70 years old male patient posted for Cataract surgery

Blood transfusion
Cirrhosis and portal hypertension
ABG
Liver and biliary system
Opioids
Diagnosis & Management of brain dead as potential donor
CKD
Post-Transplant pt for incidental surgery
TURP
70 years old male patient posted for Cataract surgery –
Dr Nandita Mehta

A cataract is an opacity of the lens of the eye that may cause blurred or
distorted vision, glare problems, or, in very advanced cases, blindness.
The word derives from the Latin "catarractes," which means "waterfall."
To the naked eye of an observer, the foamy white opacity of an
advanced cataract resembles the turbulent water of a waterfall. Cataract
is a significant cause of blindness worldwide.Cataracts occur frequently
with increasing age and may be a normal part of aging.

There has been a significant evolution in surgical technique of cataract

extraction throughout the world in the last few decades. After Ridley
introduced the intraocular lens, the challenge was to reduce the size of
incision. It was fulfilled by Kelman with the introduction of
phacoemulsification and by Mazzocco with the introduction of foldable
intraocular lens.The technical advances in phaco machines, phacotips,
and availability of ophthalmic viscoelastic devices have played a great
role in cataract surgery to be faster and more controlled and less
traumatic now than before.
As incisional size of cataract extraction has reduced, local anesthesia
techniques have also advanced significantlyfrom retrobulbar, peribulbar,
sub-Tenon’s, to topical anaesthesia. Even though, the sub-Tenon’s
anaesthesia technique reduced the risk of complications of
peribulbar/retrobulbar anaesthesia but the technique is still associated
with a possibility of damage to optic nerve, retrobulbar haemorrhage,
and ocular muscle injury.
Koller and Knapp can be considered the pioneers of local anaesthesia
for cataract surgery. Koller introduced topical cocaine in 1884 while
Knapp introduced retrobulbar anaesthesia in 1884. In the beginning of
19th century, orbicularis block was introduced by Van Lint, O’Beriens,
and Alkinson. In last 25 years, local anaesthesia techniques have
progressed from posterior peribulbar to “no anaesthesia” techniques.
Evolving surgical techniques have reduced the need for akinesia. In
1992, Fichman reintroduced topical anaesthesia for cataract surgery.
Topical anaesthesia is used to block the afferent nerves of the cornea
and the conjunctiva (long and short ciliary nerves, nasociliary nerves).
This technique eliminates the possible complications of injectable
anaesthesia. However, it does not eliminate pain sensitivity of the iris,
the zonule, and the ciliary body which is achieved by intracameral
technique of anaesthesia with preservative free 1% lidocaine.
In 1998, Amar Agarwal introduced the technique of “no anaesthesia” for
cataract extraction. In this technique, no topical or intracameral drugs
are used. Although without any side effects, the stress for the surgeon is
increased.
Due to increased stress on surgeon, the “no anaesthesia” technique has
not gained popularity world over.
In 1999, Gutierrez–Carmona modified “no anaesthesia” technique and
introduced Cryoanalgesia for cataract surgery. In this technique, all
solutions to be used during surgery are cooled to 4° C.

The ideal anaesthesia would be one that provides adequate pain relief
during surgery and postoperatively, be easy to administer and have
minimal complications. For doing cataract surgery, the anaesthesia
could be local or general. Majority of cataract patients are operated
under local anaesthesia (infiltration, topical, intracameral).
The general anaesthesia has its own complications in elderly cataract
patients. Most of the patients have co- morbidities like COPD, diabetes,
hypertension, heart diseases or combination of them. These patients
maybe on many drugs like bronchodilators, oral hypoglycemics,
antihypertensives, anti arrhythmics, anti-platelet drugs and blood
thinners etc. The elderly patients are prone to intra and postoperative
problems like respiratory complications, poor glycemic control,
arrhythmias, myocardial infarction, cognitive dysfunction. On the other
hand, in local anaesthesia there is no need of fasting before or after
surgery, and also no need of intubation or using any systemic
medications. Still it is very important to stop antiplatelet drugs
preoperatively, in order to avoid haemorrhage due to the needle.

The million dollar question is: which anaesthesia to select for cataract
surgery? Only two persons can decide this—the patient, who is
undergoing cataract surgery and the ophthalmic surgeon, who is going
to operate. For the same patient, different surgeons may select different
techniques of anaesthesia. The skill and experience of surgeon, co-
operation of patient, type of cataract, associated ocular co-morbidity like
corneal opacity, pupillary dilatation, facilities available etc. are important
factors while deciding upon the type of anaesthesia.
Is there any role for general anaesthesia in modern cataract surgery? Of
course yes—for paediatric cataracts and for some adult patients with
parkinsonism, deaf mutes, mental retardation, patients under active
psychiatric treatment need general anaesthesia in order to perform
cataract surgery safely and comfortably. Other indications for this
anaesthesia would be the previous occurrence of retrobulbar
haemorrhage, patient’s request inspite of explaining the advantages of
local anaesthesia.
Proper pre-operative workup and optimising of patient is important
irrespective of type of anaesthesia, making sure that all anticoagulants
are stopped according to guidelines.
For general anaesthesia fasting should be ensured( ERAS protocol).
All patients should receive a proton pump inhibitor and an antiemetic
either with premedication or at the time of surgery. It is advisable to
avoid long acting sedatives in the elderly as that can lead to respiratory
depression and increased incidence of post operative cognitive
dysfunction.
The concept of providing different pharmacological agents for balanced
anaesthesia, i.e., for analgesia, muscle relaxant, abolishment of all
reflexes including somatic reflexes, and somnolence has removed the
use of very potent, toxic, and long-acting agents. The drugs used
include: Opioids (μ receptor agonist): Fentanyl, Remifentanil, Alfentanil,
Benzodiazepine (sedative/hypnotic): Midazolam, etizolam, Inhalational
agent : Isoflurane, Sevoflurane, and intravenous anaesthetic agent
Propofol (which in low dose can be used as sedative with topical
anaesthesia also).

Various Blocks

Routinely, all the blocks are performed by the ophthalmologists only but
in some centres where there is availability of anaesthesiologist and
trained anaesthesia nurses the blocks are administered by them.

Retrobulbar Block
The technique was first described in 1884 by Knapp and was very
popular block for cataract surgery till 25 years back. The main goal of
this procedure is to obtain anaesthesia of the cornea, uvea, and
conjunctiva, as well as akinesia of the extraocular muscles by blocking
the ciliary nerves and the II, III, VI cranial nerves, which all go through
the retroconal space. This was the oldest mode of local anaesthesia
practiced all over the world for cataract surgery where the anaesthetic
solution (2-3 mL) was injected into the retrobulbar space of the orbit by
passing a thin (25 G) long (1.5 inch) needle through the lower eyelid at
the level of temporal limbus. Intermittent pressure is applied with the
closed eyelids for the dispersion of anaesthetic solution. Complications
occur in 1-3% of patients, ranging from mild to severe like: retrobulbar
haemorrhage, ocular perforation, rarely subarachnoid or intradural
injection, postoperative ptosis, diplopia secondary to myotoxicity,
cardiorespiratory distress, injury to optic nerve, vascular retinal
occlusion .
Life threatening complications include brainstem anaesthesia
(central block), acute seizure activity, and cranial nerve block. Sight
threatening complications include retro- and peribulbar haemorrhage,
ocular penetration and perforation, retinal vascular spasm, optic nerve
injury, and ocular myotoxicity. The block induced bleeding can be
subcategorizedinto three groups: (1) minor haemorrhage caused by
damage to a vein or small artery that produces a palpable elevation in
intraocular pressure (IOP); (2) arterial haemorrhage producing rapid
proptosis and raised IOP; and (3) concealed haemorrhage in which
blood remains within the muscular cone and produces elevations in IOP
without visible evidence of orbital haemorrhage.

Peribulbar Block
Peribulbar anaesthesia was discovered late in the 1980s by David and
Manda and gradually replaced the retrobulbar injection technique. The
anaesthetic solution is injected into the extraconal compartment of the
eye. Thus, most of the complications associated with retrobulbar
anaesthesia are avoided.
Addition of clonidine and dexmedetomidine to local anaesthetic
drugs like ropivacaine, bupivacaine or lignocaine not only decreases the
total volume of peribulbar anaesthetic solution to be used but also
augments early onset and prolonged offset of sensory analgesia as well
as provides smooth operating conditions with a wider safety margin of
anaesthesia . It also provides sedation which enables full cooperation
and potentially better operating conditions and also decreases the
intraocular pressure significantly.
There is no difference in pain perception during surgery with either
retrobulbar or peribulbar anaesthesia as both are equally effective.
Conjunctival chemosis is more common after peribulbar block and lid
haematoma is more common after retrobulbar block.
 Sub-Tenon’s anaesthesia
Stevens described sub-Tenon’s anaesthesia for cataract extraction
in 1992. A small incision is made in the conjunctiva below the lower
limbus in the temporal quadrant, exposing the sclera. The anaesthetic
solution (2 mL) taken in a syringe is injected using a special blunt tipped
curved needle (configuring the globe curvature) into the peribulbar space
beyond the equator. Because of its easy administration under direct
visibility of the needle insertion, it became more popular than the
previous methods of giving anaesthesia for cataract surgery.
The sub-tenon’s anaesthesia is less painful at the time of its
administration, provides better akinesia and leads to smaller rise in
intraocular pressure just after the injection than peribulbar anaesthesia.
The addition of clonidine 1 μg/kg to 2 % lidocaine in sub-Tenon’s
anaesthesia for cataract surgery increased the duration of sensory
anaesthesia, ocular akinesia, and the duration of analgesia.

Topical Anaesthesia
Topical anaesthesia is used to block the afferent nerves of the cornea
and the conjunctiva (long and short ciliary nerves, nasociliary nerves).
This technique eliminates the possible complications of injectable
anaesthesia. Advantages of topical anaesthesia include no risk of ocular
perforation, extraocular muscle injury, or central nervous system
depression. Vision returns almost immediately, and patients are able to
leave the operating room without being patched post-operatively
because no eyelid block is used. However, it does not eliminate pain
sensitivity of the iris, the zonule, and the ciliary body.

Intracameral anaesthesia
Gills introduced intracameral technique of anaesthesia, wherein 0.25 mL
of preservative free 1% lidocaine anaesthetic solution is injected into the
anterior chamber on the surface of iris. Topical and intracameral
techniques are not absolutely safe as epithelial and endothelial toxicities
are reported with them.
Combined topical and intracameral anaesthesia without sedatives is well
tolerated for most phacoemulsification patients. It is also effective in
cases when complications or adverse events occur. Although topical
anaesthesia alone provides acceptable anaesthesia for manual small-
incision cataract surgery, combined topical and intracameral
anaesthesia decreases patients’ discomfort and increases their
cooperation during the operation. Most of the pain during cataract
surgery under topical anaesthesia is due to extension of the anterior
chamber by irrigation such as too much hydration during hydro-
dissection.

No Anaesthesia

Amar Agarwal introduced the technique of “no anaesthesia” for cataract

extraction in 1998. In this technique, no topical or intracameral drugs are
used. A question that arises is that cornea is supplied by a dense plexus
of sensory nerves,then how it is possible to do cataract surgery without
any anaesthesia? Possible explanations are: peripheral and superior
cornea is less sensitive than central cornea; dark-brown eyed Indians,
Chinese, and blacks have a corneal sensitivity that is four times less
than blue-eyed Caucasians; people in developing countries like India are
more exposed to ultraviolet rays which may result in a significant loss of
corneal sensitivity. Due to increased stress on surgeon, the “no
anaesthesia” technique has not gained popularity.

Cryo Analgesia
Gutierrez–Carmona modified “no anaesthesia” technique and
introduced cryoanalgesia for cataract surgery. In this technique, all
solutions to be used during surgery are cooled to 4°C except povidone
drops. Before surgery, an eye mask of cold gel is placed over the eye for
10 min. During the surgery, the eye is irrigated with cold balanced salt
solution. The advantage of performing phaco with irrigation at low
temperature is that it partially avoids the heat generated by the phaco
tip, eliminating pain. Further, using cold fluids reduces postop
inflammation, the risk of endophthalmitis and the endothelial trauma
caused by the heat of the phaco tip. Although known to be a safe
technique for clear cornea phacoemulsification with acceptable level of
pain, it is not suitable for all cataracts and all patients.
Compared with retrobulbar/peribulbar, topical anaesthesia does not
provide the same excellent pain relief in cataract surgery; however, it
achieves similar surgical outcomes. Topical anaesthesia reduces
injection related complications and alleviates patients’ fear of injection.
With the advent of phaco emulsification the need for complete akinesia
of the globe has been eliminated. Still, the choice of topical anaesthesia
is not suitable for patients with a higher initial blood pressure or greater
pain perception. Peribulbar anaesthesia provides significantly better
patient satisfaction in comparison with topical anaesthesia when used
for cataract surgery.
Complications
Various complications and side effects have been reported in the world
literature following the various blocks given for cataract surgery in the
adults which may either be due to the technique of block or due to
allergic reactions to the drugs used.
Although peribulbar anaesthesia is considered to be a safer alternative
to retrobulbar anaesthesia for cataract surgery, transient or serious
complications have been reported in the literature such as amaurosis,
contralateral cranial nerve III (ptosis, and medium-sized pupils
unresponsive to light stimulus) and VI nerve paralysis , central retinal
artery occlusion and transient complete visual loss. Necrotizing fasciitis
after local retrobulbar anaesthesia injection and facial block for cataract
surgery have also been reported.
Sub-Tenon anaesthesia although safe, showed more intraoperative and
postoperative complications than topical anaesthesia like significant
redness due to subconjunctival haemorrhage.
Long-term visual compromise secondary to needle misadventure,
resulting in penetration or perforation of the globe, is the most feared
complication in ophthalmic anaesthesia. So blocks can be performed
under ultrasound guidance which include real-time visualization of
needle trajectory and spread of injected local anaesthetic, resulting in
blocks of improved quality and safety.

Conclusion

The type of anaesthesia has to be decided on the type of cataract

surgery to be performed in the patient. Topical with intracameral
anaesthesia appears to be safe mode of practice for phacoemulsification
procedure for experienced surgeons. Otherwise, sub-Tenon’s
anaesthesia is also safe. Peribulbar/sub-Tenon’s anaesthesia is better
for extracapsular cataract extraction. In view of the dangerous
complications of retrobulbar anaesthesia, it is practiced much less
currently. General anaesthesia is reserved only for patients where it is
really indicated as most of these patients have one or more co-
morbidities. Monitored anaesthesia care maybe helpful if facilities are
available.
MCQ

1. Regional anaesthesia for cataract surgery include all

except

A) Facial nerve block

B) Ophthalmic nerve block
C) Peribulbar block
D) Parabulbar block.

2. Complications of Retrobulbar block include

A) Amaurosis
B) Optic nerve sheath injury
C) Perforating eye injury
D) All of the above.
A
P
P
E BLOOD
C
TRANSFUSION Dr. Jyotsna Agarwal

2 Associate Professor
0 Anaesthesiology
Hamdard Institute of
2 Medical Sciences and
1 Research, New Delhi
OVERVIEW
 Background
 Patient Blood Management
 Strategies to manage surgical bleeding and reduce transfusion
 Preoperative
 Intraoperative
 Blood products transfusion- PRBC, Platelets, Plasma, Cryoprecipitate
 Massive blood transfusion
 Point of care testing- TEG, ROTEM
 Complications
DEFINITIONS

 Haemovigilance – Procedure cover the entire blood transfusion chain and used to
standardize the use of blood in healthcare

 Patient blood management (PBM) - Timely application of evidence-based

medical and surgical concepts designed to maintain hemoglobin concentration,
optimize hemostasis and minimize blood loss in an effort to improve patient
outcome
The Society for the Advancement of Blood Management
GOALS OF PATIENT BLOOD MANAGEMENT (PBM)

 Balance the threats posed by two independent risk factors of patient outcome-
Anemia and Transfusion
 Hemoglobin alone is not a sufficient indicator for transfusion, overall patient
condition should be considered
MEASURES TO MINIMIZE BLOOD TRANSFUSION

 PREOPERATIVE MEASURES
 INTRAOPERATIVE MEASURES
PREOPERATIVE STRATEGIES TO MANAGE SURGICAL BLOOD LOSS

 Manage anemia, medications that affect hemostasis

ANEMIA
 Independently associated with increased risk of transfusion
 Severe anemia impacts oxygen delivery to vital organs
 because of reduced cardiac output (CO) due to hypovolemia, reduced oxygen
carrying capacity due to anemia
 Compensatory ability depends on patients cardiopulmonary status
PREOPERATIVE STRATEGIES TO MANAGE SURGICAL BLOOD LOSS

Elective surgical procedures — It may be appropriate to postpone an elective

procedure when there is a reversible cause of anemia or coagulopathy that can be
corrected in a reasonable period of time
PREOPERATIVE STRATEGIES TO REDUCE BLOOD TRANSFUSION

 Iron deficiency anaemia

Treat with iron rather than transfusion, unless the anemia is extremely severe and
there is risk of organ ischemia
PREOPERATIVE STRATEGIES TO MANAGE SURGICAL BLOOD LOSS

 Screening tests for bleeding disorders

 Hemoglobin
 Platelet count
 Screening tests of coagulation (prothrombin time [PT] with international normalized
ratio [INR] and activated partial thromboplastin time [aPTT])
 Liver function tests, Renal function tests
 Lab tests for patients receiving anticoagulants
 PT/INR for those on warfarin
 Creatinine for those on a dabigatran or Direct factor Xa inhibitor
PREOPERATIVE STRATEGIES TO REDUCE BLOOD TRANSFUSION

Routine screening tests of coagulation are not indicated unless a bleeding disorder
is suspected

The American Society of Anesthesiologists, The British Committee for

Standards in Hematology ,The European Society of Anaesthesia

 Preoperative screening should be done early enough to allow time for diagnosis and
treatment of pathologies
 INTRAOPERATIVE STRATEGIES TO MANAGE SURGICAL BLEEDING
Fluid management in bleeding patients
 Maintenance of normovolemia throughout the perioperative period
 During acute bleeding, Hb values are only slightly decreased initially
 Large volumes of crystalloid resuscitation is
 Associated with dilutional anemia and coagulopathy, tissue edema and adverse
outcomes
Traditionally crystalloid : blood loss – 3:1
Practice is towards using lower crystalloid : blood loss ratio
~1.5 : 1 (1.5 volumes of crystalloid for every 1 volume of lost blood)
1 : 1 (equal volume of colloid to volume of lost blood)
Fodor, G.H., et al. Optimal crystalloid volume ratio for blood replacement for maintaining hemodynamic stability and lung
function: an experimental randomized controlled study. BMC Anesthesiol 19, 21 (2019)
INTRAOPERATIVE STRATEGIES TO MANAGE SURGICAL BLEEDING
Maintenance of normothermia : Hypothermia should be avoided throughout the
perioperative period in noncardiac surgical patients

Hypothermia causes coagulopathy due to impairment of platelet aggregation and

reduced activity of enzymes in the coagulation cascade leading to REDUCED
CLOT FORMATION

Even mild (eg, 1°C) hypothermia can increase blood

Rajagopalan S et al. Anesthesiology. 2008;108(1):71.
loss by ~20 %

Use blood warmer for transfusion of all thawed or refrigerator-temperature blood

products, fluid and patient warming devices
 INTRAOPERATIVE STRATEGIES TO MANAGE SURGICAL BLEEDING

