is
required to define the exact criteria and benefits of such an approach.

The Open Abdomen

The primary aim in any abdominal surgery is definitive management of pathology, followed by primary
sheath closure. This is not always possible or safe, and the advent and widespread acceptance of damage
control surgery has presented surgeons with another challenge; that of the open abdomen. This is reflected
in the development of a grading system for open abdomens (Biforck et al, 2009)20. Most authors on damage
control surgery advocate delaying fascial closure until after definitive management of intra-abdominal
injuries has been achieved. Abbreviated / damage control surgery in general surgical abdominal emergencies
has also resulted in a large number of open abdomens.

Complications of the Open Abdomen

Fistula 18, 20, 21
A problem unique to the open abdomen is the entero-atmospheric fistula. The lack of a fistula tract and of
‘quality’ overlying tissue virtually precludes spontaneous fistula closure. This is exacerbated by continuous
efflux of enteric content, systemic catabolic state, local and systemic sepsis, fluid and electrolyte challenges,
nutritional (especially protein) deficiencies, complications of nutrition delivery, and prolonged hospital
admissions to produce a condition with high mortality.
Risk factors for the development of fistulae in DCS are not fully understood; however large bowel resection,
large volume crystalloid resuscitation, and increasing number of re-explorations are all independent risk
factors for the development of fistulae, whilst some data suggests that abdominal sepsis increases risk. Type
of anastomosis (stapled vs handsewn or anatomic configuration) has not been shown to impact fistulation.
Early closure protects against fistula formation.

Bowel Obstruction
Bowel obstruction following damage control surgery and an open abdomen is usually “adhesive”. Early
obstruction is likely mechanical and should prompt consideration for re-exploration. Late obstruction (>7-10
days) is more challenging, and due to the risks of adhesiolysis in a frozen abdomen (bleeding, enterotomies,
fistulae, prolonged surgery) this is often managed conservatively with nasogastric decompression and
parenteral nutrition.

Ventral Hernia17,18
The inevitable consequence of non-closure of the abdominal aponeurosis is a ventral hernia. An increasing
delay to attempted closure increases the risk of ventral hernia. Once the sheath is deemed to not be
“closeable” it may be allowed to granulate and epithelialize, or be covered with a split thickness skin graft
(SSG). No robust data exists regarding the optimal method to achieve epithelial continuity across a ventral
hernia. SSG may allow earlier return to pre-morbid function in settings where a wound dressing would be
inhibitory (eg scholar), but granulation with epithelialisation from the wound edge may result in a smaller

6
ventral hernial defect. Regardless of the method employed, both result in a significant future challenge,
which is likely to entail prolonged and technically challenging surgery to achieve sheath closure.

Temporary Abdominal Closure15-21

Temporary abdominal closure (TAC) is one of several terms used to describe the method of abdominal
containment employed between the primary laparotomy and relook laparotomy or laparotomies until fascial
closure is achieved. Several methods of TAC have been described in literature, and there is frequently more
than one method employed in one patient;
Negative Pressure Wound Therapy (NPWT) or vacuum assisted closure (VAC)
Bogota Bag
Skin Closure only
Opsite sandwich
Temporary mesh closure
Fascial tension methods (eg Wittman patch, VAMMFT)

Negative Pressure Wound Therapy (NPWT) involves a negative pressure dressing placed onto the skin
overlying an abdomen in which some sort of visceral protective layer has been inserted. It is attractive in that
it does not injure skin or sheath with suturing, and deals with abdominal effluent by means of the negative
pressure. This removed effluent contains inflammatory mediators. The major drawback of NPWT is the
propensity for evisceration of abdominal content with increases in intra-abdominal pressure or loss of
suction. This has limited its use locally.

A ‘Bogota Bag’ is a clear plastic bag (commonly fashioned from a Vacoliter bag) that is secured to the skin
edges by means of continuous non-absorbable monofilament. It is cheap, easy to apply, and prevents
evisceration even with coughing/mobilizing; this makes it an attractive option in our environment and is
currently the first line TAC method utilized locally. The major negative of the Bogota bag it that is does not
prevent retraction of the abdominal aponeurosis and thus increases the risk of failure of sheath closure.

Skin closure (with sheath left open) is not commonly employed and results in a ventral hernia; however is a
viable option, especially where there is loss of sheath owing to injury or sepsis/necrosis. It is relatively
protective against fistula formation (compared to a granulated ventral hernia), and may facilitate earlier
oncological therapy in selected patients.

Fascial Traction Methods have seen rising popularity in the literature of the past two decades. Wittman first
described a Velcro-like closure device sutured to each sheath edge, which allowed for easy re-opening and
easy tightening, and produced a proprietary device first commercially available in 1992 in Europe. He showed
increased delayed primary closure rates than previously used methods and reported decreased mortality
than expected based on APACHE-II scores. Since then several combinations of methods have been described,
perhaps the most successful of which is VAMMFT.
Vacuum Assisted Mesh Mediated Fascial Traction (VAMMFT) uses a commercially available wound closure
system in conjunction with a non-absorbable mesh. A perforated polyprolpylene sheet is placed over the
abdominal viscera and into the paracolic gutters to ensure easy separation of the viscera and abdominal wall
at future closure. The mesh is sutured to the sheath by continuous, large non-absorbable monofilament
sutures, and then run through with non-absorbable sutures in a shoe-lace fashion to allow future tightening.
The entire wound is then covered with a topical VAC dressing. At 48 hour intervals the mesh is tightened,

7
and a new VAC applied. This is done in the ward/ICU with analgesia, thus avoiding the frequent returns to
theatre described in literature for other methods. Once deemed feasible, the patient is taken to the OT for
Delayed Primary Fascial Closure, with/without a lateral release to achieve tension free closure. VAMMFT has
demonstrated up to 80% delayed primary closure rates in literature, with relatively low morbidity and
mortality. A such, it is currently the TAC method of choice for those patients in whom sheath closure is not
attainable at the first relook laparotomy

References
1. HH Stone, PR Strom, RJ Mullins Management of the major coagulopathy with onset during laparotomy.
Ann Surg, 197 (1983),
2. Shapiro, M.B. et al. Damage Control: Collective Review Journal of Trauma. 2000. 49
3. Lee, J.C, et al. Damage control laparotomy. Current Opinion in Critical Care. 2006. 347–350.
4. Hirshberg A, Mattox K, TOP KNIFE: The Art & Craft of Trauma Surgery
5. Carlos A.O. et al. A comprehensive five-step surgical management approach to penetrating liver injuries
that require complex repair. J Trauma Acute Care Surg. 75(2
6. Diederik V. et al. Acute Management of Hemodynamically Unstable Pelvic Trauma Patients: Time for a
Change? Multicenter Review of Recent Practice. World J Surg. 2008. 32: 1874–1882.
7. Peep T. et al. Civilian Duodenal Gunshot Wounds: Surgical Management Made Simpler. World J Surg.
2006. 30
8. Badger A.S. et al. Management of Liver Trauma. World J Surg. 2009. 33:
9. Manchev V. Damage control and Abdominal Compartment Syndrome. Surgical Seminar. June 2015.
10. Sharrock AE et al. Management and closure of the open abdomen after damage control laparotomy for
trauma. A systematic review and meta-analysis. Injury (2016) 296-306
11. Bleszynski MS et al. Open abdomen with negative pressure device vs primary abdominal closure for the
management of surgical abdominal sepsis; a retrospective review. American Journal of Surgery (2016)
211; 926-932
12. Weinberg JA et al. Closing the open Abdomen: Improved success with Wittmann patch staged abdominal
closure. Journal of Trauma (2008) 2:65:345-348
13. Smith BP, Adams RC et al. Review of Abdominal Damage Control and Open Abdomens; Focus on
Gastrointestinal Complications. J Gastrointestin Liver Dis (2010) 19:4:425-435
14. Steenkamp CJ et al. A selective vacuum assisted mesh mediated fascila traction approach following
temporary abdominal containment for trauma laparotomy is effective in achieving closure. S Afr J Surg
(2018) 56:4:28-32
15. Bruhin A et al. Systematic review and evidence based recommendations for the use of Negative Pressure
Wound Therapy in the open abdomen. Int J Surgery (2014) 12: 1105-1114
16. Bradley MJ et al. Independent Predictors of Enteric Fistula and Abdominal Sepsis after Damage Control
Laparotomy. JAMA Surg (2013) 148:10:947-954
17. Person B et al. Abbreviated emergency laparotomy in the non-trauma setting. World J Emerg Surgery
(2009) 4:41
18. Stawicki et al. The concept of damage control; extending the paradigm to emergency general surgery.
Injury (2008)39:93-101

8
 THORACIC AND VASCULAR TRAUMA
Drs IN Waliaula, M Alkilani, C Anauth
Moderator: Ms T Mbebe 29th June 2019

Introduction

Despite major advancements in emergent care, diagnostic imaging modalities and standardized protocols of vascular
trauma, uncontrolled hemorrhage remains the leading cause of mortality in the critically ill patient. Timely
identification of life or limb threatening vascular trauma is crucial to survival and functionality. This seminar aims to
highlight the principles and practice of vascular trauma1.

BASIC PRINCIPLES & PRACTICAL APPROACH TO A PATIENT WITH VASCULAR TRAUMA

Evaluation of a patient with suspected vascular injury2
The following aspects should be elicited when evaluating a patient with suspected vascular trauma:
1. High-risk mechanism of injury
Significant blunt-force loading and anatomic extent across major vessels.
Penetrating path in proximity to major vessels.
2. Blood loss at the scene
3. Bleeding indicators
Prehospital hypotension and trauma in proximity to a major vessel
Unexplained shock, with non-bleeding extremity or neck lacerations
4. Physical Examination
Pulsatile hemorrhage, copious venous oozing, or a large hematoma.
Absent extremity pulses and doppler signals.
Bruit or thrill over injury site.
Major peripheral nerve deficit in proximity to a major vessel.
5. High-risk fractures or joint dislocations
Cervical spine fracture—vertebral artery injury.
Thoracic spine fracture—thoracic aortic injury.
Supracondylar humerus fracture—brachial artery injury [common in the pediatric population].
Knee dislocation—popliteal artery injury.
Tibial plateau fracture—below-knee popliteal artery injury and/or lower limb compartment syndrome.

Table 1 Hard and soft signs of a vascular injury.

Principles of management1,2
1. Hemorrhage control
a. Direct pressure.
b. Temporary Tourniquet.
c. Hemostatic dressings/ Foleys catheter-preferred option.
2. Damage control resuscitation under extreme circumstances following poor patient physiology
3. Evaluation and diagnostic investigations
a. Isolated penetrating trauma that have hard signs do not need any vascular imaging studies.
b. Patients with soft signs, imaging studies deemed appropriate
4. Strategies to minimize ischemic time e.g. utilizing temporizing shunts.

Principles of surgical management1

Adequate exposure to allow proximal and distal control of injured vessels. In some circumstances minimally
invasive balloon tamponade may assist by inducing an interim mechanical tamponade.
Systemic heparinization.
Evaluate antegrade and retrograde flow by assessing arterial back bleeding and passing a Fogarty catheter
to extract intraluminal debris followed by focal heparin saline flush of the arterial segments.
Tension-free repair (10 anastomosis, venous patch, interposition graft (autogenous versus prosthetic graft).
Ensure adequate soft tissue coverage.
Other associated injuries are addressed once vascular continuity is established.

Table 2 illustrates the natural history and sequelae of different vascular injuries.

1
 COMMON VASCULAR INJURIES
Cervical vascular trauma3, 4
Accounts for 7% injury in the neck after penetrating trauma with a reported stroke rate of 27% and mortality rate of
7% to 50%.
Figure 1 & Table 3 demonstrate the anatomical zones of the neck and prescribed imaging modalities.
Carotid artery
Penetrating carotid trauma accounts for 90% of carotid injuries whilst blunt trauma accounts for <1% of injuries.
Clinical evaluation involves establishing clinical signs of a vascular injury, neurological deficits & associated aero-
digestive tract injuries which occur in 1- 7% of patients.
Please refer to the seminar on Thoracic & Vascular Trauma 3rd June 2017.

Carotid Injuries with a focal neurological deficit3

Management of patients with established neurology remains controversial. [arterial repair versus ligation].
Pre-hospital delays and accurate assessment of the patient’s neurological status (confounded by prevailing
hypotension, hypoxia, alcohol inebriation and or traumatic brain injury) presents a therapeutic dilemma. Current
literature advocates surgical repair of the carotid artery under certain circumstances. Surgical repair of the carotid
artery is based on the concept of restorating cerebral blood flow to the “ischemic penumbra”,thereby potentially
decreasing the area of ischemic infarction.
Indications for ligation:
Established infarct on imaging.
Severe cerebral oedema.
Coma for 4-6 hrs
Absent distal flow of the carotid stump at surgery.
Technically challenging distal control for base of skull lesions.
Local policy : Ligation of carotid artery is indicated where poor physiology, dense neurology and established major
cerebral infarction on imaging .

Vertebral artery1, 2
Vertebral artery trauma is increasingly recognized due to liberal imaging of patients with cervical trauma.
Penetrating injuries occur more frequently than blunt injuries. Anatomically the V2 segment is most
vulnerable to blunt trauma due to its fixed nature within the foramina. Figure 2 demonstrates the anatomical
aspects of the vertebral artery.
80% of patients are typically asymptomatic following injury as a result of the rich collateral circulation.
Patients may present acutely with hemorrhage, hematoma or features of an ipsilateral Horner’s syndrome.
Evaluation of vertebral artery trauma is similar to carotid artery injuries. A high index of suspicion should be
maintained for concomitant aero-digestive tract injuries. Definitive management entails:
Non-Operative Management
Advocated only in blunt trauma. Symptomatic and asymptomatic patients are treated with anti-
coagulation therapy for 3 to 6 months followed by radiographic surveillance.
Operative management
Surgical control of the vertebral artery is technically challenging; thus most advocate unilateral proximal
ligation of the V1 segment. Endovascular stenting is advocated as a salvage procedure in cases of an
absent or hypo-plastic contralateral vertebral artery. Embolization of the proximal and distal ends of a
transected vessel (extravasation/pseudo-aneurysm) maybe performed after angiographic evaluation of
the contralateral vertebral artery.
Local policy:
First line management entails endovascular therapy (coiling versus stenting) pending the type of
pathology: intimal injury, dissection, transections and pseudo-aneurysms.
Thrombosed vertebral artery: No vascular intervention warranted

2
Thoracic vascular trauma1, 5, 6
Trauma to the great vessels within the thoracic cavity is devastating, with a high pre-hospital mortality.
Penetrating trauma accounts for 90% of injuries and associated with an 80% mortality.
The aorta is the most commonly injured great vessel in the thoracic cavity after blunt trauma with a mortality
rate of 80-90%. Most injuries occur at the aortic isthmus, distal to the left subclavian artery.
Rupture of the aorta is thought to occur in 2 phases:7
Rupture of intima and media followed by adventitial rupture. These 2 phases occur sequentially with a time
lag that is indeterminate lasting from seconds to years. This time lag represents the residual tensile strength
in the aorta, affording further evaluation and treatment of these injuries prior to a fatal rupture.
Table 4 Features of a suspected thoracic aortic injury on plain radiography.
Computerized angiography (CTA)
Primary diagnostic modality in suspected blunt thoracic aortic injury. This modality is preferred to
conventional angiography for penetrating trauma in hemodynamically stable patients.
Figure 3 & Table 5 demonstrates grading of aortic injuries based on CTA features.
Medical Management7
Anti-impulse therapy: Comprises anti-hypertensive therapy to reduce the risk of extending the injury (intimal,
medial, or adventitial) and rupture, and potentially reduces the volume of blood loss if ruptured. Calcium
channel blockers are prescribed if Beta blockers are contra-indicated. These agents are used to regulate the
blood pressure & rate control with targets of systolic blood pressure <100mmHg, MAP of < 60mmhg and a heart
rate < 100 beats /minute.
Surgical management
Urgent surgical intervention is indicated for frank aortic ruptures, hemodynamic instability, increasing
hemorrhage from chest tubes, and radiographic evidence of an expanding hematoma. Open surgical
repair is associated with mortality rates ranging between 10- 35%.
Thoracic Endo-Vascular Aneurysm Repair (TEVAR) is currently the standard of care for acute traumatic
aortic injuries with reported lower mortality rates of 4.8%.
Table 6: Criteria for anatomic suitability for endovascular repair.
Complications of TEVAR:
1. Device related include endoleaks, migration, endograft and collapse
2. Neurological:
Spinal Cord Ischemia; Reported in 2.5 -10% of patients
Stroke: 3.1% reported especially after coverage of the left subclavian artery
Left upper limb ischemia due to coverage of the subclavian artery
3. Access related: The large size of the TEVAR device delivery systems may predispose patients to :
Groin hematomas Dissection
Pseudo-aneurysms Rupture
Retroperitoneal haemorrhage Occlusion
AV Fistula
Local policy:
Blunt trauma: injury grades 1 / 2: Anti-impulse therapy, anticoagulation x1/12, bedrest.
Grade3 injury: TEVAR.
Grade 4 injury: Surgery via a thoracotomy.

Brachial artery1, 8
Clinical suspicion of an injury is determined by absent or discrepant pulses.
In blunt injuries the associated fracture or dislocation should be reduced prior to evaluating the pulse
status. If the distal pulse returns the patient should be treated expectantly with regular evaluation,
however if the limb remains ischemic or pulseless the vessel should be explored with a view to arterial
repair followed by a planned orthopedic intervention.
In isolated penetrating trauma, patients with pulse discrepancies should be explored.
Operative management includes:
Primary repair (In 50% of cases the artery can be repaired primarily due to its great mobility.
Interposition graft (For arterial defect >5mm, preferably the reverse saphenous vein)
Intra-operative assessment for concomitant nerve injuries and their repair should be performed

3
 The functional outcome of the upper limb is governed not only by re-establishing luminal vessel patency
but also neural repair as well (ulnar, radial or median nerve). Failure to achieve this relegates the limb
to a cosmetic appendage and a resultant Volkmann’s ischemic contracture.
Local policy:
Open repair of brachial artery injuries presenting acutely, whilst associated fractures and nerve injuries
are managed simultaneously in conjunction with the orthopaedic surgeons.
With delayed injuries, provided there is no pseudo-aneurysm or extravasation of contrast on imaging
and no limb threat, can be managed conservatively.
Mangled extremities require an ablation with emphasis on preserving limb length
Septic lesions warrant vessel ligation

Subclavian artery 4, 9
Subclavian artery trauma is associated with significant morbidity & mortality, mostly as a result of
penetrating trauma.
The upper limbs are rarely ischemic due to collateral circulation, with long term morbidity secondary
to brachial plexus injuries.
Approach to injuries is dependent on hemodynamic stability. Unstable & actively bleeding patients
require immediate exploration. Stable patients require appropriate imaging to localize the exact site of
injury and plan further management.
Operative management
Open surgery is technically challenging and is reserved for:
Hemodynamically unstable patients
Technically unsuitable injuries (1st part of subclavian requires sternotomy for proximal control)
Endovascular repair using covered stent grafts is considered the primary treatment modality [in our
unit] providing immediate technical resolution of pseudo-aneurysms, lacerations and arteriovenous
fistulae. Advantages include:
Decreased morbidity of operative exposure and nerve injury
Avoids dissection at base of neck, which is median sternotomy and thoracotomy respectively.
If active bleeding seen on angiography, temporary balloon tamponade can be performed with
open repair/stenting
Non-Operative management
Non-flow limiting intimal disruptions and dissections maybe managed with clinical observation and
anti-coagulation (Enoxaparin 1mg/kg) or antiplatelet therapy; antithrombotic therapy should
embolic symptoms develop.
Local policy:
Endovascular therapy is first line treatment for acute and delayed subclavian artery injuries that satisfy
technical imaging criteria and stable patient physiology.
Hybrid procedures are reserved for difficult access and pathology that poses technical challenges.
Surgical intervention for unstable patients or where endovascular intervention is contraindicated.

Popliteal artery1, 2, 10, 11

Popliteal artery injuries are devastating - associated with local amputation rates of up to 37.5%. A high index
of suspicion and prompt management is advocated.
Mechanism of Injury
Penetrating: Low velocity (stab wounds), High Velocity (gunshot wounds).
Blunt force: Knee dislocations, Tibial plateau fractures.
Diagnostic Evaluation
X-ray: Essential to evaluate contiguous dislocations or fractures.
Duplex Doppler: Presence or absence of Intimal flap, AVF and pseudo-aneurysms.
CTA: Allows evaluation of inflow as well as outflow vessels, associated soft tissue & osseous injuries.
Conventional angiogram rules out diagnostic doubt (retained foreign body) or motion artefacts on
CTA.
Vascular Pathology
Occlusive Injuries include vessel transection and thrombosis.
Non-occlusive Injuries include intimal flaps, pseudo-aneurysms and AVF

4
 Management11
Hard signs of vascular Injury: surgical intervention
Soft signs: imaging to characterize injury
Operative management
Open exploration: Primary repair, saphenous vein interposition grafts and shunting maybe utilized
Endovascular therapy: Stenting of pseudo-aneurysms and AVF as bridging therapy.
Non-operative management: anticoagulant or anti-platelet therapy is advocated for non-occlusive injuries.
Local policy: Figure 4 provides an algorithm for management of popliteal injuries after knee dislocation.
Patients with a knee dislocation and a viable limb should have definitive imaging.

Pitfalls to avoid in managing peripheral vascular injuries12

Avoid limiting skin preparation and draping.
Control external hemorrhage during skin preparation and draping, followed by surgical exposure: proximal and
distal vascular control.
Avoid straight incisions across axillo-brachial area, antecubital fossa and medial or posterior popliteal area.
Obtain proximal and distal vascular control through short incisions around large peripheral hematomas.
Avoid prolonged vascular repair when an indication for temporary intraluminal shunt is present in a physiologically
unstable patient.

Pelvic trauma13
Mortality from pelvic ring injury is secondary to pelvic exsanguination.
Disruption of the pre-sacral venous plexus and hemorrhage from displaced fractures are the main contributors to
exsanguination.
Arterial injuries are present in 10-60% of hemodynamically unstable patients. These injuries mostly involve
branches of the internal or external iliac artery.
Preperitoneal packing can be used as a temporizing measure followed by angio-embolization and pelvic fixation.
Figure 5 provides an algorithm for management of pelvic vascular trauma

Local policy: On table angiogram with a view to stenting or angio-embolisation

Special circumstances
Principles of management of peripheral venous injuries14
The optimal management of venous injury remains controversial. The venous system is a low flow system thus venous
repairs are prone to post-operative venous thrombosis. Techniques employed when embarking on repair include:
Lateral venorrhaphy Patch venoplasty
End-to-end anastomosis Interposition graft (autologous vein or prosthetic)
In the stable patient liberal ligation of venous injuries is well tolerated with minimal long-term morbidity. Special
considerations are given to internal jugular vein (IJV) and popliteal veins where repair should be considered if there is pre-
existing pathology to the contralateral IJV & technically feasible popliteal vein repair.
Local policy:
Arterial injuries take precedence over venous injuries
Simple injuries are repaired
Complex injuries are ligated

Compartment syndrome15
Acute Compartment Syndrome (ACS) refers to a critical interstitial pressure increase within a confined osteo-fascial
space causing a decline in the perfusion pressure to the tissue within.
A delta pressure of 30 mmHg is recommended for decompression with minimal complications.
ACS is a clinical diagnosis and the most important determinant of outcome is early recognition and expeditious
management.
Figures 6 to 9 detail the pathophysiology, management algorithm and surgical approaches to fasciotomies in the different
anatomical locations.

5
 Complications of ACS
Myonecrosis
Reperfusion syndrome
Neurovascular injury
Infection
Amputation
Death
Figure 9: Lower limb fasciotomy
Figure 8: Upper limb fasciotomy

6
Technological advances: Specialized skill5, 9, 17
Endovascular stenting (covered stents)
Minimally invasive.
Reduced morbidity and length of stay in hospital.
Decreases morbidity over arteries associated with difficult exposure via standard operative technique
Beneficial irrespective of injury and hemodynamic status in the case of using intravascular balloon for
proximal control i.e. RELIANT balloon.
Less Ischemic time.
Avoidance of complications related to surrounding structures especially the brachial plexus.
Disadvantages:
Long term follow-up.
Lack of compliance with follow up as most of our patients are from a disadvantaged background
Skillset deficit of conventional open repair for the trainee.
Endovascular embolization:
Embolotherapy aims to obtain hemostasis through thrombosis of flow distal to the arterial and arteriolar
collateral supply without causing tissue necrosis.
Embolization agents used include:
Resorbable gelatin sponge (temporal proximal control)
Coils (permanent)
Liquid agents
Local policy
Selective embolization is achieved by use of coils, gelfoam and microparticles.
Choice of embolic agent is determined by vessel diameter and anatomical location.

Paediatric vascular trauma1

Iatrogenic injuries has the highest incidence in the neonatal age group. These injuries occur mainly during intra-
venous line insertion, arterial line (for arterial blood gas sampling and monitoring). Non-Iatrogenic injuries
commonly occur after penetrating injuries affecting mostly the upper limbs. The following factors should also
be considered when planning therapy.
1. Vessel diameter
2. Vessel spasticity
3. Expected axial growth
Treatment options includes:
1. Conservative management: Most favoured approach. Adverse outcomes include distorted limb growth,
gait disturbances & amputation.
Local policy: Conservative management entails use of anticoagulation in selective patients.
2 Surgical exploration
Open Approach
Primary Repair
Interposition graft
Vessel Ligation
Endovascular techniques have a limited scope in paediatric patients.

Conclusion
Prompt recognition of the patient with vascular trauma is invaluable to reducing the morbidity and mortality
from vascular injuries. Although imaging modalities are useful adjuncts in the evaluation of vascular trauma
patients, they should not delay decision making and appropriate management of vascular injuries. The
emergence and continued evolution of endovascular therapy has increased the armamentarium of the vascular
surgeon in management of trauma patients and in combination with open surgical techniques is projected to
enhance favourable outcomes.

7
 APPENDICES
Table 1: Clinical Features of suspected vascular trauma
HARD SIGNS SOFT SIGNS

Pulsatile hemorrhage History of hemorrhage

Expanding hematoma Wounds of neck or extremities and unexplained hemorrhagic shock
Bruit / thrill over area of injury Neurologic deficit of peripheral nerves in proximity to vessels
Absent extremity pulses High-risk fracture, dislocation, or penetrating proximity wound

Table 2: Sequelae according to mechanism of injury

Injury Type Natural History Complication
Penetrating Injury
Laceration Pseudo-aneurysm or thrombosis Ischemia, rupture, embolization
Contusion Stenosis, thrombosis Ischemia, embolization
Arteriovenous fistula Increase in size & flow “Steal” syndromes, heart failure
Blunt
Intimal dissection or thrombosis Spontaneous resolution None unless progression
<25%
Intimal dissection or thrombosis Pseudo-aneurysm, thrombosis Rupture, Ischemia
>25%
Pseudo-aneurysm Increase in size Rupture, embolization
Thrombosis Occlusion, recanalization Ischemia, stenosis
Arteriovenous fistula Increase in size & flow “Steal” syndrome, pseudo-aneurysm
Transection Thrombosis, pseudo-aneurysm Ischemia, compartment Syndrome
Table 3: Imaging options for cervical vascular trauma

Zone of Injury Imaging modality

I CT angiography
II Duplex ultrasound
III CT angiography

Table 4: Features of an aortic injury on plain radiography

Mediastinal Findings Widened mediastinum >8cm Lateral displacement of trachea
Obliteration of Aortic knob Deviation of naso-gastric tube
Depression of left main bronchus Calcium layering of aortic knob
Loss of paravertebral pleural line
Fractures Sternum Scapula & clavicular fractures in Polytrauma
1st and 2nd ribs Thoracic spine
Apical Cap
Massive left Hemothorax
Ruptured diaphragm
Anterior displacement of trachea
Loss of aorto-pulmonary window
Table 5: CTA grading of aortic injuries
GRADE IMAGING FEATURES TREATMENT
I Intimal Tear Medical therapy
Repeat imaging in 6 weeks
II Intramural Hematoma Medical therapy
III Pseudo-aneurysm Elective TEVAR*
IV Rupture Emergent TEVAR*
Table 6: Criteria for TEVAR
Access vessels Femoral or iliac Arteries
Anatomic suitability Native aorta 16 to 42mm
Landing zones 2cm Proximal & distal landing zones

8
Figure 1: Zones of neck Figure 2: Vertebral artery anatomy

Figure 3: Aortic injury grading Figure 4: Algorithm for popliteal artery injury after knee dislocation

Knee dislocation or
Multiple Ligament Inj.

Threatened Limb

On table angiogram Formal angio

Positive Negative

Revasc
Serial Neurovasc Reviews x 24 hrs

Figure 5: Algorithm for management of pelvic trauma

9
Figure 7: Algorithm for suspected compartment syndrome

References
1. Sidawy AP: In: Rutherford's Vascular Surgery and Endovascular Therapy. 9 ed: Elsevier. p7620-7840. Chapter 180-185.
2. Teixeira PGR, DuBose J. Surgical Management of Vascular Trauma. Surg Clin North Am. 2017;97(5):1133-
55.
3. Lee TS, Ducic Y, Gordin E. Management of Carotid Artery Trauma. Craniomaxillofac Trauma Reconstr.
2014;7(3):175-89.
4. du Toit DF, Lambrechts AV, Stark H. Long-term results of stent graft treatment of subclavian artery injuries:
management of choice for stable patients? J Vasc Surg. 2008;47(4):739-43.
5. Pillai J, Yazicioglu C, Monareng T. Lessons learned from the endovascular management of blunt thoracic
aortic injuries: A single-centre experience. S Afr J Surg. 2015;53(1):19-21;
6. Lee WA, Matsumura JS, Mitchell RS, Farber MA, Greenberg RK, Azizzadeh A, et al. Endovascular repair of
traumatic thoracic aortic injury: clinical practice guidelines of the Society for Vascular Surgery. J Vasc Surg.
2011;53(1):187-92.
7. Neschis D. Management of blunt thoracic aortic injury. In: Mills J, ed. UpTo Date. Waltham, Mass. UpTo
Date,2019. www.uptodate.com/contents/management of blunt thoracic aorta injury. 1st April, 2019.
8. Padayachy V, Robbs JV, Mulaudzi TV, et. al. A retrospective review of brachial artery injuries and repairs-Is
it still a "training artery"? Injury, Int J Care. 2010;41(9):960-3.
9. Naidoo NG, Navsaria P, Beningfield SJ. Stent graft repair of subclavian and axillary vascular injuries: The
Groote Schuur experience. S Afr J Surg. 2015;53(1):5-9.
10. Nair R, Abdool-Carrim AT, Robbs JV. Gunshot injuries of the popliteal artery.Br J Surg. 2000;87(5):602-7.
11. Banderker M, Navsaria P, Edu S. Civilian popliteal artery injuries. S Afr J Surg. 2012;50:119-24.
12. Feliciano DV. Pitfalls in the management of peripheral vascular injuries. Trauma Surgery & Acute Care Open.
2017;2(1):e000110.
13. Scemama U, Dabadie A, Varoquaux A. Pelvic trauma and vascular emergencies. Diagnostic and
interventional imaging. 2015;96(7-8):717-29.
14. Giannakopoulos TG, Avgerinos ED. Management of Peripheral and Truncal Venous Injuries. Front Surg.
2017;4:46.
15. Donaldson JH, Behrooz. The Pathophysiology, Diagnosis and Current Management of Acute Compartment
Syndrome. Open Orthop J. 2014;8:185-93.
16. Cakir O, Subasi M, Erdem K. Treatment of vascular injuries associated with limb fractures. Ann R Coll Surg
Engl. 2005;87(5):348-52.
17. Du Toit DFC, D. The Endovascular Management of Penetrating Carotid Artery Injuries: Long Term Follow-
up. Eur J Vasc Endovasc Surg. 2009;38(3):267-72.