 Electrosurgery devices
 Intraoperative blood salvage - also known as blood recovery
 Acute normovolemic hemodilution
 Use of hemostatic agents- Antifibrinolytic agents, Fibrinogen, PCC
INTRAOPERATIVE STRATEGIES TO MANAGE SURGICAL BLEEDING
Used prophylactically to reduce surgical blood loss and transfusion
Antifibrinolytic agents
 Tranexamic acid (TXA), Epsilon-aminocaproic acid (EACA), Aprotinin
Fibrinogen concentrate
 In low plasma fibrinogen level (<150 to 200 mg/dL)
 Recombinant activated factor VII (rFVIIa) – in intractable bleeding
 Desmopressin (DDAVP) - in vWD, mild hemophilia A , acquired platelet defects
 Prothrombin complex concentrate (PCC)
INTRAOPERATIVE STRATEGIES TO MANAGE SURGICAL BLEEDING

Prothrombin complex concentrate (PCC)

 Typically indicated for Emergency reversal of warfarin
 All PCCs contain factors II, IX and X
 Also contain low doses of heparin, variable amounts of protein C and protein S-
avoid in HIT
 4-factor PCCs - contain therapeutic levels of factor VII
 Supplemental factor VII administered with 3 factor PCC
INTRAOPERATIVE STRATEGIES TO MANAGE SURGICAL BLEEDING

PCC (contd)
 Advantages of PCCs over fresh frozen plasma (FFP)
 Rapid administration in a small volume, avoidance of volume overload and
transfusion reactions
 More rapid reversal of the anticoagulant effect

 activated PCC (aPCC; eg, FEIBA) contain activated factor VII

BLOOD PRODUCT TRANSFUSION
INFECTIOUS DISEASES TESTING IN BLOOD TRANSFUSION
 Infectious Disease Tested for Blood Transfusions : 2018
 Human immunodeficiency virus (HIV) , Hepatitis C virus (HCV) , Hepatitis B virus
(HBV)
 Human T-cell lymphotropic virus (HTLV)
 West Nile virus , Zika virus
 Serologic test for syphilis

Infectious Diseases Theoretically Transmissible by Blood Transfusion for Which No

Test Is Available: 2004
Malaria, Severe acute respiratory syndrome (SARS), Variant Creutzfeldt-Jakob disease
BLOOD PRODUCT TRANSFUSION
BLOOD PRODUCT TRANSFUSION
Recipient Can receive BLOOD donated
from
 RED CELL COMPONENTS Group O Group O (Universal Donor)
Group A Group A and O
In red cell transfusion, there must be
ABO and RhD compatibility between Group B Group B and O
the donor’s red cells and the Group AB Group AB, A, B and O
recipient’s plasma. (Universal recipient )
 PLASMA AND COMPONENTS
CONTAINING PLASMA PLASMA donor Can be given to (recipient)
Group AB plasma (no any ABO group patients
In plasma transfusion, group AB
antibodies) (Universal Donor)
plasma can be given to a patient of
any ABO group because it contains Group A plasma (anti-B) Group A and O
neither anti-A nor anti-B antibody Group B (anti- A) Group B and O
Most blood products should be given Group AB Group O only
ABP compatible as much possible (anti -A, anti-B)
RED CELL CONCENTRATE (‘PACKED RED CELLS’, ‘PLASMA-REDUCED
BLOOD’ TRANSFUSION

Clinical points
 150–200 ml red cells from which most of the plasma has been
removed
 Haematocrit ~ 55-75%
 Haemoglobin ~ 20 g/100 ml
 Administration of PRBCs is facilitated by utilizing crystalloid or
colloid as a carrier - both Lactated Ringer and Normal Saline are
compatible and equally acceptable
Miller Anaesthesia 9 edi
PRBC TRANSFUSION DECISION MAKING (CONTD)
At rest, oxygen delivery = 4 x oxygen consumption Oxygen delivery is expected to be adequate
enormous reserve present until the hematocrit (packed cell volume) falls
below 10 percent

During bleeding –
Increase cardiac output + increased oxygen extraction can
compensate for the decrease in arterial oxygen content However, increase cardiac output
requires more oxygen
Provided intravascular volume is maintained, and
cardiovascular status is normal

Leftward ODC shift of stored blood is

So the “critical point” is the Hct where oxygen normalized within 6 to 24 hours after
consumption becomes delivery dependent – At this Hct transfusion as transfused RBCs regenerate 2,3-
transfusion is required BPG to normal levels
PRBC TRANSFUSION DECISION MAKING (CONTD)

Surgical patients
In patients without significant ongoing bleeding
Hgb threshold <7 to 8 g/dL (hematocrit~ ≤21 to 24 percent)
[Restrictive policy]

In patients with significant ongoing bleeding, known acute coronary syndrome, signs of
myocardial or other organ ischemia
Hgb threshold of <9 g/dL (hematocrit~ ≤27percent) [Liberal policy]

 General consensus- PRBC indicated if Hgb <6 g/dL, and transfusion is rarely
indicated if Hgb >10 g/dL
Practice guidelines for perioperative blood management: an updated report by the American Society of
Anesthesiologists Task Force on Perioperative Blood Management. Anesthesiology. 2015;122(2):241.
PRBC TRANSFUSION DECISION MAKING (CONTD)
 These strategies do not describe the indications for administration of subsequent
units of blood, repetitive transfusions
REPEAT TRANSFUIONS
Transfuse 1 unit of packed red cells at a time
Expected Hemoglobin increase ~1 g/dL and hematocrit by 3%
Follow up by checking post-transfusion hemoglobin
Post-transfusion Hgb level can be assessed after 15 minutes PRBC administration (in
the absence of bleeding)
For repeat red cell transfusion- send new blood sample for compatibility testing

 Future development of more sensitive indicators of tissue oxygenation (intramucosal

pH) may reduce the need of surrogate markers (such as hemoglobin) for transfusion
trigger
 PLATELET TRANSFUSION

CLINICAL POINTS
 Administered as
 Single donor platelets - Apheresis platelet pack harvested from a single donor
 Random donor platelets - Pooled units of whole blood derived platelets
(manufactured from whole blood donations from 4-6 different donors)
 Stored at room temperature, can be used up to 7 days
 Infused over < 30 minutes
PLATELET TRANSFUSION (CONTD)

Risks of Platelet Transfusion

 Bacterial infection - due to storage at room temperature
 For any patient who develops a fever within 6 hours after receiving platelets, sepsis
from platelets should be considered
PLATELET TRANSFUSION DECISION MAKING

INDICATIONS
• <50,000 / microL - in surgical patients

• <100,000 / microL - Surgical patients involving central nervous system bleeding,

ocular surgeries
- Surgical patients when qualitative platelet defects present
• <20,000 / microL - Minor invasive procedures (CVP line)
• Component of massive transfusion protocols

Each platelet dose (one apheresis unit) increase the platelet count by ~ 30,000/microL
to 50,000/microL in a non-bleeding adult
Cochrane Database Syst Rev. 2018;9:CD012779. Epub 2018 Sep 17.
PLASMA

 Most commonly ordered and transfused hemostatic agent in the world

Fresh Frozen Plasma (FFP)
 The fluid portion of 1 unit of human blood that has been centrifuged and separated
and then frozen at -18°C (or below) within 6 hours of collection
Plasma Frozen within 24 Hours of Collection (PF24)
 For plasma processed and frozen within 8 to 24 hours of collection
 PF24 is similar comparable to FFP, with slight reduction in factor V and 25% decrease
in factor VIII
PLASMA

FFP and PF24 thaw can store at 1 °C to 6 °C for up to 24 hours

If prepared in a closed system and

not transfused within 24 hours

Can be stored at 1 °C to 6 °C for up to 5 days

Relabelled as ‘Thawed Plasma’
PLASMA

 FFP- Contains all labile and stable coagulation factors and is indicated for
multiple coagulation deficiencies
 Most clotting factors remain stable for 3 months if stored at <−24°C
 FFP has all of the clotting factors at their normal concentrations when administered
within 6 hours of thawing
 After that interval, the levels of the labile factor V and VIII begin to diminish
PLASMA
 Indications
 Component of massive transfusion protocols
 Emergency surgery in patients with severe bleeding
 INR >2
 Replacement of deficient coagulation factors
 Reversal of warfarin , if a prothrombin complex concentrate (PCC) is not
available

 Do not use in stable nonbleeding patients solely to "correct" a mildly elevated

INR (<2)
 The recommended initial dose of FFP is 10 to 15 mL/kg
CRYOPRECIPITATE

 Concentrate of high-molecular-weight plasma proteins that precipitate when frozen

plasma is slowly thawed at 1-6°C
 Volume of one unit ~ 5 to 20 mL . Contains
 Fibrinogen , von Willebrand factor, Factor VIII, Factor XIII
 Used to treat fibrinogen deficiency, von Willebrand disease and hemophilia A (factor
VIII deficiency)
CRYOPRECIPITATE

Cryodepleted plasma ("cryosupernatant")

 Is deficient in high molecular weight vWF multimers and FVIII

Administration of cryoprecipitate
 Infusion should be completed within 6 hours of thawing, warming not required
HB-BASED O2 CARRIERS (HBOCS)

 Oxygen therapeutics are labeled as Hb-based O2 carriers (HBOCs)

 Fluosol-DA , Perfluorooctyl bromide , HBOC-201, Hemopure
 Failure in clinical trials- increased adverse events myocardial infarction and death
Parameter Synthetic blood products Allogenic Transfusion
Oxygen delivery Rapid and consistent Dependent o 2,3 DPG
Risk for disease transmission None Many
Storage Room Temperature Refrigeration
Shelf life 1-3 years 42 days
Preparation Ready to use Cross match
Compatibility Universal Type specific
Duration of action 1-3 days 60-90 days
MASSIVE BLOOD TRANSFUSION
 Defined as replacement by transfusion of 10 units of red cells in 24 hours
Alternative definitions
 3 units of red blood cells over one hour or
 any four blood components in 30 minutes

 Dilution of coagulation factors and platelets will occur following administration of

large volumes of replacement fluids. Massive or large volume transfusions can
therefore result in disorders of coagulation
MASSIVE BLOOD TRANSFUSION

Emergency surgery with massive blood transfusion

RBCs, Fresh Frozen Plasma (FFP), and apheresis platelets transfused in 1:1:1 ratios
apheresis platelet unit

Physiology supporting the 1:1:1 (FFP:platelets:RBCs) approach

With this ratio, effective concentrations transfused are
 Plasma coagulation factor concentration of 65 percent, platelet count of 55 x 109/L,
hematocrit of 26 percent
 Thus, giving blood products, and nothing but blood products, barely keeps levels
above conventional transfusion triggers
MASSIVE BLOOD TRANSFUSION

RBCs, Fresh Frozen Plasma (FFP), and apheresis platelets 1:1:1 ratio (contd)

 More of any one product merely dilutes the other two

 Any crystalloid solution administered will further dilute all three blood components
 Patients who are likely to require massive transfusion – should receive a 1:1:1 ratio
of FFP to platelets to RBCs at the outset of their resuscitation and transfusion
therapy
 Complications – discussed subsequently
POINT OF CARE TESTING FOR BLOOD TRANSFUSION
INTRAOPERATIVE DIAGNOSTIC TESTING
 Standard coagulation tests Take atleast 45 to 90 minutes
 Platelet count
 Fibrinogen concentration

 Point-of-care tests - Provides more timely information compared with standard

tests allowing more rapid decision-making
POINT OF CARE TESTING FOR BLOOD TRANSFUSION

 Hemoglobin or hematocrit measurements - Arterial blood gas, instruments for

Hb measurement
 Overall hemostatic function- Thromboelastography (TEG), Rotational
thromboelastometry (ROTEM) (adaptation of TEG)
 Allow rapid assessment of coagulopathy and responses to interventions
 Test overall hemostatic function
 Transfusion algorithms guided by viscoelastic testing (TEG, ROTEM) reduces RBC
and platelet transfusions compared with standard care in cardiac and liver
surgeries, trauma
International Society on Thrombosis and Hemostasis
POINT OF CARE TESTING FOR BLOOD TRANSFUSION

 With TEG or ROTEM tests, a tracing result provides

information regarding clot initiation, kinetics of clot
formation, clot strength, and fibrinolysis
 Primary fibrinolysis
 Secondary hyperfibrinolysis
 Thrombocytopenia
 Clotting factor consumption
 Hypercoagulability
COMPLICATIONS OF BLOOD PRODUCT TRANSFUSION
COMPLICATIONS OF BLOOD PRODUCT TRANSFUSION
 Hemolytic transfusion reactions
 Febrile non-hemolytic transfusion reactions (FNHTRs)
 Transfusion-related acute lung injury (TRALI)
 Transfusion-related circulatory overload (TACO)
 Transfusion-transmissible infections (bacterial, viral, or parasitic)
 Transfusion-associated graft-versus-host disease (ta-GVHD)
 Transfusion-related immunomodulation that may lead to postoperative infection
 Massive transfusion may result in additional complications (citrate toxicity with
hypocalcemia, hyperkalemia, acidosis, hypothermia)
COMPLICATIONS OF TRANSFUSION

Transfusion related fatalities

COMPLICATIONS OF TRANSFUSION

Clinical Presentation
 In an unconscious or anaesthetized patient – difficult to identify
 hypotension and uncontrolled bleeding , or oozing
 Acute reactions can occur with transfusion of 5‐ 10 mL of blood
 Strict monitoring for the first 15 minutes of each unit should be done
TRANSFUSION-RELATED ACUTE LUNG INJURY (TRALI)

 ARDS caused by blood transfusion

 Manifests as noncardiogenic pulmonary edema, NO VOLUME OVERLOAD PRESENT
 S/S- Within 6 hours after transfusion, clear temporal relationship to the transfusion
 Fever, dyspnea, fluid in the endotracheal tube, and severe hypoxia
 All blood components, especially FFP implicated, larger transfused blood volumes
have higher incidence – less with cryoprecipitate and PCC as compared to FFP
 Management- Stop transfusion, supportive measures
TRANSFUSION ASSOCIATED CIRCULATORY OVERLOAD (TACO)

 Excessive administration volume of blood leading to pulmonary edema with evidence

for increased left-sided cardiac filling pressures (in contrast to TRALI)
 Management- Lung protective ventilation, diuretics
 Incidence is less with leucoreduced blood
COMPLICATIONS- ACID-BASE ABNORMALITIES
 pH of stored blood is low (<7 by day 35)
 storage media is very acidic (pH 5.5 for CPD)
 accumulation of lactic and pyruvic acids by RBC metabolism and glycolysis
 carbon dioxide partial pressure (Pco2) of 150 to 220 mm Hg (cannot escape
through plastic bags)
 Acidosis in a patient receiving a large volume transfusion
 Under normal circumstances, the body can easily neutralize acid load from
transfusion
 Mostly due to inadequate treatment of hypovolemia instead of effects of
transfusion
COMPLICATIONS- ACID-BASE ABNORMALITIES

The routine use of bicarbonate or other alkalizing agents, based on the number of units
transfused, is unnecessary
COMPLICATIONS OF CITRATE INFUSION

 Large amounts of citrate transfusion can cause Metabolic alkalosis

 Metabolism of each mmol of citrate generates 3 mEq of bicarbonate (~ 23 mEq of
bicarbonate in each unit of blood)
 Metabolic alkalosis can occur if underlying renal disease (prevents the excess
bicarbonate excretion)

 Citrate intoxication and metabolic alkalosis can lead to

 hypocalcemia, hypokalemia , dysrhythmia, and hypotension
COMPLICATIONS- HYPERKALEMIA

 Hyperkalemia
 Very rare as a result of transfusion
 Can occur in patients with impaired renal function and neonates
COMPLICATIONS- COAGULATION ABNORMALITIES

 Major trauma or blood loss will initiate a cascade of coagulation abnormalities

 This coagulopathy is caused by a combination of factors
 consumptive coagulopathy
 dilution of coagulation factors

 S/S- oozing, hematuria, bleeding from venipuncture sites

 D/D- DIC, dilutional thrombocytopenia, deficiency of factors V and VIII, transfusion
reaction
COMPLICATIONS- COAGULATION ABNORMALITIES

 Management based on - Point of care testing preferentially

 If available, Fresh blood is extremely effective in treating transfusion-induced

coagulopathies
 Low levels of fibrinogen, factor V, VIII- supplemented by FFP, cryoprecipitate
administration
COMPLICATIONS - HYPOTHERMIA

 Administration of blood stored at 4°C - can cause hypothermia

 Hypothermia can
 Impair coagulation factors and platelet function
 Ventricular irritability and cardiac arrest
 Shivering increases metabolic demands
 Management- Warm blood through blood warmers, plastic coils or plastic cassettes
in a warm water (37°C-38°C) bath or warming plates
COMPLICATIONS- HEMOLYTIC TRANSFUSION REACTION

 Intravascular hemolysis
 Occurs due to direct attack on transfused donor cells by recipient antibody and
complement
 Can occur with even 10 mL of blood
 Under GA- Hemoglobinuria (presenting sign), bleeding diathesis, hypotension
 Acute renal failure
 Management- Maintain urinary output >75 mL/h, alkalization of the urine
DELAYED HEMOLYTIC TRANSFUSION REACTION (IMMUNE
EXTRAVASCULAR REACTION)

 Decrease in the posttransfusion Hematocrit 2-21 days later

 Occurs in recipients sensitized to RBC antigens by previous blood transfusions or
pregnancy, more common in females
 Occur when the level of antibody at the time of transfusion is too low to be
detected
 RBC destruction occurs only when the level of antibody is increased after a
secondary stimulus (i.e., anamnestic response)
NONHEMOLYTIC TRANSFUSION REACTIONS

Febrile reactions
 Very common
 The transfusion usually does not need to be discontinued in minor allergic and febrile
reactions
 Use of leukoreduced blood has lowered the incidence of febrile reactions
NONHEMOLYTIC TRANSFUSION REACTIONS (CONTD)
 Allergic reactions can be minor, anaphylactoid, or anaphylactic
 S/S- Urticaria, itching, facial swelling
 Management- Antihistamines

 Anaphylactic allergic reactions

 Dyspnea, hypotension, laryngeal edema, chest pain, shock
 Does not involve red cell destruction, occurs very rapidly, with few ml of blood or
plasma
 Give transfusions with washed RBCs in such patients
TRANSFUSION-ASSOCIATED GRAFT-VERSUS-HOST DISEASE

 Donor lymphocytes from transfused blood products initiate an immune reaction

against recipient tissues
 Generalized rash, leukopenia, and thrombocytopenia, sepsis, death can occur
 Irradiation of blood can prevent transfusion-associated GVHD
TRANSFUSION-RELATED IMMUNOMODULATION

 Homologous (allogeneic) blood transfusion exerts a nonspecific immunosuppressive

action on the recipient
 Effects are contradictory
NONINFECTIOUS RISKS OF BLOOD TRANSFUSIONS

 Microchimerism: More than one cell line in an individual organism

 Posttransfusion purpura- due to recipient alloantibodies attacking donor platelet
antigens, treated with IVIG
 Alloimmunization: Can lead to platelet counts become refractory to transfusions .
RBC alloantibodies can also form rarely
 Iron overload: Can result from chronic transfusion therapy, fatal liver or heart
dysfunction can occur
PERIOPERATIVE PATIENT BLOOD MANAGEMENT DURING THE
COVID-19 PANDEMIC

 During the COVID-19 pandemic- shortages of blood products caused by decreased

blood donations
 Perioperative PBM - VITAL to balance supply and demand for blood products
Dr. Nisha Kachru
Anatomy
— Largest internal organ – weight
600-1800gms

— Traditionally divided into 4 lobes

— Couinaud model - functional

segments (8), based on hepatic
vascular supply and biliary
distribution.
— Hepatic resection
Microscopic anatomy
Blood supply
— 20- 25% of the resting CO (1500ml/min)
— Hepatic Artery -25% SpO2-98%
— Portal Vein- 75% SpO2-60-70%
— Oxygen supply 50:50