10
 SURGERY FOR HYPERTENSION
Drs SR Sibiya, MFF Elfirgani
Moderator: Ms S Ntloko 6th July 2019

Uncontrolled hypertension is characterized by cardiovascular, cerebrovascular and renal complications with

resultant mortality. Majority of patients present with primary hypertension whilst the remaining 5–10% have
secondary hypertension. Appropriate diagnostic timing and intervention for secondary hypertension may have
curative intent, however the challenge relates to screening. The Renin-Angiotensin-Aldosterone system (RAAS)
is an important pathophysiological mechanism underlying most causes of secondary hypertension.
Basic definitions
Resistant hypertension: BP >140/90mmHg despite 3 anti-hypertensive agents including a diuretic
Severe hypertension: Systolic > 180/110 or systolic BP > 180mmHg or diastolic BP > 110mmHg
Common causes of secondary Hypertension:
Vascular: Renal artery stenosis, coarctation of the aorta and Takayasu’s arteritis.
Endocrine: Primary aldosteronism, Pheochromocytoma, Cushing’s disease and hyperparathyroidism.
Others: Renal parenchymal disease, drugs e.g. cocaine, Obstructive sleep apnea

RENAL ARTERY STENOSIS 1, 2

Renovascular hypertension (RVH) arises from severe renal artery stenosis. This pathology leads to reduced
kidney perfusion, loss of kidney function together with a reduced nephron mass, and eventual ischemic
nephropathy. Renal artery stenosis (RAS) has a bimodal age variation: The elderly manifest with
atherosclerosis and young females usually present with fibromuscular dysplasia (FMD). Other causes include:
Takayasu’s arteritis, dissections and trauma.

Pathophysiology of hypertension:
Poor renal perfusion leads to the circulatory release of Renin which cleaves angiotensinogen into inactive
angiotensin I. The Angiotensin I is then converted by Angiotensin Converting Enzyme (ACE) (residing
predominantly in the lungs) to generate the active peptide Angiotensin II (AT 2). AT 2 regulates renal sodium
balance, aldosterone synthesis and vascular resistance. It also has wide ranging actions on the vascular smooth
muscle.
Differences between unilateral (‘two kidney-one clip’) and bilateral (‘one kidney-one clip’) RAS:
The release of renin produces elevated arterial pressures, sodium retention and decreased blood flow and
glomerular filtration rate in the affected kidney. The contralateral normal kidney is exposed to increased
arterial pressures and undergoes “pressure natriuresis” and increased urinary sodium excretion to prevent
hypervolemia. The hypertension is therefore Renin-dependant or Angiotensin II mediated.

In bilateral RAS, the reduced pressure to the kidney activates the RAAS but because the contralateral kidney is
absent or diseased, the sodium-retaining mechanisms are activated and expand the circulatory volume
returning the renal perfusion pressure to nearly normal. As a result, plasma renin activity falls and arterial
pressure does not depend on the pressor effect of Angiotensin II. The hypertension is therefore volume-
dependant and the influence on Angiotensin II can only be demonstrated if sodium is decreased or depleted.

Classification of renal artery stenosis

RAS can be classified anatomically as:
Ostial (involving the origin)
Truncal (>10mm from the renal artery origin)
Segmental (stenosis in the segmental branches of the renal artery)
Mixed type and renal artery occlusion.
The severity of RAS can either be mild (<30%), moderate (30-69%) and high grade (>70%).
A haemodynamically significant stenosis exceeds 60%.

1
 Investigations
The following objectives should be considered when investigating RVH.
To assess function/physiology of the RAS especially in activating the RAAS.
To identify the presence and degree of the stenosis.
To predict the benefit from revascularization.
Functional studies of the RAAS
- Peripheral renin activity measurements are unreliable (sensitivity of 36%). Variability in sensitivity
emanates from changes in sodium intake, volume status, renal function and drug interactions.
- Renal vein renin assay is useful in lateralising the stenosis. A ratio of >1.5 between the renin activity of
the stenotic kidney and the non-stenotic kidney is used. The greater the lateralization, the more likely
the clinical BP benefit will accrue with revascularization.
Presence and degree of stenosis
Duplex Doppler provides anatomic and haemodynamic assessment of the stenosis. A Peak systolic
velocity (PSV) of >180cm/sec at the level of stenosis and a Renal aortic ratio (RAR) > 3.5 are diagnostic
of a haemodynamically significant stenosis. Renal Resistive Index (PSV-EDV)/PSV) >0.8 indicates
critical stenosis of the renal artery or severe parenchymal disease The abnormal ratio denotes a poor
response to revascularization as a result of associated intrinsic renal disease.
CT Scan / MRI can be used to anatomically locate the stenotic renal artery lesion.

Assessing renal function

Traditionally, instrumenting the individual ureters was performed to obtain the GFR (glomerular filtration rate)
but in modern practice, radio-isotopes e.g. Technetium 99 can be used to estimate the fractional blood flow
and filtration by each kidney.
A useful imaging strategy comprises a Duplex scan of the renal arteries and a subsequent CTA to obtain
anatomical & haemodynamic data. If the Duplex scan is unavailable or equivocal, a Captopril renogram can be
obtained to assess haemodynamic significance of the renal artery stenosis. A Split Renal Function provides
qualitative information pertaining to renal salvage.

RAS causes and pathology

Disease Atherosclerosis FMD Vasculitis Dissection Occlusion

Key Usually located in Affects distal 1/3 May occur with May be Collaterals resent
characteristics proximal segment with “string of aortic involvement. associated with usually from supra-
beads” Macaroni sign Aortic dissection renal arteries

Management
Medical therapy: ACE-I or ARB and a diuretic. It is important to monitor the renal function once an ACE-I is
commenced due to the potential worsening of renal failure. Randomized trials have shown that
supervised antihypertensive drug treatment results maybe similar to endovascular therapy outcomes.
Surgical intervention: resistant hypertension, a haemodynamically significant stenosis > 70%, kidney size >
8cm, deteriorating renal function and a life-expectancy of approximately 2 years post intervention.
Contraindications: Chronic dialysis patients, RAS < 70% and a short life expectancy.
Endovascular treatment
Renal angioplasty +/- stenting has gained momentum over the years.
Deployment route: Femoral or brachial access - for ostial lesions the stent should extend 1-2mm into
the aortic lumen.
Potential complications: Contrast-induced nephropathy, renal embolization, and renal artery
dissection or rupture.
There is controversy regarding the use of a distal protection devices.
Post procedure medication: DAPT for 4 weeks, aspirin indefinitely.

2
Open Surgery
Indications: patients requiring concomitant abdominal aortic surgery (e.g. AAA repair) and failed
endovascular therapy.
Options include aorto-renal bypass, extra-anatomical bypass
Nephrectomy: If renal function is <10%; a small shrunken/ scarred kidney <8cm and extensive disease.

Local policy: Endovascular - first strategy is used with open repair being reserved for the paediatric population.
Reported trials:
STAR (Stent Placement and blood pressure and Lipid lowering for the prevention of progression of
Renal Dysfunction Caused by Atherosclerotic Ostial Stenosis of the Renal Artery)
ASTRAL (Angioplasty and Stenting for Renal Artery Lesions) and
CORAL (Cardiovascular Outcomes in Renal Atherosclerotic Lesions)

Management algorithm for Renal artery stenosis

ENDOCRINE HYPERTENSION 3, 4, 5
Primary aldosteronism and Pheochromocytoma.
A high index of suspicion is required for diagnosis.
Surgical management: adrenalectomy maybe performed laparoscopically or traditional open surgery.

Primary hyperaldosteronism
Primary hyperaldosteronism (PA) is a group of disorders where aldosterone production is inappropriately high
for the sodium status. This productivity is relatively autonomous of its major regulator (Angiotensin II) and is
non suppressible by sodium loading.
It exists as idiopathic hyperaldosteronism (IHA); aldosterone producing adenoma (APA); adrenal carcinoma
and familial hyperaldosteronism. IHA involves both adrenal glands and accounts for 60-66% of cases whereas
APA is unilateral and accounts for 30-35% of cases.
Mechanism of Hypertension
Pathological unregulated (RAAS) production of Aldosterone.
Increased sodium and water uptake, increased volume load and cardiac output.
Sodium reabsorption is accompanied by potassium excretion. Aldosterone can also cause
vasoconstriction.
Hypertension is dependent on the plasma volume expansion and systemic vasoconstriction.

3
 Urinary loss of potassium and hydrogen ions, exchanged for sodium at the distal nephron, may result
in hypokalaemia and metabolic alkalosis.

The disease is important because patients have a higher cardiovascular morbidity and mortality than age and
gender matched patients with primary hypertension and the same magnitude of BP elevation.
Indications for screening
Hypokalemia
Resistant or severe hypertension
Hypertension in the presence of an incidental adrenal mass
Young onset (age<40yrs) hypertension
Those being evaluated for other causes of hypertension

Diagnosis
Biochemical hallmark features of PA: hypokalaemia, high aldosterone and low renin. Hypokalaemia (9-37% of
patients) and its absence should not rule out hyperaldosteronism.
The diagnosis involves the following:
Detection
Confirmation
Diagnosis and subtype classification

Screening test:
Morning sampling of plasma aldosterone and renin levels. Aldosterone Renin Ratio (ARR) is the gold standard
screening test with superior results. A ratio of >30-50 is indicative of PA. Spironolactone adversely affects the
ARR. Threshold ARR values depend on whether the plasma aldosterone concentration is measured in
conventional or system international units.
Locally an ARR ratio of > 91 is diagnostic.

Confirmation
A positive ARR should prompt a confirmatory test. There are 4 options: oral sodium loading test, saline
infusion test, Fludrocortisone stress test and Captopril challenge test. Locally the Saline infusion test is used.
Patients are admitted and 2L normal saline is infused over 4 hours whilst patient is seated. Plasma aldosterone
levels are taken at the start and thereafter hourly. Aldosterone should be suppressed to <10ng/dL. Values
elevated above the designated suppressive value confirms PA
Subtype classification
Adrenal CT scan is the imaging modality of choice.
Ultrasound is unreliable for the detection of smaller lesions. Adrenal carcinoma is suspected if unilateral
heterogeneous lesions > 4cm found on CT scan.
APA may appear as small hypodense nodules (usually <2cm).
For bilateral adrenal lesions, Adrenal vein sampling (AVS) is indicated to localise the functional lesion and
should only be performed in patients planned for surgery.

Distinguishing between unilateral and bilateral disease is important because unilateral adrenalectomy in
patients with APA or unilateral disease corrects the hypertension however medical treatment is indicated
in bilateral disease.

4
Management
Medical
Aldosterone receptor antagonists e.g. Spironolactone and Eplerenone should be provided to all patients
especially those with bilateral disease. The drug of choice is Spironolactone 12.5-25mg daily and should be
titrated to regulate the blood pressure. Adverse effects includes gynaecomastia.
Surgery
Laparoscopic adrenalectomy should be performed in patients with unilateral disease following potassium
and blood pressure control.
30-60% of patients with a unilateral aldosterone tumour maybe cured whilst some patients will still
require medical management and commenced on a single antihypertensive agent.
The predictors of hypertensive resolution post operatively include: patients on 2 or less antihypertensive
drugs; a BMI of < 25kg/m2; hypertension of < 6years and female sex.

Post-operative
Plasma aldosterone and renin activity shortly after surgery should be measured as an indicator of early
biochemical response. Spironolactone can be discontinued day 1 post op and the anti-hypertensives should be
reduced. A generous sodium diet is recommended to avoid the hyperkalaemia that can develop from
hyperaldosteronism due to contralateral adrenal gland suppression. Blood pressure typically normalises in 1- 6
months after adrenalectomy.

5
Pheochromocytoma
Pheochromocytomas are chromaffin-cell tumours that usually produce catecholamine’s (epinephrine,
norepinephrine and dopamine)
80-85% of these lesions arise from the adrenal medulla.
Paragangliomas arise from the paravertebral ganglia of the sympathetic chain (5% - 20%).
Both the catecholamine producing tumours accounts for 0.2-0.6% of all causes of secondary hypertension
and have similar clinical presentation and management.
Diagnosis
The classic triad: episodic headache, sweating and tachycardia are not always present.
Hypertension (sustained or paroxysmal) is the commonest sign found in 80-90% of patients.
Orthostatic hypotension, secondary to a decreased blood volume caused by persistent vasoconstriction
and diminished sympathetic reflex, may commonly occur in patients with pheochromocytoma.
Clinicians should have a high index of suspicion in patients younger than 25yrs with new-onset
hypertension.
Measuring urine and plasma catecholamine and metanephrines is diagnostic.
Most patients with pheochromocytomas have fluctuating levels of catecholamine whereas the
metabolism of catecholamines into metanephrines is constant.
Locally, the use of two consecutive 24 hr urinary catecholamine samples with values greater than twice the
upper limit of normal are diagnostic.

Imaging
Uncontrasted CT scan (sensitivity of 85-94%) detects adrenal lesions approximately 0.5cm. The
assessment of Hounsfield units (HU) can differentiate a benign from a malignant tumour. The
characteristic findings for pheochromocytoma includes: increased uptake with 40-50 HU; delayed
washout with necrosis and calcifications.
Functional imaging with MIBG or PET scan is indicated in patients with larger tumours (>10cm),
paragangliomas, metastatic disease and tumour recurrence.

Management
Treatment goals: normalize BP and heart rate; restore volume depletion and prevention of intra-operative
hypertensive crisis.
The PPGL guidelines recommends the following:
Pre-operative medical therapy to normalize blood pressure and heart rate alpha adrenergic blockade
+/- Beta blockade.
Pre-operative blockade of functional pheo/paraganglioma to prevent cardiovascular complications.
A high sodium diet and fluid intake is suggested to prevent severe hypotension following tumour removal.
Laparoscopic adrenalectomy should be performed and open resection reserved for very large or invasive
pheochromocytomas.

Locally, pre-operative blood pressure control is obtained by using Doxazosin (short-acting selective alpha
blocker) for at least 2 weeks prior to surgery. The target systolic blood pressure <110-120mmHg and diastolic
< 60-70mmHg. Beta blockers should not be commenced at the outset because the absence of alpha blockade
will exacerbate the epinephrine-induced vasoconstriction by blocking the vasodilator component of beta 2.
They should be started once optimal alpha blockade is achieved with the aim of reducing the tachycardia
aiming for a heart rate of 60-80 beats/min.

Surgical outcome
Approximately 80% of patients may become normotensive following adrenalectomy. Post-operative
hypertension may persist as a result of residual tumour, metastatic disease, intra-operative injury of the renal
artery or acquired renovascular changes due to pre-op hypertension. Plasma catecholamine or urinary

6
metanephrines should be measured initially 2 weeks following surgery, followed by 3 monthly sampling for the
first year and thereafter annually.
Laparoscopic adrenalectomy is generally considered to be the standard technique for removal of adrenal
tumours with open surgery reserved for lesions > 5cm.
Laparoscopic adrenalectomy
Laparoscopic adrenalectomy is contraindicated for tumours >5cm and those with a high likelihood of
malignancy. Laparoscopic adrenalectomy can be performed using a transabdominal, retroperitoneal and
robotic approach.
The transabdominal approach was the first technique described for this operation but the retroperitoneal
technique is employed locally. The major benefit of the retroperitoneal approach is that the surgeon does not
need to move any other organs out of the way because the adrenal gland lies posteriorly against the ribcage.
This approach is associated with less post-operative pain, shorter operative time, reduced blood loss, shorter
hospital stay and reduced risk of surgical access site herniation.

Open adrenalectomy
Open adrenal surgery can be done via the anterior, posterior, and thoraco-abdominal approach. Anterior
approach is the most commonly favoured approach comprising a midline incision or more commonly a
subcostal incision and is ideal for very large adrenal tumours, particularly when a malignancy is suspected as it
allows excellent exposure and resection of invaded structures.

COARCTATION OF THE AORTA 6

Aortic coarctation predisposes to hypertension in young children but may also manifest for the first time in
adulthood. It is defined as a constricted segment of aorta that occurs in the thoracic aorta.
The classical location is the thoracic aorta just distal to the left subclavian in the region of the ligamentum
arteriosum.
This pathology may occur in the distal thoracic aorta and the abdominal aorta. The pathogenesis is poorly
understood but it is thought to be related to the presence of abnormal ductus arteriosus tissue. The stenosis is
usually extreme with a remnant pinpoint lumen.
Blood reaches the distal aorta via collateral connections between branches of the subclavian, scapular and
intercostal arteries, and via the anastomosis between the internal thoracic and inferior epigastric arteries.
Although the blood supply to the lower part of the body is diminished, patients with coarctation seldom have
peripheral gangrene.
The danger of coarctation is due to the effects of hypertension proximal to the coarctation with cerebral
haemorrhage and left ventricular failure
Mechanism of hypertension
Is probably due to the relatively poor blood supply to the kidneys, which results in the release of renin and
subsequent renal-mediated hypertension

Diagnosis
The characteristic sign is radio-femoral pulse and a large difference in blood pressure between the arms and
legs. Chest X-ray will often show a figure “3 sign” notching of the posterior fourth to eighth ribs due to dilated
collateral intercostal arteries. Definitive diagnostic confirmation requires a CT angiogram.

Management
Medical
Beta-blockers are usually used to reduce the upper extremity hypertension. Dosage should be titrated since
lowering the BP may further reduce the lower limb perfusion pressures.
Surgery
Patch aortoplasty, resection with interposition grafting, bypass grafting without resection. The safety
after interposition grafting is excellent and associated with a >60% resolution of the hypertension and a
<2% re-coarctation rate.
Endovascular repair:

7
 Balloon angioplasty +/- stenting. Endovascular repair has become popular as an alternative to surgery
and also used in patients with recurrent coartcation. Placement of a bare-metal stent can prevent
recoil of the aorta following balloon angioplasty but carries a complication of intimal hyperplasia.
Using a covered stent protects against immediate rupture during angioplasty and may prevent the
long-term complication of aneurysm formation.
Locally, an endovascular first approach is favoured with a view to deploying a covered stent as the long term
results with angioplasty are poor. The alternative is open repair by means of an end to end anastomosis.
Patient follow up
Unrepaired coarctation: lifelong follow-up by cardiologist
Post repair: Follow-up should be annually. Imaging of the repair should be performed every 5 years to
assess for complications of aortic aneurysm or recoarctation.

TAKAYASU’S ARTERITIS7
Takayasu’s arteritis (TA) is an idiopathic, granulomatous, large-vessel arteritis that predominantly involves the
aorta, its major branch arteries and the pulmonary arteries. It is the 3rd common cause of vasculitis in the
paediatric age group representing the leading cause of stenotic aorto-arteriopathy and one of the most
prevalent causes of renovascular hypertension in childhood. The overall incidence has been estimated to be
2/1,000,000 per year. The causes of hypertension include renal artery stenosis (often bilateral and involves
the ostia), middle aortic syndrome and dysfunction of the carotid baroreceptors.

Diagnosis
There is a broad clinical spectrum, hence TA is a diagnosis made with a high index of suspicion.
Signs and symptoms: Hypertension, vascular bruits and asymmetric blood pressure between limbs or
asymmetric arterial pulses in extremities, sometimes accompanied by fever, malaise or musculoskeletal
symptoms. Haematological investigations: Elevated Erythrocyte Sedimentation Rate [ESR], C - reactive protein
[CRP] and normochromic normocytic anaemia. The diagnosis is confirmed on imaging with the demonstration
of lesions in the aorta or its major branches

Management
Medical
The aim of medical treatment is to control the active inflammation, minimize arterial injury and prevent the
development of vascular complications. Early initiation of corticosteroid therapy for induction of remission,
use of immunosuppressive agents as adjunctive therapy, and clinical monitoring of therapy with inflammatory
markers has been used to successfully treat patients.
Surgical Treatment
There are no clear guidelines to direct the choice between open and endovascular intervention. The practice is
largely determined by local practice, availability of expertise, the site and lesion location.
Surgical intervention whether open or endovascular is delayed until the patient is deemed as having inactive
disease.
Indications include uncontrolled hypertension as a consequence of renal artery stenosis, cerebrovascular
disease, and coronary artery disease, severe coarctation of the aorta, aortic aneurysms, renovascular
hypertension, end-organ ischemia, and progressive aneurysm enlargement with associated risk of rupture or
dissection.
Percutaneous transluminal angioplasty with balloon or stenting
In RAS angioplasty is successful with resolution of hypertension in up to 96% with patency rates ranging from
92.7-100% at 1-5 years. Stent placement is reserved for restenosis or arterial dissections post angioplasty.
Open Surgery
Both reliable and durable in selective patients with inactive disease not requiring immunosuppression at the
time of surgery. Some centres prefer open surgical revascularization using renal artery bypass grafting.

8
 RENAL DENERVATION 8
Renal denervation (RDN) is a catheter based procedure that uses radiofrequency pulses in the adventitial
layers of the renal arteries to ablate the sympathetic nerves in the vascular wall.
This is used in resistant hypertension and BP reduction (20-30mmHg) has been shown in excess of 3 years.
The development of renal artery stenosis as a complication of the treatment is uncommon.
Symplicity 1 and 2 trials had shown benefit in RDN however the recent Symplicity 3 trial showed no benefit
using this mode of therapy. Based on these recent results, this form of therapy is currently not offered locally.

Conclusion
It is important to be aware of the clinical clues that suggest secondary hypertension: severe or resistant
hypertension age less than 30yrs and elevated blood pressure developing acutely in a patient with previously
stable readings. These clinical scenarios should prompt further investigations to establish the cause and plan
appropriate treatment namely endovascular therapy for the vascular causes and adrenalectomy for the
endocrine hypertension.

Summary of diagnosis of secondary hypertension in different age groups

9
References
1. Safian RD, Textor SC. Renal artery stenosis. N Engl J Med 2001; 344(6):431-442
2. Bloch MJ, Basile J. Diagnosis and management of Renovascular disease and Renovascular hypertension. J
Clin Hypertens 2007;9(5):381-389
3. Funder JW, Carey RM, Mantero F et al. The management of primary aldosteronism: Case detection;
diagnosis and treatment: an endocrine society clinical practice guideline. J Clin Endocrinol Metab
2016;101(5):1889-1916
4. Lenders JW, Duh QY, Eisenhofer G et al. Pheochromocytoma and paraganglioma: an endocrine society
clinical practice guideline. J Clin Endocrinol Metab 2014;99(6):1915-1942
5. Thomas RM, Ruel E, Shantavasinkul PC, Corsino L. Endocrine hypertension: An overview on the current
etiopathogenesis and management options. World J Hypertens 2015; 5(2):14-27
6. Eskandari MK, Morasch MD, Pearce WH, Yao JST. Contemporary Vascular Surgery 2012;227-235
7. Mason JC. Takayasu arteritis: surgical interventions. Curr Opin Rheumatol 2015;27:45-52
8. Esler M. Renal denervation for treatment of drug-resistant hypertension. Trends Cardiovasc Med 2015;
25(2):107-115

10
 CONSCIOUS SEDATION AND THE CONTROL OF PAIN
Dr M Jali, Dr S Thaver, Dr M Ramaphoko
Moderator: Ms L Cronje 13th July 2019

The management of pain is central to the care of the surgical patient. Collaboration between
anaesthetists and pharmacologists has ensured that advances in pain management are available to the
surgical patient. This seminar will address the surgeon’s role in the management of acute pain, aspects
of sedation and chronic pain

Acute pain
In 2010, the cost of treating pain and revenue lost due to decreased productivity in the USA was >$750
billion, more than that of heart disease, cancer or diabetes.(1) 2019 is the Global Year Against Pain in the
Most Vulnerable, highlighting pain as a human right and lack of pain treatment in low- and middle-
income countries. Thus, economic and humanitarian factors point to the importance of research,
education and training in prevention and treatment of pain. Pain is defined by the International
Association for the Study of Pain (IASP) as an ‘emotional experience associated with actual or potential
tissue damage, or described in terms of such damage’, and is further characterised by: i) an inciting
event, ii) is of sudden onset, iii) is time limited and iv) has the potential to develop into a pathological
condition.(2) The experience of pain is subjective, differing from patient to patient in intensity and
duration, acute pain typically lasting from 1 to 6 months.(1, 3)

Mechanism of pain (3-5)

1. Inflammatory pain – Either nociceptive or neuroplastic. It is a heightened pain sensitivity in
response to tissue damage or inflamation

2. – due to nerve injury or altered sensory transmitting system in spinal cord

Sensory loss- –
negative sensory phenomena
Paradoxical hypersensitivity –

Management(1-5)
Post-operative pain management has evolved from sole opioid administration to a multimodal
approach, lowering individual drug side effects and reducing opioid use and dependency. The
ladder is still relevant today, with an added fourth step of advanced modalities e.g. local/ regional
anaesthesia as well as patient controlled anaesthesia (PCA) pumps (fig 1).(6)

Figure 1: Modified WHO pain ladder

1
The general principle is to start with simple analgesics, climbing up the ladder if pain persists and
deescalated depending on response (see table 1 for drugs, table 2 for blocks). In post-surgical pain, a
step-down approach is used. Pain management should be: procedure and patient specific; given at
regular intervals ( ) via least invasive route; measured and adjusted according to
response. Pain scale charts are used quantify the severity of pain (fig 2).

Figure 2: Universal Pain scale charts are used to quantify the severity of pain

Table 1. Common analgesic drugs and basic pharmacology(1, 5)

Drug Class/Action Route Common Dose Caution

Paracetamol Anti-pyrexial/ 0,5-1g per dose 6 Liver failure
hourly max 4g/day
Ibuprofen 200-400mg 4-6 Peptic ulcer disease
inhibitor hourly Renal disease
Diclofenac Standard 50mg tds Peptic ulcer disease
inhibitor Extend 100mg/dly Renal disease
Codeine Weak opioid 15-60mg 4 hourly, Constipation,
max 360mg/day dependence
Tramadol*** Atypical opioid 50-100mg 6 hourly Constipation
agonist Max 400mg/day -3 antiemetics and
SSRI - CI
Morphine Strong opioid 0.05-0.2mg/kg*
Ketamine 0,2-0,5mg/kg ** Dissociative state
* Dose dependant on route of administration
**Dose for sedation and induction of anesthesia differs
*** Tramadol is a centrally acting weak µ-opioid receptor analgesia but also a noradrenaline
and serotonin reuptake inhibitor. Tramadol's serotonin and norepinephrine reuptake inhibitory effects
may result in two adverse events: serotonin syndrome and seizures. Prevalence is modest in the
general population, but if left untreated, the morbidity and mortality can be high; therefore, prompt
recognition and management is essential. Treatment is supportive with benzodiazepines use for
seizures.(7)

Some current acute pain concept

1.) Preventive acute pain management has replaced the concept of “pre-emptive analgesia” (which had
scantly evidence)(8) and shows promise in both better acute pain modulation and prevention of
transition to chronic pain.(2) Preventive interventions are where the effect on postoperative pain and or
analgesic consumption exceeds the duration of action of the medicine. Preventive strategies include:
use of ketamine
may reduce opioid consumption by up to 24%); local anaesthetic infusions of lignocaine; neuraxial and
peripheral neve block regional techniques; use of gabapentinoids (calcium channel 2 ). These
drugs in combination with traditional multimodal analgesics, and psychological support are crucial
elements.(1, 2, 9)

2
2.) Opioid-sparing / or opioid free techniques and protocols. Whilst opioids are still an central
component of managing severe pain, opioid-sparing approaches have become popular for several
reasons:
i) Enhanced recovery after surgery(10)
ERAS is an evidence-based, multimodal 3 phases approach (preoperative, perioperative and post-
operative)
Shown to reduce both recovery time and postoperative complications, whilst being cost effective.
First published in 2005 for elective colorectal surgery, ERAS protocols now apply for a variety of
surgeries and although not all items are implementable in the emergency setting, Lohsiriwat et al.
demonstrated improved outcomes in emergency surgeries.(11)
Managing the analgesic component of ERAS is essential for successful implementation and involves
reduction of opioids with use of regional anaesthesia and preventive pain strategies (see above).
Peripheral nerve blocks are gaining in popularity compared to neuraxial techniques, especially in
patients on anticoagulant therapy.
ii). Opioids and cancer.(2, 9, 12) The evidence for increased cancer recurrence with use of opioids and
protective effect of regional
newer preventive pain strategies, reducing perioperative opioid use during cancer surgery is feasible
and may be beneficial, although adequate pain management may need inclusion of opioids.
iii). Opioid-induced hyperalgesia (OIH) is defined as a state of nociceptive sensitization caused by
exposure to opioids. Patients present with paradoxically increasing pain, despite increased opioid use.
Treatment is by tapering or reducing the dose of the opioid and instituting alternative pain strategies.

of patients.(13)
iv). Opioid dependent patients: May require much higher doses of medication to achieve pain control.

3.) Acute neuropathic pain. There is increasing recognition that acute neuropathic pain is common and
overlooked after surgery and trauma. This is important as acute perioperative neuropathic pain needs
rapid intervention to prevent development of chronic pain. Ketamine, opioids (including tramadol)
and 2 are the preferred systemic treatment options.(9)

Table 2. Regional anesthesia as modality in pain control peri-operatively 1 ,2

NEURAXIAL BLOCKS PERIPHERAL BLOCKS
Types Agents Types Agents
Bupivacaine Bupivacaine
Intrathecal/spinal Lignocaine Peripheral nerve blocks Lignocaine
Epidural Tetracaine Intra-articular blocks Tetracaine
Caudal block Ropivacaine Infiltration on incision Ropivacaine
Adjuncts Adjuncts
iods Epinephrine
Epinephrine Dextrose
Dextrose

Sedation- Procedural Sedation

Definition
Sedation is a drug-induced depression of consciousness, with a continuum varying from minimal
sedation and anxiolysis to moderate sedation and analgesia, to deep sedation and finally general
anaesthesia.(14, 15)
Types of sedation: the continuum of sedation and sedation end-points.(14)

3
Aims
Reduce patient fear, anxiety and distress
Minimize physical discomfort and pain
Allow procedure to be carried out effectively and safely
Maintain and monitor physiological parameters
Return patient to state for safe discharge

Pre-Sedation Assessment(14)
Good history taking and examination to find contra-indication to conscious sedation
le and drugs used)
Chronic drugs (drug interaction)

Airway assessment is critical -

Safe Standards
Patient factors(14, 16)
Consider patient’s risk factors and physiology: ASA Grading
Aspiration risk need to be considered e.g.
Appropriately fasted even though controversial
Informed consent and escort available
Patient’s ability to co-operate (Children, elder
Procedures undertaken
Personnel (14, 16)

Members should be competent in Airway management, ACLS, Managing complications

Must possess adequate knowledge of drugs and effect of drugs on patient
Complex cases shouldn’t be done by a operator sedationist alone i.e.: elderly, inexperience, ASA
II, combination sedation, prolonged sedation
Facility (14-17)
Full equipped resuscitation trolley needs to be available
Monitoring equipment: BP monitoring, pulse oxim
Presence of adjuncts: supplemental oxygen, suction,
Availability of appropriate sedatives and anxiolytics and appropriate reversals
noea

with opioid use

Failed Sedation
Failure to achieve adequate level of sedation necessitating in abandoning the procedure or
converting to general anaesthesia
Causes: Inadequate initial assessment, under dosing of drugs, patient factors, drug factors, operator
factors.