— HABR (hepatic arterial buffer response) – reduction in PBF, matched

by increase in HABF to maintain oxygen delivery
Functions of the Liver
1. Metabolic and storage- carbohydrate, protein, fats

2. Detoxification- alcohol, drugs, ammonia

3. Synthetic- bile, heme, coagulation factors, albumin, cholesterol

4. Immunologic – Kupfer cells, NK cells , T & B lymphocytes

5. Homeostatic- glucose/volume homeostasis, hormone synthesis and

degradation
Liver Function Tests
— Hepatocyte function- Liver enzymes - AST, ALT, LDH,GST

— Detoxification and excretory function –S. Bil (indirect/direct),

S.Ammonia, U. bilirubin

— Synthetic function - S. Albumin, S. globulin, coagulation factors-

PT/INR

— Cholestasis - Alk Phosphatase, GGT

Hepatic dysfunction and LFTs
Hepatic Causes S. Bilirubin Aminotransferas Alkaline
dysfunction es Phosphatase
Prehepatic Hemolysis, Increased Normal Normal
Hematoma unconjugated
resorption,
Bilirubin overload
post blood
transfusion
Hepatic / Viral, alcoholic, Increased Markedly increased Normal to slightly
hepatocellular drug induced, conjugated increased
sepsis, hypoxemia,
cirrhosis
Posthepatic / Biliary tract stones, Increased Normal to slightly Markedly increased
cholestatic stricture, tumour conjugated increased
Cirrhosis
— pathological end point of chronic inflammatory liver disease
— steady or recurrent parenchymal inflammation, necrosis & and
fibrosis
— formation of regenerative nodules
— distortion of normal liver architecture with increased resistance
to intrahepatic blood flow
— portal hypertension
Causes
Portal hypertension
Chronic increase in portal venous pressure

— HPVG ( Hepatic Venous Pressure Gradient) maintains flow

— HPVG = WHVP-HFVP (wedged-free HVP)
— Normal HPVG 1-5mm Hg
— Mild PHT - 5-10mm Hg
— >10mmHg clinically significant
— Shunt formation
Portal Hypertension
— !P = R X Q

— Increased resistance to intrahepatic blood flow (R)

— Peripheral & splanchnic NO & neural, humoral and
endothelial factors like prostaglandins, VIP, glucagon etc →
splanchnic vasodilatation → increased portal inflow (Q)
— exacerbation of PHT

— Formation of collaterals, ascites, splenomegaly

Systemic effects of cirrhosis
— Hematological
— Coagulation
— Cardiac
— Renal
— Pulmonary
— CNS
— Gastrointestinal
— Hepatocellular Carcinoma
Hematological
Anemia
— Chronic illness
— Malnutrition
— Blood loss
— Hypersplenism
— Bone marrow depression
Coagulopathy
1. ↓ synthesis of

— procoagulant except tissue thromboplastin (III), calcium (IV) and

von Willebrand factor(VIII)
— anticoagulant factors (protein C, S, antithrombin III)
— clearance of activated factors
Coagulopathy
2. Thrombocytopenia due to

— Splenic sequestration (splenomegaly)

— decreased level of thrombopoietin
— immunologic mechanism,
— direct bone marrow suppression
Coagulation
3.Vitamin K deficiency

4. Dysfibrinogenemia

5. Fibrinolysis – accelerated fibrinolysis

Need blood component therapy, Vitamin K, tranexamic acid

Cardiac Manifestations
1. Hyperdynamic circulation with low SVR, high CO, low BP
2. PAP raised, PVR normal,
3. Systolic dysfunction – impaired contractility
4. Diastolic dysfunction- delayed LV filling
5. ECG abnormalities –prolonged QT
6. Ionotropic & chronotropic response to stress impaired
7. Underlying CAD, cardiomyopathy
Renal dysfunction
— Hypovolemia → Renal hypoperfusion with ↓ GFR →
- activation of RAAS ( renin angiotensin aldosterone) &
vasopressin → Na & water retention
- Precipitated by pre/ intraoperative hypovolemia, diuretics

— Prone to parenchymal renal disease, sepsis

— Coexisting diabetes, immune complex nephropathies,

amyloidosis
Hepatorenal Syndrome (HRS)
— Functional renal failure with no renal pathology in patients with
cirrhosis, reversible
— water retention- ascites, oedema, azotemia, oliguria, electrolyte
imbalance
— Type 1 - rapid onset (1-2 weeks), precipitating cause present e.g.,
surgical stress, GI bleeding, SBP, LVP, poor prognosis, survival 2-4
weeks
— Type 2- gradual onset, progression of RAAS and vasopressin
systems, better prognosis, survival 6 months
Management
— Maintain renal perfusion
— Avoid nephrotoxic drugs like NSAIDs, aminoglycosides, ACE
inhibitors, ARBs
— Elimination of underlying cause

— HRS
- Increase renal perfusion pressure with octreotide, terlipressin or
norepinephrine infusions combined with volume expansion with
albumin
- Dialysis
- Liver Transplantation
Pulmonary Complications
Vascular
— Hepatopulmonary syndrome (HPS)
— Porto pulmonary hypertension (PoPH)

Mechanical
— Hepatic hydrothorax
— Ascites/ Pleural effusion
Hepatopulmonary Syndrome (HPS)
— Defined as abnormal alveolar-arterial oxygen gradient (≥15mmHg)
while breathing room air in sitting position
— Intrapulmonary vasodilatation V:Q mismatch
— Impaired HPV
— Clubbing, cyanosis, spider naevi
— Platypnoea –shortness of breath which is worse in standing position
and relieved by lying down
— Orthodexia- fall in PaO2 by 4mmHg or 5% on moving from supine to
erect position
HPS contd..
— Severity depends on PaO2
- >80mmHg - mild
- 60-80mmHg - moderate
- 50-60mmHg - severe
- <50mmHg- very severe
— Diagnosis –’saline bubble test’ on ECHO - intrapulmonary vasodilatation,
Tc99m albumin scintigraphy
— Management –
— Oxygen supplementation to maintain SpO2 over 88%
— Liver Transplant
Portopulmonary Hypertension
— Pulmonary artery hypertension in a known case of liver disease
with PHT
— Cause – pulmonary endothelial smooth muscle proliferation or
thrombus in situ
— Diagnosis – TTE/ right heart catheterization showing
-PAP > 25mmHg, PVR> 240dynes/s/cm5, PAWP <15 mmHg
— Classification
- mild-PAP 25-35mm Hg
- moderate 35-45mm Hg
- severe > 45mm Hg
PAP > 45 mmHg –Absolute CI for LT

Management
Phosphodiesterase inhibitors, prostacyclin analogues to reduce PVR
Hepatic Hydrothorax
— Passage of ascitic fluid from peritoneal to pleural space
— Through defects in diaphragm, usually on right
— Reduced FRC, atelectasis, hypoxia

— Diagnosis – Chest X-ray, thoracocentesis

— Management
— Sodium restriction, diuretics
— Trans jugular Intrahepatic portosystemic shunt (TIPS)
Hepatic encephalopathy
— Neuropsychiatric manifestations in patients with significant liver
disease- acute or chronic

— Sign of decompensated liver disease

— Neurotoxins/ ammonia produced in the gut reach the brain due to

portosystemic shunting and failure of the liver to detoxify them

— Precipitated by GI bleeding, infection, portosystemic shunts,

diuretic overdose, sedatives, high protein diet
West-Haven Criteria
Grade Description

I Trivial lack of awareness, shortened attention span, disordered

sleep
II Lethargy, behavioral change, asterixis

III Somnolence, confusion, gross disorientation, bizarre behavior

IV Coma
Management
— Elimination of precipitating cause

— Restriction of protein intake

— Oral lactulose or neomycin/rifaximin

— Avoid GA, sedatives, opioids

— Protection of airway
 Ascites
Causes
— Hypoalbuminemia → Decreased oncotic pressure
— Activation of the RAAS with sodium water retention
— Increased portal hydrostatic pressure

— Classification
Mild (detectable only by ultrasound)
Moderate (moderate symmetrical abdominal distention)
Large –severe abdominal distention
Effect
— Diaphragmatic splinting so decreases pulmonary compliance
— Decreases renal perfusion
— Spontaneous bacterial peritonitis (SBP)
— Falsely high CVP
— Predisposes to aspiration
— Abdominal wound dehiscence/herniation
Treatment - Salt restriction
- Diuretics- spironolactone/frusemide
- Nonspecific beta blockers to reduce PHT

Refractory ascites
- midodrine for refractory ascites
- Large volume paracentesis- albumin 8gm/l
- Trans jugular Intrahepatic portosystemic shunt (TIPS)
- Liver Transplant
Varices
— Portosystemic collaterals- bypass liver
— Most commonly at lower oesophagus and stomach
— Upper end of anal canal
— Umblical
— Bare area of liver
— Retroperitoneal
— Risk of spontaneous rupture and bleeding- mortality -25-50%
— Diagnosis
esophagogastroduodenoscopy

— Management
Non-selective betablockers
Endoscopic ligation with sclerotherapy
Management of acute variceal bleeding
— Airway protection
— Volume Resuscitation to maintain UO
— Correction of coagulopathy/ Tranexamic acid/Vitamin K/blood
products
— Vasoconstrictors - vasopressin, terlipressin, octreotide, somatostatin
— Antibiotics
— Balloon tamponade-difficult intubation/ventilation
— Endoscopy with variceal ligation/banding/glue/sclerotherapy
— TIPS
Anesthetic management
Types of surgeries
— Gall stone disease
— Hepatic resection
— Shunt procedures
— Liver transplant
— Others
Preoperative assessment
History
— gradual onset
— nonspecific- loss of appetite, malaise, fatigue, disrupted sleep,
cognitive decline
— alcoholism, recreational drug use, medical drugs
— blood transfusion
— history of jaundice, GI bleeding, abdominal distention pruritis,
altered colour of urine, stool
— Family history of genetic diseases
Examination
— General – cachexia, muscle wasting,drowsiness,confusion
— CNS – asterixis, tremors
— Head –icterus, fetor hepaticus, spider naevi
— Chest - gynecomastia, spider naevi
— Abdomen – ascites, hepatic size, splenomegaly, caput medusae
— Hands – clubbing, palmer erythema
— Genitalia - testicular atrophy
— Lower limbs- edema, petechiae

— Involvement of renal/pulmonary/cardiac systems

Laboratory evaluation
— CBC — PT/INR, S. fibrinogen
— B. glucose — Chest X ray, USG
— B.urea, S. Cr — ECG, ECHO, Stress ECHO
— Electrolytes- Na, K, Mg, PO4 — PFT/ABG
— S. bilirubin, Transaminases, S. — Viral markers
Albumin
Aminotransferases in hepatic disease
Liver disease Aminotransferses

NAFLD AST & ALT normal to < 5 X normal

AST:ALT < 1
Acute viral hepatitis > 25 X normal
Chronic viral hepatitis Normal to 10 X normal
Alcoholic hepatitis AST & ALT normal to < 8 X normal
AST:ALT - 2:1
Shock liver AST & ALT normal to > 50 X normal
AST:ALT - 1:1
Child-Pugh Scoring system
Sign of Hepatic 1 point 2 points 3 points
dysfunction

Encephalopathy grade None Grade I-II Grade III-IV

Ascites Absent Mild Severe
Bilirubin (mg/dl) <2 2-3 >3
Albumin (gm/dl) > 3.5 2.8-3.5 < 2.8
INR < 1.7 1.7 -2.3 > 2.3
Total Score 3-15

Class A 5-6 -mild risk 2-10% mortality

Class B 7-9 - moderate risk 12-31% mortality
Class C >10 - poor risk 50-82% mortality, contraindication for elective surgery
— MELD – 3-month mortality, organ allocation, perioperative
mortality
Logarithmic formula- INR, S. Creatinine, S. Bilirubin
MELD < 10 - CTP A
10-14 - CTP B
>14 - CTP C

— Na MELD includes S. Na
— iMELD-integrated MELD - Age & S. Na
— PELD
Evaluation risk for surgery
Patient factors
— ASA grading
— extent of liver disease- CTP C, Acute hepatitis, fulminant hepatic
failure

Surgical factors
— type of surgery-emergency / elective
— nature of surgery - intra-abdominal, major, -high risk
- laparoscopic cholecystectomy in CTP-B/C
Preoperative optimization
— Nutrition- low protein, high — metabolic and electrolyte
calorie diet derangements
— optimize hydration — treatment of active infections
— renal status — hypoglycemia
— encephalopathy — minimize ascites/hydrothorax
— coagulopathy
OT preparation
— Universal precautions for Hepatitis B, C
— Hypothermia- fluid and other warming devices
— Large bore IV access-(7/8 Fr gauge sheath)
— Hemorrhage - rapid infusion systems, blood conservation
techniques
— Invasive monitoring
— Asepsis
— Blood & blood products
— Inotrope infusions
Anesthesia concerns
— Maintenance of hepatic blood flow, oxygenation
— Altered pharmacology-increased sensitivity, large volume of
distribution, increased free drug, reduced hepatic clearance,
active metabolites
— Avoid I/M injections, nasal intubations, nasal/oesophageal
probes/ NG tubes
— May be on beta blockers for PHT
— Hyporesponsive to vasopressors
Factors reduce hepatic blood flow
— Hypoxia — Intravenous agents
— Hypocarbia — Volatile anesthetics
— Haemorrhage — IPPV/PEEP
— Mesentric traction — Regional anesthesia
— Increased IAP — Sepsis
Premedication
— avoid sedation- encephalopathy
— avoid diazepam, midazolam
— lorazepam/oxazepam safe
— dose reduction
— prolonged duration of action
Induction

— sensitivity to the CNS depressant effect

— thiopentone - decreased binding
— propofol maintains HABR/extrahepatic metabolism/less
encephalopathy, normal recovery
Inhalational Agents
— reduce MAP & CO → ↓HBF
— avoid halothane/enflurane
— HABR preserved with isoflurane, sevoflurane, desflurane
— desflurane safest- rapid emergence, less hepatic metabolism, less
↓CO
— N2O may be avoided-reduce hepatic blood flow
Opioids
— Morphine - free drug increased, action prolonged
— Pethidine/alfentanil/ buprenorphine- elimination reduced
— Fentanyl – large doses accumulate
— Remifentanil safest
Muscle Relaxants
— Scoline –RSI (ascites), pseudocholinesterase ↓– prolonged duration
— Non depolarizing agents
- slower onset of action
- duration prolonged
- Vecuronium/rocuronium- hepatic metabolism
— Atracurium/cisatracurium -safe

— Neostigmine – unaffected
Intraoperative monitoring
— ECG — Biochemical & hematological
— SpO2 monitoring
— NIBP, EtCO2, — glucose
— Temperature — hematocrit
— U.O. — electrolytes
— Blood loss — calcium
— Arterial pressure monitoring — ABG
— CVP monitoring — TEE/ Pulmonary artery
— Neuromuscular monitoring
catheterization/ SVV
— TEG/ Thromboelastometry
Postoperative care
Analgesia
- Avoid epidural catheters
- Regional analgesia- hematoma
- PCA fentanyl
- NSAIDS not recommended
- Acetaminophen up to 2gm/day
- Tramadol- low dose
— ICU care- CTP-B/C
— Signs of decompensation – encephalopathy, jaundice
Role of neuraxial anesthesia
— coagulopathy/ thrombocytopenia
— post hepatic resection coagulopathy
— hypotension and reduction in hepatic blood flow
— non-responsive to catecholamines
— decreased LA requirements
Considerations for special procedures
TIPS (Transjugular Intrahepatic Portosystemic Shunt)
— Interventional radiological procedure
— create a shunt between portal vein and systemic circulation(hepatic vein)
through the liver parenchyma
— Indicted in refractory ascites, variceal haemorrhage, reduce gradient
— Contraindications -CHF, severe TR, mod-severe pulmonary HT, sepsis,
biliary obstruction
— Complications - vascular injury, dysrhythmias, hemorrhage, trauma,
encephalopathy, renal failure
Anesthetic concerns
— Complete evaluation and optimization
— Remote location
— Access to the patient
— L.A/Sedation/G.A.
— Ability to lie supine
— Encephalopathy
— Airway protection
— Ventilation compromised
Spleno-Renal Shunt- Anesthesia concerns
— Pediatric patients
— Non cirrhotic portal HT/ Extra hepatic portal venous
obstruction/Budd Chiari syndrome
— Shunt from splenic to left renal vein
— Variceal bleed
— Massive splenomegaly with pancytopenia
— Liver functions usually normal
— Ascites- minimal
— Growth retardation/ decreased muscle mass
Liver transplantation
Surgical stage Surgical considerations Anesthetic considerations
Preoperative Transplant evaluation, MELD Preoperative evaluation, Arrangement of blood
score products, vascular access
Dissection Mobilization of liver, vascular Hemodynamic instability due to loss of ascitic fluid,
structures, bile duct haemorrhage, decreased venous return
Anhepatic Clamping of hepatic A, portal Hemodynamic instability due to IVC clamping,
V, removal of liver, hypoglycemia, hypothermia, hyperkalemia, metabolic
anastomoses of donor portal acidosis, hypocalcemia
V to IVC

Reperfusion Anastomosis of hepatic A, Hemodynamic instability, hyperkalemia, acidosis,

reperfusion of new liver arrythmias, cardiac arrest
ICU Hemostasis, graft function Haemodynamic instability, extubation, ICU care.
Thank You
 2/8/21

Disclaimer

• Enthusiastic approach may lead to too much information

ABG
• Will try to stick to Simple and basic approach
• May omit few fancy things which are not so commonly required

Dr Prashant Kumar
Professor
M .D.,PDFN A (N euroanaesthesia & Critical Care)
M BA (Hosp Adm in)
Com m onwealth Fellow U.K. (Belfast)
Dept of Anaesthesiology & Intensive Care
Pt BDS, PGIM S at University of Health Sciences
Rohtak, Haryana, India

Objectives Introduction:

• Introduction

• Basics of analysis of blood gases Arterial blood gas (ABG) is a crucial skill
ABG interpretation is especially important in critically ill patients.
• Must knows technical errors
Stepwise approach helps ensure a complete interpretation of
• Steps for analysis every ABG.
• Case based example and discussion

Applications of ABG ABG Equipment

• To document respiratory failure and assess its severity

• To monitor patients on ventilators and assist in weaning

• To assess acid base imbalance in critical illness

• To assess response to therapeutic

• interventions and mechanical ventilation

• To assess pre-op patients

1
 2/8/21

ABG – Procedure and Precautions ABG Equipment

• Where to place -- the options 3 electrode system that measures

• Radial
• Three fundamental variables - pO2, pCO2 and pH
• Dorsalis Pedis
• Femoral
• All others like, HCO3, computed by software using standard formulae
• Brachial

Technical Errors Technical Errors…

Air Bubbles WBC Counts

• pO2 150 mm Hg & pCO2 0 mm Hg • 0.01 ml O2 consumed/dL/min
• Contact with AIR BUBBLES
• ↑pO2 & ↓ pCO2 • Marked increase in high TLC/plt counts : ↓ pO2
• Seal syringe immediately after sampling • Chilling / immediate analysis
Body Temperature
• Affects values of pCO2 and HCO3 only
ABG Syringe must be transported earliest via COLD CHAIN
ABG Analyser controlled for Normal Body temperatures

Technical Errors Internal consistency of the values

Excessive Heparin The Henderseon-Hasselbach equation:

• Ideally : Pre-heparinised ABG syringes
• Syringe FLUSHED with 0.5ml 1:1000 Heparin & emptied
• DO NOT LEAVE EXCESSIVE HEPARIN IN THE SYRINGE

pKa H2CO3 is the negative logarithm (base 10) of the acid dissociation constant of carbonic
acid. It is equal to 6.1 at normal body temperature.

If the pH and the [H+] are inconsistent, the ABG is probably not valid.

2
 2/8/21

pH and H+
pH Approxim ate [H+]
(nm ol/L)
• At a pH of 7.4, the concentration of hydrogen ions is 40 nanomoles/litre.
7.00 100
7.05 89
7.10 79

• For every 1 nanomoles/litre change in hydrogen ion concentration, the pH changes by 7.15 71
7.20 63
0.01 unit. 7.25 56
7.30 50
7.35 45
7.40 40
7.45 35
7.50 32
7.55 28
7.60 25
7.65 22

Is there alkalemia or acidemia present? Is the disturbance respiratory or metabolic?

• pH < 7.35 acidemia • Look for Relationship between the direction of change in the pH
pH > 7.45 alkalemia and the direction of change in the PaCO2?
• This is usually the primary disorder In primary respiratory disorders, the pH and PaCO2 in opposite directions;

• Remember: an acidosis or alkalosis may be present in metabolic disorders the pH and PaCO2 change in the same direction.

even if the pH is in the normal range (7.35 – 7.45)

Need to check the PaCO2, HCO3- and anion gap

Condition 1

• pH ↓ • pH 7.20

• PaCO2. ↑ • pCO2 69
• HCO3. ↑ • HCO3 26
• Resp acidosis
• Partial compensated
Low Acidic
Resp acidosis
Uncompensated Resp Acidosis

3
 2/8/21

Selected etiologies of respiratory acidosis Condition 2

• pH ↑
Airway Sleep Incorrect
Increased
obstruction CN S disordered N eurom uscular Ventilatory CO2 productio
m echanical • PaCO2. ↓
- Upper depression breathing (OS im pairm ent restriction ventilation
n:
- Lower A or OHS) settings
• HCO3. ↓
shivering,
COPD • Resp Alkalosis
rigors,
• Partial compensated
seizures,
asthma

malignant
hyperthermia,

other obstructive
lung disease hypermetabolism,

increased intake
of carbohydrates

Selected etiologies of respiratory alkalosis

Hypoxemia or Stimulation of Pregnancy, liver Incorrect

• pH 7.5 CNS stimulation: hypoxia: chest receptors: Drugs, hormones: disease, sepsis,
hyperthyroidism
mechanical
ventilation settings

• pCO2 16 fever, lung disease, pulmonary

edema, salicylates,

pain, profound anemia, pleural effusion, catecholamines,

• HCO3 24
fear, low FiO2 pneumonia, medroxyprogester
one,
anxiety, pneumothorax, progestins

CVA, pulmonary
embolus
cerebral edema,

brain trauma,
Resp Alkalosis
brain tumor,
No compensation
CNS infection

Condition 3 Selected causes of metabolic alkalosis

• pH ↑ Hypovolemia with Cl- depletion Hypervolemia, Cl- expansion

• PaCO2. ↑
•GI loss of H+ •Renal loss of H+: edematous
• HCO3. ↑ •Vomiting, gastric suction, states (heart failure,
• Metabolic Alkalosis
villous adenoma, diarrhea cirrhosis, nephrotic
• Partial compensated
with chloride-rich fluid syndrome),
•Renal loss H+ hyperaldosteronism,
•Loop and thiazide diuretics, hypercortisolism, excess
ACTH, exogenous steroids,
post-hypercapnia
(especially after institution hyperreninemia, severe
hypokalemia, renal artery
of mechanical ventilation) stenosis, bicarbonate
administration

4
 2/8/21

interpretate Condition 4

• pH ↓
pH 7.51,
pCO2 40, • PaCO2. ↓
HCO3- 31: • HCO3. ↓
• Metabolic acidosis

• Partial compensated

Normal
Uncompensated metabolic alkalosis
Partially compensated respiratory acidosis
Uncompensated respiratory alkalosis

Selected etiologies of metabolic acidosis Anion Gap

• Elevated anion gap:

• AG = [Na+] - [Cl- +HCO3-]
• Normal anion gap: will have increase in [Cl-]
• Elevated anion gap represents metabolic acidosis
• Normal value: 12 ± 4 mEq/L
• Major unmeasured anions
• albumin
• phosphates
• sulfates
• organic anions

Anion Gap? Anion Gap

• AG= [Na+]-( [Cl-] + [HCO 3-] )-12 ± 2

• Normal anion gap ≈ 12 meq/L. Increased Anion Gap Normal Anion Gap
• Diabetic Ketoacidosis
• In patients with hypoalbuminemia, the normal anion gap is lower than 12 meq/L; the “normal” • Diarrhea
anion gap in patients with hypoalbuminemia is about 2.5 meq/L lower for each 1 gm/dL • Chronic Kidney Disease
• Renal Tubular Acidosis
decrease in the plasma albumin concentration • Lactic Acidosis
• Addisons Disease
• patient with a plasm a album in of 2.0 gm /dL would be approxim ately 7 m eq/L.) • Alcoholic Ketoacidosis
• Carbonic Anhydrase
• If the anion gap is elevated, consider calculating the osmolal gap in compatible clinical • Aspirin Poisoning
• Inhibitors
situations. • Methanol Poisoning
• Elevation in AG is not explained by an obvious case (DKA, lactic acidosis, renal failure, • Ethylene Glycol Poisoning
Toxic ingestion is suspected • Starvation

• OSM gap = measured OSM – (2[Na+] - glucose/18 – BUN/2.8

• The OSM gap should be < 10

5
 2/8/21

S e le cte d m ix e d a n d co m p le x a cid -b a se d istu rb a n ce s

Base Excess Mixed Disorders

D is o rd e r C h a ra c te ris tic s S e le c te d s itu a tio n s

R e s p ira to ry a c id o s is w ith m e ta b o lic a c id o s is ↓ in p H •C a rd ia c a rre s t
↓ in H C O 3 •In to x ic a tio n s
↑ in P a C O 2 •M u lti-o rg a n fa ilu re

R e s p ira to ry a lk a lo s is w ith m e ta b o lic a lk a lo s is ↑ in p H •C irrh o s is w ith d iu re tic s

↑ in H C O 3- •P re g n a n c y w ith v o m itin g
↓ in P a C O 2 •O v e r v e n tila tio n o f C O P D

R e s p ira to ry a c id o s is w ith m e ta b o lic a lk a lo s is p H in n o rm a l ra n g e •C O P D w ith d iu re tic s , v o m itin g , N G s u c tio n

↑ in P a C O 2, •S e v e re h yp o k a le m ia
↑ in H C O 3-

R e s p ira to ry a lk a lo s is w ith m e ta b o lic a c id o s is p H in n o rm a l ra n g e •S e p s is

↓ in P a C O 2 •S a lic yla te to x ic ity
↓ in H C O 3 •R e n a l fa ilu re w ith C H F o r p n e u m o n ia
•A d v a n c e d liv e r d is e a s e

M e ta b o lic a c id o s is w ith m e ta b o lic a lk a lo s is p H in n o rm a l ra n g e •U re m ia o r k e to a c id o s is w ith v o m itin g , N G s u c tio n , d iu re tic s , e tc .

H C O 3- n o rm a l

Is there appropriate compensation for the primary Compensation.

disturbance?
• Usually, compensation does not return the pH to normal (7.35 – 7.45).

Bicarbonate Buffer Respiratory Regulation

6
 2/8/21

Compensation.. Compensations..

• Bicarbonate Buffer System

• Acts in few seconds

• Respiratory Regulation
• Starts within minutes good response by 2hrs,
• complete by 12-24 hrs

• Renal Regulation
• Starts after few hrs, complete by 5-7 days

Compensation Compensation 1,2,3,4,5

Disorder Expected compensation Correction factor

Metabolic acidosis PaCO 2 = (1.5 x [HCO 3-]) +8 ±2

Acute respiratory acidosis Increase in [HCO 3-]= ∆ PaCO 2/10 ±3
Chronic respiratory acidosis (3-5 Increase in [HCO 3-]= 3.5(∆ PaCO 2/10)
days)
Metabolic alkalosis Increase in PaCO 2 = 40 + 0.6(∆HCO 3-)

Acute respiratory alkalosis Decrease in [HCO 3-]= 2(∆ PaCO 2/10)

Chronic respiratory alkalosis Decrease in [HCO 3-] = 5(∆ PaCO 2/10) to

7(∆ PaCO 2/10)

If the observed compensation is not the expected compensation, it is likely that more than one acid-base disorder is present.

Determinants of PaO2

• PaO2 is dependant upon Age, FiO2, Patm

OXYGENATION • As Age ↑, expected pO2 ↓

• PaO2 = 109 - 0.4 (Age)

• As FiO2 ↑ the expected PaO2 ↑

7
 2/8/21

Berlin criteria for ARDS severity Scenario 1

• PaO2 / FiO2 ratio Inference • 68-year-old female, admitted with shortness of breath.
• The patient appears drowsy and is on 10L of oxygen via a mask.
• PaO2 : 52.5 mmHg (82.5 – 97.5 mmHg)
• pH: 7.29 (7.35 – 7.45)
• PaCO2 : 68.2 mmHg (35.2 – 45 mmHg)
• ARDS is characterized by an acute onset within 1 week, bilateral radiographic
pulmonary infiltrates, respiratory failure not fully explained by heart failure or volume • HCO3 –: 26 (22 – 26 mEq/L)
overload, and a PaO2/FiO2 ratio < 300 mm Hg • Base excess: +1 (-2 to +2)

Scenario 2 Scenario 3

An 89-year-old patient presents with fever, rigors, A 22-year-old female is brought into A&E by ambulance with a 5-day history of vomiting and
lethargy.
hypotension and reduced urine output, confused. History of disorientated and looks clinically dehydrated. At present, looks very unwell from the end of
catheterization for long. the bed.
•PaO2: 93 mmHg (82.5 – 97.5 mmHg) IV access, routine inv, fluids. increased respiratory rate, low blood pressure and
tachycardia.
•pH: 7.29 (7.35 – 7.45) •PaO2 : 97.5 mmHg (82.5 – 97.5 mmHg)
•PaCO2: 41.2 mmHg (35.2 – 45 mmHg) •pH: 7.3 (7.35 – 7.45)
•PaCO2 : 30.7 mmHg (35.2 – 45 mmHg)
•HCO3-: 15 (22 – 26 mEq/L) •HCO3 -: 13 (22 – 26 mEq/L)
•BE: – 4 (-2 to +2) •BE: -4 (-2 to +2)

Thanks
Best Wishes

8
LIVER AND THE BILIARY SYSTEM

 Liver is the largest internal organ weighing about 1.7 kgs in an average 80
kg man.
 Located in right upper quadrant beneath the diaphragm and is protected
by the rib cage.
 Divided into right and left lobes and then further into eight segments.
Blood supply to liver

 Total blood flow(25% of cardiac output)

 The liver has a dual blood supply.
Hepatic artery(20%) Hepatic portal vein(80%)

❑ Suppiles the non parenchymal ❑ Partially deoxygenated blood carrying

structures of liver with arterial blood. nutrients absorbed from small intestine.
❑ It is derived from the coeliac trunk ❑ The dom inant blood supply to liver
❑ Supplies around 30-50% of oxygen parenchyma
requirement. ❑ Allows the liver to perform its gut related
functions(such as detoxification)

Nerve Supply
Hepatic Plexus which contains Sympathetic(coeliac plexus ) and
paraympathetic (vagus nerve) nerve fibres
Main functions of liver

▪ Maintenance of core body temperature

▪ pH balance and correction of lactic acidosis
▪ Synthesis of clotting factors
▪ Glucose metabolism, glycolysis and gluconeogenesis
▪ Urea formation from protein catabolism
▪ Bilirubin formation from haemoglobin degradation
▪ Drug and hormone metabolism and excretion
▪ Removal of gut endotoxins and foreign antigens
Routinely available tests of liver function

Test Normal Range

Bilirubin 5-17micromol/L
Alkaline phosphatase 35-130IU/L
Aspartate transaminase(AST) 5-40IU/L
Alanine transaminase(ALT) 5-40IU/L
Gama glutamyl transpeptidase(GGT) 10-48IU/L
Albumin 35-50g/L
Prothrombin time 12-16s
Bilirubin metabolism
 Pathway of bilirubin excretion
 BILURUBIN PARENCHYMAL CHOLESTASIS
OVERLOAD(Hemol DYSFUNCTION
ysis)
Aminotransfera Normal Increased Normal (maybe
ses (maybe normal increased in
or decreased in advanced
advanced stages)
stages)
Alkaline Normal Minimal increase Marked
phosphatase Increased
Bilirubin Increased Increased Increased
unconjugated conjugated and conjugated
unconjugated

Serum proteins Normal Decreased Normal (maybe

decreased in
advanced
stages)

Prothrombin Normal Normal in early Normal in early

Time stages and stages &
prolonged in late Prolonged in
stages advanced
 BILURUBIN PARENCHYMAL CHOLESTASIS
OVERLOAD(Hemoly DYSFUNCTION
sis)

Urine urobilinogen High Present Absent

Urine bilirubin Absent present Present

Urine Bile salts and Absent Present Present

pigments
Stool stercobilins High Present Absent

GGT/ 5’- Normal Normal Increased

nuleotidase
How to differentiate clinically between different
causes of obstructive jaundice?

Obstructive jaundice due to galls stones will present with

colicky pain in the right hypochondrium that is aggravated
with fatty meal. It is often associated with fullness and bloating.

Obstructive jaundice due to cholangitis – Reynold’s Pentad:

septic shock, mental confusion, Charcot’s triad (fever,
abdominal pain and jaundice). No significant relation with
meals. H/o ERCP, surgery, parasitic infection usually present.

Obstructive jaundice due to malignancy is associated with

significant weight loss. Very gradual, progressive in nature.
Palpable, non-tender mass may be present (Courvoisier’s law)
Causes of obstructive jaundice
Surgical resection for carcinoma head
of pancreas

 PPPD(pylorus preserving pancreaticoduodenectomy)(Removal of duodenum and

pancreatic head including distal part of bile duct)
 Whipples procedure(to achieve a clear resection margin)- (Structures removed)
▪ Cancerous parts of pancreas
▪ Duodenum
▪ Common bile duct
▪ Distal part of stomach
▪ Anastomosis performed- pancreaticojejunostomy,gastojejunostomy
▪ and hepaticojejunostomy
EFFECTS OF OBSTRUCTIVE JAUNDICE ON
VARIOUS ORGAN SYSTEMS
CARDIOVASCULAR EFFECTS
Bradycardia due to direct effect on SA node.

Impaired cardiac contractibility

Impaired response to beta agonist drugs

Decreased peripheral vascular resistance

Hypotensiv e patient prone for circulatory collapse

Net result Exaggerated hypotensive response to bleeding
More prone to perioperative shock
 RENAL SYSTEM

An increased incidence of acute kidney injury.

Mediated by endotoxemia as a result of sepsis and loss of bile salts to

the vascular space.

Loss of intestinal bile salts which normally prevent bacterial overgrowth,

leads to portal and systemic endotoxemia, leading to kidney injury

Kidney injury exacerbated by induced diuresis and impaired

myocardial contractility.

Refractoriness of tubules to ADH and Increased levels of ANP resulting in

hypovolemia
  Ed synthesis of clotting factors →
Deranged prolongation of prothrombin time
Vit. K deficiency d/t biliary obstruction →
coagulation 
defective γ- carboxylation – def of vit K
dependent factors
 Endotoxin, hypersplenism →
thrombocytopenia
 Endotoxin → ed fibrinolysis, low grade DIC
IMMUNE SYSTEM
Defects in cellular immunity

• Depressed function of RE system i.e Kupffer cells

• Impaired T cell proliferation
• Decreased neutrophil chemotaxis
• Defective bacterial phagocytosis

Can lead to Sepsis

• Under normal physiological conditions, sphincter of oddi

presents a barrier to retrograde translocation of bacteria of
intestine
• Portal and systemic endotoxemia ( increased bacterial
translocation)
Delayed wound healing
and High incidence of
wound dehiscence due to
defective collagen
synthesis.
Anaesthetic considerations
pertaining to:

liver dysfunction and

Surgery
 Due to liver dysfunction:

Hypoproteinaemia and reduced levels of drug binding proteins

Altered volume of distribution and increased TBV
Coagulopathy
Alterations in drug metabolism and clearance
Hypoglycemia
Electrolyte imbalance
Anaemia ,leucopenia and thrombocytopenia
Deficiency of fat-soluble vitamins (A,E,D,K)
Increase in serum cholesterol and atheromatous changes
Due to surgery

Major surgery- long duration with

increased blood loss and fluid shifts

Roof top incision- post op analgesia.

Epidural- blockade above T5, decrease

in hepatic blood flow
 Preoperative assessment and optimisation

❑ Informed patient consent

❑ High morbidity and mortality associated

❑ Post operative complications(primary pancreatic fistula,haemorrhage,abscess)

❑ Preoperative risk assessment

❑ Complete history, physical , laboratory examinations and assessment of surgical risks

❑ Physiologic and operative severity score for enumeration of mortality and morbidity(POSSUM Model)

❑ Evaluation and optimisation of preoperative physical conditions and medications

❑ Age- independent risk factor of postoperative mortality and complications

❑ Infection
❑ Cardiac and pulmonary diseases

❑ Renal dysfunction

❑ Prior medical and surgical history

❑ Medications

❑ Coagulopathies

❑ Nutritional status
Intraoperative management

 Combined general and epidural anaethesia

 Thoracic epidural anaesthesia – decreases sympathetic activity)
 Excellent pain relief
 Deceases incidence of pulmonary complications
 Decreases cardiac metabolic demand
 Decreases risk of thromboembolic complications
 Prevention of surgical site infections(second most common
nosocomial infections after urinary tract infections)
 Antibiotics(first dose should begin within 30-60 min of skin incision)
 Normothermia)decreased subcutaneous tissue perfusion mediated by
vasoconstriction)
 Normoglycemia
❑ Intraoperative fluid management
❑ Intravenous fluids to replace fluid deficits , third space losses and blood loss to
maintain adequate cardiac output, blood pressure and urine output.
❑ Fluid excess— negativ e impact on cardiac , pulmonary and bowel function
tissues oedema and anastomotic breakdown
❑ Goal directed fluid therapy( central v enous pressure- most widely
used),transesophageal echocardiography,pulmonary artery
catheterisation,oesophageal doppler guided fluid boluses,arterial waveform
analysis
❑ Appropiate use of fluids, v asopressors and inotropes.
❑ Intraoperative ventilation
❑ Protectiv e mechanical v entilation using reduced tidal v olumes<8ml/kg
❑ PEEP(6-12mmhg) to prev ent alv eolar collapse and atelectasis
❑ Recruitment manoeuv res

❑ Intraoperative thromboprophylaxis
❑ Intraoperative use of graduated compression stockings and intermittent
pneumatic compression
Postoperative management
 Post operative care in ICU/HDU
❑ High risk patients(comorbidities, elderly , major abdominal surgery)
❑ Extended haemodynamic monitoring
❑ Post operativ e invasive/non invasive v entilation
❑ Postoperative inv estigations v iz complete blood count, KFT, LFT, serum
electrolytes, coagulation profile, CXR.
 Pain relief/non opioid analgesia
❑ Thoracic epidural with local anaesthetics(midthoracic lev el catheter T8/9
achiev es both analgesic and sympathetic blocks)
❑ NSAIDS
 Postoperative ambulation and prevention of venous thromboembolism(LMWH
started 12 hrs or more postoperatively)
 Respiratory rehabilitation
❑ Deep breathing and direct coughing
❑ Chest wall physiotherapy
❑ Mechanical breathing dev ices(incentive spirometry,blow bottles, CPAP)
THANK YOU
PRESENTER- DR VIBHOR GUPTA
ASSISTANT PROFESSOR
DEPARTMENT OF ANAESTHESIA
UCMS,GTB HOSPITAL
DELHI
 Opioids have been the mainstay of pain treatment for thousands
of years, and they remain so today.