4
Drugs(14)
Class Name Dose Onset of action Effect Reversal
Opioid Morphine 0.05-0.1mg/kg IV Analgesia
(Max dose
10mg)
Fentanyl 0.25-2ug/kg IV 3-6 mins Analgesia
Tramadol 50- 40 mins Analgesia
1-2mg/kg IV 20 mins
Benzodiazep Midazolam 0.05-0.1mg/kg IV 3-5 mins Sedation Flumazenil
ines Amnesiac 10ug/kg
Anxiolytic
Anaesthetic Propofol 0.5mg/kg 45-90 seconds Sedative

Ketamine 0.5-1mg/kg IV 1.5mins Analgesic

2-4mg/kg IM 2-5mins Dissociative
4- >5mins
IV-Intravenous; IMI- Intramuscular injection

Propofol
Must be used with caution. Patient selection very important p
Cardiorespiratory depressant
- Lead to general anaesthesia easily

Must always be used with analgesic agent

Ketofol ( Propofol/Ketamine) (18, 19)
Combination allow lower doses of each drug as well as dose dependent side effects
ratio propofol: Propofol: Ketamine 10:1
Leads to deeper sedation easier lower doses
Propofol/Fentanyl (18, 19)
Greater risk of respiratory depression that Ketofol
Better analgesic effect than ketofol
Assessment of Sedation(14)
Must be recorded on monitoring chart
Subjective scales: University of Michigan Sedation Scale ( UMMS) which is preferred or the Wilson
Sedation Scale
Can assist in determining which part of the continuum patient is in.

The University of Michigan Sedation Scale

Paediatric Considerations(14)
Children <5 years can’t be sedated by person who isn’t qualified in paediatric airways

5
 Avoidance of procedural sedation within 6weeks of URTI (reactive airways)
Fasting and hypoglycaemia to be considered
Child’s weight clearly documented and drugs given according to weight
Airway (definitive and rescue) and equipment available for weight and age
Upper Airways obstruction must be at the forefront of the practitioner’s mind

Discharge Criteria(14)
Must be recovered with appropriate staff and equipment

Must be accompanied by responsible person and clear discharge instructions

Chronic Pain
Chronic pain is a major source of suffering and disability world-wide.
Definition: has been simplified to “pain that persists or recurs for more than 3months”.(20)
Chronic pain may be classified into:
Chronic primary pain: represents chronic pain as a disease in itself. Characterized by disability or
emotional distress and not better accounted for by another diagnosis of chronic pain. Includes
chronic widespread pain, chronic musculoskeletal pain, primary headaches, chronic pelvic pain and
irritable bowel syndrome.
Chronic secondary pain: pain is a symptom of an underlying condition. It is organised into 6
categories:(20)
I. Chronic cancer-related pain: is due to cancer or its treatment, e.g. chemotherapy.
II. Chronic postsurgical or post-traumatic pain: develops or increases in intensity after tissue
trauma (surgical or accidental); persists beyond three months.
III. Chronic neuropathic pain: caused by a lesion or disease of the somatosensory nervous
system. May be peripheral or central.
IV. Chronic secondary headache or orofacial pain: contains the chronic forms of symptomatic
headaches. Also includes chronic dental pain.
V. Chronic secondary visceral pain: is secondary to an underlying condition originating from
internal organs of the head, neck, thoracic, abdominal or pelvic regions.
VI. Chronic secondary musculoskeletal pain: pain in bones, joint and tendons arising from an
underlying disease classified elsewhere.

Mechanism of Chronic Pain

The exact mechanisms involved in the pathophysiology are not well understood. It is thought that rapid
and long-
modulation of pain following injury:
Peripheral sensitization takes place in inflammatory pain, in some forms of neuropathic pain and in
ongoing nociceptive stimulation. During peripheral sensitization, inflammatory mediators enhance
the pain sensation in response to stimuli by decreasing the threshold and prolonging the firing of
nociceptors.
Central Sensitization occurs in inflammatory, functional and neuropathic pain. It is caused by the
increase in excitability of central nociceptor transmission neurons of the spinal cord.

Persistent Post-operative Pain

Also referred to as chronic post- ; defined as “pain persisting at
least three months after surgery, that was not present before surgery, or that had different
characteristics or increased intensity from preoperative pain, localized to the surgical site or a referred
area, and other possible causes of the pain were excluded (e.g., cancer recurrence, infection).” (21)
CPSP may affect 11% of patients at one-year post surgery, but may be as high as 50-85% for certain
types of surgery e.g. limb amputation.(21)

6
Risk Factors for Developing Persistent Post-Operative Pain
Risk factors based on type of surgery:(21)
Abdominal: Increased risk in liver transplant surgery, redo surgery for anastomotic leakage,
emergency laparotomy for bowel obstruction
Breast (11-57% CPSP): Age <65 years, breast-conserving surgery, axillary lymph node dissection,
radiotherapy
Inguinal hernia (5-63% CPSP): Age < 60, anterior mesh repair (compared to endoscopic posterior
mesh repair) or a second recurrent repair resulted in a higher incidence
Thoracic: video-assisted thoracic surgery: lower incidence compared to open thoracotomy (up to
65% CPSP)
Thyroid: increased risk with robot-assisted surgery

Risks may be further classified as follows: (21, 22)

Pre-operative Factors Post-operative factors Other

Preexisting Pain: Increased severity of Intensity of Acute Anaesthetic technique:

pre-existing pain associated with Postoperative Pain. protective regional
increased risk of CPSP blockade and adjuvant
analgesia
Preoperative Opioid Exposure Risk:
Surgery. Doses of Remifentanil.

Genetics Immune Activity

Psychologic Factors.
Demographics: F>M, Age

Management (21, 22)

Risk factor identification
Preventative strategies:

damage during surgery and injury to the nerves during dissection or retraction. Preventative
options include minimally-invasive surgery and less extensive surgery.
Treatment of pre-operative pain
Modification of anaesthetic technique
Pharmacological treatment
Psychological intervention: adequate preoperative counselling regarding the surgery and
expected outcomes can alleviate stress and help prevent CPSP.

Management options(23)
Depends on the proper identification of the aetiology and type of pain (neuropathic vs nociceptive)
via a thorough history-taking and physical examination. Pain existing from the preoperative period,
postoperative complications or the recurrence of the primary disease should be ruled out before
labelling it as CPSP.
I. Pharmacotherapy:
the first line of treatment for most patients.
I. Pain interventions: nerve blocks, nerve ablation and neuromodulation
II.
resection of neuromas (in breast, thoracic, and upper abdominal surgery)
re-implantation of proximal ends of cut nerves deep into muscle tissue
in CPSP following inguinal hernia surgery
Triple neurectomy of the ilioinguinal nerve, iliohypogastric nerve and genitofemoral
nerve; or removal of the fixation material and the mesh.

7
 Scar excision or autologous fat graft to the dermo-hypodermal junction at painful scar
III. Lifestyle modification: massage, physiotherapy, and acupuncture.
IV. Psychological interventions

Complex Regional Pain Syndromes (CRPS)(24, 25)(up to dte)

CRPS is a debilitating condition which may have a profound and debilitating effect on the patient’s life.
Defintion: Chronic neurological condition involving the limbs characterised by severe pain along with
sensory, autonomic, motor and trophic impairment. It may be induced by surgery, trauma or minor
injury. There are 2 types (although this may no longer be completely accurate):
Type I (previously known as reflex sympathetic dystrophy) corresponds to patients with CRPS
without evidence of peripheral nerve injury and represents the majority of clinical presentations.
Type II (formerly termed "causalgia") refers to cases in which peripheral nerve injury is present.

Diagnostic criteria (The Budapest consensus criteria for the clinical diagnosis):(25)
Continuing pain, which is disproportionate to any inciting event
1 symptom in each of the 4 categories on history; 1 sign in 3 of the 4 categories on examination:
Sensory: hyperesthesia/ hyperalgesia, allodynia
Vasomotor: temperature asymmetry(>1°C), skin colour changes/asymmetry
Sudomotor/edema: edema, sweating changes, sweating asymmetry
Motor/trophic: decreased range of motion; motor dysfunction (weakness, tremor,
dystonia); trophic changes (hair, nail, skin).
There is no other diagnosis that better explains the signs and symptoms

Potential aetiologies(24-26)
There are numerous theories but aetiology is poorly understood, complex and is likely a
combination of factors
Amongst these are: “exaggerated” inflammation theories, sympathetic nervous mediation,
central sensitization and cortical reorganisation, ischaemia-reperfusion, small fibre neuropathy,
and an
auto-immune disorder.

Management(24, 26)

Management must be with a specialized multidisciplinary team including the surgeon with pain
physicians, physiotherapists and psychologists. There are unfortunately few RCT data to guide therapy.

Medical Management Interventional procedures Other

NSAIDs Trigger point/tender point Psychosocial and behavioral
Anticonvulsants injections management
Antidepressants Regional sympathetic Physical occupational therapy
Bisphosphonates nerve block
Topical lidocaine or capsaicin Spinal cord stimulation Patient education
Nasal calcitonin
Oral glucocorticoids Epidural clonidine Immunomodulation
Alpha-adrenergic antagonists and Surgical sympathectomy
agonists
Ketamine infusion Botulinum toxin-A
IV Immunoglobulin Plasma exchange
Opioids

8
Surgical
Sympathectomy: likely to provide complete pain relief for patients demonstrating transient complete
relief with paravertebral sympathetic ganglion blockade (SGB). may be
offered prior to SGB and has shown successful outcomes.(27)
Amputation of the affected limb only in patients with severe hyperpathia in combination with a non-
functional or severely recurrently infected limb

References

1. Edward R M. Management of Acute Perioperative Pain. UpToDate, May 2019, (accessed 19 April
2019).
2. Tighe P, Buckenmaier
medicine in the United States: a status report. Pain Medicine. 2015;16(9):1806-26.
3. Raff M. Acute pain guidelines. South African Family Practice. 2016;58(5):20-41.
4. Engelbrecht C. Ac
Zealand. (Accessed 19 April 2019).
5. South African Acute Pain Guidelines. South African Journal of Anaesthesia and Analgesia. 24-03-
2017:S1-S137.
6. Vargas- nalgesic ladder still valid?: Twenty-four years of experience.
Canadian Family Physician. 2010;56(6):514-7.
7.
syndrome and seizures. The American journal of medicine. 2018;131(11):1382. e1-. e6.
8. Dionne R. Preemptive vs preventive analgesia: which approach improves clinical outcomes?
-4, 6.
9. ell R, Trinca J. Acute pain management: scientific
evidence, 2015. Medical Journal of Australia. 2016;204(8):315-7.
10.
perioperative care in elective colonic surgery: Enhanced Recovery After Surgery (ERAS®) Society
recommendations. World journal of surgery. 2013;37(2):259-84.
11. Lohsiriwat V. Enhanced recovery after surgery vs conventional care in emergency colorectal
surgery. World Journal of Gastroenterology: WJG. 2014;20(38):13950.
12.
reports. 2018;3(2).
13. Velayudhan A, Bellingham G, Morley- -induced hyperalgesia. Continuing
Education in Anaesthesia, Critical C -9.
14. South African Society of Anaesthesiologists Sedation Guidelines 2015. Guidelines for the safe
use of procedural sedation and analgesia for diagnostic and therapeutic procedures in adults: 2015.
South African Journal of Anaesthesia and Analgesia. 2015;21(2)S1-S36.
15. Dr I Waliaula, Dr R Singh and Dr SR Sibiya; Department of Surgery Seminar: Conscious sedation
and the control of pain (2017) 1- 10.
16. Frank R et.al; Procedural sedation in adults outside the operating room; Uptodate 2019.
(Accessed May 2019.).
17. Wood-
emergency centre. African Journal of Emergency Medicine. 2019;9(1):8-13.
18. uss BS. Clinical practice guideline for
emergency department procedural sedation with propofol: 2018 Update. Annals of emergency
medicine. 2019;73(5):470-80.
19. .
Propofol–fentanyl versus propofol–ketamine for procedural sedation and analgesia in patients with
trauma. The American journal of emergency medicine. 2018;36(10):1766-70.

9
20. Treede R-D, Rief W, Barke A, Aziz Q, Bennett MI, Benoliel R, et al. Chronic pain as a symptom or
a disease: the IASP Classification of Chronic Pain for the: International Classification of Diseases:(: ICD-
11:). Pain. 2019;160(1):19-27.
21. Thapa P, Euasobhon P. Chronic postsurgical pain: current evidence for prevention and
management. The Korean journal of pain. 2018;31(3):155.
22. Correll D. Chronic postoperative pain: recent findings in understanding and management.
F1000Research. 2017;6.
23. Preventative
Pharmacologic Considerations. Anesthesiology: The Journal of the American Society of
Anesthesiologists. 2018;129(3):590-607.
24.
trauma. 2017;5(1):2.
25. Ganty P, Chawla R. Complex regional pain syndrome: recent updates. Continuing Education in
-84.
26. Birklein F, Dimova V. Complex regional pain syndrome–up-to-date. Pain reports. 2017;2(6).
27. Singh B, Moodley J, Shaik AS, Robbs JV. Sympathectomy for complex regional pain syndrome.
Journal of vascular surgery. 2003;37(3):508-11.

10
 NEONATAL MALFORMATIONS OF THE ALIMENTARY TRACT
Dr R Singh, Dr R Bux, Dr S Govender
Moderator: Dr S Govender 3rd August 2019

INTRODUCTION
Neonatal malformations of the alimentary tract may be associated with abnormalities of other organ
systems namely VACTERL (Vertebral, Anorectal, Cardiac, Tracheo- Esophageal, Renal and Limb)

INITIAL MANAGEMENT: FLUIDS 1

Neonates with suspected obstruction must be aggressively resuscitated as a first line treatment.
Nurse all neonates or infants on the lateral position to prevent aspiration of gastric contents.

Maintenance fluids
Neonatelyte and PMS are the maintenance fluids available to us.
Daily maintenance fluids for most children can be estimated using the formula: 4 mL/kg per hour
up to 10 kg by adding 2 mL/kg per hour for 11 to 20 kg, and 1 mL/kg per hour for each additional
kilogram of body weight thereafter.
Resuscitation fluids
Modified Ringer’s lactate is the fluid of choice for resuscitation.
Initially 20mls/kg bolus is given.
Repeat boluses of 10mls/kg used to achieve urine output of 1-2mls/kg/hr. FDP bolus of 10ml/kg
is an alternative resuscitation fluid.

INITIAL MANAGEMENT: NEONATAL TRANSPORT2

Principles are based on TWO SIDES (Tube (nasogastric [NG] tube), Warmth, Oxygen, Stabilisation, IV
fluids, Documentation, Escort, Specimen)

OESOPHAGEAL ATRESIA (OA) AND TRACHEO- OESOPHAGEAL FISTULA (TOF) 3,4

Oesophageal atresia and TOF is a structural congenital abnormality characterized by incomplete
formation of the oesophagus and an abnormal communication between the oesophagus and the
trachea. Associated with VACTERL.
Embryology
During the 4th to 6th weeks of embryogenesis the trachea and oesophagus develop from a common
foregut derivative. The tracheo-oesophageal fold fuses to form a septum that divides the foregut into
a ventral laryngotracheal tube and a dorsal oesophagus. Deviation of this septum results in OA and /
or TOF. Isolated oesophageal atresia is rare.
GROSS CLASSIFICATION

Long gap OA (>2 vertebral bodies gap) occurs when there is no distal fistula and the distance between
the blind oesophageal ends is considerable (type A and B).

OA without OA with OA with OA with TOF without

TOF proximal TOF distal TOF double fitulae OA (H Fistula)

1
Presentation
Prenatal: Maternal polyhydramnios
Postnatal: Marked drooling / copious, white frothy bubbles. Tachypnoea/ coughing/ choking.
Worsening of symptoms especially while feeding. Abdominal distension.

Investigations / Diagnosis
Prenatal ultrasound: absence of stomach gas, distended oesophageal pouch (diagnostic)
Diagnosis is suspected when a NG tube will not pass further than 10-12 cm from alveolar ridge.
Plain CXR / AXR: curling up of the tube in proximal pouch. Air below the diaphragm or within the
bowel confirms TOF (diagnostic). Absence of gas = no distal fistula.
Chromosomal studies: important are Trisomy 13, 18 and 21.
Investigations to identify VACTERL anomalies:
Babygram: assessment of the vertebrae, ribs, limbs.
Echocardiography: to define the severity of the cardiac lesion and a right sided aorta as
the approach for the repair of the atresia should be a left thoracotomy
Renal ultrasound: to exclude renal pathology

Management
Medical
Includes resuscitation, lateral positioning
Insertion of a Replogle tube (a double lumen tube, where one lumen is for drainage of saliva
and the other functions as an air vent placed in the upper oesophageal pouch and connected
to continuous low pressure suction of -15 to -35 cmH20 to aspirate saliva and prevent
aspiration)
Intravenous H2-antagonists or proton pump inhibitor to increase gastric pH. Broad-spectrum
antibiotics and chest physiotherapy.
Surgery
Rigid bronchoscopy allows us to confirm the site of the fistula, to assess the trachea, and to
take specimens for microbiology.

Spitz classification (Risk stratification & Prognostication to direct timing of operative intervention)
Birth weight Associated anomaly Timing Survival rate
>1.5kg Without major cardiac anomaly Immediate repair 97%
<1.5kg +/- Major cardiac anomaly Delayed repair 59%
<1.5kg With Major cardiac anomaly Staged repair 22%

Definitive surgery
Short gap Involves division of the fistula with primary anastomosis of the oesophagus.
Long gap with or without TOF may be approached with a Livaditis myotomy/ fokers 2 staged
procedure/ multistage extra thoracic oesophageal elongation/ cervical oesophagostomy and
gastrostomy with oesophageal replacement.
A chest drain may be inserted and a trans-anastomotic tube nasogastric tube placed.
A postoperative contrast study is usually performed (locally on day 5) to rule out an anastomotic
leak prior to commencing feeds.
An extrapleural anastomosis is preferred (reduced chance of empyema in the case of an
anastomotic leak)
Primary anastomoses should be delayed to 7-10 days in premature neonates

2
Complications
Early: Anastomotic leak /stenosis or stricture, gastrooesophageal reflux (GOR), recurrent fistula,
tracheomalacia, recurrent LRTI.
Late: oesophageal dysmotility, dyspepsia, dysphagia, food impaction, strictures.

DUODENAL ATRESIA4,5
Congenital duodenal obstruction may arise due to an atresia, stenosis or web. The obstruction most
commonly occurs in the second part of the duodenum. Bilious vomiting occurs if the obstruction is
distal to the ampulla of Vater (occurs in 90% of patients). There are associated conditions or anomalies
including trisomy 21, cardiac defects, malrotation and multiple intestinal atresias.

Embryology
By the 8th week of gestation failure of recanalization of the duodenal lumen occurs, however
hypertrophy of the primitive duodenal villi leads to occlusion. An annular pancreas, a pre-duodenal
portal vein, or malrotation and Ladds bands may cause extrinsic duodenal obstruction.

Classification
Type I: Intraluminal membrane/web causing obstruction.
Type II: Short fibrous cord connecting blind-ending proximal and distal segments.
Type III: Complete separation of the proximal and distal segments with associated ‘V’ shaped
mesenteric defect.

Presentation
Prenatal: polyhydramnios
Postnatal: vomiting in the first 48 hours. If stenosis present it results in a delay in diagnoses with
feed intolerance

Investigations / diagnosis
Prenatal ultrasound: ‘double bubble’
Plain radiography: classic ‘double bubble’ with absence of distal gas (usually not present)
Contrast meal: makes diagnosis, rules out malrotation and volvulus

Management
Supportive: Resuscitation (Correct hypokalemic, hypochloremic metabolic alkalosis) / nasogastric
decompression/ thermoregulation.
Surgery: Confirm position of the DJ flexure and assess for distal atresias/malrotation.
Duodeno-duodenostomy: proximal and distal duodenal pouches are opened and
anastomosed in a ‘diamond’ shape bypassing the atretic segment.
Ladd Procedure: If malrotation present
Complications
Early: anastomotic leak, bile duct injury, sepsis.
Late: peptic ulceration secondary to alkaline reflux, blind – loop syndrome with duodenal stasis,
recurrent obstruction.

JEJUNO-ILEAL ATRESIA4-6
Jejuno-ileal atresias can be associated with gastroschisis/ malrotation/ cystic fibrosis and concurrent
duodenal or colonic atresia. They most commonly present in the proximal jejunum (30%) and distal
ileum (35%)
Aetiology
Develops as a result of an antenatal vascular insult leading to ischemia and necrosis of the affected
segment of the bowel. The use of maternal vasoconstrictive medications, smoking, and drug abuse in

3
the first trimester has been shown to increase the risk of small bowel atresia.

Classification

Modified Louw and Barnard

Type I
a mucosal web/stenosis (32%)
Type II
atretic bowel ends separated by a
fibrous cord (25%)
Type III
atretic bowel separated by a ‘V’-
shaped mesenteric gap (15%)
‘apple peel’ appearance, distal atretic
bowel coiled around the ileocolic
artery (11%)
Type IV
multiple atresias (6%)

Clinical Features
Prenatal: polyhydramnios
Postnatal: bilious vomiting/ abdominal distension/ delayed passage of meconium

Investigations / Diagnosis
Prenatal ultrasound: multiple dilated bowel loops
Radiography: abdominal x-ray: “triple bubble”. Proximal atresias show dilated loops and few air
fluid levels and absence of distal air. Distal lesions will reveal more air fluid levels.
Upper GI contrast study: confirms level of obstruction and can exclude a malrotation.

Management
Supportive: Resuscitation / nasogastric decompression/ thermoregulation.
Surgery: At laparotomy position of the DJ flexure confirmed. The dilated proximal end is resected
and anastomosed to the distal portion. Saline is injected to assess for distal atresias. It is essential
to preserve bowel length. If limited bowel length or a grossly dilated proximal jejunum, a tapering
enteroplasty is favored.
Post-operative: management of potential complication; short bowel syndrome, ileus,
complications associated with parenteral nutrition and multiple surgeries.

COLONIC ATRESIA6,7
Colonic Atresia is the rarest form of Intestinal Atresia. The incidence is approximately 1 in 20 000 live
births. Sites of colonic atresia are ascending colon 28%, hepatic flexure 3%, transverse colon 23%,
splenic flexure 25%, descending and sigmoid colon 20%. In one third of patients there are associated
congenital lesions and in rare cases there may be associated Hirschprung’s Disease.
Aetiology
Related to antenatal vascular accidents or defects in the fibroblast growth factor 10 pathway.

4
Classification
The most widely used classification divides Colonic Atresia into 3 types:
Type I: consists of mucosal atresia with an intact bowel wall and mesentery
Type II: the atretic ends are separated by a fibrous cord
Type III: the atretic ends are separated by a V-shaped mesenteric gap (most common)

Clinical Presentation
Postnatal: Infants usually present with failure to pass meconium, abdominal distension and bilious
vomiting.

Investigations / Diagnosis
Prenatal ultrasound: diameter of colon may be larger than expected for gestational age.
Plain radiograph: Multiple air-fluid levels and dilated loops of large bowel. The dilation may be
massive and mimic pneumoperitoneum
Contrast enema: Shows the calibre of the distal bowel lumen. A small diameter distal colon that
comes to an abrupt halt at the level of the obstruction is diagnostic.

Management
Treatment depends on the extent and location of the lesion and the clinical presentation of the
patient. Care should be taken to avoid perforation secondary to severe distension.
A staged approach is adopted consisting of colostomy with a mucous fistula as the initial surgery.
This is generally preferred as the proximal and distal lumen ends adjacent to the atresia are
discrepant and it is necessary to exclude distal pathology such as Hirschprung’s Disease.
Ileocolic or colocolic anastomosis should be performed as a second procedure 3 to 6 months later.

Prognosis
When diagnosed early and in the absence of other serious co-morbidities the overall prognosis for
Colonic Atresia is excellent.

ANORECTAL MALFORMATIONS (ARM)6-8

ARMs consist of a wide spectrum of defects, it occurs in 1 in 5000 livebirths and is slightly more
common in males. Is associated with VACTERL.

Embryology
The embryological basis includes failure of descent of the urorectal septum. The rectum fails to
descend through the external sphincter complex, ending above or below the levator ani muscle and
may fistulate with the bladder (males) and vagina (females) or the perineum.

Clinical Presentation
Post-natal: absence of anus, or the presence of an anal fistula and abdominal distension early in
neonatal period.
Often a period of 16 to 24 hours is needed before the defect can be properly identified.
If meconium is seen on the perineum, a perineal fistula is present. If there is meconium present
in the urine, a recto-urinary fistula exists.

Investigation / Diagnosis
Prenatal: diagnosis of ARM cannot be confirmed antenatally but associated anomalies can
Plain radiography: A prone cross table lateral view is done after 24hrs if the defect is not properly
identified, to assess the level of the defect. AXR shows dilated loops of bowel with multiple air-
fluid levels and absence of rectal gas.

5
 VACTERL abnormalities should be excluded.
Renal Ultrasound: to assess the urinary tract.
Spinal ultrasound: to detect associated spinal abnormalities if < 6 months of age
Spinal MRI: to detect associated spinal abnormalities if > 6 months of age

Classification
Currently ARMS are classified according to the Krickenbeck classification which is a therapeutic and
prognostic orientated and based mainly on the presence or absence of fistulas and their type and
location, as well as the position of the rectal pouch.

KRICKENBECK CLASSIFICATION OF ANORECTAL MALFORMATIONS

MAJOR CLINICAL GROUPS RARE/REGIONAL VARIANTS
Perineal (Cutaneous) fistula Pouch colon
Rectourethral Fistula Rectal atresia/stenosis
Bulbar Rectovaginal fistula
Prostatic H-type fistula
Rectovesical Fistula others
Vestibular Fistula
No Fistula
Anal Stenosis

Management
During the first 24 hours: - fluid resuscitation is commenced
- Antibiotic therapy is commenced
- NG tube to decompress the abdomen and prevent aspiration
- evaluate for associated VACTERL defects
If associated anomalies or complications (gross abdominal distension, sepsis or perforation):
a colostomy is performed followed by a definitive pull-through procedure at 3-6 months of
age.
If no anomalies or complications a single stage procedure is performed (lower morbidity and
mortality, better continence, easier dissection)
The decision for colostomy vs primary anoplasty are based on the type of fistula/ level in
relation to the sphincters and clinical condition of the patient.

Male Newborn
Rectoperineal Fistula: Posterior sagittal anoplasty (PSARP) or limited PSARP.
Rectobulbar, Rectoprostatic Fistula: initial colostomy followed by a PSARP or Laparoscopic
assisted PSARP for high rectoprostatic fistula
Recto-bladder neck fistula: Abdominal approach is required, Laparoscopic assisted ASARP

Female Newborn:
Rectovestibular Malformation: (Most common) Diversion colostomy and delayed definitive
repair by PSARP. A primary PSARP or primary anterior sagittal anorectoplasty can be performed
in selected cases.
Cloaca (Single opening): a diversion colostomy is performed. Definitive repair is through:
Posterior saggital anorectourethrovaginoplasty (PSARUVP ) if the common channel is <3cm
Abdominoperineal approach if common channel >3cm as it may be difficult to mobilize the vagina
through PSARP.

6
 Post-operative issues:
- In patients with a rectourethral fistula a Foley’s catheter must be left in-situ for 5-7days to
allow the fistula to heal.
- At 2 weeks post op anal dilation must begin – mum is taught how to dilate twice daily. Locally
a candle is used for this purpose.
- Once an appropriate size is reached, the colostomy may be closed. Dilations are continued
thereafter until the child is passing stool comfortably and at regular interval.

Long Term
Faecal continence is the major goal regarding correction of the defect. Approximately 75 %
maintain continence.
Constipation is common postoperatively especially in children with lower anorectal
malformations. Lower bowel washouts – may be required for children with incontinence
(true/pseudo) to achieve continence

HIRSCHPRUNG’S DISEASE (HD) 9-11

HD also known as ‘congenital megacolon’ is a developmental disorder. It is characterized by the
absence of ganglion cells in the myenteric and submucosal plexus from the anorectum, resulting in a
functional obstruction. Occurs in 1:5000 live births.

Embryology
Ganglion cells are derived from the neural crest. By 13 weeks post-conception, the neural crest cells
have migrated from proximal to distal through the GIT after which they differentiate into mature
ganglion cells. There are two main theories why this process is disturbed in children with HD.
Neural crest cells do not reach the distal intestine due to early maturation or differentiation into
ganglion cells. (Arrest of Aboral neuroblast migration)
Neural crest cells reach their destination, but fail to survive or differentiate into ganglion cells due
to an inhospitable microenvironment.

Types
Short segment disease (80%): transition zone in rectum or rectosigmoid colon. M:F ratio 4:1
Long segment disease (10%): proximal colonic. M: F ratio 1:1
Total colonic aganglionosis (10%): variable involvement of the distal small intestine

Clinical Presentation
Early Presentation:
Delayed passage of meconium beyond the first 24 hours (present in approximately 90%)
Abdominal distension, bilious vomiting, and feeding intolerance.
Caecal or appendiceal perforation may be the initial event occasionally
Fever, abdominal distension, and diarrhoea due to Hirschsprung-associated enterocolitis (HAEC),
which can be life threatening (Approximately 10% of neonates)

Late Presentation:
Patients presenting later in childhood have chronic severe constipation.
Clinical features pointing to the diagnosis include delayed passage of meconium at birth, failure
to thrive, abdominal distension, and dependence on enemas without significant encopresis.

Investigations
Plain X-Rays: show dilated bowel loops throughout the abdomen.

7
 Water-soluble contrast enema: shows a transition zone between the normal and aganglionic
bowel (pathognomonic finding of HD). Irregular contractions and mucosal irregularity is also seen.
Retention of contrast on x-ray 24hrs post enema is highly suggestive of HD.
Anorectal manometry: the absence of a recto-anal inhibitory reflex is a classical finding.
Suction rectal biopsy: may be less reliable in older children because of a higher risk of sampling
error (sensitivity > 90%, specificity > 95%). Not done locally due to lack of facilities.
Full thickness rectal biopsy: the gold standard for the diagnosis is the absence of ganglion cells in
the submucosal and myenteric plexuses on histological examination. Hypertrophic nerve fibres
(2cm above dentate line)

Management
Initial Management:
IV fluids and electrolyte replacement, NG tube decompression, IV antibiotics if sepsis /
enterocolitis suspected, colonic lavage using large bore rectal tube
Operative Management:
The surgical treatments aim to remove the aganglionic bowel and anastomose the normal
bowel to the anus while preserving sphincter function.
Surgical techniques:
Swenson, Duhamel and Soave procedures (main techniques)
Total transanal endorectal pull-through (TERPT) and the laparoscopic assisted pull-through
procedures (now preferred)
Procedure depends on age of presentation. Neonates - TERPT, older child – levelling
colostomy
Total colon aganglionosis:
These patients are managed with an initial small bowel enterostomy, followed 6 to 12 months
later by a laparoscopic assisted Duhamel procedure. The Duhamel technique offers the
advantage of creating a larger rectal reservoir in these patients.
Long Term Complications
Faecal incontinence( true/pseudo), constipation, enterocolitis

INTESTINAL MALROTATION (IM)6,12

IM is defined as either non-rotation or incomplete rotation of the intestine around the superior
mesenteric artery. It involves anomalies of fixation as well. It is seen in 1 in 6000 live births.