 The word opium is derived from the Greek word for juice “opios”.

 The term “opioid” is used to denote all exogenous substances

natural and synthetic, that bind to any of the several opioid
receptors .

 Opiate is the term used for drugs derived from opium.

-On the basis of source

 Naturally occuring
 Phenanthrene :Morphine, Codeine ,Thebaine
 Benzylisoquinoline: Papaverine
 Semisynthetic
 Heroin
 Dihydromorphone
 Thebaine derivatives: Buprenorphine.
 Synthetic
 Phenylpiperidines: Meperidine, Fentanyl, Sufentanil,
Alfentanil, Remifentanil.
 Morphinan compounds:Levorphanol, Butorphanol.
 Phenyl-heptylmines: Methadone, Diphenylpropylamine.
 Benzomorphans: Pentazocine
 On the basis of action

Opioid Agonists Opiod Agonist- Antagonist

 Morphine  Pentazocine
 Meperidine  Butorphanol
 Fentanyl  Nalbuphine
 Sufentanyl  Buprenorphine
 Remifentanyl
 Alfentanyl
 Codeine
 Hydromorphone
 Methadone  Opiod Antagonist
 Tramadol
 Heroin  Naloxone
 Naltrexone
 Nalmefene
 Endorphins:
 Primarily μ agonist

 Enkephalins:
 Primarily μ and δ agonist

 Dynorphins:
 Potent κ agonist

 Endomorphins:
 Binds to the µ-receptor with high affinity and high selectivity.
 μ receptor κ receptor δ receptor

Location μ1 – supraspinal spinal Spinal

µ2 - spinal Supraspinal Supra-spinal

Effects Analgesia Spinal analgesia Spinal analgesia

Respiratory depression Dysphoria Affective behaviour
Sedation Sedation (Supraspinal)
Euphoria Psychomimetic Respiratory depression
Miosis
Bradycardia,
Hypothermia
Physical dependence

Agonists Morphine, Codeine, Pentazocine, Enkephalins

Fentanyl
Pentazocine(weak)
Endorphins
Dynorphins
-Brainstem

-Medial thalamus

-Spinal cord: receptors

located in the substantia
gelatinosa .

-Hypothalamus

-Limbic system

-Peripheral nerve
fibers
 Opioid receptors belong to a super family of G-protein coupled
receptors.
 All three opioid receptor classes couple to G-proteins and inhibit
adenyl-cyclase. The subsequent reduction of intracellular cAMP
results in opening of K+ channels and supression of N type of Ca2+
channels.
 The resultant hyperpolarization prevents excitation and
propagation of action potential.
 The reduced intracellular Ca2+ leads to suppression of
neurotransmitter release – NA, DA, 5-HT, GABA and Glutamate.
Pre-synaptic Neuron
• Activation of opioid receptor decreases

Ca2+ influx in response to incoming AP

•Decrease in level of neuroexcitatory

transmitters like Glutamate NA, DA, 5-
HT.

Post-synaptic Neuron
• Increase in the K+ efflux

•Resultanthyperpolarization prevents
propagation of action potential
Analgesia

 Produces strong analgesia without

loss of consciousness.

 Increases the threshold of pain.

 Sedation:

 Drowsiness and indifference to surroundings.

 Inability to concentrate and extravagant imagination
 Larger doses produce sleep – EEG resembles normal
sleep

 Mood effects:

 Opioids produce euphoria, tranquility.

 In persons with pain & addicts sense of
wellbeing– euphoria.
 In normal persons these sensations may be
unpleasant in absence of pain – dysphoria.
 Respiratory Depression

 Pontine and medullary ventilatory centre – Both rate

and depth of respiration is diminished.
 Vasomotor centre – High doses cause fall in BP.

 Stimulation

 Edinger Westphal Nucleus – miosis .

 Vagal centre – Bradycardia .
 Hippocampal cells – convulsions (inhibition of
GABA release).
 Neuro-endocrine:

 FSH, LH and ACTH levels are lowered.

 Decrease in levels of Sex hormone and
corticosteroids, but no infertility.
 Increases ADH release – oliguria..

 CVS:

 No direct action on the myocardium.

 Histamine release, depression of vasomotor centre
and decrease in the sympathetic tone of blood
vessels may cause vasodilatation leading to
hypotension.
 Metabolism:

 Conjugation with glucuronic acid in hepatic and extra

hepatic sites esp. the kidneys.

 Morphine-6-glucuronide (5-10%): Agonist action at µ–

receptors produces analgesia and depression of
ventilation.

 Excretion:
 Via Urine, Plasma t1/2 = 2-3 hrs

 Completely eliminated in 24 hrs.

 Analgesic:

 Surgical analgesia, post operative analgesia, long bone fracture,

burns.
 Myocardial infarction.
 Palliative therapy in cancer.
 Visceral pains – pulmonary embolism, pleurisy, acute
pericarditis.

Other Uses

 Pre-anaesthetic medication
 Head Injury

 Bronchial asthma

 Shock – Hypotension

 Renal Failure, Liver diseases .

 Unstable personalities
Phenylepiperidine derivative
having structural similarities
with that of local anaesthetics.

Pharmacokinetics

 1/10th as potent as morphine.

 Rapid but short duration of action (2-3 Hrs)

 In equal analgesic dose it produces as much sedation, euphoria

and respiratory depression as morphine.

 Less histamine release – safer in asthmatics.

Clinical Uses:

 For labour analgesia and post operative analgesia.

 Effective for suppression of post operative shivering.

Adverse Effects:

 Similar to morphine.
 Atropine like effects – dry mouth, blurred vision,
tachycardia.
 Overdose – tremors, mydriasis, delirium and
convulsion due to norpethidine accumulation.
Phenylpiperidine derivative
synthetic opioid structurally
related to meperidine

 Pharmacokinetics
 75 to 125 times as potent as morphine.
 Rapid onset and shorter duration due to greater lipid
solubility.
 Rapidly redistributed to inactive storage sites such
as fat and skeletal muscles.
 75% of the initial dose undergoes first-pass
pulmonary uptake.
 Analgesia: Low IV dose 1-2 µg/kg

 Adjuvant to anaesthetics (2-20 µg/kg)

 As a component of Total Intravenous Anaesthesia (TIVA) –

Dose 50-150 µg/kg.

 Intrathecal fentanyl may be used to provide labour analgesia

and as an adjuvant for spinal and epidural anaesthesia.

 Oral transmucosal fentanyl 5- 20 µg/kg may be used to decrease

pre-operative anxiety and facilitate induction.

 Transdermal fentanyl patch delivering 75 - 100 µg/hr may be

used for treatment of chronic pain in cancer patients.
Adverse Effects:

 Similar to morphine

 Persistent/ recurrent respiratory depression

 Carotid sinus baroreceptor reflex control is

markedly depressed- caution in neonates.

 Bradycardia is more prominent than in

morphine.

.
Fentanyl As a Sole Anaesthetic Agent

Advantages

-Lack of direct myocardial depressant effects.

-Absence of histamine release.

-Suppression of stress respone to surgery.

  Thienyl analogue of fentanyl.

 Pharmacokinetics:

 Potency is 5 to 10 times that of fentanyl.

 Lipophilic nature permits rapid penetration into the BBB and onset of
CNS effects.

 Metabolism :

 Extensively metabolised by hepatic microsomal enzymes.

 Context-sensitive half time is shorter than that of alfentanyl for

continuous infusion up to 8 hrs due to the large Vd.
 Longer analgesia and less ventilatory depression.

 More rapid induction.

 Earlier emergence and earlier tracheal extubation

 Fentanyl analogue with lesser potency and shorter duration of
action.

 Despite its lower lipid solubilty it has a more rapid onset of

action due to the higher degree of non-ionisation.

 It is used to provide analgesia when the noxious stimulation is

acute but transient as in laryngoscopy, tracheal intubation and
performance of a retrobulbar block.

 Associated with a lower incidence of PONV.

 Selective μ agonist with potency similar to fentanyl.

 Predictable onset and termination of effect because of

 Rapid clearance
 Smaller Vd
 No significant redistribution to inactive storage sites

 Unique ester-linkage

 Metabolised by non-specific plasma and tissue

esterases. Safe in hepatic and renal failure.
  Short intense analgesia
 Suppressing transient sympathetic response to laryngoscopy of at risk
patients.
 Intermittent administration as PCA during labour and delivery.
 Sedation in mechanically ventilated patients.
 Sedation and analgesia during monitored anaesthesia.

Side effects:.
 Termination of analgesic effect on accidental stoppage of infusion.
 Nausea and vomiting
 Depression of ventillation
 Decrease in B.P and H.R.
 Time taken for blood plasma concentration of a drug to
decline by one half after an infusion designed to
maintain a steady state (i.e. a constant plasma
concentration) has been stopped.

 The “context” in this case is the duration of infusion.

 Centrally acting analgesic with moderate affinity for μ receptors and
weak κ and δ activity.

 Dual mechanism of action

 Opioid agonist effect.

 5-HT and NA uptake inhibition

 Effective both orally and IV .

 Uses
 Effective for the treatment of chronic pain.
 Can be used where NSAIDS are contraindicated.
 Post-operative shivering.

 Disadvantages
 Seizures have been demonstrated.
 High incidence of nausea and vomiting.
 Produce analgesia with
limited ventilatory
depression and low potential
These drugs bind to μ- for producing physical
receptors where they act as dependence.
partial agonist or competitive
antagonist and exhibit partial However they can attenuate
agonist actions at other the efficacy of subsequently
receptors. administered opioid agonists.
Ceiling effect present.
 Benzomorphan derivative.

 Weak μ-receptor antagonist, but agonist of κ and δ receptor.

 One of the commonly used agents, given orally and IM.

Uses:
-Moderately severe pain in injury, burns, trauma and
orthopaedic manuevers .
Disadvantages:

 Depresses myocardial contractility.

 Increases blood catecholamine levels thus increasing B.P, H.R,

SVR.

 High incidence of PONV.

 Limited analgesia.

 Partially antagonizes other opioids.

 Naloxone , naltrexone, nalmefene.

 Higher affinity for μ-receptors results in

displacement of the opioid agonists from the
receptor sites.
 Non-selective antagonist of all types of opioid receptors
Uses
 Treat opioid induced depression of ventilation in post-
operative period .
Diagnostic- To confirm physical opioid dependence.

Adverse Effects
 Antagonizes analgesic actions of opioids.
 Nausea/ vomiting .
 Increased sympathetic nervous system activity
 Balanced Anaesthesia
Neuraxial opioids
TIVA
High-Dose Opioid for Cardiac Surgery

DEPT OF ANAESTHESIA MKCG

Monday, March 9, 2015 MEDICAL COLLEGE 53
 PCA using opioids is now the cornerstone of post-operative
analgesia.
 Morphine remains a rational choice for PCA therapy. However it
is slow in onset and does not allow rapid titration of effect.
 Meperidine (50-100) mg produces variable degree of pain relief
and not always effective in patients with severe pain.
 IV opioids can produce potent and short-lasting analgesia.

Bolus Dose Infusion Rate

Fentanyl 1-3 µg/kg 0.01-0.05 µg/kg/min
Alfentanil 10-20 µg/kg 0.25-0.75 µg/kg/min
Sufentanil 0.1-0.3 µg/kg 0.0015-0.01µg/kg/min
Remifentanil - 0.05-0.25µg/kg/min
 Morphine (0.75 µg/kg/min) is the most frequently used IV
agent in the ICU.
 Remifentanil (0.15 µg/kg/min) allows more rapid emergence
from sedation and earlier extubation while providing
comparable level of sedation.

Balanced Anaesthesia
 Opioid as a component of balanced anesthesia:
 Reduce post-operative pain and anxiety.
 Decrease the autonomic responses to airway
stimulation.
 Improve haemodynamic stability.
 Reduce the dose of sedative agents.
 Reduce the requirement of inhalational agents.
 Loading Maintenance Dose Comments
Dose
Bolus Infusion
Fentanyl 2-6 µg/kg 25-50 µg/kg 0.5-5.0 Risk of significant
µg/kg/hr depression of
spontaneous ventilation

Alfentanil 25-50 µg/kg 5-10 µg/kg 0.5-2 Propofol decreases

µg/kg/min elimination clearance
and distribution

Sufentanil 0.25 - 0.1 - 0.25 0.5-

2µg/kg µg/kg 1.5 µg/kg/hr

Remifentanil 1 - 2 µg/kg 0.1-1.0 During emergence and

µg/kg/min post-operatively
alternative analgesia
should be administered
or low-dose infusion
continued
 Useful when delivery of inhalational agents are compromised
or contraindicated.
 Most commonly an opioid is combined with another drug more
likely to provide hypnosis and amnesia.
 Combination of alfentanil and propofol produces excellent
TIVA.
 Alfentanil: Provides analgesia, haemodynamic stability and
blunting of responses to noxious stimuli.
 Propofol: Provides hypnosis and amnesia and is anti-emetic.

Induction Maintenance
Alfentanil 25 to 50 µg/kg 0.5 - 1.5 µg/kg/min

Propofol 0.5 to 1.5 mg/kg 80 to 120 µg/kg/min

 Introduced as a stress-free anesthetic method for cardiac surgery.

 First performed with morphine. However, fentanyl and sufentanil

were recommended later.

 Advantage of providing stable haemodynamics due to

 Lack of myocardial depressant effect.
 Supression of stress response to surgery.

 Several factors have diminished the popularity

 Lack of evidence substantiating any significant outcome benefit
 added drug costs.
 Possible awareness.
 Postoperative depression of ventilation.
 Induction Infusion Comments
Dose
Fentanyl 5-75 µg/kg 0.1 -1.0 Naloxone infusion with
µg/kg/min individual dose titration is
needed for reversal.

Alfentanil 150 µg/kg 2 to 12 µg/kg/min Associated with more

(+/- cardiovascular adverse
thiopental) effects than is the case with
fentanyl and sufentanil.
Sufentanil 2 to 20 µg/kg 1.0 to 2.0 µg/kg/hr More rapid induction and
more stable haemodynamics
intraoperatively and
postoperatively.
Remifentanil 2 µg/kg 0.25 -0.5 µg/kg/min Appropriate anaesthesia for
minimally invasive coronary
(+Propofol) (+ propofol, artery bypass surgery.
3 mg/kg/hr) High incidence of muscle
rigidity.
-Used during epidural/spinal anaesthesia alongwith
local anaesthetics for intra and postoperative
analgesia.

-Chronic cancer or non-malignant pain.

-Resistant intractable pain to other treatment options.

 Pharmacokinetics:

-Uptake from epidural space into : epidural fat,systemic absorption

or diffusion across dura into CSF.

-Lipid solubility determines onset of action and cephalad movement

of opioids.

-Highly lipid soluble: fentanyl,sufentanyl

-Poorly lipid soluble: morphine.(delayed depression of ventilation

due to cephalad movement of drug).
-Nausea,vomiting

-Pruritis

-Depression of ventilation

-Urinary retention

-Sedation

-CNS excitation,GI dysfunction

Preoperative

1. Evaluation

2. Identification: Identify factors such as total opioid dose

requirement

3. Consultation: Meet with addiction specialists and pain

specialists with regard to perioperative planning.

4. Reassurance: Discuss patient concerns related to pain

control, anxiety, and risk of relapse.

5. Medication: Calculate opioid dose requirement and modes

of administration.
1. Maintain baseline opioids (oral, transdermal, intravenous).

2. Increase intraoperative and postoperative opioid dose to

compensate for tolerance.

3. Consider neuraxial analgesic techniques when clinically

indicated.

Postoperative

1. Plan preoperatively for postoperative analgesia.

2. Maintain baseline opioids.
3. Use multimodal analgesic techniques.
After discharge:

-If surgery provides complete pain relief, opioids should be slowly

tapered, rather than abruptly discontinued.

-Develop a pain management plan before hospital

discharge.Provide adequate doses of opioid and nonopioid
analgesics.

-Arrange for a timely outpatient pain clinic follow-up or a visit with

the patient’s addiction specialist.
Transdermal Therapeutic System
 Fentanyl is available in a transdermal therapeutic
system.

 Advantages include no first-pass drug metabolism

by the liver; improved patient compliance,
convenience, and comfort; and consistent analgesia.

 In cancer pain

 Use for postoperative analgesia is not recommended

due a high incidence of significant respiratory
depression.
 Iontophoresis: Technique by which drug
passage through the skin is augumented
with an external electric current.

 When in need of pain medication,patient

double clicks the button

 Advantages
 Avoids the risk of complications from needle-related injuries and
infection.
 Pre-programmed electronics eliminate the potential for manual
programming errors and excessive dosing.
 Compact size of the system enables greater patient mobility after
surgery.
 Eliminates hepatic first-pass
metabolism and improves patient
comfort, convenience, and compliance.
 Opioids with high lipid solubility,
such as buprenorphine, fentanyl are
readily absorbed from sublingual
mucosal tissues.

 Oral transmucosal fentanyl citrate Buccal Lozenge

(OTFC) is a solid dosage form of
fentanyl that consists of fentanyl
incorporated into a sweetened lozenge on a stick.

-OTFC may be ideally suited to treat breakthrough cancer pain

-In children it may be used.
 Computer controlled
infusion pumps (CCIP)

 Target conc. Set

instead of infusion
rate

 CCIP calculates infusion

rate from target
concentration and
delivers required volume

 Therapeutic plasma conc

for a particular opioid for
a particular effect needs
to be known
 Combine the advantages of
continuous infusion with flexibility
of bolus doses according to
patient’s need.

 Activating a switch – Disposable PCA Pump with a switch

delivers bolus dose.

Lockout interval:
Minimum time that would have to elapse
between two activations
 Administration of
background infusion
superimposed on
patient controlled
boluses.
 Help to maintain
plasma concentration
in between boluses.
 Opioids are widely used in the practice of anaesthesia
for pre-anaesthetic medication, systemic and spinal
analgesia and supplementation of general anaesthetic
agents.

 A proper understanding of the

pharmacokinetic and pharmacodynamic
properties of opioids, is essential for their
judicious use.

 New opioid delivery systems are continually being

developed. Such systems allow more flexibility in
providing analgesia, both inside and outside the
operating room.
DIAGNOSIS AND MANAGEMENT OF
BRAIN DEAD AS POTENTIAL
DONOR

Dr.$$PUNEET$KHANNA$
Associate))Professor)
Anaesthesiology,)Pain)Medicine)and)Cri6cal)Care)
All)India)Ins6tute)of)Medical)Sciences)
New)Delhi)
• The)problem)
• Organ)donor)screening))
• Management))
The problem?
)

)Over)147,913)fatali6es)were)aHributed)to)road)traffic)accidents)in)India,)in)

the)year)2017.)

In)nearly)40–50%)of)road)accident)fatali6es,)the)cause)of)death)was)head)

injury.))

If)5–10%)of)all)brainQdead)pa6ents)are)considered)for)organ)harves6ng,)

there)would)be)no)requirement)for)a)living)person)to)donate)organs.)
The problem?
•  Transplanta6on)of)human)organ)bill)–)August)1992)
•  Transplanta6on)of)human)organ)act)–)1994)
)
)
)
)
18.)3)per)million ) ))))25.6)per)million ) )))))))32)per)million)
.36)per)million)
• 85000)liver)failures) ) ) )3%)
• 200000)kidney)failure ) )8000)

• Hearts)and)lungs? ) ) )1%)
 Screening and management
Donor$

Living$donor$ Deceased$Donor$
Who$is$Poten;al$Brain>dead$Donor$(PBDD)?)