Embryology
It is divided into 3 stages.
Stage I: (5-10 weeks): foregut, midgut and hindgut herniate from the abdominal cavity where they
then undergo a 270º counter-clockwise rotation around the superior mesenteric vessels.
Stage II: (10-11 weeks): the bowel returns to the abdominal cavity.
Stage III: (11 weeks to term): fixation of the duodeno-jejunal loop to the left of the midline (left
of the SMA) and the cecum in the right lower quadrant

Types
Non-rotation occurs due to arrest in stage I. The normal anatomical locations of the
duodenojejunal and the caecum are lost. The mesentery forms a narrow base as the gut lengthens
on the SMA without rotation, leading to clockwise twisting and midgut volvulus.
Incomplete rotation occurs due to arrest in stage II. The peritoneal bands (Ladd's bands) running
from the misplaced caecum to the mesentery compress the third portion of the duodenum, often

8
 causing duodenal obstruction. The mesenteric base may be narrow and a midgut volvulus can
ensue. Internal herniations and right mesocolic (paraduodenal) hernias may occur.
Incomplete fixation: Failure of retroperitoneal fixation of the mesentery may result in formation
of potential hernial pouches such as a mesocolic hernia. Failure of fixation of the caecum may
result in volvulus of the terminal ileum, caecum, and proximal ascending colon.

Presentation
Acute
Sudden onset of bilious vomiting is the cardinal sign of neonatal intestinal obstruction, and
malrotation with volvulus must be the presumed diagnosis until proven otherwise.
Abdominal distention with peritonitis if vascular compromise to the completely obstructed
bowel develops with abdominal wall erythema and shock as a late sign.
Chronic
Patients present less dramatically.
Presentation is nonspecific: failure to thrive, gastroesophageal reflux, early satiety, and mild
abdominal discomfort.
Partial volvulus can lead to mesenteric venous and lymphatic obstruction and subsequently
impaired nutrient absorption.
Diagnosis
Water soluble contrast meal : (gold standard) duodenojejunal flexure to the right of the
spine, obstruction of the duodenum, and the ‘coil spring,’ ‘corkscrew,’ or ‘beak’ appearance
of the obstructed proximal jejunum.
Plain abdominal x-ray: the double bubble sign that is associated with the duodenal atresia
may be seen, however the presence of distal gas excludes duodenal atresia.
Colour Doppler Ultrasound: Inversion of the superior mesenteric vessels (SMV on the left of
the SMA. ‘Whirlpool sign’- appearance of the SMV, bowel and the mesentry wrapping
around the SMA.

Management
There has been little change from Ladd's original description of the operative technique for
correction of malrotation, with or without volvulus.
Six key elements intra-operatively are as follows:
Entry into abdominal cavity and evisceration
Counter clockwise detorsion of the bowel
Division of Ladd caecal bands

9
 Broadening of the small intestine mesentery
Incidental appendectomy (Controversial, not performed locally)
Placement of small bowel along the right lateral gutter and colon along the left lateral
gutter
• Midgut Volvulus: patients should be aggressively resuscitated, given intravenous broad-
spectrum antibiotics, and taken to the operating room for immediate exploration.

REFERENCES:
1. Hackam DJ, Grikscheit TC, Wang KS, et al. Brunicardi FC(ed). Schwart’z Principles of Surgery.
9th ed. New York: Mcgraw-Hill; 2010.
2. Puri P(ed). Transport of the surgical neonate. In: Newborn Surgery, 4th ed. Boca Raton: CRC
Press; 2017.
3. Teague WJ, Karpelowsky J. Surgical management of oesophageal atresia. Paediatric
Respiratory Reviews. 2016(19):10-15
4. Adams SD, Stanton MP. Malrotation and intestinal atresias. Early Human Development. 2014
Dec; 90(12): 921-5
5. Lodwick DL, Minneci PC, et al, editors. Intestinal atresia. In: Fundamentals of Pediatric Surgery,
2n ed. Springer; 2016.
6. Townsend CM, Beauchamp RD, Evers BM, Mattox KL et al, editors. Sabiston Textbook of
Surgery. 20th ed. eBook: Elsevier; 2017.
7. Holcomb G, Murphy JP, Ostlie D et al. Ashcraft’s Pediatric Surgery. 6th ed. eBook:
Elsevier;2014.
8. Gangopadhyay AN, Pandey V. Anorectal malformations. J Indian Assoc Pediatr Surg. 2015 Jan;
20(1):10–5
9. Butler Tjaden NE, Trainor PA. The developmental etiology and pathogenesis of Hirschsprung
Disease. Transl Res. 2013 Jul; 162(1): 1–15
10. Granéli C, Dahlin E, Börjesson A, Arnbjörnsson E, Stenström P. Diagnosis, Symptoms, and
Outcomes of Hirschsprung’s Disease from the Perspective of Gender. Surg Res Pract. 2017.
11. Green HL, Rizzolo D, Austin M. Surgical management for Hirschsprung disease: A review for
primary care providers. Journal of the American Academy of Physician Assistants. 2016 Apr;
4(16):24-29
12. Elumalai G., Logeshwaran A. Malrotation of midgut, embryological basis and clinical
significance. Elixir Embryology. 2017.

10
 PAEDIATRIC SURGICAL EMERGENCIES
Drs M Kadwa, S Parthab, C Naidoo

Moderator: Ms J Sewlall 17th August 2019

Introduction

Paediatric surgical emergency is an acute injury or illness that poses an immediate risk to a paediatrics’
life or long-term health. The management of these conditions as well as paediatric resuscitation is
important to the general surgeon.

Meckel’s Diverticulum 1,2,3

Meckel’s diverticulum (MD) is a common congenital anomaly of the gastrointestinal tract. MD
represents a persistent remnant of the omphalomesenteric duct which connects the midgut to the yolk
sac in the foetus. It is a blind ending true diverticulum containing all layers of the ileum.

The Rule of Two’s is a classic description of the essential features of MD:

Male-to-female ratio of 2:1
Occurs in approximately 2% of the population
Located within 2 feet from the ileocecal valve(+- 60cm)
Approximately 2 inches in length(+- 5cm)
Approximately 2- 4 % of patients develop a complication over the course of their lives, typically
before the age of 2.

Anomalies of the omphalomesenteric duct

a Umbilical polyp/granuloma
b Meckel's diverticulum.
c Fibrous band.
d Omphalomesenteric duct cyst.
e Patent omphalomesenteric duct.
f Patent omphalomesenteric duct with prolapse

Clinical presentation
MD is usually asymptomatic but can be found incidentally or can present with a variety of clinical
manifestations, the commonest of which is gastrointestinal bleeding. The classical presentation is
painless rectal bleeding in a child <2yrs. GIT related to MD is caused by ulceration of the small bowel
due to acid secretion by ectopic gastric mucosa within the diverticulum. The site of mucosal ulceration
and bleeding is adjacent to or close to the diverticulum, and not from the mucosa or ectopic tissue
1
within the diverticulum. Small bowel obstruction, diverticular inflammation and perforation are other
complications that may occur. A Littre’s hernia is a herniated Meckel’s diverticulum into any hernia sac.

Investigation
The majority of cases are diagnosed incidentally. A technetium 99 pertechnetate scan (‘Meckel scan’) is
the investigation of choice and shows enhancement of the ectopic gastric mucosa in the diverticulum.
Small bowel enteroclysis and mesenteric angiography can be considered but are rarely used.

Meckel's scan is a nuclear medicine study

in which technetium 99pertechnetate is
used to identify areas of ectopic gastric
mucosa. Theoretically, the scan should
identify only those diverticula that
contain ectopic gastric mucosa, which
occurs in less than 25 percent of cases.
Meckel's diverticula lacking gastric
mucosa will not be seen on a Meckel's
scan.

Management
Symptomatic patients should undergo surgical resection, which can be facilitated by either simple
diverticulectomy (excision of the diverticulum at its base) or by segmental small bowel resection and
primary anastomosis. Management of an incidental MD remains controversial with most literature
suggesting resection in young healthy patients with anatomical risk factors (length >2 cm, palpable
abnormality within the diverticulum and the presence of a fibrous band)

Intussusception 2,3,4
Intussusception is the telescoping or invagination of one segment of bowel (intussusceptum) into an
immediately adjacent segment of bowel (intussuscipiens). Mesenteric congestion of the intussusceptum
leads to venous obstruction and an oedematous bowel wall causing arterial insufficiency which
ultimately leads to ischaemia of the intestinal mucosa. This results in bowel obstruction with shedding
of the intestinal lining giving the typical clinical presentation of “red currant jelly” stools.
Aetiology
This most frequently occurs at the ileo-caecal junction in children aged 6-12 months. The majority of
cases in children are idiopathic. In children outside the stated age group or with recurrent
intussusception, a pathologic lead point causing the intussusception is more likely. Likely lead points are
polyps, lymphomas, granulomas and a Meckel’s diverticulum.
Investigation
Ultrasound: Investigation of choice and shows a mass with a “target” sign or a “pseudo-kidney” sign.
Plain AXR: Obstructive pattern with dilated loops of bowel and air fluid levels.
Clinical presentation
Colicky abdominal pain, bilious vomiting and blood stained mucoid stool (red currant jelly) is the classic
presentation. An abdominal mass may be present on digital rectal examination.

2
The Brighton Collaboration Intussusception Working Group clinical diagnostic criteria
Major Criteria Minor Criteria
Level 1 (Intestinal Obstruction) Bile stained vomit Abdominal pain
Abdominal distention Vomiting
Air/fluid levels, Dilated loops Lethargy
Level 2 (Intestinal Abdominal/rectal mass Pallor
Invagination) Intestinal prolapse Hypovolemic shock
Soft tissue mass on imaging < 1 year male
Level 3 (Intestinal Vascular PR bleeding Non-specific abnormality on x-
compromise) ‘Red currant jelly’ stool ray

Diagnostic scoring: probable if 2 or more major criteria, or 1 major and 3 or more minor criteria.
Possible if 4 or more minor criteria
Management
Non-operative reduction is the treatment of choice but is usually only successful in patients that present
early. This is done via a contrast enema using either air (pneumatic) or hydrostatic.
Contra-indications to a contrast enema in these patients are signs of peritonitis or intestinal perforation.
Operative reduction can be achieved via laparoscopy or a laparotomy.

Hypertrophic Pyloric Stenosis 3

Infantile hypertrophic pyloric stenosis (IHPS) is characterised by hyperplasia of smooth muscle fibres of
the pylorus leading to narrowing of the pyloric canal and gastric outlet obstruction.
Aetiology
The aetiology of IHPS is unclear but is probably multifactorial, involving genetic predisposition and
environmental factors. Neonatal hypergastrinaemia and gastric hyperacidity may play a role.
Clinical presentation
Progressive postprandial vomiting that is non-bilious and forceful “projectile”. Patients are emaciated
and dehydrated; may have epigastric distention with visible gastric peristalsis and a palpable “olive”
mass which is the pylorus that can be palpated in the epigastrium or to the right of the midline.
Investigation
Patients have a severe hypokalaemic, hyponatraemic, hypochloraemic metabolic alkalosis with a
paradoxical aciduria on dipstick.
Plain AXR shows a dilated gastric bubble.
Abdominal ultrasound is the investigation of choice (>95% specificity); demonstrates e pyloric muscle
thickness > 4mm and pyloric channel length > 16mm.
If there is still doubt, a contrast study will show delayed gastric emptying with retrograde peristalsis, a
“string sign” with contrast passing through a narrowed pylorus and an umbrella sign with contrast
spilling into the duodenum, outlining the hypertrophied pyloric muscle.
Management
HPS is a biochemical emergency - need adequate resuscitation prior to surgical intervention. A
nasogastric tube to decompress the stomach and avoid aspiration and a Foley catheter to monitor urine
output is essential to the initial resuscitation.
The Ramstedt’s pyloromyotomy is the goal standard of treatment and can be performed via
laparoscopy or an endo-umbilical skin incision. This involves a longitudinal incision of the anterior wall
of the hypertrophic pylorus with sharp and then blunt dissection down to the level of the submucosa;
relieving the constriction and allowing normal passage of stomach contents into the duodenum.

3
Acute Scrotum3,5
Acute scrotal pain with/without swelling and erythema
Anatomy of Spermatic Cord
The cord layers and their congruent abdominal layer includes the external spermatic fascia (external
oblique muscle.); cremasteric muscle (internal oblique muscle.) and internal spermatic fascia
(transversalis fascia).
Contents:
Arteries: testicular, cremasteric, deferential
Nerves: genital branch of genitofemoral n., sympathetic testicular nerves, Ilio-inguinal n. runs
superficial to external spermatic fascia
Veins: Pampiniform plexus becoming testicular v.
Vas deferens
Lymphatic vessels draining to para-aortic nodes
Tunica Vaginalis (peritoneum)

Causes of Acute Scrotum

Pathology Frequency Age at presentation
Extravaginal torsion Uncommon Perinatal
Intravaginal torsion Common Anytime, peak 13-16yrs
Testicular appendage torsion Very common Anytime, peak 11yrs (pre-pubertal)
Epididymitis Rare 0-6months
Orchitis Uncommon After puberty
Idiopathic scrotal oedema Uncommon 0-5yrs

Testicular torsion
Twisting or torsion of the testis results in occlusion of the gonadal blood supply which leads to necrosis
if not acted on urgently. There are 2 types:
Intravaginal: Occurs most commonly and is predisposed to by an abnormally high investment of the
spermatic cord by the tunica vaginalis. This anomaly is known as the Bell-Clapper anomaly and
results in a pendulous testis that has a horizontal lie and allows the testis to be readily twisted by
leg movement or cremasteric contractions. Outside the neonatal period, testicular torsion is almost
always associated with the Bell-Clapper variant.
Extravaginal: Occurs less commonly and manifests in the neonatal period. During descent of the
testis into the scrotum, there is a loose areolar plane around the testis which allows the entire
tunica vaginalis and the spermatic cord to twist.
Clinical presentation
In the newborn, antenatal torsion presents as a firm hard scrotal mass in an otherwise
asymptomatic baby. The scrotal skin characteristically fixes to the necrotic testis.
The older child will present with sudden onset of severe, progressive pain in the testis, lower
thigh, lower abdomen with a history of preceding intermittent testicular pain.
Examination findings are a typically enlarged, exceedingly tender, high-riding testis with transverse
orientation often associated with nausea and vomiting. Hemi-scrotal erythema with a usually absent
cremasteric reflex.
Blue dot sign: A bluish black spot seen through the scrotal skin is associated with appendicular torsion.
Investigation
Ultrasound doppler is used to determine blood flow to the testis. It has a sensitivity of 89.9% and
specificity of 98.8% and false positive of 1%.
Management

4
 Testicular torsion is a surgical emergency with viability of the testis directly linked to onset of
symptoms and surgical intervention. There is a high salvage rate in patients that undergo testicular
detorsion within 6 hours of onset of pain.
Manual detorsion is an option for cases with early presentation.
Midline scrotal exploration with contra-lateral orchidopexy is the recommended surgery.

Epididymo-orchitis
Epididymitis usually occurs in pre-pubertal period with orchitis occurring more commonly in post-
pubertal period.
It is usually caused by retrograde spread of infection from the urinary tract, through ejaculatory ducts
and along the vas deferens. Usually found in boys with urinary tract anomalies or those needing urinary
tract instrumentation eg. intermittent catheterizations.
Clinical Presentation
More gradual onset of pain worsening over days; associated with dysuria or urethral discharge.
Oedema may make assessment difficult however it can be differentiated by relief of pain on
lifting the affected testicle (Positive Prehn’s sign) and a normal lying testis.
May present with a reactive hydrocele.

Investigation
Doppler ultrasound shows increased blood flow to the testis
Urinary cultures reveal E coli in younger patients and N gonorrhoeae, Chlamydia, coliformc,
Mycoplasma in the sexually active.
Management
Antibiotic therapy
In patients with recurrent episodes: Ejaculatory duct reflux and underlying urinary tract
anomalies should be excluded with renal ultrasound and VCU post infection.

Idiopathic Scrotal Oedema

Rapidly developing scrotal swelling of unknown aetiology (5-9 years) beginning in the inguinal or
perineal region.
Often misdiagnosed in the setting of occult infective pathology. Treated with antihistamines,
corticosteroids with/without antibiotics.

Incarcerated Inguinal Hernia

Occurs as a result of a patent processus vaginalis.
Clinical Presentation
Prior history of an intermittent scrotal swelling.
Acute history of an irreducible groin swelling with obstructive symptoms
Diagnosis
Made on the basis of a suggestive history and clinical examination
Bile stained vomiting
Abdominal distention
Irreducible inguinal hernia that is tender and erythematous.
Investigation
AXR: Dilated loops of bowel with air-fluid levels
Ultrasound usually not necessary but can be used to distinguish between a tense or complicated
hydrocele
Management
NGT and Foley catheter to decompress the abdomen and avoid risk of aspiration
Trendelenburg position and reduce under sedation
Herniotomy after 48 hours to allow for inguinal oedema to settle

5
Oesophageal Foreign Bodies (FB) [3
Occurs most often between the ages of 18-48 months with possible devastating consequences
associated with button battery ingestion. Most FB will pass into the stomach once it has passed the
cricopharyngeus muscle. but some lodge at the mid-oesophagus level at the aortic arch (10-17%) or at
the OG Junction (5-20%). Contributing factors include male sex, lack of molars before the age of 4,
oesophageal disorders, immature coordination of swallowing or sphincter control or an unsafe
environment. 50-80% of FB are food items with coins being the next most common.
Clinical Presentation
Acute: Drooling, dysphagia, vomiting, features of oesophageal perforation
Longstanding duration: Failure to thrive, recurrent aspiration pneumonia, wheezing, acquired
tracheo-oesophageal fistula
Investigations
X-ray: AP and lateral views of the neck and chest are routine
Contrast study may be used to outline a filling defect in a patient with a suggestive history, but
no radio-opaque object seen on X-rays

Management
Foley catheter extraction may be attempted for a uniformly round object such as a coin if
the child presents in the first 24 hours
Care should be taken to distinguish between a coin and button battery on xray, with a “halo”
sign being present around a battery
Rigid oesophagoscopy is performed to retrieve a button battery, an object that is of irregular
shape or if the object has been in situ for >48 hrs. A flexible endoscopy is performed post
removal to exclude any oesophageal injury.

Caustic Ingestion 5
20% of all caustic ingestions can cause oesophageal injury with areas of maximal injury being the same
as with ingested FB impaction. Most ingestions in under 3years of age are preventable and those
occurring in adolescence is usually intentional and therefore more severe. 10% of oesophageal burns
occur in the absence of oropharyngeal injury.
Concurrent airway injury may occur due to aspiration or inhaled fumes.

Pathophysiology
Acid Alkali
Necrosis Coagulative Liquefactive
Penetration Limited mucosal Submucosa & muscle
Transit time Rapid Slow
Pathology Pyloric spasm Thrombosis and ischaemia
Injury location Stomach Oesophagus
Initial reparative phase lasts 2 weeks with re-epithelialization and scar formation occurring from 3rd week.

Management
Initial: NPO, IV Fluids
An NGT should not be inserted due to the risk of oesophageal perforation
Emetics and oral intake are not advised because most alkalis are neutralized in the stomach and
there is an associated increased risk of secondary injury.
A flexible endoscopy is performed within 48hr of ingestion to diagnose the extent of injury
If > 48hours, then a contrast swallow is performed prior to endoscopy
Technetium 99 sucralfate scan: Sucralfate adherence confirms oesphageal injury

6
Endoscopic grading
Grade Description Plan Additional
0 Normal, healthy
I Oedema and hyperaemia
IIA Scattered ulcers FU 2 - 3/52 ; swallow if symptomatic PPI, sucralfate, Mycostatin,
B
II Circumferential ulcers NGT under direct vision + Swallow 14 days, NG feeds
IIIA Scattered necrosis Antibiotic Coverage until oral tolerated
IIIB Circumferential necrosis Gastrostomy + Oesophageal
replacement

Late complications
Oesophageal stricture: Common complication with significant morbidity; requires multiple
anaesthetics and oesophageal dilations. If unsuccessful, may require oesophageal replacement.
Motility disorders
Carcinoma: Latency period 15-40 years, Low incidence

Anterior Abdominal Wall Defects 6.8

A newborn with an anterior abdominal wall defect is one of the most dramatic clinical presentations
and can be very disconcerting to both mum and medical professionals alike. The two most common
pathologies seen in paediatric surgery are Omphalocele and Gastroschisis. Understanding the
differences in the two entities is crucial to appropriate management.
Embryology
The abdominal wall is formed by infolding of the cranial, caudal and two lateral embryonic folds. Whilst
the abdominal wall is forming, the rapid growth of the intestinal tract leads to its migration outside the
abdominal cavity with its return within the abdominal cavity by the 10th-12th week of gestation.

Omphalocele 1, 3
An omphalocele or exomphalos is a midline abdominal wall defect with herniation of the abdominal
viscera covered by a biological membrane consisting of peritoneum on the inner surface, amnion on the
outer surface and Wharton’s jelly in-between. The umbilical vessels and urachus insert into the
membrane not the abdominal wall. This pathology is thought to result as a failure of the infolding of the
abdominal wall.
Clinical presentation
Infants with an omphalocele have an approximately 50% incidence of associated anomalies and
therefore need a full VACTERL work-up.
Beckwith-Wiedemann Syndrome: a combination of macrosomia, macroglossia, and an umbilical
defect. These children should be screened for hypoglycaemia.
Association with chromosomal abnormalities such as Trisomy 13, 15, 18, and 21
Other major associated anomalies include exstrophy of the bladder or cloaca and the Pentalogy
of Cantrell: Omphalocele, epigastric diaphragmatic hernia, sternal cleft, ectopia cordis, and
intracardiac defect, such as ventricular septal defect.
Management
Acute
Neonatal resuscitation as required and counselling of the mum.
It is imperative to maintain the integrity of the omphalocele sac and this includes:
Removing the umbilical clamp that can erode into the sac, and suture ligation of the
umbilical cord.
Covering the umbilical sac with cling wrap
Surgical management: Non-urgent if the sac is intact.
Management is either primary closure or staged closure, and this depends largely on
Co-morbidities and associated anomalies
Size of the defect: Minor (<5cm) or Major (>5cm or containing liver)
7
Primary Closure
Primary repair can be achieved with minor omphaloceles. This involves excision of the sac, reduction of
abdominal contents, ligation of the umbilical vessels and urachus with closure of the sheath.
Staged Approach
Used when primary closure might subject the baby to abdominal compartment syndrome or if com-
morbidities preclude the baby from a safe anaesthetic. Initially the sac is covered with a topical agent
such as silver sulfadiazine to allow granulation of the sac. Once granulated this is then managed with
compression dressings and closure of a ventral hernia later in life.
Prognosis
The overall survival for infants with omphalocele depends on the size of the defect and the severity of
associated anomalies.

Gastroschisis 6,7,8
Gastroschisis is a full thickness defect in the abdominal wall to the right of the umbilicus. There is a
normal insertion of the umbilicus into the abdominal wall. A variable amount of intestine herniates
through this defect with no covering membrane.
Aetiology
Thought to result from an ischaemic insult to the developing body wall. The right paraumbilical
area is at risk because it is supplied by the right umbilical vessels until involution of the vessels.
Associated with distinctive maternal risk factors: young age, exposure to cigarette smoking,
vasoactive drugs, and environmental toxins.
Incidence is 1:6000 - 10 000 live births. Often associated with intestinal atresia (10-15%) and
cryptorchidism (30%).
Clinical presentation
Ante-natal: can be diagnosed by an ante-natal ultrasound. Increased AFP.
Post-natal: Para-umbilical defect through which the intestine freely protrudes. Bowel is
characterised by a “peel” that is caused by direct exposure to the amniotic fluid: thickened,
oedematous, matted intestine.
Management
Acute: Neonatal resuscitation. These neonates are at increased risk of hypothermia, increased fluid loss,
and aspiration. This can be avoided by:
Removing the umbilical clamp and suture ligation of the umbilical stump
Covering the exposed bowel with cling wrap
Insertion of NGT for free drainage
IV line and maintenance IVF and boluses as needed
If signs of intestinal ischaemia, then neonate should be placed in a right lateral position to avoid
twisting/compression of the mesenteric vascular pedicle.
In cases of a closing gastroschisis

Surgical management:
Primary: Can be achieved in a well resuscitated neonate with minimal peel.
A suture-less bedside procedure can be attempted under sedation with reduction of the
intestine and closure of the anterior abdominal wall using steri-strips/hyperfix. Alternatively,
the child may be taken to theatre for formal abdominal wall closure under general anaesthesia.
Staged
Involves inserting a prefabricated spring loaded silastic silo bag and sequential reduction of
bowel into the abdomen over a period of 3 -7 days followed by later closure of the abdominal
wall defect either by closure of the sheath or using a prosthetic patch.
These patients are usually slow feeders. They are maintained on TPN and trophic feeds until
they gain bowel function. Late occurrence of necrotising enterocolitis has been reported in
patients after gastroschisis repair.

8
 In cases of associated intestinal atresia, a thick peel may preclude an immediate repair. The
abdominal wall is closed and the intestinal atresia is addressed in 6 to 8 weeks when the peel is
softer and more amenable to an anastomosis.

Necrotizing Enterocolitis 6,8

‘Inflammatory intestinal disorder primarily seen in premature infants, characterized by variable
damage to the intestinal tract, ranging from mucosal injury to full-thickness necrosis and perforation’.
Necrotizing enterocolitis (NEC) is the most frequent and lethal gastrointestinal disorder affecting the
intestine of the stressed, preterm neonate. It occurs at a rate of 0.7 to 1.1 per 1000 live births (3-7% of
NICU population). The overall mortality ranges between 10% - 50%.

Aetiology
Multifactorial aetiology, theorized to be an inappropriate inflammatory response in the preterm
neonate following an insult to the gut. Insult may be due to initiation of enteral feed, bacterial infection,
intestinal ischemia from birth asphyxia, umbilical artery cannulation, persistence of patent ductus
arteriosus, cyanotic heart disease, and maternal cocaine abuse. This leads to a mucosal injury to gut
with translocation of normal gut flora in a genetically predisposed neonate. This leads to a SIRS
response due to immature immunity with no inhibitory immune component.

Clinical Presentation

Investigations
The pathognomonic radiographic feature of NEC is pneumatosis intestinalis.
Other radiographic findings may include portal venous gas (poor prognostic sign), ascites, fixed
loops of small bowel, and free air. The distal ileum and ascending colon are the usual affected
areas, although the entire GI tract can be affected as in NEC totalis.
Management
Medical management
NPO with NGT decompression and IV Fluids
Septic screen and broad spectrum antibiotics with anaerobe cover
Bowel rest for 7-10 days with TPN
Serial AXR
Surgical management is indicated in:
Failure of medical treatment
Features of gut necrosis
Pneumoperitoneum
Fixed loop of bowel on serial AXR
9
Surgical options are:
Laparotomy and bowel resection with primary anastomosis or stoma
Laparotomy clip-and-drop (damage control) in an unstable patient
Peritoneal drainage to decompress the abdomen in neonates who are too unstable for theatre.
This is usually performed by insertion of a glove drain into the peritoneal cavity.

Prognosis
The overall mortality rate for surgically managed NEC ranges from 10% to 50%. NEC remains the most
common cause of short gut syndrome. Intestinal strictures may develop after medical or surgical
management of NEC in approximately 10% of infants. Neurodevelopmental delay is also a frequent
long-term complication.

References
1. Meckel’s Diverticulum. Uptodate. Patrick J Javid, Eric M Pauli. Feb 07,2018.
2. Schwartz Principles of Surgery, 10th edition.
3. Ashcrafts Pediatric Surgery, 5th edition.
4. World Health Organisation. State of the world’s vaccines and Immunisation 2010.
5. Coran AG et al. 2012. Paediatric Surgery. 7th edition. Philadelphia, USA. Elsevier Saunders
publishers
6. Townsend C, Beauchamp D; Evers M; Kenneth Mattox K. Sabiston Textbook of Surgery. 20th
Edition. Elsevier publishers. June 2016
7. Sekabira, J. & Hadley, G.P. Paediatric Surgery Int (2009) 25: 327-329. Gastroschisis: a third world
perspective
8. Ameh EA; Stephen W. Bickler; Lakhoo K; Nwomeh BC; Poenaru D. Paediatric surgery: A
Comprehensive Text for Africa. Volume I & II. Global Help Publishers

10
 SURGICAL ASPECTS OF GOITRE INCLUDING HYPERTHYROIDISM
Drs N Ndlovu, S Sibiya, IN Walliaula
Moderator: Mr YD Naicker 24th August 2019

Thyroid Embryology1 Arises from an outpouching of the primitive foregut at week 3 of gestation
Originates at the base of the tongue at the foramen caecum
Endoderm cells in the floor of the pharyngeal anlage thicken to form the medial thyroid anlage, which
descends into the neck anterior to structures that form the hyoid bone and larynx
During its descent, the anlage remains connected to the foramen caecum via an epithelial-
lined tube known as the thyroglossal duct.
This medial thyroid anlage gives rise to thyroid follicular cells
The lateral anlages originate from the 4th branchial pouch and are of neuro-ectodermal in origin. The
lateral anlages provide the calcitonin producing parafollicular/C-cells.
The median anlage fuses with the paired lateral anlages at week 5.
Thyroid follicles are apparent by week 8 and colloid formation by week 11.
The path the gland follows may result in developmental abnormalities:
Thyroglossal duct cyst/sinus: Week 5-8, duct obliterates but rarely it may persist. Can occur
anywhere along the migratory path but 80% occur at the hyoid bone. 1% risk of malignancy.
Lingual thyroid: failure of normal median anlage descent from the foramen caecum.
Ectopic thyroid: can occur anywhere in the neck/ mediastinum.
Pyramidal lobe: fibrous, band like remnant of the thyroglossal duct, occurs in 50% of patients.