A)poten6al)organ)donor)is)defined)by)the)presence)of)either)brainstem)death)or)a)catastrophic)and)

irreversible)brain)injury)that)leads)to)fulfilling)the)brainstem)death)criteria.)

What$is$Brainstem$Death?)

“Brainstem)death”)means)the)stage)at)which)all)brain)func6ons)are)permanently)and)irreversibly)ceased.))

However,)the)cause)of)irreversible)coma)has)to)be)established,)precondi6ons)should)be)met,)and)

confounding)factors)are)to)be)ruled)out.)
 Deceased donor management
• Stabilize!)

• Manage)
 Effective donor management

• Clinical)exper6se)
• Vigilance)
• Flexibility)

• Mul6Qtasking)
• Collabora6on)
• When)does)donor)care)start?)
) ) ) ))
) )Aber)consent)for)dona6on)has)been)obtained)
)
) ))))))Appropriate)to)think)about)it)before!)
• Revision)of)exis6ng)orders)or)placement)of)new)
medical)orders)is)intended)to:)
)
• D/C)medica6ons)no)longer)needed)or)appropriate)

• Con6nue)required)medica6ons,)or)therapy)
)
• Create)condi6onal)orders)
Death
“Death)is)the)permanent)loss)of)capacity)for)consciousness)and)all))
brainstem)func6on.)This)may)result)from)permanent)cessa6on)of)
circula6on)or)catastrophic)brain)injury”)
)
)
)
Shemie)SD)et)al.)Interna6onal)guideline)development)for)the)determina6on)of)death.)Intensive)Care)Med.)
2014;40(6):788–97.)
 Brain death
• Brain)death)is)a)clinical&diagnosis.))

• The)diagnosis)requires)demonstra6on)of)the)absence)of)both)
cor6cal)and)brain)stem)ac6vity,)and)demonstra6on)of)the)
irreversibility)of)this)state.)
Etiology of brain death
•  Severe)head)trauma)
•  Aneurysmal)subarachnoid)hemorrhage)
•  Cerebrovascular)injury)
•  HypoxicQischemic)encephalopathy)
•  Fulminant)hepa6c)necrosis)
•  Prolonged)cardiac)resuscita6on)or)asphyxia)
•  Tumors))
)
 Clinical triggers for notifying Organ
Procurement Organization
• At)the)ini6al)indica6on)that)a)pa6ent)has)suffered)a)
nonrecoverable)neurologic)injury)

• As)soon)as)a)formal)“brain)death”)examina6on)is)
contemplated)

• Before)ini6a6ng)a)discussion)that)may)lead)to)
withdrawal)of)lifeQsustaining)therapy)
Contraindications to donation?
Non)CNS)malignancies:)
• Choriocarcinoma ) ) )93%)
• Malignant)melanoma)))) )74%)
• CA)lung ) ) ) ) )43%)
• RCC) ) ) ) ) ) )63%)
)
Buell)JF,)Beebe)TM,)Trofe)J,)et)al:)Donor)transmiHed)malignancies.)
Ann)Transplant)2004;)9:53–56)
• CNS)malignancies)
• Over)all)transmission)rate)is)23%)
NOT$AN$
• Risk)factors)for)transmission:)
ABSOLUTE$
• highQgrade)malignancy)(grades)III–IV))
• Previous)craniotomy)
CONTRAINDICATION$
• Presence)of)a)ventriculoperitoneal)or)
ventriculoatrial)shunt.)
Donor septicaemia/Bacteremia
•  Donor)bacteremia))20%)
NOT$AN$
•  Actual)transmission)rate)low)
•  Adverse)1)year)outcomes)without)treatment)
ABSOLUTE$
•  Pathogen)specific)an6bio6cs)

CONTRAINDICATION$
 Absolute contraindications
• Undiagnosed)febrile)illness)
• Meningi6s,)encephali6s)of)unknown)e6ology)
• Flaccid)paralysis)of)unknown)e6ology)
• HBsAg)posi6ve)
• HIV)posi6ve)
 Pathophysiology
Loss)of)brain)stem)func6on:)
)
• Loss)of)vasomotor)control)leads)to)a)hyperdynamic)state.)
• Cardiac)arrhythmias))
• Loss)of)respiratory)func6on))
• Loss)of)temperature)regula6on)
• Hormonal)imbalance)Q)DI,)hypothyroidism)
 Perioperative management
Following)declara6on)of)brain)death)and)consent)
• Treatment)emphasis)shibs.)
• Focus)should)be)on:)
• Providing)hemodynamic)stabiliza6on.)
• Support)of)body)homeostasis.)
• Maintenance)of)adequate)cellular)oxygena6on)and))))))
donor)organ)perfusion.)
Autonomic/ sympathetic storm
Release)of)catecholamines)
from)adrenals)
(Epinephrine)and)
Norepinephrine))results)in)
a)hyperQdynamic)state:)

•  Tachycardia)
•  Elevated)C.O.)
•  Vasoconstric6on)
25>32%$
•  Hypertension)
Hypothalamus
• Impaired$temperature$regula;on$>$hypothermia$or$
hyperthermia$

• Leads$to$vasodila;on$without$the$ability$to$
vasoconstrict$or$shiver$(loss$of$vasomotor$tone)$
$
• Leads$to$problems$with$the$pituitary$...$
Normal pituitary gland
•  Controlled)by)the)
hypothalamus)

•  Releases)ADH)to)conserve)
water)

•  S6mulates)the)release)of)
thyroid)hormone)
Pituitary failure
• ADH)ceases)to)be)produced)=)Diabetes)Insipidus)

• Can)lead)to)hypovolemia)and)electrolyte)imbalances)

• Leads)to)problems)with)the)thyroid)gland))
Thyroid gland
•  Produces hormones that
increase the metabolic
rate and sensitivity of the
cardiovascular system

! Levothyroxine (T4)
! Triiodothyronine (T3)
Thyroid failure
Leads to:

!  Cardiac instability

!  Labile blood pressure

!  Potential coagulation problems

•  Brain death leads to sudden reduction in circulating
pituitary hormones

•  May be responsible for impairment in myocardial cell

metabolism and contractility which leads to myocardial
dysfunction

•  Severe dysfunction may lead to extreme

Cardiovascular system

• Loss)of)vasomotor)tone)

• Arrhythmias)

• Myocardial)damage)
Neurogenic pulmonary edema
! Lungs highly susceptible

! Left-sided heart pressures

exceed pulmonary pressure,
temporarily halting pulmonary
blood flow
! Lung injury!
13>18%$
Coagulation defects
!  Results from the passage of
necrotic brain tissue into the
circulation
!  Leads to coagulopathy and
sometimes progresses further
to DIC
!  DIC may persist despite factor
replacement requiring early
organ recovery
29>55%$
Organ donor management
•  Hypertension " Hypotension
•  Excessive Urinary Output
•  Impaired Gas Exchange
•  Electrolyte Imbalances
•  Hypothermia
Hypotension$
! Fluid)Bolus)–)NS)or)LR)(Followed)by)MIVF)NS)or).45)NS))
! Consider)colloids)(seriously))
! DDobutamine)
!  opamine)
! Norepinephrine)
! Vasopressin)
! Thyroxine)(T4)protocol))
)
“Rules of 100’s”
•  Maintain SBP >100mm Hg

•  HR < 100 BPM

•  UOP > 100ml/hr
•  PaO2 > 100mmHg
Vasopressin
•  Low dose shown to reduce inotrope use
•  Plays a critical role in restoring vasomotor tone

Vasopressin Protocol

!  4 unit bolus
!  1- 4 u/hour – titrate to keep SBP >100 or MAP >60
Diabetes insipidus
Posterior pituitary damage
Rule of thumb – 500 ml UOP
per hour x 2 hours is DI

Goal is UOP 1-3 ml/kg/hr

46>78%$
Diabetes insipidus
! Treatment is aimed at correcting hypovolemia
! D esmopressin (DDAVP) 1 mcg IV, may repeat x 1 after 1
Vasopressin)infusion)
hour.

! Replace hourly U.O. on a volume per volume basis with

MIVF to avoid volume depletion

! Leads to electrolyte depletion/instability monitor closely to

avoid hypernatremia and hypokalemia
Impaired gas exchange
•  Maintain PaO2 of >100 and a
saturation >95%
•  Monitor ABG’s q2h or as
requested by OPO
•  PEEP 5 cm, HOB up 30o
•  Aggressive pulmonary toilet
•  CXR
•  Bronch? CT Chest?
Most organ donors are referred with:
! Chest trauma
! Aspiration

! Long Hospitalization

! Impending Neurogenic Pulmonary Edema

Brain Death contributes to and complicates

all of these conditions
Impaired gas exchange: Goals
• Maintain)lung)health,)op6mize)organ)oxygena6on)

• Avoid)overQhydra6on)
• Lung)protec6ve)ven6la6on)strategies)
• Avoid)oxygen)toxicity,)FiO2)<)1.0,)PIP)<)30)cm)H2O)
Metabolic imbalance
• Hypokalemia)
Serum)Potassium)<)3.5)meq)/)L)
)
• Hypernatremia)
Serum)Sodium)>)155)meq/L)
)
• Calcium,)Magnesium,)Phosphorus))
• Hyperglycemia)
Hypothermia
• Con6nuous)temperature)management)
• Central)vs.)Tympanic,)Skin,)Axillary,)etc)
• Hypothermia)blanket)
• If)temperature)less)than)32)C)
–  warming lights
–  covering patient’s head with blankets
–  hot packs in the axilla
–  warmed IV fluids
–  warm inspired gas
Anaemia

• Hematocrit)trigger)is)30%)
• Helps)in)oxygen)delivery))
• Assess)for)source)of)bleeding)
T4 protocol
Bolus:
!  15 mg/kg Methylprednisone
!  20 mcg T4 (Levothyroxine)
!  20 units of Regular Insulin
!  1 amp D50W
Infusion:
!  200 mcg T4 in 500 cc NS Oral)Levothyroxine))
!  Run at 25 cc/hr (10 mcg/hr) 300Q400)mcg/8)hourly)
!  Titrate to keep SBP >100
Monitor Potassium levels closely!
 Organ donation process
•  Evaluate)organ)func6on))
•  Labs)(&)UA))within)6)hours)of)surgery)
•  Type)and)Screen)
•  Consent)signed)
•  Serology)tes6ng)
•  Medical)Social)History)
•  Locate)poten6al)recipients)
•  Manage)hemodynamics)
•  Arrange)opera6ng)room)
THANK$YOU$

Thank you!
CHRONIC KIDNEY DISEASE

DR. ANUPAMA GILL SHARMA

MBBS, DA, DNB,IDCCM
ASSOCIATE PROFESSOR
A.B.V.I.M.S. & DR. R.M.L. HOSPITAL,
NEW DELHI
CHRONIC KIDNEY DISEASE (CKD)……

Defined as kidney damage or glomerular filtration rate (GFR) <60 mL/

min/ 1.73 m2 for 3 months or more, irrespective of cause

ESRD (End Stage Renal Disease)

GFR < 25 mL/hr
Requirung dialysis, Renal Transplantation
Ref: www.kdigo.org/clinical_practice_guidelines/pdf/CKD/KDIGO_2012_CKD_GL.pdf
PATHOPHYSIOLOGY
MULTISYSTEM DYSFUNCTION

Cardiovascular

Respiratory

Coagulation

Neurological

Musculoskeletal

Metabolic
 CARDIOVASCULAR
• CARDIO-RENAL SYNDROME
CARDIAC FUNCTION RENAL FUNCTION

1. Hypertension -
• Intravascular volume expansion
• Retention of sodium and water and
• Activation of the renin-angiotensin- aldosterone system.
 CARDIOVASCULAR

2. Congestive cardiac failure 5. Uraemic Cardiomyopathy

• Diastolic failure • Pericardial effusion/Pericarditis
• Left Ventricular hypertrophy • High index of suspicion for pericarditis
whenever patients with ESRD
3. Dilated cardiomyopathy complain of chest pain, as up to 20%
experience it at some point
• with systolic heart failure
6 . Risk of CAD / MI
4. Arrythmia
• Atrial fibrillation - common in
patient with ESRD (13-27%)
• Risk of stroke
 RESPIRATORY
• Pulmonary edema - fluid overload , hypoalbunemia
• Pleural effusion
• Ventilation can be affected due to Ascites.
• Fibrinous pleuritis
• Pulmonary calcification
• Predisposition to tuberculosis.
 COAGULOPATHY

• Increased tendency to bleed despite normal platlets count .

-Altered interaction of vWF with Gly 2b 3a receptor.

-Decreased factor 3 and ADP activity

• Uraemic thrombocytopathy, Thrombasthenia(Qualitative platlet dysfunction)

- Improves with dialysis

• Risk of GI bleed ,epistaxis,hemorrhagic pericarditis, subdural hematoma

• Increased tandency of thrombosis of vascular access.

 COAGULOPATHY

• Emergency treatment of coagulation abnormalities with

Von willibrand factor 0.3 mcg /kg nasal or IV

Conjugated estrogen

Blood transfusion
 NEUROLOGICAL SYMPTOMS

• Impaired abstract thinking

• Uraemic neuropathy and encephalopathy

• Lassitude

• Uremia related dementia

• Insomnia and Depression

• Psychosis, Coma

• Distal symmetric mixed motor and sensory polyneuropathy

 RENAL OSTEODYSTROPHY
• Secondary hyperparathyroidism

• Decreased vit D production

• Bone demineralization

• Advised low phosphate intake ,oral calcium and vit D

supplementation,

• Accumulation of aluminium in bone

 ANEMIA IN CKD

• Normocytic,normochromic type

• Erythropoietin-50-150 U/kg/wk IV or SC (once, twice, or three times per

week )

• Also improves bleeding diathesis, impaired mentation, lethargy

• Intermittent iron injections can be given.

 CAUSES OF ANEMIA IN CKD
• Relative EPO deficiency • Uraemic millieu (Bone marrow
suppression)
• Iron deficiency
• Blood loss tendancy

• Vitamin defeciencies • Hyperparathyroidism

• Shortened RBC life span • Inflammation and infection risks

 DIALYSIS RELATED PROBLEMS

• Hypotension

• Dialysis dementia

• Peritonitis

• Systemic anticoagulation

• Dialysis Disequilibrium syndrome ( DDS)

- treatment by reducing the rate of

dialysate fluid.

- Decrease the surface area of dialysis

membrane
  IMMUNOSUPPRESSIVE DRUGS
• Prevent acute and chronic T cell autoimmune reactions

•Four classes
-corticosteroids
-calcineurin inhibitors
-antimetabolites and
-azathioprine target of rapamycin inhibitor Sirolimus

• Intraoperatively induction agent given to eliminate lymphoid cells

RENAL TRANSPLANT
 HISTORY

• Renal transplantation was first attempted in 1906

• Since the use of chemical immunosuppression in the 1960s ,it has

become the preferred treatment for ESRD.

• Pre emptive kidney transplantation ( before dialysis complications

occur, shown to improve graft survival.
SURGICAL TECHNIQUE
Step A. Renal artery anastomosis performed end-to-side to the external iliac artery.

Step B. Renal vein anas- tomosis performed end-to-side to the external iliac vein.

Step C. Ureteral anastomosis to the bladder mucosa.

 PREOP-EVALUATION

• Etiology of CKD

• Frequency of dialysis and last performed

• Associated comorbidities

• Organ functions evaluation

• Correct coagulopathy

• Optimise acid base ,fluid and electrolyte balance

 PRE- OPERATIVE ORDERS

• NPO from 12 midnight

• Review all investigations, Acid base status

• Anti-aspiration prophylaxis - Tab Ranitidine 150 mg midnight and morning

• Anxiolysis - Tab Alprazolam

• Continue all antihypertensive and immunosuppressive drugs

• Preop dialysis

• Adequate blood products to be arranged ( leukodepleted

RBC s)

• Post op ICU bed to be kept

CLINICAL ABNORMALITIES IN CKD AND THEIR RESPONSE TO DIALYSIS
IMPROVED NOT IMPROVED VARIABLE RESPONSE

• Volume status • Splenomegaly • Hyperuricemia

• S. Na ; S. K levels • Lymphocytopenia • Secondary

• Metabolic acidosis Hyperparathyroidism
• Sleep disorder
• Hyperphostaemia • Peripheral neuropathy
• Pruritis
• Hypocalcemia
• Arterial Hypertension
• Hypothermia • Infertility and sexual
• Pericarditis dysfunction • Cardiomyopathy

• Coma • GI bleeding
 CHOICE OF ANAESTHESIA

• Recepient - Balanced general anaesthesia with ETT using opiods,volatile

anesthetics and muscle relaxant .

• Donor - GA with epidural analgesia , adequate hydration important.

 INTRA OPERATIVE GOALS

• Adequate padding of fistula, care of potential fistula sites

• Neuromuscular monitoring

• Maintain renal blood flow

• Avoid hypotension, maintain euvolemia.

• Careful managment of fluid ,acid base and electrolytes.

 Intraoperative course
• Premedication- Fentanyl,Glyco ,Midazolam
• Atracurium / Cis - atracurium.

• Propofol / Thio - sudden hypotension

• Desflurane / Isoflurane

• Thiopentone- large volume of disttribution and decreased • Cautious use of local anaesthrtics
protein binding

• Renal excretion of neostigmine is 50 %.

• Laryngoscopic response to be blunted.
 Anaesthesia drugs that depend signifanctly on renal elimination

Completely dependent Partially dependent

• Intravenous anesthetics— barbiturates
• Digoxin
• Others—aminoglycosides, vancomycin, cephalosporins,
and penicillins
• inotropes
• Muscle relaxants— pancuronium

(used frequently; monitoring of blood • Anticholinergics— atropine, glycopyrrolate

levels indicated in chronic renal failure)
• Cholinesterase inhibitors— neostigmine, edrophonium

• Others—milrinone, hydralazine, cycloserine,

sulfonamides, and chlorpropamide
ANAESTHETIC AGENTS
HEMODYNAMIC MONITORING
 MONITORING

• Care of AV FISTULA • CVP

• 12 lead ECG • Urine monitoring

• Arterial BP/NIBP • Temp

• Spo2 • Sugars

• EtCO2 • Role of TEE in complicated cases

 FLUIDS and ELECTROLYTES
• CVP guided fluid management • NS/ RL / BSS (plasmalyte)
( > 15 cm usually)
• Blood sugar at the time of
• Avoid large sudden fluid reperfusion preferably be <
adminstration 160 mg/dl.

• Careful correction of acid and • Mannitol 20% before

balance intraop reperfusion.
Potential hyperkalemia is corrected • Controversial role of furosemide
Transplanted kidney function is
supported
 FLUIDS and ELECTROLYTES

• Urine catheter and monitoring must.

• Replace urine with fluid if patient has any

• Warm fluids,regular k and ABG

• Evenly distribution of fluid better than sudden bolus before

reperfusion
 Role of colloids

• Routine use of albumin not recommended.

• Colloids like HES, Gelatin,dextrans not recommend ,may cause AKI.

• HES induced renal dysfunstion - swelling and vascuralization of

tubular cellas and obstruction due to production of hyperviscous
urine
 BLOOD TRANSFUSION

• Transfuse if PCV is < 25%. leukodepleted RBC

• Role of immunomodulation in early 70s was described.

• Also reports of higher graft rejection with blood

• Lower transfusion trigger

• Risk of infection, fluid overload, pulmonary edema, immune

sensitization.
 VASOACTIVE AGENTS

• Risk of artery vasoconstricion ,graft rejection

• Recheck volume status

• Role of Dopamine—not recommended

• Dobutamine for low cardiac output states with advanced

hemodynamic monitoring

• If needed noradrenaline can be used

 ISCHEMIA TIME

• Donor warm ischemia time : Time from clamping of the aorta or

renal artery to cold perfusion.