Anatomy1
Normally 2 lobes connected by an isthmus. Lies posterior to the strap muscles. Weight +/-20g
Enveloped in investing fascia that condenses posteriorly to form the ligament of Berry which attaches it to
the trachea posteriorly.
The parathyroid glands in the superior posterior region of the thyroid are in close approximation with the
thyroid gland and function independently, may range from 2-6.
Blood supply
Superior thyroid arteries- arise from the External Carotid Arteries
Inferior thyroid arteries- arise from the thyrocervical trunk (a branch of the SCA)
Thyroid ima artery- arise from the aorta or innominate artery (1-4% occurrence)
Venous drainage is via the superior, middle (which drain into the IJV) and inferior thyroid veins
(which drain into the brachiocephalic vein).
Nerves
Sympathetic innervation from the superior, middle and inferior cervical ganglion
Superior Laryngeal nerves
Internal branch: sensation to supraglottic larynx
External branch innervates Cricothyroid muscle.
Cernea classifies variations in which the external branch crosses the superior thyroid pole
Intra-operative appreciation of the Space of Reeves and Joll’s triangle in order to prevent
injury

Joll’s triangle

1
 Recurrent laryngeal nerves (RLN)
Motor innervation to all the intrinsic muscles of the larynx except cricothyroid muscle
Sensory innervation to the subglottic region
A non-recurrent RLN may be present in nearly 1 % of patients.
Injury to one RLN leads to paralysis of the ipsilateral vocal cord. Bilateral RLN injury may
lead to airway obstruction.
Landmarks of the RLN: tubercle of Zuckerkandl , Simons triangle, Inferior thyroid artery,
Berry’s ligament, tracheo-oesophageal groove
Lymphatic drainage is to the regional lymph nodes. Level VI nodes are the primary zone of drainage.

Physiology and Function of the Thyroid2

Thyroid hormone biosynthesis and secretion are maintained within narrow limits by regulatory mechanisms
that are sensitive to small changes in circulating hormone concentrations. Iodide is absorbed from the GIT and
taken up by the acinar cells where it is combined with mono-iodotyrosine (MIT) and diiodotyrosine (DIT). These
are coupled to form active hormones T4 & T3 stored in the colloid and secreted into the plasma. T4 is solely a
product of the thyroid gland, whereas most T3 is produced in peripheral organs from de-iodination of T4.
Thyroid hormone secretion: Release of the hormones into the bloodstream involves the negative feedback
system of the hypothalamic-pituitary-thyroid axis.
Thyroid hormone affects almost every system in the body:
CNS: Determinants of brain and somatic development in infants and of metabolic activity in adults
Cardiac: Positive inotropic and chronotropic effects
Respitatoty: Maintains normal hypoxic and hypercapnoeic drive in respiratory centre
GI: Increase GI motility
Musculoskeletal: Increase bone and protein turnover and speed of muscle contraction and relaxation
Increase glycogenolysis, hepatic glucogenesis, intestinal glucose absorption
2 consumption, basal metabolic rate and heat production (stimulation of Na/K ATPase)
Increase cholesterol synthesis and breakdown

Goitre 2,3,4
The term goitre simply refers to the diffuse or nodular enlargement of the thyroid gland. The presence of a
goitre does not necessarily mean that the thyroid gland is malfunctioning. A goitre can occur in a gland that is
euthyroid, hyperthyroid and hypothyroid. One of the most common causes of goitre formation worldwide is
iodine deficiency.
Pathophysiology
TSH stimulates thyroid cellular growth and differentiation, as well as thyroid hormone production.
Sustained stimulation of TSH receptors on the thyroid either by endogenous TSH, TSH receptor antibodies,
or TSH receptor agonists (Human chorionic gonadotropin).

Aetiological factors involved in the evolution of goitre can be divided into primary and secondary factors.
Primary factors
Genetic heterogeneity of normal follicular cells and acquisition of new inheritable qualities by
replicating epithelial cells. Familial goitre present an autosomal dominant pattern of inheritance.
Female gender and age are likely to interact with or trigger the genetic susceptibility.

Secondary factors
Iodine deficiency or impairment of iodine metabolism may be due to congenital or environmental
factors leading to increase in TSH secretion. Stimulation of new follicle generation seems to be
necessary in the formation of simple goitre.
In pregnancy there is increase need for iodine and elevated renal clearance of iodine which requires
thyroid hypertrophy to increase iodine uptake that might otherwise satisfy minimal needs.
Natural goitrogens are substances in the diet or drugs that give for other conditions. The goitrogen
thiocyanate potentiates the effect of severe iodine deficiency in endemic areas of Africa.
Inborn errors of thyroid hormone synthesis
2
 Smoking, stress, certain drugs
Other thyroid-stimulating factors (IGF-1 and others)

Classification of goitre
Simple goiter ( Euthroid)
Multinodular goiter
Toxic-diffuse
Toxic adenoma
multinodular
Neoplastic
Benign
Malignant
Diffuse hyperplastic
Physiological
Pubertal
Pregnancy
Inflammatory
Autoimmune
Granulomatous
Fibrosing
Infective

Goitres should be monitored by examination and biopsy for possible malignant transformation, which may
be signaled by a sudden change in size, pain, or consistency. A goitre may present in various ways:
Incidentally, as a swelling in the neck discovered by the patient or on routine physical examination
On imaging studies performed for a related or unrelated medical evaluation
Local compression causing dysphagia, dyspnea, stridor, plethora or hoarseness
Pain due to hemorrhage, inflammation, necrosis, or malignant transformation
Signs and symptoms of hyperthyroidism or hypothyroidism
Thyroid cancer with or without metastases

WHO Grading of Goitre

0 Goitre not palpable or visible when the neck is extended
1a Goitre detected on palpation
1b Goitre palpable and visible when neck extended
2 Goitre visible when neck is in the normal position
3 Large goitre visible from distance

Diagnostic work-up of goiter 2,3,4

Laboratory investigations
Initial screening should include TSH, in the absence of symptoms of hyper or hypothyroidism further
testing is not required
Further tests based on presentation/suspicion:
Thyroid peroxidase antibody (TPO): Grave’s disease, Hashimoto’s thyroiditis
Anti-thyroglobulin: differentiated thyroid cancer, Hashimoto’s thyroiditis
Calcitonin: an individual at high risk for medullary carcinoma of the thyroid
Imaging
X-ray may show compression of surrounding structures
Ultrasonography to assess goitre size, consistency and nodularity. Risk of neoplasm can be effectively
assessed with US and can be used to localize nodules for US guided biopsy. Features suggestive of
malignancy: solitary lesion, heterogeneous composition, poorly defined margin, central calcification, taller
than wide and increased vascularity.

3
TI-RADS (risk stratification system described by the American College of Radiology)
TI-RAD 1 Normal thyroid gland
TI-RAD 2 Benign lesions
TI-RAD 3 Probably benign lesions
TI-RAD 4 Suspicious lesions (sub classified as 4a, 4b, and later 4c 4 with increasing risk of malignancy)
TI-RAD 5 Probably malignant lesions (more than 80% risk of malignancy)
TI-RAD 6 Biopsy proven malignancy
TI-RADS 4a has 5-10% risk of malignancy, 4b and 4c may have 10-80% risk of malignancy. TI-RADS 5 category
lesion have >80% risk of malignancy

Radionuclide uptake scan allows determination of the function of a nodule and has both diagnostic and
therapeutic roles. It is indicated if TSH levels are subnormal or for post-thyroidectomy screening purposes.
Two radionuclides are mainly used for the evaluation of patients with thyroid nodules Tc 99m and I123. I123 is
both concentrated and organified within the gland, whereas Tc 99m is only concentrated. According to the
2015 American Thyroid Association (ATA) guidelines if a thyroid scan is performed I123 should be preferred
over Tc99m. Iodine I131 best used for therapy for functional lesions and metastatic lesions.
Hot nodule: 4% risk of malignancy
Iso-functioning nodule: 9% risk of malignancy
Cold nodule: 16% risk of malignancy
Roentgenography assesses extent of goitre and presence of calcification. Replaced by ultrasonography.
Elastography evaluates the stiffness of the tissue since all thyroid nodules that are firm on palpation are
suspicious for malignancy, which adds diagnostic value in respect of malignancy prediction. However,
elastography is not widely used in clinical practice and not included in the major guidelines.
Computed tomography (CT) scan is more precise than roentgenography. CT scanning can be used to
delineate size and goitre extent as well as to assess the effect of goiter on nearby structures.
CT is useful in the follow-up of patients with thyroid cancer that shows evidence of recurrence.
Indirect laryngoscopy is used to exclude recurrent laryngeal nerve palsy.

Biopsy techniques
Fine-needle aspiration biopsy is used for cytology. US guidance is the gold standard
Core biopsy in the form of U/ guided core biopsy
Diagnostic lobectomy/thyroidectomy according to Bethesda system

Retrosternal Goitre (RG)5

The ATA defines a RG as thyroid extension beyond the sternal notch with the patient in supine position detected
either clinically or radiologically.
Presentation: Most patients are asymptomatic, and this persists until compression of surrounding relations
occurs. Symptoms include dysphagia, dyspnea, orthopnea, cough, globe sensation & hoarseness.
Evaluation: Clinical, biochemical and imaging findings as in cervical goitres are evaluated. Cross-sectional
imaging in the form of CT scan and or MRI are recommended to characterize lesions, evaluate proximity to
mediastinal relations and plan surgical approach.
FNAB is precluded by the retrosternal location, which limits access & accuracy of specimens obtained.
Management: Medical management achieves partial reduction in glandular size & is thus advocated mainly as
a pre-operative adjunct. Surgery in the form of a Total Thyroidectomy is considered the treatment of choice for
symptomatic RGs. Management of asymptomatic RGs remains highly topical.

Classification and approach for retrosternal goitre

Grade Anatomical location Approach
1 Above aortic arch (above T4) Cervical
2 Aortic arch to pericardium Manubriotomy
3 Below right atrium Full sternotomy

4
Hyperthyroidism6
Clinical state induced by excessive synthesis and secretion of thyroid hormones by an overactive gland.
Clinical: Heat intolerance, hyperactivity, palpitations, tachycardia, tremors, arrhythmias, weight loss.
Biochemical: TSH and Radio-Iodine uptake
Overt: Suppressed TSH level with elevated T3 and T4 levels.
Sub-clinical: Persistently subnormal TSH levels with T3 & T4 within normal ranges.
Causes
Increased hormone synthesis Increased release of stored hormone

Grave’s disease Thyroiditis

TMNG Iatrogenic Thyrotoxicosis
Toxic Adenoma
Drug induced
Thyroid cancer

Grave’s Disease7, 8
Commonest cause of hyperthyroidism. Highest incidence seen in females; peak incidence at 40-60 years. 50%
patients have a positive family history of auto-immune thyroid disease.
Pathogenesis: Autoimmune mediated production of Thyrotropin Receptor Antibodies (TRAb) stimulating TSH
receptors to synthesize excessive thyroxine. Chronic stimulation of follicular cells leads to goitre.
Presentation: features of hyperthyroidism described above plus features of Graves ophthalmopathy (eyelid
retraction, lid lag, proptosis, exophthalmos, motility disorders, thyroid acropachy, pre-tibial myxoedema)
Diagnosis: Combination of clinical, biochemical & radiologic findings are used to make a diagnosis.
Biochemical
Low TSH;
Elevated T3 and free T4;
Positive Anti TRAb
Imaging: Thyroid ultrasound: Enlarged, hyper vascular gland with heterogenous texture
RAIU: Diffuse homogenous uptake.
Management
Treatment Type Indications Contraindications Advantages
High likelihood of remission Allergy Well tolerated
Pregnancy (PTU only) Liver dysfunction PTU safe in pregnancy
Anti-thyroid drugs
Thyroid storm Rapid return to
euthyroidism
Large thyroid gland Pregnancy/ Lactation Avoids Surgery
Suspicious/ confirmed Possible restoration of
RAI malignancy euthyroidism
Poor patient compliance
Ophthalmopathy
Confirmed/ suspicion of Not fit for OT Rapid resolution of
malignancy 1st/ 3rd trimester hyperthyroidism
Surgery- Near
Compressive symptoms pregnancy Safe in 2nd trimester
total
CI or Inability to tolerate anti- pregnancy
Thyroidectomy thyroid drugs Easier screening
Pronounced ophthalmopathy

Toxic Adenoma (TA) 7, 10

TAs are single autonomously functioning thyroid nodules causing clinical & biochemical thyrotoxicosis often
surrounded by normal parenchyma that is functionally suppressed.
Pathogenesis:
proliferation & function of thyroid follicular cells.
5
Presentation: Patients typically present with features of thyrotoxicosis. Compressive symptoms are rare.
Evaluation:
Biochemical
Low TSH
elevated T3 and free T4
positive Anti TRAb
Imaging: Thyroid ultrasound: A solitary nodule and a small contralateral thyroid lobe
RAIU: Uptake in a single nodule increased with concomitant suppression in surrounding gland
FNAC: For normal or increased TSH, US guided if posteriorly located
Management:
Radioactive Iodine for smaller nodules with mild/well tolerated hyperthyroidism
Surgery indicated if (Ipsilateral lobectomy +/- isthmusectomy):
Compressive symptoms
Suspicion of cancer
Co-existing hyperparathyroidism requiring surgery
Large Goitre (>80g, substernal or retrosternal extension)
RAI insufficient for therapy
Need for rapid correction of thyrotoxicosis
Alternative treatment modalities include percutaneous ethanol injection, thermo-ablation, or
radiofrequency ablation.

Toxic Multi-Nodular Goitre7, 10

This refers to a goitre with multiple autonomously functioning nodules.
Clinical presentation & diagnostic approach mirrors that of a toxic adenoma.
Evaluation:
Biochemical: - Low TSH; elevated T3 & Free T4; TRAb (Negative in up tp 90%)
Imaging: Thyroid U/s: Enlarged thyroid with non-homogeneity (nodularity); cysts & calcifications
RAIU: ‘Hot’ & ‘Cold’ nodules demonstrated
Cytology: Image guided FNAB of dominant nodules (as per Bethesda system).

Management
Treatment Advantages Disadvantages Comments
Surgery Significant goitre reduction Not all patients eligible Standard therapy in large goitres/
Rapid achievement of Surgical morbidity need for rapid decompression
euthyroidism Treatment of choice if RInot feasible
Allows pathologic
evaluation
Anti- Easiest treatment option Lifelong treatment needed Indicated before surgery &
Thyroid Mainly in preparation for Small chance of remission radioiodine especially in older
Drugs surgery or RI Adverse effects in 5% patients & those with comorbidities.
(ATD) Continuous goitre growth Long term treatment recommended
when surgery & RI cannot be used.
RAI Effective in rendering Gradual reversal of Standard , unless goitre > 100g
patients euthyroid & hyperthyroidism High dose RI offered to patients with
reducing thyroid volume. Gradual reduction of goitre a very large goitre not fit for, or who
Few subjective side 5% risk of transition to decline surgery
effects. Grave’s
15% 5yr risk hypothyrodism
Treatment may need to be
repeated in some patients

6
Subclinical Hyperthyroidism7
Biochemical state of persistently low TSH level with free thyroid hormones within normal reference ranges.
0.5-7% of patients develop overt hyperthyroidism, while 5-12% revert to normal TSH levels.

Aetiology and differential diagnosis of subclinical hyperthyroidism

Endogenous Exogenous Transient Subclinical Causes of Low TSH

Hyperthyrodism (Not Subclinical Hyperthyroidism)
Grave’s Excessive thyroid Anti-thyroid drugs Pituitary/Hypothalamic
Disease replacement Thyroiditis Insufficiency
Toxic Thyroid Hormone Subacute Psychiatric Illness
Adenoma suppressive therapy Painless Drugs
TMNG Severe Non-thyroidal illness
Late 1st Trimester Pregnancy
Smoking

Evaluation: Thyroid function tests are used to establish disease severity [Mild: TSH 0.1-0.4, Severe: TSH <0.1]
and possible aetiology.
Management: Treatment is recommended for symptomatic patients with severe disease to prevent
progression to overt hyperthyroidism & decrease morbidity & mortality from associated cardiovascular &
osteogenic disease. Choice of treatment is largely dictated by the aetiology, comprising of ATDs, RAI or surgery.

Surgical Treatment of a Goitre6

Surgery is an attractive treatment modality as it offers definitive therapy through removal of the goitre.
Indications include:
Compressive symptoms
Suspicion of malignancy
Failed response to other treatment modalities
Prevention of complications from progressive enlargement
Cosmesis

The surgical options available are tabled below

Surgery Description Indication

Lobectomy Removal of diseased thyroid lobe Toxic Adenoma
Lobectomy + Removal of diseased lobe + Isthmus Toxic Adenoma
Isthmusectomy
Subtotal Thyroidectomy Removal of diseased & Non-diseased lobes + Toxic Multi-Nodular
Isthmus leaving 2-3g of thyroid tissue bilaterally Goitre
Large Goitre
Hartley Dunhill Subtotal Total lobectomy & Isthmusectomy on diseased Toxic Multi-Nodular
Thyroidectomy side + Subtotal resection on Non-diseased side Goitre
(4g left) Large Goitre
Near Total Thyroidectomy Total lobectomy & Isthmusectomy on diseased Toxic Multi-Nodular
side + Subtotal resection on Non-diseased side Goitre
(1g left) Large Goitre
Total Thyroidectomy Complete removal of all thyroid tissue. Grave’s Disease
Hashitoxicosis
Complications include
Hemorrhage and post-op hematoma <1%
Transient Hoarseness; 5-10%
Transient Hypocalcemia; 10-20%
7
 Long term voice complications; 1-2%
Permanent Hypocalcemia; 1-2%

Thyroid Storm7, 9
This refers to a rare acute & severe life-threatening complication of thyrotoxicosis characterized by a systemic
hypermetabolic state. It involves organ systems. Risk factors include thyrotoxicosis, uncontrolled Grave’s
disease and thyroid nodules. Precipitation factors include trauma, surgery, infection and drugs (anticholinergic
and adrenergic)
Evaluation: Diagnosis is largely clinical using the Burch-Wartofsky Point Scale (BWPS) system.
Management: The following algorithm gives a description in management of Thyroid storm

Thyroid Nodule (STN) 10

STN refers to a discrete lesion that is radiologically distinct from the surrounding thyroid parenchyma. Clinical
relevance is derived from the reported 5-15% risk of malignancy in these lesions. Imaging & cytological
characteristics are evaluated for risk stratification & defining treatment options.
Imaging: The ATA & ACR TIRADs systems are commonly used to evaluate lesions.
Cytology: Image guided FNA of lesions remains the recommended procedure for evaluating STNs.

The Bethesda System

Diagnostic Category Risk of Malignancy Usual Management

I. Non-Diagnostic or Unsatisfactory 1-4% Repeat FNA with U/s Guidance
II. Benign 0-3% Clinical follow-up
III. AUS OF FLUS 5-15% Repeat FNA
IV. Follicular Neoplasm or Suspicious 15-30% Surgical lobectomy
for a follicular Neoplasm
V. Suspicious for Malignancy 60-75% Near total thyroidectomy or Lobectomy
VI. Malignant 97-99% Near total thyroidectomy

8
 Management Algorithm

Solitary Thyroid Nodule

Clinical Ass. & TSH Level

Normal or High
Low TSH TSH

Thyroid US
123
I or 99Tc

Hot Nodule High Intermed. Low Very Low Benign or

Suspicion Suspicion Suspicion Suspicion Size <1cm

Treat as FNA >1.5cm FNA if >2cm

FNA if > 1cm No FNA
hyperthyroidism

Cytology Bethesda Classification

Non-diagnostic Benign Indeterminate FN/SFN Suspicious Malignant

Repeat FNA No Surgery US Risk/ Immunohistochemical stains/Molecular Test/Surgery Surgery

References
1. Brunicardi F, Andersen D, Billiar T, Et al. Schwartz's Principles of Surgery, 10e. pg 1502-1520
2. Chiaw Ling Chng et al. Diagnostic performance of ATA, BTA and TIRADS sonographic patterns in the
prediction of malignancy in histologically proven thyroid nodules. Singapore Med J. 2018 Nov; 59(11):
578–583
3. M.B Zimmermann et al. Iodine deficiency and thyroid disorders.The Lancet Diabetes & Endocrinology.
April 2015;3(4): 286-295
4. Khatawkar AV, Awati SM. Multi-nodular goiter: Epidemiology, Etiology, Pathogenesis and Pathology.
IAIM, 2015; 2(9):152-156
5. Charles T. Huins et al.A new classification system for retrosternal goiter. International Journal of
Surgery(2008) 6,71-76
6. Chen AB, V. Carty, S. American Thyroid Association Statement on Optimal Surgical Management of
Goiter Thyroid. 2014;24(2):181-9.
7. Ross DB, H. Cooper,D. 2016 American Thyroid Association Guidelines for Diagnosis and Management
of Hyperthyroidism and Other Causes of Thyrotoxicosis. Thyroid. 2016;26(10):1-79.
8. Gan T, Randle RW. The Role of Surgery in Autoimmune Conditions of the Thyroid. Surg Clin North Am.
2019;99(4):633-48.
9. Satosh TI, O. Suzuki,A. Guidelines for the Management of Thyroid Storm from The Japan Association
and Japan Endocrine Society. Endocrine Journal. 2016;63(16):1025-64.
10. Haugen BA, E. Bible, K. 2015 American Thyrioid Association Management Guidelines for Adults
Patients with Thyroid Nodules and Differentiated Cancer. Thyroid. 2016;26(1):1-274.

9
 NEOPLASMS OF THE THYROID GLAND
Dr L Jafta, Dr KSB Chiliza, Dr MO Ramawela
Moderator: Mr B Olotu 31st August 2019

Introduction
The incidence of thyroid cancer has increased globally without associated increased in mortality,5-
year survival rate of more than 85%, the increase is attributed to the increased detention of thyroid
cancer as a result of improved imaging modalities. (1)

Thyroid nodule
The American Thyroid Association (ATA) defined thyroid nodule as a discrete lesion within the thyroid
gland that is radiologically distinct from the surrounding parenchyma. May be solitary, multiple, cystic
solid or complex mass which may be functionally active or inactive.
Assessment of a thyroid nodule
Clinical evaluation: most thyroid nodules are asymptomatic and discovered by the patient and
physicians during routine neck examination neck. Characteristics of a suspicious thyroid nodule
includes:
History
Family history for MEN, MTC, and PTC
History for head and neck radiation
History for Hodgkin and non-Hodgkin’s lymphoma
Age < 20 or > 70
Male sex
Iodine intake (either insufficient and excessive quantities)
Physical examination
Firm nodule
Nodule fixed to adjacent structure
Large nodules (> 4cm)
Growth of nodule, especially during L-thyroxine therapy suppression
Symptoms of compression: hoarseness, dysphagia, dysphonia, dyspnoea and cough
Abnormal cervical lymphadenopathy
Paralysis of vocal cords
Biochemistry
TSH: Basal TSH concentration should be obtained
Suppressed TSH concentration will necessitate the determination of free thyroxine
(fT4) and free triiodothyronine (fT3). This may indicate a hot nodule.
A normal TSH should be followed up by FNA
A high TSH indicate hypothyroidism and anti-thyroid peroxidase antibodies must be
obtained to confirm Hashimoto’s thyroiditis
Calcitonin
Is a sensitive and specific tumour marker used in the diagnosis, surveillance, and
prognosis of MTC. However, routine serum calcitonin levels are not recommended in
the ATA’s guidelines.

Thyroid ultrasonography: readily available, highly effective and sensitive in the evaluation of thyroid
nodule. Some of the ultrasonographic features suggestive of the malignancy includes:
Microcalcification
Intranodal hypervascularity (evaluated by Doppler)
Hypo-echogenicity
Nodule with irregular border
Cervical lymphadenopathy

1
 Vascular invasion.
Taller than wider
Absence of halo sign

Elastography
Dynamic techniques that uses USS to provide an estimation of tissue stiffness by measuring the degree
of distortion under the application of an external forces, it is score 1-5, score 4 & 5 are highly
suggestive of malignancy. It is 97% sensitive and 100% specific.

Score Thyroid elastography

1 Elasticity in the whole nodule
2 Elasticity in a large part of the nodule
3 Elasticity at the peripheral of the nodule
4 No elasticity in the nodule
5 No elasticity in the nodule and the posterior shadowing

Genetic testing
Genetic markers such as BRAF, RAS can be performed on cytology specimen, this increases the
diagnosis of malignancy in thyroid nodule and prevent unnecessary surgery when cytology is
inconclusive or indeterminate, this has improved the pre-operative diagnosis of thyroid cancer
particularly when performed in conjunction with routine thyroid cytology.
TIRADS
Thyroid imaging and data reporting system was proposed by Horvath et al in 2009 like BIRADS in
breast, it has been validated in many prospective studies to be accurate and achieving similar
sensitivity and specificity as elastography but is cumbersome to use and only fines its place in medical
literature

Thyroid scintigraphy
Uses one of the radioisotopes of iodine (usually I-123/ i131 or technetium-99 pertechnetate (99Tc) to
determine thyroid nodule activity
functional or hot: when there is a tracer uptake greater than the surrounding normal thyroid
iso-function or warm: when the tracer uptake is equal to the surrounding normal thyroid
parenchyma
non-functioning or cold: when the tracer uptake is less than the surrounding thyroid parenchyma
Scintigraphy is recommended for patients with supressed TSH and provides functional rather than
morphological information. It has two major roles:
1. to identify hyperfunctioning nodules when a low TSH is found on initial testing
2. to determine which nodule to sample in patients with multiple nodules

FNA Cytological evaluation

This forms the cornerstone for thyroid nodule evaluation and are classified according to the Bethesda
classification, refer appendix
According to ATA guidelines, FNA may be performed with or without ultrasound guidance.

2
 THYROID MALIGNANCY SUB-TYPES
Types Papillary Follicular Medullary Anaplastic Hurthle Cell Lymphoma
Carcinoma Carcinoma Carcinoma Carcinoma Cancer
Incidence 80% 10% 5% 2% 3-10% < 1%

Age 35-40 years 30-60 years Isolated: > 60 years 50-60 years 60 years
40-50 years
Genetic:
10-20 years
Sex Female (2:1) Female (3:1) Female (1,5:1) Female (3:1) Female Female

Cell Well differentiated Well differentiated Intermediately Poorly Well Non epithelial
Differentiation differentiated differentiated differentiated
(C cells)
Histology Orphan Annie nuclei Capsular/ vascular Amyloid Giant cells
Psammoma bodies invasion May secretes calcitonin, Spindle cells
Papillary architecture Invasion influences ACTH, Serotonin
prognosis
Mode of Lymphatic Haematogenous Lymphatic/ Lymphatic Lymphatic Lymphatic
Spread Haematogenous

Symptoms None Same as papillary, Solitary nodule with Rapidly Asymptomatic Painless, rapid
May have: except swollen cervical lymph nodes. enlarging May often be enlarging neck
- hoarseness lymph nodes are Compression symptoms neck mass, multifocal and mass with cervical
- swollen lymph rare and distance metastasis dyspnoea, bilateral adenopathy
nodes dysphagia,
neck pain
Other features P’s -papillary cancer F’s M’s More Non-Hodgkins
Popular (most Follicular cancer Medullary cancer common in 4.1 female
common) Far away mets Multiple endocrine elderly predominance
Palpable LN Female 3.1 neoplasia (MEN IIa or 70% in Hx of Hashimoto’s
Positive I131 uptake FNA not usually IIb women thyroiditis
Post op I131 scan to adequate aMyloid 20-30% Hx increases risk x 60
guide treatment Favourable Median node dissection differentiated
Positive prognosis prognosis thyroid ca
(mostly
papillary)
Nodular
goitre or
rapidly
enlarging
neck mass

Treatment Surgery Surgery Surgery Early: Surgery Surgery R-CHOP*

Adjuvant
Radioiodine I131 Radioiodine I131 Median lymph node radiotherapy Radioiodine Radiotherapy
dissection Chemotherap I131
TSH suppression TSH suppression y Thyroidectomy
Screen asymptomatic - doxorubicin TSH for relief of
family member - cisplatin suppression airway
obstruction
Kinase inhibitors Late:
- vandetanib Palliative care
- cabozantinib
Prognosis Near 100% 97% 90% 7% 97% Stage dependent
(5-year
survival)

*R-rituximab, C-cyclophosphamide, H-Adriamycin, O-oncovin (vincristine), P-prednisone

3
Staging systems
There are several staging systems ranging from AMES, AGES, TNM being the most widely accepted
staging system. Please refer to appendix.

Surgical management of Differentiated Thyroid Carcinoma

Ipsilateral Lobectomy vs Total Thyroidectomy

Indications for Total Thyroidectomy Indications for Lobectomy
Known distant metastases Papillary microcarcinomas provided no previous
Extrathyroidal extension* radiation exposure
Tumour >4cm No other risk factors
Cervical lymph node metastases Tumour <1cm, unifocal & confined to thyroid without
Poorly differentiated vascular invasion
Bilateral nodularity
*invasion into surrounding structures such as strap muscles, trachea, larynx, vessels, oesophagus,
RLN

Completion thyroidectomy recommended in any of the following:

Tumour >4cm diameter, positive resection margins, gross extrathyroidal extension, macroscopic
multifocal disease, macroscopic nodal metastases, confirmed contralateral disease, or vascular
invasion.
Lymph node dissection.
The most common site of nodal metastases is in the central neck, which is cervical level VI. The role
of therapeutic lymph node dissection for treatment of thyroid cancer nodal metastases is well
accepted for cN1 disease. However, the value of routine prophylactic level VI (central) neck
dissection for cN0 disease remains unclear, although this may detect a substantial number of
patients with pN1 disease.

Recommendations
Therapeutic central-compartment (level VI) neck dissection for patients with clinically involved
central nodes should accompany total thyroidectomy to provide clearance of disease from the
central neck.(2)
Prophylactic central-compartment neck dissection (ipsilateral or bilateral) should be considered
in patients with papillary thyroid carcinoma with cN0 nodes who have advanced primary
tumours (T3 or T4) or cN1b, or if the information will be used to plan further steps in therapy.
Thyroidectomy without prophylactic central neck dissection is appropriate for small (T1 or T2),
non-invasive, cN0 papillary thyroid cancer and for most follicular cancers.(3)
Therapeutic lateral neck compartmental lymph node dissection should be performed for patients
with biopsy-proven metastatic lateral cervical lymphadenopathy.(4)

Post-Operative Management of Thyroid Cancer

Role of TSH suppression (5)
Differentiated thyroid cancer
TSH stimulates proliferation of normal thyrocytes and most thyroid cancer cells
TSH reduction reduces recurrence and cancer-related mortality
Amount of suppression and the duration needed to achieve these goals remain
unclear
High risk: <0.1mU/L
Intermediate risk: 0.1 – 0.5mU/L
Low risk with undetectable Tg level: 0.5 – 2mU/L
Low risk with low level Tg: 0.1 – 0.5mU/L

4
 Low risk with lobectomy: 0.5 – 2mU/L
TSH induced subclinical hyperthyroidism can negatively affect bone
(osteoporosis in postmenopausal women) and heart (angina in patients with IHD
and AF in elderly)
Medullary
Thyroid hormone replacement needed but not suppression of TSH.

Radioactive Iodine (6)

Differentiated thyroid cancer
Previously RAI after total thyroidectomy
Facilitate identification of persistent or recurrent neoplastic disease with
¹³¹I scintigraphy and serum thyroglobulin assays
Adjuvant treatment with aim of improving long-term outcomes by
eradicating occult microscopic foci of neoplastic cells
o Both practices recently challenged
Current guidelines recommend selective RAI use based on individual risk, with
lowest activity needed to ensure successful treatment
Not routinely recommended after thyroidectomy in low risk DTC,
unifocal papillary microcarcinoma or multifocal papillary
microcarcinoma in absence of other adverse features
Adjuvant therapy considered in intermediate risk and routinely
recommended in high risk DTC
Shown to improve survival with distant metastases and improved local
control if no distant metastatic disease.

Local therapy (Embolization/ Radiotherapy)

Differentiated thyroid cancer
No role for routine adjuvant EBRT to the neck in DTC after initial complete
surgical removal of tumour
Considered for progressive disease, thereby delaying need for systemic
treatment (e.g. EBRT or embolization for bony or liver metastases)
EBRT indicated in unresectable disease or following palliative surgery with no 131I
uptake
Medullary
EBRT used sparingly as may limit future surgical intervention with induction of
fibrosis and may reduce QOL
Consider EBRT to neck if extensive nodal disease, residual MTC or extension of
MTC beyond thyroid
Real therapeutic role still controversial because of absence of prospective
randomized trials comparing EBRT to observation.

Systemic therapy (Kinase inhibitors) (7)

No role for routine systemic adjuvant therapy in patients with DTC
Tyrosine kinase inhibitors are the best systemic option to RAI refractory progressive
disease and metastatic medullary thyroid cancer with progressive disease over past 12-
14 months
Disease progression assessed with thyroglobulin (DTC) or calcitonin (MTC)
doubling times and standardized imaging (every 6-12 months) – calculated with
RECIST
Exceptions to the rule include large tumour burden, irresectable distant sites
(e.g. trachea, spinal cord, brain) or a high level of 18-FDG uptake

5
 Differentiated thyroid cancer
Sorafenib and lenvatinib approved for use (multikinase inhibitors with
antiangiogenic properties)
Improved disease-free survival shown for sorafenib (DECISION trial - 2013) with
lenvatinib (SELECT trial - 2015)
Subgroup analysis showed significant improvement in overall survival in
older (>65 years) compared with younger patients (SELECT trial)
Previously, advanced RAI refractory progressive disease treated with
doxorubicin +/- cisplatin
Very limited efficacy and associated with serious adverse events
including cardiac and haematological toxicities
Medullary cancer
Tyrosine kinase inhibitors used in progressive and symptomatic unresectable,
locally advanced or metastatic MTC
Cabozantinib and Vandetanib licenced for use
Common adverse effects include hypertension, hand–foot skin reaction,
diarrhoea, rash, fatigue, weight loss, stomatitis and raised TSH levels
Anaplastic cancer
EBRT recommended soon after resection, preferably with radio-sensitising drugs
such as combinations of taxanes with or without platin or anthracyclines
(chemo-radiation)
Palliative chemo-radiation also for unresectable primary tumours without
detectable distant metastases
Most challenging cases present with advanced distant metastatic disease (stage
IVC). Requires balance of local control of primary tumour vs treatment of distant
metastases
If locoregional disease is imminent treat with chemo-radiation first
If airway secured, systemic chemotherapy with cytotoxic drugs or,
preferably, enrolment in clinical trial considered.

Surveillance Differences between Medullary Thyroid Cancer and Others

Differentiated thyroid cancer
Neck US with serum thyroglobulin (on thyroid hormone replacement) are best initial
diagnostic modalities in low to moderate-risk cancers
Tg measurements reach nadir 3-4 weeks post operatively
Cervical U/S to evaluate central and lateral compartments depending on risk and
Tg status every 6 to 12 months (1-3 years in low risk, longer in high risk)
Risk estimate updated continually and revised based on follow-up
77% of recurrences discovered during first 5 years after surgery
Radioiodine whole-body scans vital in months after surgery among patients with disease
stage justifying thyroid remnant ablation or with suspected metastatic disease
Whole-body scanning typically performed 2 to 12 weeks postoperatively in patients
whose clinicopathological staging may justify postoperative 131I therapy
Requires withdrawal of Thyroid hormone treatment for 4 weeks
123
I the preferred radioisotope because emissions are suitable for planar and single-
photon emission CT (SPECT)/CT imaging but do not “stun,” that is, subtly injure,
thyrocytes and limit ability to concentrate subsequent therapeutic 131I dose
131
I used for posttreatment scan more sensitive for detection of metastatic disease
due to higher administered dose and longer physical half-life, which permits imaging
at later time points when background activity has dissipated

6
 Unfortunately, many refractories to RAI (usually poorly differentiated disease -
not effective for either detection or treatment of distant disease)
CT, MRI and 18F-FDG PET make important contributions in localizing residual
disease and monitoring progression and responses to therapy in suspected
distant metastases (in appropriate setting).

Medullary thyroid cancer

Pre-operative calcitonin level serves as marker of disease burden, and
postsurgical reduction indicates success in eradicating tumour
Tumour markers (calcitonin and CEA) should be checked no earlier than 3
months after surgery to establish persistent disease
Patients with undetectable tumour markers and normal imaging after surgery
followed up annually; those with persistent tumour markers followed up closely
for progression
Calcitonin and CEA doubling times useful measures - predictive of outcomes and
aggressive tumour behaviour
Patients with calcitonin and CEA doubling times within 6 months have
shorter overall survival
Locally recurrent disease managed with observation or surgery, depending on
risk of tumour threatening vital structures and other patient factors.

Lymph Node Dissection

Differentiated thyroid cancers (8, 9)
Therapeutic central-compartment (level VI) neck dissection for clinically involved central
nodes with TT to provide clearance of disease from central neck (Strong
recommendation, Moderate-quality evidence)
Prophylactic central-compartment neck dissection (ipsilateral or bilateral) considered
with papillary thyroid carcinoma with cN0 central nodal disease but advanced primary
tumours (T3 or T4) or cN1b lateral nodes, or if information used to plan further therapy
(Weak recommendation, Low-quality evidence)
Thyroidectomy without prophylactic central neck dissection appropriate for small (T1 or
T2), non-invasive, cN0 PTC and most follicular cancers (Strong recommendation,
Moderate-quality evidence)
Therapeutic lateral neck compartmental lymph node dissection performed for biopsy-
proven metastatic lateral cervical lymphadenopathy (Strong recommendation,
Moderate-quality evidence).
Medullary Thyroid Cancer (10)
Preferred surgery is total thyroidectomy with bilateral central neck dissection (in
absence of substantial distant metastatic disease)
Dissection of lateral neck compartments recommended only if metastatic disease
suspected by neck U/S and confirmed by FNA cytology
ATA guidelines recommend contralateral neck dissection with lateral neck disease based
on calcitonin concentrations >58 pmol/L
Recommendation remains controversial
Incidental, sporadic MTC with no evidence of residual disease might be safely observed
after less extensive resections
Requires genetic testing, neck U/S, tumour markers (CEA, Calcitonin)

Conclusion
Although the prognosis of DTC is relatively good, 30–40% of patients with distant metastases
develop resistance to RAI therapy due to tumour dedifferentiation. With increased understanding of

7
thyroid carcinogenesis, biologically targeted therapeutic agents for radioiodine refractory DTC (RR-
DTC) have changed the therapeutic landscape and provide encouraging options for patient going
forward.

References
1. Davies L, Welch HG. Increasing incidence of thyroid cancer in the United States, 1973-2002.
Jama. 2006;295(18):2164-7.
2. Haugen BR, Alexander EK, Bible KC, Doherty GM, Mandel SJ, Nikiforov YE, et al. 2015
American Thyroid Association management guidelines for adult patients with thyroid nodules and
differentiated thyroid cancer: the American Thyroid Association guidelines task force on thyroid
nodules and differentiated thyroid cancer. Thyroid. 2016;26(1):1-133.
3. Denlinger CS, Sanft T, Baker KS, Baxi S, Broderick G, Demark-Wahnefried W, et al.
Survivorship, version 2.2017, NCCN clinical practice guidelines in oncology. Journal of the National
Comprehensive Cancer Network. 2017;15(9):1140-63.
4. Boolaky KN K-ML, Alkilani M. Seminar 2017.Neoplasms of the thyroid gland. UKZN
5. Cabanillas ME, McFadden DG, Durante C. Thyroid cancer. The Lancet.
2016;388(10061):2783-95.
6. Grani G, Lamartina L, Durante C, Filetti S, Cooper DS. Follicular thyroid cancer and Hürthle
cell carcinoma: challenges in diagnosis, treatment, and clinical management. The Lancet Diabetes &
Endocrinology. 2018;6(6):500-14.
7. Valerio L, Pieruzzi L, Giani C, Agate L, Bottici V, Lorusso L, et al. Targeted therapy in thyroid
cancer: state of the art. Clinical oncology. 2017;29(5):316-24.
8. Shah P, Reddy C, Lawrence R, Sudarshan P, Wilne S, Daniel M. Medullary thyroid cancer
presenting with airway obstruction. International Journal of Pediatric Otorhinolaryngology Extra.
2016;14:1-3.
9. O’Neill C, Vaughan L, Learoyd D, Sidhu S, Delbridge L, Sywak M. Management of follicular
thyroid carcinoma should be individualised based on degree of capsular and vascular invasion.
European Journal of Surgical Oncology (EJSO). 2011;37(2):181-5.
10. Randle RW, Bates MF, Schneider DF, Sippel RS, Pitt SC. Survival in patients with medullary
thyroid cancer after less than the recommended initial operation. Journal of surgical oncology.
2018;117(6):1211-6.

8
 PARATHYROID PATHOLOGY AND MEN SYNDROME
Dr JP Singh, Dr J Khan, Dr S Govender
Moderator: Mr M Kgatle 7th September 2019

Understanding the embryology and appreciating the surgical anatomy of the parathyroid glands is central
to the surgical management of hyperparathyroidism as this guides the surgeon to the many anatomical
variations associated with parathyroid glands.1
Parathyroid gland function1
The parathyroid glands produce parathyroid hormone (PTH) which modulates calcium and phosphate
homeostasis; PTH also stimulates the conversion of calcidiol (25-hydroxyvitamin D) to calcitriol (active
vitamin) in renal tubular cells, thereby stimulating intestinal calcium absorption.
Parathyroid gland cell types
The parathyroid gland contains two cell types, chief cells and oxyphil cells. Chief cells are predominant;
produce and secrete PTH in response to low extracellular calcium levels.
Oxyphil cells are larger, appear at onset of puberty, but have no known function. With nuclear medicine
scans, selectively take up Technetium-sestamibi radiotracer to allow delineation of glandular anatomy.
Parathyroid gland embryology
Arise from endodermal epithelial cells, in conjunction with the thymus (Figure 1). Most (84%) patients
have 4 parathyroid glands, 2 superior and 2 inferior. Additional glands are found in 13% of patients and
2

Figure 1: Embryological development of parathyroid glands

Superior parathyroid glands
Derived from 4th branchial pouch, closely related with lateral lobes of the thyroid.
Lie under the thyroid superficial fascia, posterior to the recurrent laryngeal nerve
Can reside inside thyroid capsule, superior and medial to posterior tubercle of Zuckerkandl of thyroid.
Usually 1-2 cms cranial to jjunction of recurrent laryngeal nerve with the inferior thyroid artery and
within 1 cm of entry of recurrent laryngeal nerve into the ligament of Berry and the cricoid cartilage.
Inferior parathyroid glands
Derived from the 3rd branchial pouch, closely associated with the thymus and have a longer
embryologic descent, which leads to more variability in their anatomic position.
Can be found in the carotid sheath, in the anterior mediastinum or even pericardium.
Majority found near the inferior pole of the thyroid, anterior to the recurrent laryngeal nerve.
Often found in thyrothymic tract, or just inside the thyroid on the inferior portion of the lobes.

Parathyroid gland blood supply

The superior parathyroid glands receive most of their blood supply from the inferior thyroid (ITA) and
branches of the superior thyroid artery (15-20%) when in proximity to superior pole of the thyroid.

1
 The inferior parathyroid glands receive their end-arterial blood supply from the ITA. Ligation of the
branches of the ITA artery close to the thyroid parenchyma and medial to the recurrent laryngeal
nerve may help preserve parathyroid vascularity.
Venous drainage is to superior, middle, and inferior thyroid veins that drain into the internal jugular vein
or the innominate vein.
The embryology and surgical anatomy is relevant in the context of a missed parathyroid gland, a common
cause for persistent hypercalcaemia following surgery for hyperparathyroidism.

Parathyroid gland size, variations in location and numbers 3

Normal parathyroid glands are approximately 5 x4 x2 mm and weigh 35-50 mg.
Ectopic parathyroid glands
Ectopic parathyroid glands that fail to fully migrate are termed "undescended."
Ectopic sites (in decreasing frequency) are paraesophageal, mediastinum, intrathymic, intrathyroidal,
carotid sheath and a high cervical position.
Supernumerary (>4) parathyroid glands occur in 2.5-15% of individuals
Can range from 5 to 8 in number.
Can reside anywhere from behind the thyroid to and including within the thymus, representing the
line of descent of thymic tissue during embryogenesis.
Mostly located within the thymus or in relation to thyrothymic ligament (two thirds of cases).

Causes of Hyperparathyroidism 4
Primary (PHPT)
Parathyroid adenoma, hyperplasia, carcinoma
Rare familial disorders
Normocalcaemic hyperparathyroidism
Secondary (SHPT)
Renal failure, impaired calcitriol (bioactive vitamin D) production, hyperphosphatemia
Decreased serum calcium
Inhibition of bone resorption
Tertiary (THPT)
Observed most commonly in patients with chronic SHPT on dialysis for years.
The hypertrophied parathyroid glands enlarge over time and continue to over secrete PTH,
despite Se Ca levels that are within the reference range or even elevated.
The hypertrophied glands become autonomic and cause hypercalcemia, even after
withdrawal of calcium and active vitamin D therapy.
May also become resistant to calcimimetic treatment

Differential diagnosis of primary hyperparathyroidism5

Note that thiazide diuretics and lithium reduce urinary calcium excretion and can cause mild
hypercalcemia; lithium also decreases parathyroid gland sensitivity to calcium.

2
 Primary Hyperparathyoidism (PHPT) 6
Most common cause of hypercalcemia in the outpatient clinical setting
Prevalence ranges from 1 to 4/ 1000 population
Female: male ratio: 2:1 to 3:1, with incidence increases with age
Postmenopausal women have an incidence 5x higher than general population
Parathyroid adenoma or carcinoma
Single gland adenoma: 75-85%
Multigland adenoma; 2 glands: 2-12% , 3 glands <1-2% , 4 or > glands: 1-15%
Parathyroid carcinoma: 1%
Lower pole adenomas are more common than upper pole adenomas
Sizes range 1 - 3 cm and weights from 0·3 g to 5 g; may be more than 25g.
Largest reported weighted 120g adenoma. Largest number was 8.
Rare Familial Disorders
Multiple endocrine neoplasia (MEN) type 1 (infra vide)
MEN type 2A syndromes – (infra vide)
Familial Hypocalciuric Hypercalcemia - autosomal dominant- mutation of CaSR gene
Familial HPT –jaw tumour syndrome- HRPT2 gene; autosomal dominant
Familial isolated hyperparathyroidism
Normocalcemic hyperparathyroidism
Present during evaluation for low bone mineral density (BMD).
PTH levels are found to be elevated in the absence of hypercalcemia.
For diagnosis of normocalcemic hyperparathyroidism, all secondary causes for
hyperparathyroidism excluded.

Familial Hypocalciuric Hypercalcemia vs Primary Hyperparathyroisism (PHPT)

FHH PHPT
Mechanism CaSr gene on chromosome 3: makes PTH less sensitive to Adenoma Hyperplasia
calcium; higher calcium level required to reduce PTH Carcinoma
secretion
Family history Autosomal dominant Syndromes rare
PTH Mildly high in 15-20% High normal - high
Urine Ca/Mg ratio Low Normal - high
Symptoms - +/-
Management Conservative Parathyroidectomy
Age < 40 years >50 years
Sex Male = female Female

Clinical Presentation of PHPT

Asymptomatic incidental hypercalcemia noted in 70-80%; in most patients, mean Se Ca < 0.25
mmol/L above the upper normal range
Normocalcemic hyperparathyroidism: when low BMD, osteoporosis, or fragility fractures.
Symptomatic hypercalcemia: classically “Stones, Bones, Groans, Psychiatric Moans”
- Renal manifestations include nephrolithiasis (15-20%), nephrocalcinosis, polyuria, renal insufficiency,
acute hypercalcaemic crisis with nephrogenic diabetes insipidus, dehydration when calcium >3·0
mmol/L
- Psychiatric moans include neuropsychiatric, lethargy, decreased cognitive and social function,
depressed mood, psychosis, neuromuscular weakness and myalgia
- GIT manifestations include constipation, nausea, vomiting, anorexia, PUD or acute pancreatitis

3
- Bone manifestations include bony pain, low bone mineral density, fragility fractures , osteitis fibrosa
cystica ( <5 percent of patients ), proximal muscle weakness.
- Cardiovascular: features are shortened QT interval , vasoconstriction, arrhythmias in severe
hypercalcemia, deposition of calcium on valves, in coronaries, and myocardium
- Other Manifestations include arthralgia, synovitis, arthritis

Diagnosis of PHPT
Serum calcium
Repeat Se Ca2+ to confirm, correct for low serum albumin; if the ionized Ca2+ not measured, the
interpretation of total calcaemia should consider serum albumin.
"Corrected" Ca (mmol/L) = Ca measured (mmol/L) + 0.020 or 0.025 (40 - albumin (g/L))].
Longstanding asymptomatic hypercalcemia is suggestive of PHPT; in young individuals, should
raise the possibility of FHH.
PTH
Elevated above normal range in approximately 80- 90% in PHPT
Modest elevation (x2 normal in parathyroid cancer and SHPT associated with renal failure
In 10-20%, minimally elevated or normal; given the patient's hypercalcemia, measurement of 24-
hour urinary Ca excretion may help distinguish PHPT from FHH
When PTH below or in the lower end of the normal range, non-PTH-mediated causes of
hypercalcemia should be investigated
24-hour urinary calcium
Not always required for the diagnosis of PHPT
Measured in asymptomatic PHPT to assess risk of renal complications (when urine Ca2+ is high).
When hypercalcemia and PTH only minimally elevated or inappropriately normal, 24-hour urinary
Ca2+ helps to distinguish PHPT from FHH.
If urinary Ca2+ excretion >200-300 mg/day Ca2+ , FHH excluded.
If urinary Ca2+ excretion <200 mg/day, FHH or PHPT with concomitant vitamin D deficiency are
possibilities. Lower urinary Ca2+ values may be seen in patients with PHPT whose Ca2+ intake is
low
75% of FHH excrete <100 mg of Ca2+ in urine daily
Serum 25-hydroxyvitamin D
May be useful to distinguish PHPT from other conditions in the following circumstances:
Differentiation of FHH from mild PHPT with vitamin D deficiency; patients have elevated
serum PTH and Ca2+ but normal or low 24-hour urinary Ca2+ excretion.
Differentiation of SHPT due to vitamin D deficiency from normocalcemic PHPT; low in the
former and normal in the latter.
Supporting findings
Include low P04, high chloride, high urine pH (>6) and high alkaline phosphatase
Localization studies (infra vide)
Following the biochemical diagnosis of PHPT, localisation studies such as ultrasonography,
technetium-99m sestamibi, CT scan, MRI scans should not be used to establish the diagnosis of PHPT
or to determine management - should be performed only when surgery is being planned.

Secondary hyperparathyroidism (SHPT)

SHPT is the overproduction of PTH secondary to hypocalcemia, typically a result of vitamin D deficiency
and/or chronic kidney disease (CKD), as listed among the cause, below:
Renal failure, impaired calcitriol (bioactive vitamin D) production, hyperphosphatemia
Decreased calcium
Low oral intake
Vitamin D deficiency

4
 Malabsorption
Renal calcium loss on Lasix therapy
Inhibition of bone resorption
Biphosphonates
Hungry Bone Syndrome
Definition of problem
CKD is arguably the commonest cause of SHPT and varies based on estimated glomerular filtration rate
(GFR). In milder forms of CKD, elevations in PTH levels occur in about 10% of patients, while being seen in
90% of individuals with severe CKD approaching the need for dialysis.
SHPT Pathophysiology in Renal failure
Calcium and phosphorous homeostasis is regulated between bone, kidney and parathyroid gland;
Key modulators include FGF-23, 25-hydroxyvitamin D, 1, 25-dihydroxyvitamin D, and PTH.
FGF-23 is released from bone due to increasing serum phosphorus levels and acts in the kidney to
increase phosphorous excretion and decrease 1 alpha hydroxylation of 25-hydroxyvitamin D.
FGF-23, along with serum phosphorous, also decreases PTH secretion, to maintain calcium and
phosphorous balance.
In CKD, stages 3-5 (GFR < 59 mL/min), FGF-23 levels increase, initially leading to phosphaturia and
decreased PTH excretion.
As the CKD progresses, there is a resistance in the kidney and parathyroid gland to FGF-23 and a
deficiency in the kidney of 1 alpha hydroxylation of vitamin D, both of which result in reduced
phosphorous excretion, resulting in hypocalcemia and hyperphosphatemia, thereby maintaining
stimulation of PTH synthesis and parathyroid gland hyperplasia.
Clinical presentation
Virtually all patients with CKD have hyperparathyroidism to some degree; there is no unique clinical
presentation that is a hallmark of SHPT.
In patients with SHPT due to vitamin D deficiency, the symptoms are mainly due to vitamin D
deficiency (osteomalacia with increased fracture risk, myopathy); in advanced cases, some may have
bone pain.

Laboratory studies
Measure serum PTH, calcium, phosphorus, and 25-hydroxyvitamin D.
Usually have a low-normal calcium and elevated PTH.
Phosphate level higher with reduced kidney function and lower values with vitamin D deficiency.
Imaging studies
Radiographic evaluation is limited to assessments of the bone disease.
Radiographs of sites of bone pain; hand x-ray may show characteristic subperiosteal erosions.
Imaging of parathyroid glands is not indicated unless primary hyperparathyroidism is suggested.

Hyperparathyroidism Issues in Management7-11

Primary Hyperparathyroidism
Medical Treatment
The treatment aims are to improve bone mineral density and to balance Calcium homeostasis.
Currently no drugs specifically approved as first line treatment for PHPT.
Surgical Intervention
Surgical intervention indicated in all patients with biochemically confirmed symptomatic Primary
Hyperparathyroidism. Parathyroidectomy is the only definitive cure for PHPT.
Specific guidelines for surgical treatment include:
Age younger than 50 years
Significant Hypercalcemia ( >2.80mmol/l)
Silent Nephrolithiasis or nephrocalcinosis

5
 Patients who are unable to comply with surveillance protocols
Patients with high risk for cardiovascular sequelae other than hypertension
Creatinine clearance reduced by 30% or more
24 hour total urinary calcium excretion greater than 10mmol (400mg)
Osteoporosis
Serum adjusted Calcium more than 0.25mmol/L above the upper limit
Patient request
Role of Localization
Avoids erroneous exploration that may impair patient quality of life.
Now routine to localize hyperfunctioning parathyroid glands before parathyroidectomy.
One should be mindful of the different pathologies that can affect parathyroid surgery such as:
parathyroid single adenoma vs multiple adenomas; parathyroid cancer vs thyroid nodule; ectopic
parathyroid vs lymph node metastasis.
Non-Invasive Localization Studies
Ultrasound: Non-invasive, inexpensive. An enlarged parathyroid gland appears as a hypoechoic
homogenous extrathyroidal mass; normal parathyroid gland is typically too small to be visualized.
CT Scan: Used when the probability of ectopic glands is high such as patients with recurrent or
persistent hyperparathyroidism. Localizes adenomas located in the retro-tracheal, retro-
oesophageal and mediastinal spaces better than ultrasound.
4D parathyroid computed tomography (4DCT): The 4th dimension is the perfusion information
derived from multiple contrast phases. Hyperfunctioning parathyroid glands typically display
rapid uptake and washout of contrast.
Sestamibi Technetium-99m scintigraphy: most commonly used localization study for parathyroid
disease. Uptake is by the mitochondria in parathyroid tissue. It can be used to localize
parathyroid adenomas in 85-95 % of patients.
MRI: Sensitivity equivalent to that of parathyroid scintigraphy. Useful when parathyroid
scintigraphy is negative or equivocal or when it suggests an ectopic gland.
Single-photon Emission Computed Tomography (SPECT): Can provide true 3D imaging. Improves
imaging of ectopic sites otherwise difficult to explore such as retro-oesophageal space or
mediastinum. Favoured in patients with recurrent hyperparathyroidism after prior surgery.

Invasive Localization Studies

Selective Venous Sampling of PTH: is the more commonly used invasive modality, it is highly
sensitive and specific localization procedure in persistent or recurrent PHPT.
Angiogram: Combines selective transarterial hypocalcemic stimulation with nonselective venous
sampling . Considered positive if PTH levels increases X1,4 or if a blush is noted on arteriography.
Ultrasound guided FNA: Used to discriminate thyroid nodules from enlarged parathyroid glands
Ultrasound guided Jugular venous sampling

Operative Approaches
Bilateral Cervical Exploration (BCE)
Historically, BCE with examination of all 4 glands was the standard option
In the hands of experienced endocrine surgeons >95% success rates with minimal morbidity.
In 4-gland hyperplasia (multigland disease), subtotal parathyroidectomy can be performed.
BNE parathyroid localization studies not available or if they fail to identify any abnormal
glands.
Secondary and Tertiary Disease
Focused Parathyroid Exploration: Performed if imaging suggests a single parathyroid adenoma.
When performed with IOPTH monitoring, focused parathyroidectomy results in excellent outcomes
comparable with bilateral cervical exploration.

6
 Minimally Invasive Parathyroidectomy (MIP): Shorter operative time compared to BCE, equivalent
success rates, improved cosmesis (smaller incision) and decreased pain.
Minimally Invasive Radio guided Parathyroidectomy: Radio-guided parathyroid surgery is started
30min to 3hr after 99m Tc Sestamibi administration. A small incision is made directly over the
presumed location of the adenoma.
Endoscopic parathyroidectomy (less commonly used). Does not offer significant advantages over
open focused parathyroidectomy.

Intra-operative parathyroid Localization

99m
Tc Sestamibi may used to identify parathyroid adenomas by radio-guidance.
Intra-operative gamma probe localization of an adenoma is most successful within a very narrow time
window of 2-3 hours after tracer injection.
The surgical bed canned again to ensure complete removal of the adenoma.
This technique eliminates the need for intra-operative frozen sections and hormone assays.

Role of Nerve Monitoring: Typically used for complex or re-operative cases.

Intra operative parathyroid hormone monitoring: May be used to indicate when all hyperfunctioning
parathyroid tissue has been removed. A baseline PTH value is obtained and a reduction of 50 % in PTH
level is an accepted standard for successful removal of the suspected adenoma.
Role of Frozen Section: May be used intra-operatively, to determine whether a nodule removed is
actually parathyroid tissue, since thyroid nodules, small lymph nodes, aberrant thymic tissue, and fat may
be mistaken grossly for parathyroid tissue.
Persistent Hypercalcemia post-operatively
PHPT considered biochemically cured if they maintain eucalcemia 6 months after parathyroidectomy.
Some patients develop persistent disease (within 6 months of initial exploration) or recurrent disease
(>6months from initial exploration).
Greater risk of complications associated with reoperation such as recurrent laryngeal nerve injury and
permanent hypoparathyroidism.
Indications for reoperation include include nephrolithiasis, osteoporosis, serum calcium level >12mg/dl,
hypercalciuria and a 30% decrease in renal creatinine clearance

Relative contra-indications to Surgery

A known contra-lateral recurrent laryngeal nerve (RLN) injury or vocal cord dysfunction.
Symptomatic cervical disc disease
Familial Hypocalciuric Hypercalcaemia

Secondary Hyperparathyroidism9-11
Medical Management
Low phosphate diet, phosphate binders, adequate intake of calcium and 1.25-dihydroxy vitamin D and a
high calcium, low aluminium dialysis bath and calcimimetics.
Surgical Management
PTH elevations in combination with persistent hypercalcaemia (>2.6mmol/l – absolute indication),
significant calciphylaxis (calcium deposition in skin - absolute indication), uncontrolled
hyperphosphataemia, elevated alkaline phosphatase levels (>300u/L) and evidence of bone erosion.
Additional indications - poorly controlled hypertension, refractory pruritis, peripheral neuropathies,
erythropoietin resistant anaemia.
Pre-operative imaging in SHPT is controversial
Operative Approach

7
 Surgical management involves a bilateral cervical exploration plus thymectomy. A subtotal
parthyroidectomy (3 and a half gland resection) is the optimal surgical approach for patients with
SHPT.
Total parathyroidectomy with the removal of all 4 glands and auto transplantation of parathyroid
tissue into the forearm has fallen into disuse.
In patients who undergo total parathyroidectomy, cryopreservation of excised tissue is performed as
the parathyroid autograft may prove to be non-functional.

Tertiary Hyperparathyroidism (THPT)9-11

Medical Management: Calcimetic agents, low phosphate diet, phosphate binders, adequate intake of
calcium and 1.25-dihydroxy vitamin D, a high calcium, low aluminium dialysis bath may be implemented.
Indications for surgery
Biochemically, the picture is similar to PHPT. THPT usually resolves within a year after renal
transplant. Thus patients are observed for at least 1 year before considering parathyroidectomy.
If the patient has frank hypercalcaemia in the immediate post-transplantation period,
nephrocalcinosis or renal stones with persistently raised serum calcium, surgery isindicated.
Severe Hypercalcemia (Calcium > 12.5mg/dL)
Persistent Hypercalcemia > 2 years after renal transplantation, assosciated with:
- Decline in renal function, without graft rejection
- Nephrolithiasis
- Progressive Bone disease
- Pancreatitis
Operative Approach in patients with THPT, a subtotal parathyroidectomy is the preferred approach.

Multiple Endocrine Neoplasia Syndromes12-15

There are 3 distinct forms of MEN syndromes, each characterized by their symptoms, the hormones
produced and genes involved. The workup and management of each of the types differs, as the spectrum
of associated tumours is different with each.
Multiple Endocrine Neoplasia Type 1 (MEN-1)
Comprises endocrine tumours of parathyroid, endocrine pancreas-duodenum, and anterior pituitary
(3p’s). Also increased incidence of foregut carcinoids, adrenocortical hyperplasia and non-endocrine
tumours.
Parathyroid tumours
PHPT is the commonest detected endocrine pathology in MEN1, occurring in up to 95% of
patients.
Patients generally present between the 3rd-5th decade; symptoms similar to sporadic PHPT
Diagnosed by raised ionized or total-albumin corrected Se Ca together with inappropriately raised
serum PTH
Screening with Se Ca in patients with pancreatic or pituitary tumours, or foregut carcinoids may
reveal MEN-1.
Surgery is the treatment of choice. Conventional open BNE with subtotal parathyroidectomy (3 to
3 and half gland resection) is recommended operation, with concurrent trans-cervical
thymectomy.
Total parathyroidectomy with forearm (or subcutaneous thoracic/abdominal) auto
transplantation is less commonly performed.
Pituitary tumours
Occurs in 30-60% of patients
Pituitary tumours comprise prolactinomas, somatotrophinomas, corticotrophinomas, as well as
non-functioning adenomas in 15% of cases.
The majority of these tumours are solitary benign macroadenomas.