• Cold ischemia time : Time from cold perfusion of the kidney to the
start of the venous anastomosis

• Recepient warm ischemia time : Removal of the kidney from

storage ice till the initiation of graft reperfusion, hence depending
on the anastomosis time of renal vessels.
 POST OPERATIVE CARE
• Atenuate extubation response • Avoid Nephrotoxic drugs,
Optimsed fluid therapy
• Extubate fully awake, complete
recovery of neuromuscular • Immunosupressant
blockade medication to be continued

• Care in HDU /ICU • Delayed graft function and

adverse cardiovascula
• Analgesia - Opioids , role of events are the most common
TAP block
Take home message..
 REFERENCES

• Millers Anesthesia 8th edition; Ronald D. Miller

• Stoelting’s Anesthesia and Coexisting Disease; 7th edition ; Roberta

L. Hines , Katherine E. Marschall
THANK YOU
POST-TRANSPLANT PATIENT FOR
INCIDENTAL SURGERY

DR. KAPIL GUPTA

PROFESSOR, ANESTHESIA & CRITICAL
CARE
VARDHAMAN MAHAVIR MEDICAL
COLLEGE & SAFDARJUNG HOSPITAL
 CASE
HISTORY

• 60 Yrs Male, 5 ft, 10 inch ht, 50 kg

• H/O Fall
• Fracture Left Femoral condyle
• Planned for ORIF
• H/O Kidney Transplant 3 months ago
• H/O DM, Hypertension
• No loss of consciousness/ any other organ injury
• Medications- Metformin, Telmasartan, Amlodipine, Tacrolimus, Predisolone, Mycophenolate
 PHYSICAL EXAM

• Conscious, oriented, GCS- 15/15

• PR- 102/ min
• BP- 90/60mmHg
• RR-16/min
• Chest - B/L clear, AE equal
• CVS- S1, S2 Normal
 INVESTIGATIONS

• Hb- 8 gm%
• Platelets- 3 lakh/cumm
• TLC/DLC- Normal
• PT/APTT- Normal
• LFT/KFT/ Electrolytes- Normal
• Blood sugar- 150mg/dl, HB1AC- 6%
• ECG- Normal
• Chest X ray- Normal
 RESUSCITATION

• Two 18 G IV cannula secured

• Adequate resuscitation- 1 liter Plasmalyte/ 2 units Packed red cells
• Air warmer and fluid warmer used
• BP - 130/80 mmHg (NIBP)
• PR- 78/min (Pulse oximeter)
• ECG- Normal rhythm
• Chest X ray - Normal
• ABG- Normal
 ANESTHETIC PLAN

REGIONAL OR GA ?
 COMBINED SPINAL EPIDURAL
FEMORAL NERVE BLOCK

• All immunosuppressants continued peri-operatively

• UNDER ALL ASEPTIC PRECAUTIONS
• Femoral nerve block- Positioning- 10 ml of 0.5% Bupivacaine (isobaric) - side of fracture
• After 20 mins, patient positioned lateral
• 2.0 ml of 0.5% Bupivacaine with 10 ug Fentanyl intrathecal - Spinal Block - L2-3 level
• Epidural Catheter secured
• T8 level achieved
• Paracetamol 1 gm IV
 INTRAOPERATIVE COURSE

• IV Fluids- Crystalloids 1 liter plasmalyte

• Oxygen- Ventimask - 6 L/min
• Temperature- 35 degrees
• Intraoperatively vitals stable
• Blood loss - 600 ml
• 1 unit packed cell transfused
• Urine- 500 ml
• Duration of surgery- 3 hrs
 POSTOPERATIVE
PACU

• Air warmer used

• Strict asepsis maintained

• Epidural top up- 2 mg Morphine in 6 ml 0.125% Bupivacaine

• Paracetamol - 1 gm TDS

• Vitals Stable
 SURVIVAL POST KIDNEY TRANSPLANT

• 1 Year- 90-95%

• 10 Year- 70-75%
 KIDNEY TRANSPLANT- INTRODUCTION

• MC TRANSPLANT RECIPIENT FOR NON-TRANSPLANT SURGERY

• Only 62% of recipients recover fully

• ALL on immunosuppression

• Increased infections
 POST-TRANSPLANT STATUS

• A NEW CHRONIC ILLNESS

• AFFECT PHYSIOLOGICAL FUNCTION

• REQUIRES A TAILORED ANESTHETIC MANAGEMENT PLAN

IS KIDNEY FUNCTION COMPLETELY
RESTORED POST-TRANSPLANT ?
 POST-TRANSPLANT

• Lower GFR

• GFR decreases by 1.4- 2.4 ml/min/yr

• National Kidney Foundation stage 2 or 3 CKD

• Prolonged drug action and excretion

 SURGERIES

• Early or late complications post-transplant

• Elective surgery

• Emergency surgery
 ANESTHESIA CONSIDERATIONS

• REJECTIONS
• INFECTIONS
• TOXICITY/SIDE EFFECTS OF IMMUNO-SUPPRESSANTS
• DRUG INTERACTION WITH IMMUNO-SUPPRESSANTS
• FUNCTIONAL STATUS OF TRANSPLANTED ORGAN
• FUNCTIONAL STATUS OF OTHER ORGANS
• PRESENCE OF CONCOMITANT DISEASES
 KIDNEY REJECTION
PATHOLOGY

• Inflammation with specific pathologic changes in allograft

• Due to recipient’s immune system recognizing non-self antigen in allograft
• With or without dysfunction of allograft
• Innate & adaptive immune systems play a significant role
• T lymphocytes are principal cells that recognize allograft
• Other co-stimulatory molecules & cytokines also play a major role
 HYPERACUTE REJECTION

• Mins after transplant

• Due to preformed antibody or ABO incompatibility

• Rarely seen now due to very sensitive cross-match tests performed before transplant
 ACUTE REJECTION
Within days to weeks

• A) Antibody-mediated rejection- antibody mediated injuries to kidney

- inflammation of glomeruli (Glomerulitis) or
- peritubular capillary (peritubular capillaritis)

• B) Acute T-cell mediated rejection- lymphocytic infiltration of tubules,

interstitium & arterial intima
 CHRONIC REJECTION

•> 3 months post-transplant

• Chronic antibody-mediated or T cells mediated rejection

 REJECTION- CLINICAL MANIFESTATIONS

• Increasing serum creatinine

• Hypertension
• Oliguria
• Proteinuria
• Fever, pain at graft site, hematuria & dysuria
• Anesthetic drug’s pharmokinetics & pharmacodynamics altered
• Prevention of graft rejection- Maintain Renal Perfusion Pressure
 WORKUP
GRAFT DYSFUNCTION

• Tissue biopsy is key for diagnosis

• Donor-derived free DNA detection test is emerging as a noninvasive tool for diagnosing
rejections but not validated to date
• Rule out prerenal causes: Check orthostatic vital sign, blood pressure & volume status
• Rule out post-renal causes mainly obstructive uropathy in older adults by bladder scan, renal
USG
 WORKUP
GRAFT DYSFUNCTION

• CBC: Look for anemia and thrombocytopenia

• Electrolyte abnormality related to CKD, AKI
• UA & urine culture: rule out infection as a cause of AKI
• Check for proteinuria
• Check BK Virus, CMV PCR in clinically indicated patients
• Testing for donor-specific antibodies
• Transplant renal ultrasound with doppler for renal arterial & venous indices
 TREATMENT OF REJECTION

• Plasma Exchange
• IV immunoglobulin (100 to 200 mg/kg)
• Rituximab
• Bortezomib
• Methyl Prednisone IV (250 to 1000 mg daily)
• rATG - Rabbit anti-thymocyte globulin IV (1 to 1.5 mg/kg) targeting T cell receptors
 INFECTIONS

• Immunosuppression- prone to infection

• Viral, fungus, protozoal, bacterial

• MC- Candida, Aspergillus, Cytomegalovirus

Operation Recommended antibiotic prophylaxis

Cefazolin, cefuroxime, or cefamandole.

Cardiothoracic surgery
If patient has a β-lactam allergy: vancomycin or clindamycin

Cefazolin or cefuroxime.
Vascular surgery If patient has a β-lactam allergy: vancomycin with or without gentamycin,
or clindamycin

Oral: neomycin plus erythromycin base, or neomycin plus metronidazole.

Colon surgery
Parenteral: cefoxitin or cefotetan, or cefazolin plus metronidazole

Cefazolin or cefuroxime.
Hip or knee arthroplasty
If the patient has a β-lactam allergy: vancomycin or clindamycin

Vaginal or abdominal
Cefazolin, cefotetan, cefoxitin or cefuroxime
hysterectomy
 POST-TRANSPLANT MALIGNANCIES

• Epithelial malignancies

• Colon, skin, vulva, bladder, lung, testes

 NEUROLOGICAL COMPLICATIONS

• 30-60% of recipients

• Due to immunosuppressive regimens & shifts in fluids/electrolytes

• Seizures, peripheral neuropathy, brain infarcts, haemorrhages

 IMMUNOSUPPRESSION

•Antibodies
• Corticosteroid (Methylprednisolone, Prednisolone)

• Calcineurin Inhibitor (Cyclosporin, Tacrolimus)

• Antiproliferative agent (Azathioprine, Mycophenolate, Cyclophosphamide, Methotrexate)

• Continued - 6-12 months

• 90% graft survival and acute rejection rate <20%

 IMMUNOSUPPRESSION

• Aggravate risk factors for CAD like hypertension, diabetes & hyperlipidaemia

• Continue during peri-operative period

• Plasma drug levels monitored

• Stress of surgery- affect absorption & metabolism of these drugs- altering plasma levels
• Know - actions, interactions & potential side effects
 ANTIBODIES
Polyclonal, monoclonal

• Ideal immunosuppressant

• Lowest toxicity

• Specific activity

• Prolonged effect
 OKT3

• Murine Monoclonal Antibody

• Prevents T lymphocyte function- directed against CD3 component of T cell receptor

• Acute administration- Cytokine release syndrome

• Fever, headache, dyspnoea, GI effects, life threatening pulmonary oedema

 ANTI-IL-2 RECEPTOR MONOCLONAL ANTIBODIES
BASILIXIMAB, DACLIZUMAB

• Block IL-2 mediated T cell activation

• Minimal toxicity

• GI upset
 THYMOGLOBULIN
POLYCLONAL ANTI-THYMOCYTE ANTIBODY

•Induction agent (immunosuppression)

•Treatment of rejection- Course of upto 10 days
•Causes lymphocyte depletion
•Cytokine release syndrome (milder form)
•Side effects- thrombocytopenia, leukopenia & serum sickness
 mTOR INHIBITORS
SIROLIMUS (RAPAMYCIN), EVEROLIMUS

• Arrest lymphocyte cell cycle (inhibit kinase activity)

• Poor wound healing

• Pulmonary toxicity- interstitial pneumonitis, fever, haemoptysis, diffuse alveolar infiltrate

 CALCINEURIN INHIBITORS
Tacrolimus, Cyclosporine

• Bind to Calcineurin- inhibit its translocation into nucleus- decrease secretion of IL-2 by T
lymphocyte

• Narrow therapeutic index

• Nephrotoxicity, Neurotoxicity & Glucose intolerance

• Oral Cyclosporine given 4-6 hrs preoperatively

 CyA Tac Aza Ster MMF ATG OK3
Anemia – – + – + –

Leucopenia – – ++ – + +

Thrombocytopenia – – – – + –

Hypertension ++ + – + – –

Diabetes + ++ – ++ – –

Neurotoxicity + + – + – –

Renal insufficiency + ++ – – – –

Anaphylaxis – – – – – +

Fever – – – – – +
 CALCINEURIN INHIBITORS
Tacrolimus, Cyclosporine

• Metabolism dependent on Cytochrome P 450

• Drugs (NSAIDS, Amphotericin, Ranitidine, Cimetidine, Gentamycin, Vancomycin) cause

induction of P 450 enzymes - affect plasma concentration of these immunosuppressants

• Cyclosporine- interferes with metabolism of other medications (Digoxin, Prednisolone,

Lovastatin)- causing toxicity
 Effect on blood level
Drug class Drug
Adverse effect

Benzodiazepines Diazepam, midazolam, alprazolam, flurazepam, clonazepam ↑ Benzodiazepines

Antibiotics Erythromycin, metronidazole, norfloxacin, levofloxacin ↑ CyA and Tac level

Antimicrobial Rifampicin ↓ CyA and Tac level

Antimalarial Chloroquine, mefloquine ↑ CyA and Tac level

↑ CyA and Tac level
Antifungal Ketoconazole, fluconazole, itraconazole, voriconazole, amphotericin B
Renal dysfunction

Anti-retroviral Ritonavir, atazanavir, darunavir, cobicistat, delaviridine ↑ CyA and Tac level

↑ CyA and Tac level

Cardiovascular drugs Amiodarone, lidocaine, quinidine, verapamil, diltiazem, amlodipine,
QT prolongation
(antiarrhythmics ) felodipine
amiodarone and quinidine

Statins Simvastatin, atorvastatin, lovastatin, pravastatin ↑ Statin concentration

↑ Anticoagulant
Anticoagulants Apixaban, dabigatran, rivaroxaban
concentration

Oral hypoglycemics Sulfonylurea, biguanides ↑ CyA level

↑ CyA and Tac level

Renal dysfunction
 CALCINEURIN INHIBITORS
Tacrolimus, Cyclosporine

• Prolonged duration of NDMR- Decrease dose of NDMR

• Increase blood level of benzodiazepines

• Cyclosporine - Increase analgesic effect of Fentanyl

• Isoflurane - decrease gastric emptying & absorption from proximal small bowel- Increase Cyclosporine levels
 Isoflurane ↓ Clearance of oral CyA
Thiopental Nil

Benzodiazepines ↑ Blood level of benzodiazepines

Propofol Nil
Etomidate Nil

Opioids CyA ↑ analgesic effect produced by fentanyl

Muscle relaxants Prolonged neuromuscular blockade

Neostigmine Caution in heart transplant patients

Local anesthetics Bupivacaine and ropivacaine can be safely used

 ANTI-PROLIFERATIVE AGENTS
AZATHIOPRINE, MYCOPHENOLATE

• Inhibit Purine synthesis- T & B lymphocyte suppression

• Toxic- Bone Marrow, GI Tract, Liver

• Neurological Toxicity

• Haematological Toxicity (anemia, thrombocytopenia, leukopenia)

 CORTICOSTEROIDS
PREDNISOLONE, METHYLPREDNISOLONE

• Cause sequestration of CD4+ T Lymphocytes & inhibit transcription of Cytokines

• Side effects- hypertension, diabetes, obesity, osteoporosis

• Major Surgery- usual dose preoperatively & 50 mg Hydrocortisone intraoperatively and every
8 hrs for 72 hrs- then continue regular dose
 PRE-OPERATIVE EVALUATION

• Medical & surgical history

• Risks of planned surgical procedure

• Meticulous cardiopulmonary screening

 PRE-OPERATIVE EVALUATION

• Co-morbidities- CAD, Hypertension, DM & Hyperlipidaemia

• CAD- Leading cause of death (32%)- Transplants recipients

• BP / Glycaemic control- improved survival

• Assess Cardiac function- 2D Echo, ECG, Stress test

 PRE-OPERATIVE EVALUATION

• Assess kidney allograft function

• Serum BUN/ Creatinine levels

• Urine analysis

• Optimize electrolytes/ acid base status

 INVESTIGATIONS

• CBC
• PT/APTT/Platelet count
• Serum electrolytes
• LFT
• KFT
• Blood sugar
• Chest X ray
• ECG
 ELECTROLYTE IMBALANCE

• Immunosuppressive therapy

• Aggravated by surgery/anesthesia

• Monitor electrolytes - esp. Potassium & Magnesium levels

• Severe electrolyte shifts- worsen neurological complications

 GLYCEMIC CONTROL

• POST-TRANSPLANT DIABETES- 4-20% PATIENTS

• TARGET GLUCOSE LEVELS - 110-150 mg/dl

• PERI-OPERative hyperglycemia- associated with:

- electrolyte imbalance
- impaired wound healing
- nosocomial infections
 AIRWAY

• Difficult Intubation in diabetics-limitations in joint mobility - caused by glycosylation of

connective tissue within their joints
• Increased risk for lymphoproliferative disorders secondary to immunosuppressant drugs
• Lymphoproliferative growth may compromise airway & cause life-threatening airway
obstruction
• Gingival hyperplasia - due to cyclosporine
.

• Aspiration risk increased - delayed gastric emptying & gastropathy due to

immunosuppressants
 PERI-OPERATIVE GOALS

• RENAL PROTECTIVE STRATEGY

• MAINTAIN RENAL PERFUSION

• REMEMBER——DRUGS thAT RELY HEAVILY ON RENAL EXCRETION FOR CLEARANCE- Have

PROLONGED EFFECTS

• PREVENT HYPOVOLEMIA, HYPOTENSION, HYPOTHERMIA & HYPOXIA

 CHOICE OF ANESTHETIC

• Surgical condition

• Patient’s medical condition

 REGIONAL ANESTHESIA

• Case based

• Risk-benefit ratio

• ADVANTAGES- Superior analgesia over systemic opioids

- Reduced pulmonary complications
- Decreased incidence of graft occlusion
 MONITORING

• Pulse oximetry
• ECG
• NIBP
• End-tidal CO2
• Anesthesia gas analysis
• Temperature
 INVASIVE MONITORING
COMPLEXITY OF CASE

• Cardiac Output Monitoring

• Arterial line

• CVP line

• Transesophageal Echocardiography
 STRICT ASEPSIS

• ALL INVASIVE LINES- Arterial line/ CVP line/ Neuraxial blocks/ Peripheral nerve blocks/ IV lines

• IMMUNOCOMPROMISED

• RISK OF SEPSIS

• Attenuated inflammatory response may diminish typical signs & symptoms of infection
 CVP LINE

Ultrasound guided

1. Prior indwelling CVP lines- thrombus

2. Immune compromised- risk of infections

 INDUCTION

• Induction agent- Propofol/ Etomidate/ Thiopentone

• Selection of iv Anesthetics - guided by patient’s hemodynamic status, drug’s cardiovascular

effects & pharmacokinetic properties

• Stress ulcer & VTE prophylaxis

• Ketamine - metabolized via hepatic cytochrome P-450 system

 MAINTENANCE OF ANESTHESIA

• ISOFLURANE - INHALATION AGENT OF CHOICE

organ - protective characteristics
safe hemodynamic profile
• DESFLURANE/ SEVOFLURANE
• Avoid prolonged use of N2O - potential risk of bone marrow suppression & altered
immunologic response
• FENTANYL/REMIFENTANIL- OPIOID OF CHOICE; MORPHINE
• AVOID- NSAIDS
 NEUROMUSCULAR BLOCKING AGENT

• Choice - dictated by length of surgery, underlying medical illnesses (i.e. myasthenia or other
neuromuscular disorders) & functional state of patient’s kidney & liver

• ATRACURIUM/Cisatracurium— HOFMAN’S ELIMINATION

• ROCURONIUM

• NEUROMUSCULAR MONITORING
 POST-GRAFT KIDNEY

• Sub-optimal auto-regulation of Renal Blood Flow

• Susceptible to sudden BP variation

• Adequate hydration

• Hemodynamic monitoring
 POST-OPERATIVE

• Extubation preferred - decrease risk of VAP

• Multimodal analgesia

• PCA pump
• Regional Anesthesia

• Early ambulation & physical rehabilitation

 CONCLUSION

• For safe management of solid organ recipients- essential to have knowledge of:

- physiology of transplanted organ

- pharmacology of immunosuppressive drugs

- associated organ dysfunction

 29-01-2021

Case Details
Transurethral Resection of • A 78 yr old male with h/o
Prostate (TURP) • Increased frequency of micturition x 3 yr

• Urgency of micturition x 2-1/2 yr

Dr. Rashmi Salhotra
• Difficulty in initiation of micturition x 2 yr
Professor
Department of Anaesthesiology • Dribbling micturition x 2-1/2 yr
UCMS and GTB Hospital,
• No p/h/o TB, DM, HTN, IHD, COPD
Dilshad Garden, Delhi
• Non-smoker, non-alcoholic

General Examination Systemic Examination

• Conscious, well oriented to time, place, person • CVS: S1, S2 normal, no murmur
• No pallor/icterus/cyanosis/clubbing/lymphadenopathy/jaundice/ • R/S: AEBE, No added sounds
pedal oedema
• CNS: GCS: 15/15, higher functions and cranial nerves normal
• Temp: normal
• P/A: Soft, non-tender, no organomegaly
• P: 88/min, regular, no radio-radial/radio-femoral delay
• Back and spine: NAD
• BP: 138/88 mm Hg in left arm in supine position

• RR: 14/min

Differential diagnosis

• Benign Prostatic hypertrophy (BPH)

Question 1:
• Prostatic CA
What is your D/D on the basis of
• Urethral stricture
history? • Urinary tract infection

• Neurogenic bladder

• Bladder neck hypertrophy

1
 29-01-2021

• Fibromuscular glandular organ

• Weight 20g
• Conical in shape

Question 2: • Surrounds the prostatic urethra

• 1.25 in. (3 cm) long

Describe the anatomy of prostate • Base of prostate lies between the neck of the bladder
above and the apex lies against the urogenital

gland. diaphragm below

• Surrounded by a fibrous capsule
• Two ejaculatory ducts pierce the upper part of
posterior surface of prostate to open into prostatic
urethra at the lateral margins of the prostatic utricle

• 5 lobes: • Arterial Supply: • Lymphatic Drainage:

• Anterior lobe: lies in front of the urethra and is devoid of glandular • Inferior vesical artery • Internal iliac nodes

tissue • Middle rectal artery

• Internal pudendal artery

• Median or middle lobe: between the urethra and the ejaculatory
ducts • Venous drainage:
• Vesical and prostatic venous plexus
• Posterior lobe: behind the urethra and below the ejaculatory ducts
• Internal pudendal veins
• Right and left lateral lobes: on either side of the urethra
• Vertebral venous plexus

• Nerve Supply

Question 3:
What is Benign Prostatic Hypertrophy?
What is the pathophysiology of BPH?

2
 29-01-2021

• Common problem in men >50 yr • Difficulty in passing urine

• Imbalance in the hormonal control of the gland • Weak stream of urine

• Median lobe enlarges upward and encroaches within the sphincter • Back-pressure effects on ureters and kidneys

vesicae located at the neck of the bladder • Enlargement of the uvula vesicae (owing to
the enlarged median lobe) results in the
• Leakage of urine into the prostatic urethra causes an intense reflex
formation of a pouch of stagnant urine behind
desire to micturate
the urethral orifice within the bladder
• Enlargement : elongation, lateral compression and distortion of urethra
• Stagnant urine frequently becomes infected
resulting in cystitis

Non-surgical management

• Reduced fluid intake: especially during late evening

Question 4: • Anti-cholinergics
What are the management • Medical therapy

options available for this patient? • Prostatic stents

• Permanent indwelling catheter

• Balloon dilatation

Medical Therapy Surgical Procedures

• Prostatic tissue growth: androgen sensitive • Open prostatectomy: retropubic, suprapubic/transvesical, transperineal

• Androgen deprivation: decreases the size of the prostate • Endoscopic:

• Transurethral resection of prostate (TURP)
• Finasteride: 5α-reductase enzyme inhibitor
• Monopolar TURP (M-TURP)
• α-Adrenergic antagonists (terazosin, doxazosin, tamsulosin): block • Bipolar TURP (B-TURP)
adrenergic receptors in hyperplastic prostatic tissue, prostatic capsule and • Laser prostatectomy (VLAP)
bladder neck • Holmium laser enucleation of the prostate (HoLEP)
• Microwave ablation (TUMT)
• Decrease smooth muscle tone and resistance to urinary flow
• Radiofrequency needle ablation (TUNA)
• S/E: Orthostatic hypotension • Aquablation

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Investigations
• CBC with platelet count • KFT with serum electrolytes
Question 5:
• RBS • ECG
How will you investigate this
• Urine: routine, microscopy • Chest X-ray
patient before anaesthesia?
• PT/INR • BGCM

• LFT

Transurethral resection of Prostate (TURP)

• Insertion of a resectoscope

(electrically powered cutting-

Question 6: coagulating metal loop) through

What is TURP? the urethra

• Resection of prostatic tissue

• Prostatic capsule intact

Morbidity and Mortality

• Continuous irrigation of the bladder
• Elderly
• Distend the bladder
• Coexisting diseases
• Bathe the surgical site
• 30-day mortality rate (M-TURP): 0.2% to 0.8%
• Wash away blood and tissue debris
• Common causes:
• Clear operative field for surgery • Pulmonary edema

• Renal failure

• Myocardial infarction

• Morbidity rate: 18%

• Acute urinary retention, gland size greater than 45 g, resection exceeding 90 minutes, age >80 yr

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Ideal Irrigation Solution

Question 7:
• Isotonic • Rapidly excreted
What are the properties of an ideal
• Non-hemolytic • Easily sterilized
irrigation solution?
• Electrically inert • Inexpensive
Enumerate the various irrigation
• Transparent
fluids available and the possible
• Non-metabolized
complications associated with each?
• Non-toxic

Solution Osmolality (mOsm/kg) Drawback

Glycine 1.2% 175 Cardiac
Glycine 1.5% 220 Neurologic
Retinal effects
Cytal
Sorbital 3.5%
178
165 Metabolized to fructose and lactate Question 8:
Hyperglycemia

Mannitol 5% 275
Lactic acidosis
Rapid expansion of blood volume
What are the anaesthetic
Glucose 2.5% 139
Pulmonary edema in cardiac compromised patients
Severe hyperglycemia in diabetic patients
concerns/challenges in a patient
Urea 1%
Distilled water
167
0 Massive hemolysis
undergoing TURP?
Hyponatremia
Renal failure
CNS symptoms
NS/RL Highly ionized
Dispersion of high-frequency current from resecting loop

Anaesthetic Concerns Position

• Patient related
• Elderly/geriatric age group • Lithotomy with slight Trendelenburg tilt
• Associated co-morbid conditions
• Hip flexion: 80 to 1000
• Disease related
• Leg abduction: 30 to 450 from midline
• Back pressure changes
• UTI
• Knee flexion such that lower legs are
parallel to torso
• Procedure related
• Positioning • Legs placed in supports or stirrups
• Procedural complications

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• Coordinated team work Complications of lithotomy

1. Venous stasis:
• Raise legs together
• Prolonged lithotomy
• Simultaneous flexion of knees and hips to prevent torsion and lumbar spine
• Compression by equipment or at the groin due to thigh flexion
injury
• Common in those with varicose veins
• Padding of bony prominences to prevent compression against leg supports • Lower extremity compartment syndrome: rare
• Limit procedure duration
• If surgical time >2 to 3 hr: periodic lowering of legs
• Use of elastic stockings
• Intermittent leg compression devices: controversial

2. Peripheral nerve injury: 3. Cardiovascular complications:

• Obturator nerve (L2, 3, 4): • Increased venous return
• Acute flexion of thigh to groin
• Weakness or paralysis of adductors of thigh • Cardiac preload: increased

• Saphenous nerve (L 2, 3, 4) • Transient increase in cardiac output

• Compression of medial aspect of leg against knee brace
• Obese patients/abdominal mass: Obstruction of venous return
• Sensory loss to the medial side of the thigh

• Common peroneal nerve (L 4, 5-S1, 2) 4. Abdominal:

• Injury around the head of fibula
• Increased intra-abdominal pressure
• Prolonged compression of the lateral aspect of knee
• Foot drop • Diaphragm displaced cephalad

5. Respiratory:

• Reduction in lung compliance

• Decrease in lung volumes: RV, FRC, TV, VC

6. Others:
Question 9:
• Loss of curvature of lumbar spine: Risk of back pain
What monitoring would you like to
• Cerebral venous and intracranial pressure increased
do in the intra-operative period?

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• ECG

• NIBP

• Pulse oximetry
Question 10:
• Temperature
What will be the choice of
• Mentation
anaesthesia for TURP?
• Blood Loss

• Serum Electrolytes

• Spinal anaesthesia: Adequate anesthesia with relaxation of the pelvic floor

• Level: Sensory level of T10 sufficient for procedure
and perineum
• Higher sensory levels: mask the symptoms (abdominal or shoulder
• Awake patient: Early recognition of signs and symptoms (e.g., mental status pain and/or nausea and vomiting) of accidental perforation of the
changes) of TURP syndrome or the extravasation of irrigating solution bladder or prostatic capsule

• Promotes vasodilation and peripheral pooling of blood: Reduces the • Advantages over epidural anesthesia:
severity of circulatory overload • Technically easier to perform
• Reduces blood loss by lowering blood pressure during surgery • Complete block of the sacral nerves
• Postoperative analgesia

• GA: Very few indications

• Technical difficulty for SA

• Preferred in patients with coagulation abnormalities Question 11:

• Patient refusal What are the potential complications
of TURP?

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Complications TURP syndrome

Intraoperative Postoperative
• Iatrogenic form of water intoxication caused by a combination of
• TURP syndrome • TURP syndrome
excessive absorption of irrigating solution and the resultant
• Bladder perforation • Clot retention hyponatremia
• Hypothermia • Bleeding • Onset: 15 min to 24 h after the onset of resection
• Myocardial Infarction • Postoperative cognitive • Incidence rate of mild to moderate TURP syndrome is 0.78% to 1.4%
• Bleeding dysfunction
• Mortality rate: 25% with severe TURP syndrome (serum sodium
concentration <120 mEq/L)

Factors determining absorption of Irrigating Excessive Circulatory Volume, Hyponatremia

Solution and Hypo-osmolarity
• Hypertension and bradycardia
• Height of the irrigating solution above the surgical table (hydrostatic
• Hypertension + Hyponatremia net water flux along osmotic and
pressure)
hydrostatic pressure gradients out of intravascular space into the pulmonary
• Distension of bladder interstitium pulmonary edema and hypovolemic shock

• Extent of open venous sinuses • Release of endotoxins in circulation + metabolic acidosis hypotension

• Acute changes in serum sodium levels are more concerning than chronic
• Length of surgical resection time
hyponatremia
• 10 to 30 mL of fluid/min of resection time • Acute serum hypoosmolality: shift of intravascular fluid into the brain and

• 6 to 8 L in procedures lasting up to 2 hours consequent cerebral edema

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Prevention
• Bipolar resectoscope • Correct fluid and electrolyte imbalance

• Laser resection • Cautious administration of iv fluids

• Monitor fluid absorption • Limit duration of irrigation to 1 hour

• Halt surgery: 750 mL (for females) or 1000 mL (for males). Assess Na+ levels and • Maximum height of irrigation fluid bag: 60 cm
neurologic status (if awake)
• Limit intravesical pressure to <15 to 25 mm Hg or 70 mm Hg for endometrial procedures
• Terminate surgery: 1000 to 1500 mL (for females) or >2000 mL (for males), >2500 mL

(saline irrigant)

Treatment Presentation and treatment of hyponatremia

Sodium level (mEq/L) Signs/Symptoms ECG findings Treatment
• Cessation of irrigation solutions 120-125 Headache Wide QRS complex Fluid restriction
Confusion Furosemide
• Oxygen supplementation Agitation
Vomiting
• Loop diuretic to promote free water excretion Lethargy
120-115 Hypotension Wide QRS complex Hypertonic saline
• Hypertonic saline (severe hyponatremia with neurologic symptoms) CHF ST elevation
Pulmonary oedema Ventricular ectopics
• Hemodialysis (normal or marginally decreased osmolality) <110 Loss of consciousness VF, VT CPR
Seizures (Cardiac arrest)
Coma
• Seizures: BZPs, Thiopentone, Phenytoin, Magnesium sulfate Cardiorespiratory arrest

Glycine Toxicity Volume of glycine absorbed Signs and symptoms

>500 ml Visual disturbances
• Inhibitory neurotransmitter in brain >1000 ml Depressed consciousness
Abdominal pain
• Normal plasma glycine level: 0.3 mmol/L, 13-17 mg/dL
>3000 ml Diarrhoea
• Distribution t1/2: 6 min
Plasma concentration of glycine Signs and symptoms
• Termination t1/2: 40 min to several hours
5-8 mmol/L Visual disturbances
• Neurologic and cardiac effects Headache
>10 mmol/L Nausea/vomiting
• Transient blindness: Pupils are sluggish or nonreactive to light Transient blindness
• T-wave depressions or inversions on ECG >20 mmol/L Fatal

• Elevated CK-MB isoenzymes for up 24 hours after surgery

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Transient Blindness Ammonia Toxicity

• >100 μmol/L
• Transient blindness: in the OT or in PACU
• Systemic absorption of glycine and its oxidative deamination to glyoxylic acid and
• Blurred vision
ammonia
• Haloes around the light • Endogenous arginine in the liver prevents hepatic release of ammonia and facilitates
conversion of ammonia to urea
• Pupillary dilatation
• S/S: Nausea and vomiting: Within 1 hour after surgery
• Reaction: Sluggish or nonreactive to light
• Coma lasting for 10 to 12 h
• Retinal dysfunction secondary to hyperglycinemia
• Reverses at ammonia levels <150 μmol/L
• Recovery: Spontaneous after 8-48 hr • Prevention: Prophylactic administration of intravenous arginine

Bladder Perforation Transient Bacteremia and Septicemia

• Incidence ~ 1%
• Common retroperitoneal
• Prostatic bacteria invade blood stream via opened prostatic venous

• Cause: Surgical instrumentation or overdistention with irrigating solution sinuses

• Signs: Decrease in the return of irrigating solution • Indwelling catheter

• Fluid accumulation in the abdomen
• Prophylactic administration of antibiotics
• Symptoms: abdominal pain, nausea, vomiting
• Transient, symptomless and easily treated with common antibiotic
• Intraperitoneal perforations: symptoms are similar and develop sooner
combinations
• Severe shoulder pain secondary to diaphragmatic irritation
• Treatment: Open surgical repair or percutaneous drainage of the abdomen • 6% to 7% patients may develop septicemia

Hypothermia Bleeding and Coagulopathy

• Blood loss: GA vs. RA: Controversy
• Prolonged and continuous irrigation with cold/room temperature
• RA: decreased central and peripheral venous pressures
solutions
• Reduced CVP: Greater absorption of irrigating solution compared to GA
• Elderly patients: reduced thermoregulatory capacity
• Vascularity and size of the gland
• Temperature change 1-20C/hr
• Duration of procedure
• Redistribution of body heat under regional anaesthesia
• Number of open sinuses
• Monitor body temperature
• Infection and prostatic inflammation from repeated or recent catheterizations
• Warm irrigation solutions

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Treatment:
• 2 to 4 mL/min of resection time or 20 to 50 mL/g of resected prostatic
• Supplemental oxygen and ventilation support
tissue
• Cardiovascular support
• Blood loss (mL) = Hb of irrigating fluid (gm/mL) × Amount of irrigating fluid
• Look for hypercarbia, hypoglycemia and diabetic coma or drug interactions
Patient’s Hb (gm/lit)
• Collect blood samples for analysis of electrolytes, glucose, ABG, 12-lead ECG
• Careful monitoring of the patient’s vital signs
• Terminate the procedure as rapidly as possible
• Serial hematocrits to assess blood loss and need for transfusion
• Primary fibrinolysis: EACA 4 to 5 g i.v. during the first hour, followed by an infusion of 1 g/h
• Abnormal bleeding after TURP: Dilutional thrombocytopenia • DIC: Systemic absorption of resected prostatic tissue rich in thromboplastin

• Dilution of coagulation factors secondary to irrigating solution absorption • Blood products

• Volume absorbed = Preoperative S. Na × ECF – ECF

Postoperative S. Na
• Example:
Question 12: • A 60 kg man has undergone TURP. His pre-operative S. Na. was 148 mEq/L
How to calculate the amount of and post-op S. Na.= 114 mEq/L. Calculate the amount of irrigation fluid
irrigating solution absorbed? absorbed.

• ECF volume= 20% of body weight (Here, 0.2X60=12L)

• Volume absorbed = 148 x 12 – 12 = 3.57 L
114

Laser Resection: Holmium:yttrium-aluminum-

garnet laser (HoLEP)
• Solid-state, high-powered, pulsed laser

Question 13: • Precise cutting capabilities

What are the other newer modalities of • Prostatic tissue is vaporized, and the resulting heat dissipation coagulates small to
medium blood vessels
surgical interventions for prostatectomy? • Retrograde resection of entire prostatic lobes from the capsule, which are then pushed
into the bladder and removed with a soft-tissue morcellator.

• Safe for patients with larger prostatic glands, greater than 70 to 100 g

• Lower transfusion rates

• Shorter hospital stays

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Photoselective vaporization of prostate (PVP) Bipolar plasma vaporization

• Vaporization of prostatic tissue with minimal dissipation of energy
• Bipolar system: Both the active and return poles on the same electrode
• Faster vaporization and coagulation of prostatic tissue
• Energy does not transverse the patient’s body toward a return electrode pad, but
• Advantages:
• Almost bloodless field
instead it remains at the site of prostate vaporization
• Faster hemostatic closure of venous sinuses
• No direct tissue contact
• Reduced absorption of irrigation fluid

• Safe and effective in patients at high risk of discontinuing their anticoagulation therapy for the procedure • Minimal heat production

• Complications: • Concomitant vaporization and coagulation of tissue

• Capsular perforation

• Dysuria
• Plasma field vaporizes a limited layer of prostate cells with significantly reduced
• Infection (secondary to necrotic tissue that occurs with coagulation) bleeding

Transurethral microwave thermotherapy

Aquablation
(TUMT)
• Newest modality to surgically treat BPH
• Effective alternative to M-TURP
• Minimally invasive high-velocity saline ablation technique
• Minimally invasive office-based procedure
• Combines ultrasonic image guidance and robotics for targeted, heat-free removal
• Anaesthesia: Local or sacral block of prostatic tissue under general anesthesia

• Heats prostatic tissue via a specialized catheter to a temperature • Area of prostate to be resected is mapped using USG

between 45°C and 65°C • The system generates and adjusts the level of saline pressure for the controlled
ablation of the prostate tissue
• Less effective than M-TURP in reducing urinary flow long term
• Directed cautery of the resected area for hemostasis using either monopolar or
• Good alternative consideration for elderly or high-risk patients bipolar techniques

Postoperative Care
• No significant serum sodium or hematocrit changes
• Close monitoring in PACU
• Resection time is ~5 min and overall procedure time is 45 min
• Watch for signs of hyponatremia
• Improved safety profile
• Continue irrigation
• Preservation of bladder neck and tissue surrounding the
verumontanum • Measure sodium levels if e/o CNS irritation/cerebral oedema

• Preservation of normal sexual function • Postoperative pain: NSAIDs, Opioids

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Suggested Readings
• Miller’s Textbook of Anesthesia. 9th edition

• Stoelting’s Anesthesia and Co-existing disease. 6th Edition

• Clinical Anatomy by regions. Richard Snell. 8th edition

• Bailey and Love’s Short practice of Surgery. 24th edition

• Barash, Cullen, Stoelting. Clinical Anesthesia. 7th edition

• Yao & Artusio’s Anesthesiology. 7th edition

• Objective Anaesthesia Review. 3rd edition

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