8
 Presentation is dependent on the hormones secreted as well as local mass effect.
MRI preferred imaging modality; functional status determined with biochemical and hormone
tests
Treatment consists of medical therapy (dopamine agonists for prolactinoma; octreotide for
somatotrophinomas) or selective transphenoidal surgical hypophysectomy
Radiotherapy reserved for residual unresectable tumour tissue.

Pancreatico-duodenal tumours
Pancreatic involvement is multicentric. Numerous microadenomas are located throughout the pancreas
and occasionally the duodenum.
Gastrinoma
Over 50% are malignant and can metastasize to regional lymph nodes and the liver.
Those with MEN1 (40%) occur at earlier than sporadic tumours and follow a more benign course.
Zollinger-Ellison syndrome (ZES): triad of gastrinomas, hypergastrinemia, and severe ulcer
disease.
Presentation is multiple ulcers in atypical locations that fail to respond to medical therapy
Diagnosis confirmed by elevated gastrin level (>1000 pg/mL). A secretin stimulation test may be
performed if gastrin level is equivocal (>200pg/mL confirmatory).
Localization best performed with a combination of octreotide scan, CT and EUS.
Gastrinoma triangle: 90% located within the space bordered by cystic and common bile duct, the
junction of 2nd and 3rd portions of the duodenum, and junction of neck and body of the pancreas
Medical management includes acid suppression with PPI therapy.
Surgery may be beneficial if tumour > 2 - 3 cm, or when gastrin excess could be regionalized.
Surgery proposed when absence of liver metastases without preoperative tumour localization or
regionalization, because most (90%) MEN-1 ZES patients have solitary, or typically multiple, small
duodenal tumours causing the gastrin excess.
Surgical options include distal pancreatectomy, enucleation of lesions, regional
lymphadenectomy and duodenotomy, with local resection of any tumours found within the
duodenum.
Treatment of non-resectable tumour mass includes somatostatin analogues, biotherapy, targeted
radionuclide therapy, locoregional treatments and chemotherapy.
Insulinomas
In about 10% of MEN1 and classically presents with “Whipple’s triad” - fasting or exercise induced
hypoglycaemia, plasma glucose level <2.2 mmol/L and reversal of symptoms with glucose.
Diagnosis confirmed with monitored 72 hours fast, during which plasma glucose and insulin levels
are measured; inappropriately high insulin level with low glucose level is indicative of an
insulinoma.
Usually benign, occasionally multifocal and may be located throughout the pancreas.
Localization is best performed with CT scan and EUS.
Surgery: enucleation of lesions within head and uncinated process and with distal
pancreatectomy.

Multiple Endocrine Neoplasia Type 2 (MEN-2)

The MEN-2 syndromes are an autosomal dominant genetic disorder and occurs as a result of an aberrant
mutation in the RET gene. They are sub-classified into MEN-2A and MEN-2B:
MEN-2A is most common subtype; associated with medullary thyroid cancer (MTC) (>90%),
pheochromocytoma (40-50%) and PHPT (20%). MTC is often the initial presenting feature.
MEN-2B is the rarest subtype and is associated with MTC (100%), pheochromocytoma (50%) and
absence of PHPT. The characteristic features are ganglioneuromatosis, and typical features with
Marfanoid habitus, enlarged lips, and mucosal neuromas in the tongue, lips, and eyelids.

9
Medullary thyroid carcinoma (MTC) – refer to Seminar on Thyroid cancer (31st August 2019)
Pheochromocytoma – refer to Seminar on Surgical Aspects of Hypertension (6th July 2019)

Multiple Endocrine Neoplasia Type 4 (MEN-4)

MEN-4 is an autosomal dominant syndrome similar to MEN1 with variable age of onset. Associated
with parathyroid adenomas (81%), pituitary adenomas (42%), NET, and nonendocrine tumours
Various types of pituitary adenoma have been reported: Cushing disease, somatotropic adenoma,
prolactinoma, and non-functioning pituitary adenoma.
Cases of gastric and bronchial carcinoid tumour or ZES have also been reported. Other associated
tumours include those of the adrenals, kidneys, and reproductive organs.

References
1 Fuleihan G, Arnold A. Pathogenesis and etiology of primary hyperparathyroidism.
https://www.uptodate.com/contents/pathogenesis-and-etiology-of-primary-
hyperparathyroidism. June 2010
2 Huayue Chen H, Senda T, Emura S, Kubo K Open Anatomy Journal.2013; 5: 1-9
3 Roy M, Mazeh H, Chen H, Sippel RS. Incidence and localization of ectopic parathyroid adenomas
in previously unexplored patients. World J Surg DOI 10.1007/s00268-012-1773-z
4 Carlson D. Parathyroid Pathology: Hyperparathyroidism and Parathyroid Tumors. Archives of
Pathology & Laboratory Medicine. 2010; 134(11): 1639-1644
5 Allerheiligen DA, Schoeber J, Houston RE, MohlVK, Wildman KM.Hyperparathyroidism. Am Fam
Physician. 1998; 57(8):1795-1802
6 Fraser WD. Hyperparathyroidism. Lancet. 2009;374(9684):145-58
7 Machado NN, Wilhelm SM. Diagnosis and Evaluation of Primary Hyperparathyroidism. The Surgical
clinics of North America. 2019;99(4):649-66.
8 Liddy S, Worsley D, Torreggiani W, Feeney J. Preoperative Imaging in Primary Hyperparathyroidism:
Literature Review and Recommendations. Canadian Association of Radiologists Journal. 2016;68
9 Mallick R, Chen H. Diagnosis and Management of Hy.erparathyroidism. Advances in Surgery.
2018;52(1):137-53.
10 Jason DS, Balentine CJ. Intraoperative Decision Making in Parathyroid Surgery. The Surgical clinics of
North America. 2019;99(4):681-91.
11 Fraser S. Surgical management of parathyroid disease. Surgery - Oxford International Edition.
2017;35(10):582-8.
12 Lairmore TC, Moley JF. Sabiston Textbook of Surgery, 20th Edition. 2017; 996-1012. Elsevier Inc
13 Bagga V, Sinha S. Surgery for pituitary tumours. Surgery. 2017;35(10):56-562
14 Deguelte S et al. Sporadic pancreatic neuroendocrine tumor: Surgery of the primary tumor. Journal of
Visceral Surgery. 2018; 155(6):483-492
15 Daly AF, Beckers, A. The Pituitary, 4th Edition. Elsevier Inc 2017; 619-630.

10
 PERITONITIS & INTRA-ABDOMINAL SEPSIS
Dr S Naidu; Dr K Rugnath; Dr C Naidoo
Moderator: Ms K Moodley 14 September 2019

Introduction
The term 'peritoneum' derives from the Greek peritonaion, meaning to 'stretch around.'
The early anatomists and surgeons described the extent of the peritoneal membrane, named its
surfaces and attachments, but did not elaborate on its function or fine structure.
The peritoneal membrane became of physiological interest to anatomists after the discovery of cells.

Generalized peritonitis from intra-abdominal sepsis is one of the most common surgical emergencies
encountered across the world. Despite tremendous advancements in surgical techniques, imaging, ICU
care and pharmacology, it still carries a high level of morbidity and mortality. With a wide range of
aetiologies, peritonitis declares itself in a variety of ways.
Diverse epidemiology is noted among populations of different socioeconomic, geographic, and
climatic conditions.

The Peritoneum
A dynamic, extensive serous membrane with both epithelial and mesenchymal features and a
variety of functions.
Capable of adapting its structure and functions to various physiological and pathological
conditions.
A key element in facilitating the movements of intra-abdominal organs and in maintaining an
equilibrium in the abdominal cavity by regulation of inflammatory responses, exchange of
peritoneal fluid and prevention of fibrosis in the abdominal cavity.

Anatomy of the peritoneum 1

The peritoneum is a serous membrane, derived from the mesoderm, that lines the abdominal cavity.
It is composed of mesothelial cells which are supported by a thin layer of fibrous tissue.
The peritoneum provides support to the abdominal viscera and acts as a conduit for nerves, blood
vessels and lymphatics. There are two layers to the peritoneum with 50-100ml of serous fluid
between.
This fluid prevents friction and allows for the layers and organs to glide freely.
The parietal peritoneum, the outer layer, attaches to the abdominal and pelvic walls. It is derived from
the somatic mesoderm. The visceral peritoneum wraps around the intra-peritoneal viscera and it is
derived from the splanchnic mesoderm.
The stomach, spleen, liver, the 1st and 4th parts of the duodenum, jejunum, ileum, transverse and
sigmoid colon are considered intraperitoneal. Retroperitoneal organs include the aorta, oesophagus,
2nd and 3rd parts of the duodenum, ascending and descending colon, pancreas, kidneys, ureters and
adrenal glands. Intraperitoneal organs are usually mobile whilst retroperitoneal organs are fixed to the
posterior abdominal wall.
The mesenteries are extensions of the peritoneum that anchor the anterior and posterior abdominal
walls.
The lesser omentum is derived from the ventral mesentery and in turn makes up the gastrohepatic and
hepatoduodenal ligaments. These contain the portal triad and play a role in the control of
haemorrhage during surgery.
The dorsal mesentery gives off the gastrosplenic ligaments, the greater omentum and anchors the
mid- and foregut organs to the posterior abdominal wall.
The parietal peritoneum receives its innervation from spinal nerves T10-L1. This innervation is somatic
and allows for the localization of pain and temperature sensations.

1
The visceral peritoneum receives autonomic innervation from the Vagus nerve and sympathetic
innervation making it difficult to localised abdominal sensations triggered by organ distension.
The peritoneum divides the abdomen into various compartments and creates potential spaces.
The transverse mesocolon divides the cavity into the supra-colic compartment, which contains the
stomach, liver and spleen and the infra-colic compartment which contains the small bowel as well as
the ascending and descending colon.
The para-colic gutters allow free communication between these compartments.
The potential spaces are areas were fluid collections maybe found and are as follows:
Pelvic Cavity
Most dependant area in the peritoneal cavity. It is bounded anteriorly by the urinary bladder
and abdominal wall and posteriorly by the rectum, the bony pelvic wall and the
retroperitoneum.
In females it is further divided inti anterior and posterior compartments. Pelvic collections in
females may be found in the Pouch of Douglas (uterus)
The Para-Colic Gutters
These are the spaces between the lateral aspect of the ascending or descending colon and the
posterolateral abdominal wall.
Sub-Hepatic Space
These are dependant areas in the supine patient.
The right sub-hepatic space is known as Morrison’s Pouch. It is bounded by the posterior
abdominal wall and the right kidney with the liver above and the abdominal surface of the
diaphragm to the right.
The left space communicates through the omental foramen with the lesser sac.
The Sub-Phrenic Space
The falciform ligament divides it into right and left spaces.
The left is bounded superiorly the coronary ligament and inferiorly by the liver.
The right is bounded superiorly by the anterior layer of the left triangular ligament and the
liver below.

Physiology of the peritoneum 1

A single layer of mesothelial cells line the peritoneal cavity. They have microvilli which increase the
surface area of the peritoneum and are connected by intercellular junctions.
The peritoneal fluid, which contains water, electrolytes, proteins and cells, pass through this
mesothelial layer and interstitium into the lymphatics.
The lymphatic channels are thought to be located in the sub-diaphragmatic spaces from where the
lymph is absorbed and passes into the anterior mediastinum and the right lymphatic duct. Drainage
may also occur through the omental lymphatics into the thoracic duct.
Ultrafiltration (via a 3-pore model) down a hydrostatic pressure gradient is responsible for transport of
fluid. Intra-peritoneal bacteria and debris undergo phagocytosis by macrophages in the peritoneal
fluid and are removed from the peritoneal cavity through the lymphatic system.

Peritonitis 2,3
Intra-abdominal infections may be caused by a large number of disease entities and represent a major
cause of morbidity and mortality. Peritonitis denotes an inflammatory process involving the
peritoneum, most often but not exclusively due to infection.
Injury of the peritoneum, whether surgical, inflammatory, or ischemic, causes a complex inflammatory
reaction. The disruption of the cellular membrane through apoptosis or necrosis, causes a release of
intracellular molecules such as DNA, ATP, and IL-
as Damage-Associated Molecular Pattern molecules (DAMPs), which induce a local cascade through
activating receptors on mesothelial and local inflammatory cells.

2
The neurological pathway of the inflammatory response of the peritoneum is activated by IL-1 binding
to paraganglia cells. The “inflammatory reflex” is formed by signalling through afferent fibres of
the Vagus nerve to parasympathetic regions in the brainstem, leading to the release
of neuropeptides from efferent nerve fibres and a resultant feedback on inflammation.

Peritonitis, according to the International Sepsis Forum Consensus Conference, is classified as either
primary, secondary or tertiary.
Primary peritonitis usually occurs in the setting of ascites, without an evident source of infection,
whereas secondary peritonitis results from the loss of integrity of the gastrointestinal or genitourinary
tracts, leading to contamination of the peritoneal space and subsequent infection.
The term tertiary peritonitis has been applied in the setting of persistent signs of peritonitis and
sepsis, often in critically ill patients, despite treatment of secondary peritonitis.

Primary peritonitis – Spontaneous Bacterial Peritonitis 4

Spontaneous bacterial peritonitis (SBP) is a common and frequently fatal bacterial infection of ascites
occurring in patients with cirrhosis who have diverse symptomatology.
The diagnosis is distinct from secondary peritonitis and is made in the absence of an intra-abdominal
source of infection or inflammatory process. Although it is most often encountered in the setting of
alcoholic cirrhosis and ascites, it represents a heterogeneous entity, with cases reported in a variety of
settings, such as nephrotic syndrome, acute viral hepatitis, malignancy, and systemic lupus
erythematosus.
In advanced liver disease, normal intestinal flora can cause deleterious effects to the host through a
variety of mechanisms leading to SBP including bacterial overgrowth, increased intestinal
permeability, so-called ‘leaky gut’ and pathological bacterial translocation - all in the setting of
immune dysregulation pervasive in patients with cirrhosis. Portosystemic shunting may result in
impairment of clearance of portal bacteraemic episodes, with subsequent seeding of ascitic fluid.
Portal hypertension, splanchnic vasodilation and activation of the renin–angiotensin cascade leads to
sodium and water retention and fluid overflow into the peritoneal cavity.
Ascites is primarily a transudative fluid with poor opsonic activity which provides a favourable
environment for growth of bacteria. SBP rarely occurs without cirrhosis, but cardiac, renal,
malignancy, portal vein thrombosis and autoimmune - related infection of ascites has been reported.
Ascitic fluid infection is classified into five types based on polymorphonuclear (PMN) cell count, ascitic
fluid culture results and clinical circumstances:
classic culture-positive SBP
culture-negative SBP also known as culture-negative neutrocytic ascites (CNNA)
monomicrobial bacterascites
polymicrobial bacterascites
secondary peritonitis
The incidence of SBP ranges from 10%-30% and mortality from 10%-46% in hospitalised patients.
SBP occurring in cirrhotic patients is mono-bacterial in the large majority of cases, with gram-negative
bacilli, most often Escherichia coli, followed by Klebsiella spp., Enterococcus spp., Streptococcus spp.
and other aerobic gram-negative bacilli. Anaerobes were infrequently isolated. Gram-positive cocci
have generally accounted for less than 25% of cases of SBP, however, in recent years they are being
cultured more frequently in patients with cirrhosis and have been linked to therapeutic interventions
and chronic antibiotic usage
Diagnosis
SBP is not a clinical diagnosis, and it cannot be made without ascitic fluid analysis. Interpreting ascitic
fluid results namely cell count and differential to calculate the PMN count is paramount. In patients
with cirrhosis and ascites, SBP may be asymptomatic (an entity that has been termed "bacterascites"),
or present as fever in the absence of abdominal findings, as clinical peritonitis, or as decompensation
of previously stable cirrhosis, for example, with worsening encephalopathy.

3
Diagnostic paracentesis should be performed without delay, ideally within 6 hours of patient
evaluation, and before the use of antibiotics. Analysis of ascitic fluid allows differentiation not only of
sterile ascites from SBP, but also of primary peritonitis from perforation of the gastrointestinal tract
into ascitic fluid. Gram stain of the ascitic fluid is often negative in SBP. The current gold standard for
cell counting is by light microscopy using a manual counting chamber; however, this is operator
dependant and can produce inconsistent results. Flow cytometry has shown to be a suitable
alternative for rapid ascitic fluid cell counting with a sensitivity and specificity of 100% for detecting
PMN count >250 cells/mm3.
Ascitic fluid absolute PMN cell concentration of >250cells/mm3 and pH<7.35, alone or in combination,
have emerged as the most accurate parameters in the immediate diagnosis of SBP; normality of both
virtually excludes the diagnosis.
Risk Factors
Biochemical
Low ascitic fluid protein level (<1 g/dL)
Elevated serum bilirubin level(>3.2 mg/dL) & advanced cirrhosis
Low levels of 25-hydroxy vitamin D
Platelet count < 98 000/mm3
Clinical
Variceal haemorrhage
Genetic
Toll-like receptor 2 gene(TLR2) variations
Nucleotide-binding oligomerisation domain 2(NOD2) gene variations
Pharmacological
Proton pump inhibitors
Beta-adrenergic antagonist
Treatment
Intravenous third-generation, broad-spectrum cephalosporins are the agents of choice for SBP
treatment because of their superiority in randomised controlled trials and rare side effect profile with
minimal risk of nephrotoxicity compared to other antibiotics. Cefotaxime covers the vast majority of
aetiological pathogens, has excellent ascitic fluid penetration and achieves sterilisation in 94% of cases
after initial antibiotic dosing. Studies have confirmed no benefit exists in high-dose or extended
duration (more than 5 days) administration of Cefotaxime.
Ceftriaxone is a strongly protein bound antimicrobial, which theoretically makes it inferior to
cefotaxime as patients with cirrhosis have poor protein synthesis, however studies have shown it is
effective as primary therapy in treatment of SBP, and can be considered as second line therapy.
Alternatives to cephalosporins with comparable results to cefotaxime include:
Co-Amoxiclav
Fluoroquinolones
Ampicillin & Gentamycin
However it is important to note that aminoglycosides cause renal impairment and should be avoided
in patients with cirrhosis who have considerable risk for renal injury.
Oral antibiotics, namely Fluoroquinolones can be used in cases of uncomplicated SBP, as switch
therapy, after IV administration where an adequate response to treatment has been shown.
Albumin is imperative in select patients with SBP, in addition to antibiotics.
A randomised, controlled trial involving patients with SBP treated with cefotaxime alone compared to
cefotaxime and albumin demonstrated that by adding albumin, patients with established chronic
kidney disease had lower mortality both during hospitalisation and at 3-month follow-up after
discharge. Therefore, the recommendation is that patients with chronic kidney disease with or without
dialysis dependency who develop SBP should receive albumin therapy. In addition, albumin prevented
irreversible renal impairment when given to patients without established chronic kidney disease.

4
Prevention
Pharmacological
Norfloxacin
Ciprofloxacin
Trimethoprim–sulfamethoxazole
Probiotics(no proven benefit)
Diet
Restrict dietary sodium intake
Aim for 1.2–1.5 g of daily protein intake
Avoidance of raw food
4-6 small meals/day

Secondary peritonitis 5, 6 ,7
Secondary peritonitis results from the direct contamination of the peritoneum by spillage from the
gastrointestinal or uro-genital tracts or their associated solid organs. The aetiology and site of
perforation shows wide age related and geographical variation. Despite advancements in surgical
techniques, antimicrobial therapy and intensive care, management of secondary peritonitis continues
to be highly challenging.

Mortality in secondary peritonitis depends in part on: patients age, pre-existing cardiovascular, liver,
renal, or neurologic disease, a non-appendicular source of infection, delay in intervention beyond 24
hours, the extent of peritonitis.
Patients with four quadrant peritonitis at the time of surgery have mortality rate of 36%. Faecal
peritonitis was also a very poor prognostic factor, with an in-hospital mortality of 38%.
Intra-abdominal sepsis, although it affects all age groups, takes a greater toll on the elderly population
than it does on younger populations.
The signs and symptoms are usually typical for acute abdomen and it is possible to make a rapid
clinical diagnosis of peritonitis in most patients. Unfortunately, in majority of cases the presentation to
hospital is late, with established generalized peritonitis, purulent contamination and varying degree of
septicaemia. A loss of physiologic reserve, together with concomitant systemic illness, results in worse
outcomes for generalized peritonitis
Secondary peritonitis is usually polymicrobial. The microbiology of secondary peritonitis is influenced
by the site of perforation and by host factors, including whether the perforation is “community
acquired” or has occurred in a postoperative patient.

Aetiology

SOURCE REGIONS CAUSE

Pancreas Pancreatitis,
Trauma (blunt, penetrating, iatrogenic)
Small bowel Ischaemic bowel, Incarcerated hernia
Closed loop obstruction, Crohn’s disease, Trauma
Meckel’s diverticulum, Malignancy (rare)
Large bowel & appendix Ischaemic bowel, Diverticulitis, Malignancy, UC &
Crohn’s, Appendicitis, Volvulus, Trauma
Uterus, salpinx & ovaries PID, Malignancy, Trauma

5
Presentation

Symptoms Signs
Abdominal Pain Abdominal tenderness
Nausea & vomiting Rebound tenderness
Fever Pyrexia, tachycardia
Constipation/diarrhea Abdominal distension
Leucocytosis

Diagnosis
Laboratory testing has an established role in the diagnosis of a wide range of acute abdominal
pathologies, including pancreatitis, cholecystitis, and acute appendicitis. Some helpful, but not specific
investigations include:
White Cell Count – aid diagnosis
Base Deficit – aid diagnosis, guide resuscitation
L-Lactate – aid diagnosis, guide resuscitation
Procalcitonin – aid diagnosis
CRP – aid diagnosis
Several radiologic modalities have a role in the evaluation of intra-abdominal infection, including plain
films, ultrasonography, and CT scan; the latter has emerged as the diagnostic modality of choice for
the diagnosis of intra-abdominal abscesses, and along with ultrasonography plays a significant role in
image-guided percutaneous drainage.
However, imaging studies should be chosen judiciously to avoid delaying definitive management,. It is
important to note that patients with generalized peritonitis or localized peritonitis with hemodynamic
instability do not need imaging, as this would not alter the need for laparotomy.

Management
The principles of management of secondary peritonitis are fluid resuscitation, the use of empiric
antibiotics and control of the septic focus. Secondary peritonitis can lead to significant fluid
sequestration and hypovolemia, which maybe exacerbated by vomiting or diarrhoea. The latest
surviving sepsis management guidelines suggest:
Measure lactate level. Repeat if initial lactate is >2mmol/L
Obtain blood cultures prior to administration of antibiotics
Administer broad -spectrum antibiotics
Begin rapid administration of 30ml/kg crystalloid for hypotension or lactate 4mmol/L
Apply vasopressors if patient is hypotensive during or after fluid resuscitation to maintain
MAP 65mmHg

Surgical management principles include rapid control of contamination, abdominal lavage and
abdominal drainage. There is no single guideline for the surgical management of peritonitis, as most
strategies depend on intra-operative findings, severity of disease, time to source control and
underlying diseases.
The surgical dilemma usually concerns conservative vs operative management, and also laparoscopic
vs open surgery. Minimally invasive or conservative approaches including percutaneous and
endoscopic treatments have been advocated by many authors for the management of uncomplicated
cases (diverticulitis, cholecystitis, etc.).
Percutaneous drainage may be especially relevant in complex cases such as hostile abdomen, provided
the collections are technically drainable. In critically ill patients requiring individualised management,
one may need to perform “damage control” surgery, a concept derived from trauma and applied to
sepsis, which may include open abdomen management, exteriorization and colostomies, drainage and
stapled resections without anastomosis.

6
In low risk patients, a single definitive operation is preferred, with re-look laparotomies only ‘on-
demand’. In high risk patients with extensive contamination or initial damage control laparotomy, as
mentioned above, it is reasonable to use staged procedures and ‘second look’ re-laparotomy. There is
no way to prevent peritonitis, however, efficient surgery, modern anaesthesia and intensive care
support may offer a chance of decreased morbidity and mortality from intra-abdominal infections.

Tertiary peritonitis 8
Tertiary peritonitis is defined as intra-abdominal infection persisting >48 hours after adequate surgical
source control and is characterized by prolonged systemic inflammation, with mortality rates ranging
from 30% to 60%.
The composition of the intra-abdominal flora found in ICU patients with tertiary peritonitis may be
influenced by several factors, such as the location of the initial perforation, antibiotic pressure, and
the ICU/hospital local flora. They are mostly opportunistic and nosocomial pathogens, including multi-
drug resistant (MDR) microbes such as Enterococcus, Enterobacter, and Candida. Tertiary peritonitis
does not require surgery, but only a non-contributory reoperation can confirm the diagnosis.
Management
Supportive care of vital organs is essential in patients with tertiary peritonitis, starting before any
surgical procedure and continued for as long as necessary postoperatively. Supportive care includes
pain management, sedation, optimisation of ventilation, haemodynamic and fluid monitoring,
improvement of renal function, nutrition and anticoagulation. Patients can be stratified on the basis
of risk factors, comprising not only severity of illness (assessed by APACHE II, SOFA or Mannheim
scores) but also individual patient-related factors such as age and comorbidities (assessed by ASA or
Charlson scores) to tailor perioperative monitoring and management, and assess prognosis.

Mannheim Peritonitis Index

Risk Factor Score

Age>50 years 5
Female gender 5
Organ Failure 7
Malignancy 4
Preoperative duration of peritonitis (?24 hours) 4
Origin of sepsis not colonic 4
Diffuse generalized peritonitis` 6
Diffuse generalized peritonitis:
Clear 0
Cloudy 6
Faecal 12

Retroperitoneal infection 9
The retroperitoneum is confined by the posterior and lateral abdominal and pelvic walls.
It may be subdivided into the following spaces:
Perirenal Space
Bounded by the peri-renal fascia
It contains the adrenal glands, the kidneys and the renal vessels
Anterior Pararenal Space
Bounded by parietal peritoneum
It contains the pancreas, ascending and descending colon and the duodenum
Posterior Pararenal Space
Bounded by transversalis fascia posteriorly. It contains only fat

7
The retroperitoneal space is a potential region for infection and abscess formation.
As their presentation is heterogenous, diagnosis may be difficult and often delayed, leading to a high
mortality and morbidity. Retroperitoneal disorders include retroperitoneal abscess, retroperitoneal
fibrosis and retroperitoneal malignancies.

Most retroperitoneal abscesses originate as an inflammatory process in the kidney and GI tract.
In our setting, tuberculosis of the spine is a common cause of retroperitoneal abscess.
Retroperitoneal fibrosis is an uncommon inflammatory condition characterized by the proliferation of
fibrous tissue in the retroperitoneum.
Seventy percent of cases are idiopathic (termed Ormand Disease) whereas 30% are associated with,
infections, trauma, retroperitoneal haemorrhage, retroperitoneal operation, radiotherapy, primary or
metastatic neoplasm.
Patients with retro-peritoneal disorders present usually with a constellation of symptoms, including
abdominal or flank pain, fever and chills (in retroperitoneal abscesses), weight loss, malaise. Patients
with psoas abscesses may have referred pain to the hip, groin, or knee. Most patients with
retroperitoneal abscess often have concurrent chronic illnesses such as renal, immunocompromised
state or malignancies.
Diagnosis
Laboratory abnormalities include elevated infectious and inflammatory markers. CT scan provides
important information regarding the location of the abscess and its relationship to neighbouring
organs and the likely source of infection.
Treatment
Traetment includes appropriate antibiotics and drainage of collection. Drainage under radiological
guidance is useful. Operative drainage through a retroperitoneal approach is indicated for lesions not
amenable to percutaneous drainage or that fail percutaneous drainage.

Tuberculous peritonitis 10
Abdominal TB may involve theGIT, peritoneum, viscera or the mesenteric lymph nodes. Occasional
overlaps between these forms have been described. Peritoneum and its reflections are common sites
of tuberculous involvement.
The diagnosis of this disease continues to pose significant challenges. This is partly due to the lack of
specific clinical features that would otherwise help in pursuing the diagnosis when suspected and also
to the limited yield of the commonly used diagnostic tests. Isolation of mycobacteria from the ascitic
fluid is difficult and frequently laparoscopy is needed for the diagnosis.
Infection of the peritoneum is usually secondary to haematogenous spread of tubercles from a
pulmonary focus. Spread of the mycobacteria may rarely occur from lesions in the adjacent organs
such as the intestine or the fallopian tubes.
Intestinal TB occurs as a result of ingesting contaminated milk or swallowing the sputum of active lung
disease.
HIV infection is the strongest of all known risk factors for the development of TB. HIV patients have
impaired Th1 type immune response, a crucial defence against Mycobacterium tuberculosis. The
interaction between TB and HIV is synergistic.
The disease can present in 3 different forms:
the wet-ascitic
fibrotic-fixed
dry-plastic form
They have similar clinical manifestations except for abdominal distension which does not occur in the
dry-plastic form. Considerable does occur, whereby more than one form may coexist.

8
Presenting complaints may include

Abdominal Pain Fever

Weight Loss Night Sweats
Diarrhoea Constipation
Ascites Abdominal Tenderness
Hepatomegaly Splenomegaly

Abdominal pain is a common presenting symptom and frequently accompanied by abdominal

distension. It is usually non-localised and vague in nature. The pain is largely due to the tuberculous
inflammation of the peritoneum and mesentery.

Diagnosis
Haematological
ESR
Biochemical
Ascitic fluid
LDH above 90U/L
Total protein levels >25g/L
ADA > 30U/L
Microbiological
Sputum – AFB, GXP
Ascitic fluid – AFB , GXP, TB Culture
Radiological
CXR
Ultrasound abdomen
CT Abdomen - thickened mesentery (>15mm) with mesenteric lymph nodes seen in most
cases

Laparoscopy is the diagnostic tool of choice in patients with suspected TB abdomen when the above
investigations yield inconclusive results. Not only does it allows inspection of the peritoneum but also
offers the option of obtaining specimens for histology.
The well-described laparoscopic appearance classifies it into 3 types:
thickened, hyperaemic peritoneum with ascites and whitish miliary nodules (<5mm) scattered
over the parietal peritoneum, omentum and bowel loops (66%)
thickened and hyperaemic peritoneum with ascites and adhesions (21%)
markedly thickened parietal peritoneum with possibly yellowish nodules and cheesy material
along with multiple thickened adhesions (fibro-adhesive type 13%).
Management
Involves anti-tuberculous treatment (RHZE) with pyridoxine, over a duration of 9-12months. Surgical
intervention should only be undertaken in cases where concomitant perforation is suspected, or in
cases of bowel obstruction with evidence of intestinal compromise.

9
References:
1. Kalra A, Tuma F. Anatomy, Abdomen and Pelvis, Peritoneum. StatPearls [Internet]: StatPearls
Publishing; 201
2. Malhotra MK, Singal R, Chowdhary K, Sharma RG, Sharma S, Dhankar A. Spectrum of
Perforation Peritonitis in a Rural Medical College. Bangladesh Journal of Medical Science. 2016
Jan; 15(01): 70-73.
3. Levy MM, Evans LE, Rhodes A. The Surviving Sepsis Campaign Bundle: 2018 Update. Critical
Care Medicine Journal. 2018 Jun; 44(6): 925-928
4. Dever JB, Sheikh MY. Review article: spontaneous bacterial peritonitis – bacteriology,
diagnosis, treatment, risk factors and prevention. Alimentary Pharmacology and Therapeutics.
2015 Jun; 41(11): 1116-1131
5. Ross JT, Matthay MA, Harris HW. Secondary peritonitis: principles of diagnosis and
intervention. British Medical Journal. 2018 Jun; 361(1407)
6. - evaluation of 204 cases and
literature review. J Med Life. 2014;7(2):132–138
7. Montravers P, Blot S, Dimopoulos G, Eckmann C, Eggimann P, Guira X et al. Therapeutic
management of peritonitis: a comprehensive guide for intensivists. Intensive Care Medicine.
2016 Aug; 42(8):1234–1247
8. Ballus J, Lopez-Delgado JC, Sabater-Riera J, Perez-Fernandez XL, Betbese AJ, Roncal JA. Factors
Associated with the Development of Tertiary Peritonitis in Critically Ill Patients. Surgical
Infections. 2017; 18(5): 588-595
9. Tirkes T, Sandrasegaran K, Patel AA, Hollar MA, Tejada JG, Tann M, et al. Peritoneal and
retroperitoneal anatomy and its relevance for cross-sectional imaging. Radiographics. 2012;
32(2): 437-51.
10. Sanai FM, Bzeizi KI. Systematic review: tuberculous peritonitis – presenting features,
diagnostic strategies and treatment. Alimentary Pharmacology & Therapeutics. 2005 Oct;
22(8): 685-700

10
 ADVANCES IN ADJUNCTS IN SURGICAL TECHNIQUES
Dr R Singh, Dr JP Singh, Dr S Thaver
Moderator: Ms S Ismail 05th October 2019

The rapid development of new technology has aided the progression of surgical management by improving the
quality of surgery, decreasing operating times and improving post-operative recovery. These factors have a
positive impact on patient outcomes as well as the cost of hospital stay.

STAPLING DEVICES 1
The concern for the healing of traditional sutures lead to the development of these devices. Understanding how
staplers interact with target tissues is key to improving patient outcomes. They are based on Halsted’s principles
of surgery; i.e. gentle handling of tissue, meticulous haemostasis, preservation of blood supply, strict aseptic
technique, minimum tension on tissues, accurate tissue apposition and obliteration of dead space.
The integrity of the staple line, which depends on adequate tissue compression, is the primary factor in creating
a stable anastomosis. The thickness of each type of tissue vary as do the intrinsic biomechanical properties that
determine the ideal compressive force and pre-firing compression time for each tissue type.
Compression, staple height, tissue thickness, tissue compressibility and tissue type must all be considered by the
surgeon prior to choosing a stapler and cartridge.
Modern day staplers are more often now single-use for use in open or laparoscopic procedures. Most linear
staplers are available in 3 staple heights. They bend staples into B-shaped conformation. Staple malformation
may be due to surgeon factors (compression time and release), type of metal, bending properties or thickness,
in addition to intrinsic tissue factors mentioned above. Types of staplers include:
Linear
Circular
Contour (curved)
Endocutters (Laparoscopic)
Haemorrhoidal staplers

Primary goal: Good tissue apposition

minimizes excessive bleeding, achieve
homeostasis and tissue perfusion, decrease
anastomotic leaks.
Complications:
Staple height too high -> inadequate
tissue apposition -> bleeding, leakage
and anastomotic breakdown
Staple height too low -> ischaemia ->
serosal tearing and necrosis

Dimensions of commonly used linear staples

Colour Rows Tissue Open staple height Closed staple height
Grey 6 Mesentery 2.0mm 0.75
White 6 Vascular 2.5mm 1.0
Blue 6 Standard 3.5mm 1.5mm
Gold 6 Standard/Thick 3.8mm 1.8mm
Green 6 Thick 4.1mm 2.0mm

Tissue properties: impact on choice of stapler and stapler height

Stomach , oesophagus , colon , small bowel vary in thickness and dimensions may change based on sex,
age, location within an organ , preoperative therapies , intraoperative medications and disease state.
Biphasic nature of tissues (liquid and solid and air components) in different ratios
Biochemical properties and extrinsic blood
The physical condition of the tissues joined; adequate perfusion
1
 Optimal stapling requires adequate compression time (to decrease the fluid in the tissue) to allow
elongation of the tissue being compressed , smooth firing of the instrument and consisent staple line
formation: this must be balanced against the risk of tissue tearing and excessive tensile strength.

Consideration in specific device-tissue interactions

Recognized that more compression is advantageous and a smaller staple height was associated with lower
incidence of hemorrhage and stenosis / stricture as well as a decreased leak rate in the shorter staple group.
With respect to compression time, in stomach tissue increasing compression times decreased staple height and
increased optimal staple formation rate. So, what is the ideal compression time?
Stomach: Wide variations in tissue thickness (mean thickness 1.6 mm – 3.1 mm, increasing from OG
Junction to the pylorus) this necessitates careful choice in staple size.
Colorectal: Anastomotic leakage (incidence up to 30 %) a major issue. Tissue thickness more uniform,
however poor vascularity and tension. Higher incidence of anastomotic leak demonstrated with use of
larger diameter circular staplers. Difficult access into the narrow male pelvis may warrant use of curved
staplers as opposed to linear staplers, which would otherwise result in longer oblique staple lines. This
allows lesser chances of stool contamination and post-op leaks.

New stapler concepts – the future: Beyond the “B” 2

Commoner surgical staplers discussed above rely on the same staple form - the “B”, which necessitates a high
delivery profile (12mm). The introduction of the D staple has allowed a significant reduction in the end-effector
size for a surgical stapler because the ‘‘D’’ shape staple allows for an extremely low profile of the applicator.
Advantages
Many tissue structures, especially those in tightly confined spaces, may be more suitable for transection
by smaller staplers. Cartridge and anvil diameter decreased to 5 mm, accommodates staples which
secure tissues associated with white and blue cartridges.
Reduces the amount of tissue dissection, improving visibility and access.
Reduces the amount of closure required and closure-associated complications.
Currently animal studies using swine models showed no difference in intraoperative performance and the
chronic healing response in jejuno-jenunal anastomosis between D- and B-shaped staples.

Contour Stapler 3
This stapler was developed to cut and staple deep in the pelvis perpendicular to the rectum. The device
conforms to a patient’s natural anatomy, allowing access deeper in the pelvis during a low anterior resection,
without handle obstruction. It has a unique curved head design which provides a more precise transection and
less tissue slippage compared to similar stapling devices. The curved head allows for placement of a 40 mm
cutline in the width of a 30mm space and low pelvic access without handle obstruction - thus enabling
transection perpendicular to the rectum. It is reloadable and may be fired up to 6 times in a single procedure.

Circular Stapler 4
Invented (1977) for colorectal cancer surgery to avoid permanent colostomy. Developed for extracorporeal
anastomosis, but recently its use in intracorporeal anastomoses has increased.
Indications:
End-to-end and end-to-side anastomoses of the oesophagus, stomach, and rectum.
For laparoscopic gastrectomy: commonly during oesophagojejunostomy after total gastrectomy; less
commonly during gastroduodenostomy and Roux-en-Y gastrojejunostomy.
Selecting a Circular Stapler
The choice of a circular stapler of adequate diameter and height is important for preventing bowel injury and
anastomotic stricture:
Size Indication
21 Bariatric surgery
25–28 Oesophagojejunostomy
28–33 Gastroduodenostomy and gastrojejunostomy.
SKIN SUBSTITUTES 5

2
A heterogeneous group of biologics, synthetic, or biosynthetic materials that can provide temporary or
permanent coverage of open skin wounds.
Commonly used products, especially in the treatment of burns wounds include human skin allografts, amnionic
membrane products, and xenografts. Tissue engineering has significantly advanced the development of skin
substitutes beyond allografts.
Classification: No universally accepted classification system, however systems are based on:
Clinical features: replaced skin component - epidermis, dermis, or both
Required permanence: temporary, permanent
Composition: material used - biologic, synthetic, or both
Layering: single layer, bilayer
Cellularity: acellular, cellular
Indications/Uses: Burns, chronic wounds, diabetic foot ulcers, chronic venous ulcer, abdominal, breast and
extremity reconstruction.

Biological skin substitutes: act temporarily like a natural skin.

Advantages: Relatively abundant in supply and not very expensive. Have a more intact and native extracellular
matrix (ECM) structure allow the construction of a more natural new dermis. Presence of a basement
membrane excellent re-epithelialisation characteristics

Synthetic skin substitutes: Constructed from non-biological molecules and polymers not present in normal skin.
Properties
- Stable, biodegradable, provide an adequate environment for regeneration of tissue
- Maintain its three-dimensional structure for at least 3 weeks to allow ingrowth of blood vessels, fibroblasts
and coverage by epithelial cells.
- Biodegradation should preferably take place after 3 weeks
- Should not initiate massive foreign body reaction
- Composed of immunocompatible materials to avoid immunoreactive processes
Cost considerations: Cost analysis studies suggest that despite the high initial costs, skin substitutes can shorten
time to wound closure and result in an overall cost reduction. In the future, the focus will likely include
incorporation of stem cells into scaffolds, as well as three-dimensional printing technology.

HAEMOSTATIC AGENTS 6
Haemostasis is a complex process that involves cellular and biochemical components of blood to form a
platelet-fibrin clot. Surgical bleeding is a consequence of ineffective local haemostasis.
Topical haemostatic agents are used as peri-operative adjuncts, modulating the coagulation pathways to
achieve haemostatic control. They should not be used intra-vascular (will cause thrombosis), or in confined
spaces where expansion of the product could lead to compression. For a detailed explanation of all agents, refer
to seminar 2017.
Haemostatic agents can be classified into 4 categories 7, 8, 9

Type of Agent Example

Physical Bone Wax, Ostene , External Agents, Haemcon, Chitoflex, Quikclot
Absorbable Gelatin Matrix (Gelfoam), Oxidized regenerated cellulose (Surgicel), Microporous
polysaccharide spheres and Microfibrillar collagen
Biologically active Topical Thrombin, Fibrin sealants, Tranexamic acid, platelet gel and Light-activated
haemostatic agent
Synthetic Polyethylene Glycol Hydrogel, Glutaraldehyde Cross-Linked Albumin, Cyanoacrylates

Choice of topical haemostatic agent 10

This is largely dependent on extent and location of bleeding, surgeon’s preference, availability and cost.
Biologically active agents (topical thrombin, fibrin seal) are preferred in brisk bleeding and are more effective in
coagulopathy or in defibrinated fluid (pooled serum or cerebrospinal fluid). Fibrin sealant and bovine albumin-
glutaraldehyde tissue adhesive (eg, Bioglue) are useful in moderate bleeding not responding to other measures.
Adverse Effects
3
Related to their composition, location of placement and absorption time. Include Infection, anaphylaxis,
impaired wound healing, embolism and thrombus formation.

ENERGY DEVICES 11
Instruments that apply energy to cut, coagulate and dissect tissue with minimal bleeding . The improper use of
energy devices may increase patient morbidity and mortality.
Most commonly used devices:
Type Product name
Monopolar electrosurgery Opti4; Encision AEM.
Bipolar electrosurgery Ligasure, Gyrus Plasma Kinetics.
Ultrasonic energy Ultrasonic harmonic scalpel; Harmonic ACE; Harmonic FOCUS, Sonosurg, AutoSonix.
Laser energy Nd:YAG laser, Argon laser, CO2 laser.
Argon beam coagulator System 7550 ABC, Cardioblate.

Electrosurgery 11
It is the use of radiofrequency (RF) alternating current (AC) to raise intracellular temperature in order to achieve
vaporisation or the combination of desiccation and protein coagulation. These effects are translated into tissue
cutting and coagulation (hemostasis), but also to occlude lumen-containing structures, or to destroy large
volumes of tissue such as soft tissue neoplasms. (note: electrosurgery is not cautery).
The RF energy is applied to the tissue by using monopolar or bipolar tools and is applied through generators,
with different duty cycles. The waveforms with different duty cycles produce 4 main effects: cutting,
coagulation, desiccation and fulguration. Electrosurgical systems function above 100KHz , since muscle and
nerve stimulation ceases - hence electrocution does not occur.
General complications in electrosurgery
Sparking effect at tool tip may cause an explosion when in contact with inflammable anesthetic gasses.
The current travelling through the body can interfere with any implanted medical devices such as
pacemakers and defibrillators.
Insulation failure, due to repetitive use of the instrument, high intensity of current flow through the wire
and in repeated sterilization process.
Direct coupling – the active electrode is touched by another tool, in which case the energy is transmitted
through the other tool to the tissues.
Capacitative coupling – may occur in laparoscopic surgery when tools, tissues and trocars are in close
proximity creating the capacitance effect - causing unintended tissue damage in the immediate vicinity.
Thermal injuries to adjacent organs depend on the types of target tissue and the types of energy sources
used. Monopolar electrosurgery shown to have higher temperature and thermal spread.

Bipolar Devices
I. The Ligasure vessel sealing system:
It is a bipolar feedback-controlled sealing system that applies a precise amount of mechanical pressure
and radiofrequency energy to tissue, causing fusion of the opposing layers by creating a seal of
denatured collagen, which can be transected. Results in a permanent seal that can withstand x3 normal
systolic pressure, seals vessels up to 7 mm with thermal spread to adjacent tissues approximately 2 mm.
II. PlasmaKinetic tissue management system delivers pulsed bipolar energy, allowing intermittent tissue
cooling, which limits lateral thermal spread. Allows simultaneous cutting and coagulation.
III. EnSeal provides vessel sealing by combining a compression mechanism with thermal energy in a bipolar
sealing device. Capable of achieving seal strengths up to 7 times normal systolic pressures on vessels up
to 7 mm with thermal spread approximately 1 mm. Although consensus awaited, it is already in
widespread use among surgeons.

Ultrasonic Energy
I. Harmonic scalpel
Mechanism of ultrasonic energy: low frequency mechanical vibrations (55.5 KHz) of the tips for tissue
cutting and coagulation. In tissues with low protein density, such as the liver, cavitation effect results in
4
 denaturation of proteins and, eventually, separation of tissue. These effects are reached at tissue
temperatures of 60 - 80ºC, resulting in coagulum formation without the desiccation and charring caused
by temperatures > 80ºC (associated with traditional electrosurgical methods).
II. Thunderbeat device also adds bipolar energy for combination effect of ultrasonic and bipolar energy.
III. Sonocision device is cordless, with the generator built into the handle.
IV. Cavitron Ultrasonic Surgical Aspirator (CUSA), also known as Ultrasonic Dissector - the ultrasonic waves
generate energy to fragment and aspirate parenchymal tissue, while selectively sparing the blood
vessels and bile ducts because of poor tissue water content.
CUSA does not coagulate; need ties, clips or staplers to achieve haemostasis and biliostasis.

These devices are versatile, allowing the surgeon to dissect, cut, and coagulate using one instrument and have
been used successfully in a number of open and laparoscopic procedures. "Clipless" laparoscopic
cholecystectomy in which the cystic artery and duct are divided and sealed with the Harmonic Scalpel, is an
example of their clinical applicability.
The advantages include minimal thermal spread, decreased tissue charring and smoke formation compared with
traditional electrosurgical instruments, and no risk of electrical injury due to the absence of electrical current.
The main disadvantages are the limited ability to coagulate vessels >3-5 mm, increased cost of disposable
instruments, potential for extensive thermal spread at high energy levels for more than five seconds, and the
user-dependent nature of the instrument.

Laser — Light Amplification and Stimulated Emission of Radiation (LASER)

Offers precise application of energy without risks of lateral tissue damage and stray current associated with
standard electrosurgery.
Although widely used in ophthalmologic and dermatologic surgery, popularity of LASERS in general surgery
has declined, possibly due to the advent of alternative energy sources

STENTS IN SURGERY
In addition to applicability in General surgery, stents have a wide utility in the practice of vascular surgery,
cardiac surgery, ENT and urology). When applied appropriately, stents have the appeal of avoiding major
surgery often without a demand on the patient’s physiology.
Technological advances have seen the evolution of stent composition from plastic to self-expanding metal
stents (SEMS) and presently to biodegradable stents. At the same time indications for stent use that began with
oesophageal cancer, now include benign and malignant disorders involving many sites in the GI and biliary tract.
Physical properties of stents 12
The first stents were made of hard plastic and were used for obstructive oesophageal cancers.
Contemporary SEMS are composed of either nitinol or stainless steel. Nitinol mesh (composed of nickel-
titanium) is soft and flexible, with smoother wire ends, reducing the risk ingrowth and overgrowth; these
stents are also resistant to pressure and are highly biocompatible.
Self-expanding plastic stent (SEPS) is made of woven plastic strands
Biodegradable stent is made from commercially available polydioxanone absorbable surgical suture
material. Have shown promising results in recurrent benign strictures; can be combined with antibacterial or
antitumor agents, or equipped with drug-eluting functions.
SEMS
Available as uncovered, partially covered (PC), or fully covered (FC).
Uncovered SEMS consists of a mesh that is bare and expands into the stenosis.
PCSEMS: stent with a membrane covering with uncovered proximal and distal ends of the stent.
FCSEMS: mesh stent covered by a membrane throughout its length.
The important physical properties of uncovered stents are good radial expansile force, flexibility and
conformability. A disadvantage of uncovered stents is that they are difficult or impossible to remove
(particularly if in position for some weeks) and tumour ingrowth (20-30% of patients).
Covered stents delay tumour ingrowth, prolong stent patency but have higher migration (as high as 28%).

Common clinical application of stents 12 ,13

Oesophageal stents

5
 Oesophageal stents maybe used for malignant or benign indications in the oesophagus, gastroesophageal
junction, and gastric cardia.
In recent years, oesophageal stents have been to treat benign oesophageal strictures (peptic, radiation
induced, anastomotic, and caustic), postoperative leaks, iatrogenic perforations, external compression from
extraoesophageal tumours, and tracheoesophageal fistulas.
Presently, fully covered Polyflex SEPS is the only approved stent for benign refractory oesophageal
strictures. However, FCSEMSs are also used for benign conditions.
Adverse events
Potential adverse events of oesophageal stenting include perforation, stent migration, stent obstruction
resulting from tissue and/or tumour ingrowth or overgrowth, tracheal compression, and bleeding. Stents in
the cervical oesophagus may cause a globus sensation.
Distal oesophageal stents traversing gastroesophageal junction may cause significant reflux and increase risk
of aspiration; stents with an anti-reflux valve could be considered to reduce reflux.
Migrated stents in patients receiving neoadjuvant therapy generally indicate treatment response and can be
removed easily
Gastroduodenal stents
Gastroduodenal (GD) stent placement is a non-surgical alternative for symptom relief and improved QOL in
gastric outlet obstruction encountered in advanced malignancy of the pancreas, duodenum, and stomach.
GD stenting also reported in patients with benign GD obstruction who are poor surgical candidates.
Has been shown that stent placement is usually associated with faster ability to tolerate oral intake and
shorter duration of hospital stay, whereas surgery is associated with better long-term outcomes including a
low rate of re-intervention.
Stent placement is therefore a reasonable alternative to palliative surgery when there is a short life
expectancy, generally < 6 months.
Adverse events
Mild adverse events include abdominal discomfort, mild fever, and occasional vomiting without obstruction.
Major adverse events occurring within the first week include bleeding, perforation, stent migration, severe
pain, fever, and jaundice.
Significant late adverse events include fistula formation, stent obstruction, late perforation or bleeding,
biliary obstruction, and stent migration.
Colon stents
Colorectal cancer often causes partial or complete bowel obstruction. Management options for such
patients include surgical resection or endoscopic stent placement.
Colon stenting has become an important tool in the palliation of advanced disease and management of
acute colon obstruction as a possible bridge to surgery (i.e., converting an emergent 2-stage surgery with
creation of a colostomy to an elective 1-stage surgery).
Colon stenting has been reported to be technically successful in up to 93% with improvement in symptoms
in 85-90% of patients overall.
With the advent of newer through-the scope stents, palliation of advanced right-sided malignant
obstruction has become easier, with technical and clinical success rates >85%
There is limited data on the use of stents for the management of benign colon strictures.
Technical considerations
Colon SEMSs may be covered or uncovered; uncovered stents are advocated because of high migration
rates of covered stents.
Smaller-diameter stents generally used in the right colon and larger-diameter stents in the left colon to
prevent solid stool impaction.
Ideally, radiologic imaging study (barium enema or CT scan with rectal contrast) should be obtained before
stent placement to assess degree of obstruction and the length and location of the stricture.
A bowel preparation is often not possible or necessary in patients with complete obstruction.

Biliary stents
Stent selection depends upon the size of the duct lumen and length to be traversed
Plastic biliary stents (introduced almost 30 years ago for relief of biliary obstruction) invariably occlude
owing to bacterial biofilm and reflux of duodenal contents after 2–6 months, but can be readily exchanged.

6
 Plastic biliary stents are composed of polyethylene, polyurethane, polytetrafluoroethylene (Teflon) and
other plastic polymers. The diameters are measured in French (Fr), corresponding to 0.33 mm, and
diameters range from 5 Fr to 12 Fr.
Although larger stent diameters provide longer patency, the diameter is limited by the size of the endoscope
channel.
Biliary stents are available in varying shapes, sizes, and numbers of barbs/flanges or pigtails. Biliary stents
can be temporary (e.g., polyethylene, Teflon) or permanent (e.g., Wallstents).
Comparative studies have shown SEMS to provide a significant prolongation of patency over traditional
plastic stents for palliation of malignant biliary obstruction and facilitate bile flow for a longer period but
cause pressure necrosis and pseudo-epithelialization over time.
Uncovered SEMS
Become buried within the bile duct wall
Very difficult to extract once it has been inserted.
Risks for migration are minimized
Covered SEMS
Designed to prolong stent patency over uncovered SEMS by preventing tumour ingrowth
Have a higher migration rate and possibly an increased risk of cholecystitis and pancreatitis.
Cholecystitis and pancreatitis can be caused by obstruction of the cystic duct and main pancreatic duct,
respectively, but clinical studies indicate similar frequencies of these complications with covered stents
as with uncovered stents
Although not approved for benign disease, there are reports of treatment for benign strictures and
postoperative biliary leaks that are removed after resolution of the underlying pathology.
Animal studies have shown the feasibility of placing expandable biodegradable biliary stents for
management of bile duct leaks; human studies using these devices in benign disease is awaited.

RECONSTRUCTIVE MATERIALS IN SURGERY 14, 15

The use of reconstructive materials has gained traction in management of general surgical conditions with most
application in use of hernia surgery.
Classification
Reconstructive materials can be classified in terms of source as follows:
I. Synthetic materials
II. Natural occurring materials: Autografts, allografts & xenografts.
I. Synthetic materials
These are available in both absorbable and non-absorbable forms.
Absorbable: Olygalactin 910 [Vicryl], polyglycolic acid [Dexon])
Nonabsorbable: Polypropylene [Marlex, Prolene], expanded polytetrafluoroethylene [ePTFE, Gore-
tex]).
II. Naturally occurring materials
Autografts are harvested from the patient, with the tensor fascia lata and rectus fascia most
commonly used. Elicit minimal host response - thus are well tolerated immunologically.
However, use limited by morbidity associated with harvesting the tissue (pain, bleeding, infection,
hernia formation), inconsistent size, quantity, and quality of tissue.
Allografts are obtained from processing cadaveric fascia lata or acellular dermal matrices (ADM) of human
donors. The material is decellularized and rendered non-immunogenic by removing cellular debris, while
maintaining the integrity of the inherent connective tissue. Rarely used due to poor reinforcement ability
compared to other materials.
Xenografts - acellular collagen extracts can be harvested from bovine or porcine species with or without
additional extracellular matrix components.

Material used in surgery

Synthetic Materials (Mesh)
The reaction elicited by synthetic materials is determined by the following factors:

7
 i. Degree of Absorption: Complete degradation of absorbable meshes ranges from 30 to 90 days. The
inflammation elicited by the non-absorbable mesh persists thus producing a more sustained reaction and
thus greater re-enforcement of the native tissue.
ii. Pore Size: The degree of porosity greatly influences the host response. Macro-porous meshes (>75
Microns) have been noted to have greater penetration of the cellular components (fibroblasts) which
facilitates collagen deposition and angiogenesis, both of which are central to host colonization. Large pores
also enable penetration of macrophages & natural killer cells into the native tissue, a process essential in
mounting and maintaining immuno-protective measures by the host. It follows then that use of micro-
porous meshes is associated with higher infection rates.
iii. Constitution: Mesh fibres can be monofilament or multifilament (braided) with multifilament products
having higher rates of infection.
iv. Weight: The weight of a mesh is determined by the material used and its pore size. Macro-porous meshes
generally weigh less as less material has been used in its production per square meter. The weight also
determines the elasticity of the mesh, with light weight meshes having greater degrees of elasticity and
have also been associated with lower rates of infection.
v. Shrinkage: Contraction of the scar plate is a common occurrence, with rates of up-to 60% reported.
Shrinkage rates are highest in heavy, microporous meshes.
Complications
Infection: Though it reportedly occurs in 0.1-3%, it is a complication feared by most surgeons as it often
means removal of the implant to achieve infection control. The risk of infection is higher with use of
microporous and multi-filament meshes.
There is limited evidence to support routine use of antibiotics as a prophylactic measure; there is
documented reduction in infection rates when antiseptic impregnated meshes.
Seroma Formation: Can develop with use of any mesh but occur frequently with microporous meshes.
Adhesion Formation: Use of intra-peritoneal mesh placement in laparoscopic surgery has led to the
increased association of intra-abdominal adhesions. Extent of adhesion formation is dependent on mesh
properties (pore size, filament structure and surface area). Composite meshes confer lowest risk for
adhesion formation as they provide a non-erosive surface interposed between the bowel and mesh
before regeneration of peritoneum.
Persistent Post-surgical Pain: Mesh placement has been associated with chronic post-operative pain,
occurring in up to 50% of patients, mainly as a consequence of chronic inflammation induced by the
mesh or neuropathic pain, from nerve damage or entrapment.
Recurrence: Hernioplasty, when compared to herniorraphy, has a recurrence rate almost half as
supported by various published studies; 65% of recurrence occur at least 3 years post operatively and is
associated with infection, seroma and hematoma formation in the immediate post-operative period.
Considerations in mesh advancement 16
Reducing mesh weight reduces foreign body reaction, and therefore postoperative pain, and discomfort. A
better bio-tolerability was tried through use of composite meshes (absorbable–not absorbable).
A - rs have
been produced. Over the last 10 years various industries have developed and marketed:
I. Lightweight mesh
II. Coated mesh: oat beta glucan coated; titanium coated
III. 3D mesh
IV. Auto-adherent mesh
: biologic meshes have been
experimented with (porcine dermal extracts or bovine protein derived meshes). Unfortunately, also these
new devices, in addition to their high costs, have shown some disadvantages (wound seroma, skin
dehiscence with graft exposur

Fully reabsorbable meshes (such as vicryl meshes) were successfully used in or after repeated laparotomies,
but have a large incidence of hernia recurrence.
Biologic mesh
Biologic meshes differ based on their source (human or animal), composition (dermal, pericardial or
submucosa) and methods of processing (stripping, cross-linking). They are more durable than
absorbable non-biologic mesh, and have the potential for permanent hernia repair under the worst of
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 circumstances. Their breakdown via hydrolysis is a benefit during complex abdominal wall
reconstruction.
Biologic grafts are acellular collagen matrices that facilitate tissue ingrowth, neovascularization, and
host integration. They provide extracellular components to complete healing, allow for the
reconstruction of new and healthy tissue, and restore mechanical and functional integrity to the
abdominal wall.
There is no evidence to support the use of biologic/biosynthetic mesh for prevention of incisional or
parastomal hernias. In complex abdominal wall hernia repairs (incarcerated hernia, parastomal hernia,
infected mesh, open abdomen, enterocutaneous fistula, and component separation technique), biologic
and biosynthetic mesh do not provide a superior alternative to synthetic mesh.
Under contaminated conditions biological is no better than synthetic mesh and could have worse
outcomes. Biologic mesh should be avoided when bridging is needed

Hybrid mesh (biosynthetic mesh)

Hybrid meshes use both biologic components and synthetic components. The biological components are meant
to protect the synthetic components from their surrounding environments.
A variety of absorbable synthetic/biosynthetic meshes are now available and have emerged as a less costly and
potentially effective alternative to biologic meshes in complex hernia repairs.

Three dimensional mesh (3D mesh) (17)

Fused deposition modelling (FDM) is the most promising 3D printing technique for the manufacture of patient
specific surgical meshes. It may improve clinical outcome by enhancing technical capacity, reduce wastage and
be cost effective. Meshes with different pore sizes and shapes may be produced rapidly using various
absorbable or non-absorbable materials as well as be antibiotic loaded to minimize post hernioplasty infections.

‘The Ideal Mesh’

The question remains: How to achieve a standard?
Ideal conditions of “ideal
Ideal mesh should have low cost, low foreign body reaction, low
immunological reaction, good scar tissue reaction, resistance to infections, no induction of bowel adhesions.
The choice of mesh is dependent on the intended use, surgeon’s preference and availability.
In general, a light-weight, macro-porous, monofilament mesh with minimal surface area will suffice for most
repairs. Composite meshes are best for intra-peritoneal use.
To date there is no consensus about the ideal mesh to use for elective primary inguinal hernia repair, for
hernia recurrence and even more for incisional hernias.
- avoid the use of non-absorbable meshes
The goals of future research should be to: (a) reduce mesh discomfort; (b) improve biotolerance; (c) reduce
mesh complications; and (d) maintain surgical results

NANOTECHNOLOGY AND THE SURGEON 18

Nanotechnology involves manipulation and control of nanomaterials with at least one dimension below 100 nm.
This has vast potential in developing field of minimally invasive surgery. Other applications that either being
investigated or already used:
Nanocoated Surgical Blades
Microstructured metal coated with diamond would allow low physical adhesion to materials or tissues and
chemical/biological inertness. The micro diameter blades may be used in eye, neurosurgery and minimal
invasive surgery.
Nanoneedles
New stainless-steel needles incorporating nanosize particles by using thermal ageing techniques have been
developed for ophthalmic and plastic surgery. They have good ductility, exceptional strength and corrosion
resistance. Nanoneedles prepared from silicon may be used in cell surgery.
Catheters for Minimally Invasive Surgery
Nano-materials added to catheters increase their strength and flexibility and have an antithrombotic effect.
Other Applications of Nanotechnology
These include self-assembling nanofibres for haemostasis, nanofabricated drains, conduits for nerve repair
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 and ways of studying in vivo processes in real time.
Wound Dressings
Nano-porous silver powder has better anti-infective properties as the smaller particles result in a greater
active surface area. Other applications for nano-silver coatings include implants, indwelling catheters and
wound dressings, and for burns and other chronic wounds.
Tissue Engineering
Nanotechnology provides new possibilities for the extracellular matrix. Micro- and nanostructured surfaces
of scaffold materials have important beneficial effects on cell adhesion and proliferation to restore,
maintain or improve tissue function.

CONCLUSION
Modern surgery has benefitted greatly from technological advances that facilitate the safe and effective
outcome of surgical practice; these technological advances have favorably impacted on the core practice of
surgery to the extent that they have become necessary adjuncts to current surgical practice
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