Quemaduras Parte 2
Quemaduras Parte 2
Quemaduras Parte 2
doi: 10.1016/j.bjae.2022.01.001
Advance Access Publication Date: XXX
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Major burns, part 2
will undergo multiple subsequent operations including tem- may also be difficult, and suitable sites for i.v. access and
porising cadaveric autografts, xenografts (such as pig skin) or direct arterial monitoring may be limited.
synthetic dermal substitutes until skin coverage with auto- It is mandatory to monitor the patient’s core temperature.
grafts is possible (using unburned patient donor skin). Later Methods to minimise heat loss include minimising exposure,
elective surgical procedures are frequently required to help using forced air warmers and heat lamps, humidifying
restore function and improve cosmesis. anaesthetic gases, infusing warmed i.v. fluids and maintain-
ing an ambient temperature in theatre of 28e33 C.
Care should be taken to assess a patient’s ventilatory re-
Location of surgery quirements preoperatively and lung protective ventilation
Burns surgery should be carried out in a dedicated burns should be continued throughout the intraoperative period.
operating theatre, ideally in close proximity to intensive care Patients who have also suffered an inhalation injury may have
facilities. Theatre personnel should have appropriate training, increased requirements for oxygen and PEEP. For these pa-
experience and access to specialist equipment. It is vital that tients, it is particularly important to avoid alveolar der-
the theatre can be appropriately warmed in order to reduce ecruitment with the loss of PEEP during transfer to a transport
heat loss. Procedures such as dressing changes may be carried or theatre ventilator. As the hypermetabolic response suffered
out under sedation led by an anaesthetist, but all the neces- by patients with burns leads to increased oxygen consump-
sary resources to convert to general anaesthesia should be tion and carbon dioxide production, higher than expected
immediately available. oxygen concentrations and minute volumes may be required.
Blood loss can be as much as 3.4% of total blood volume for
each per cent TBSA excised.6 Bleeding risks are increased in
Preoperative assessment patients with infected burn tissue, deeper thickness burns
and by prolonged operative time. Bleeding risks may be
Assessment of a patient for burn surgery should include
reduced by using limb tourniquets on extremity burns, topical
knowledge of the extent of the burn, associated injuries and
adrenaline or compression bandages. The use of near-patient
details of the planned surgery, including positioning needed
coagulation studies such as thromboelastography may be
and estimated blood loss. Coagulopathy may be present,
superior to standard laboratory-based tests in detecting
driven by endothelial injury and the inflammatory cascade,
coagulation abnormalities and may be of value to direct blood
often exacerbated by secondary infection. Its extent can vary
product use intraoperatively.7
from subclinical changes to fulminant disseminated intra-
vascular coagulation (DIC). Therefore, the need for blood
products should be anticipated early.
Given the large volumes of i.v. fluids often required and the General vs regional anaesthesia
potential for associated renal injury, a thorough assessment Most patients with major burn injuries will require general
of circulating volume status and electrolyte abnormalities anaesthesia for surgical interventions. However, regional
should also be made. Nutritional support should generally be anaesthesia, either alone or in combination with general
continued throughout the operative period in patients who anaesthesia, may be suitable. Careful evaluation is required
have been mechanically ventilated before surgery, and fasting before performing neuraxial anaesthesia because of the
times kept to a minimum in those requiring airway increased incidence of coagulopathy and infection in this
intervention. patient group.
Airway assessment should include clinical examination
and a careful review of previous anaesthetics. Although me-
chanical ventilation may have already been established Intensive care management
before transfer to the operating theatre, particular care is
required to prevent accidental extubation, especially in pa- Fluid management
tients with airway burns or inhalation injuries. Formation of a Appropriate resuscitation with fluids is critical in the first
tracheostomy may be indicated for various reasons and is 24e48 h after a burn injury. Under-resuscitation may lead to
commonly required for patients with complex facial burns in impaired tissue perfusion, end organ damage and extension
order to maintain skin health around the mouth and nose. In of burn depth. However, giving excessive fluids is also harm-
addition, although burns involving the face or neck may not ful; risks include electrolyte disturbances such as hypona-
present any airway difficulties initially, subsequent contrac- traemia, exacerbation of tissue oedema, pulmonary and
tures may severely limit neck extension and mouth opening. cerebral oedema, and abdominal and limb compartment
Advanced techniques such as awake fibreoptic intubation syndromes.
may be indicated. A difficult airway trolley with equipment for The Parkland formula remains the most commonly used
emergency front of neck access should always be immediately tool to calculate fluid requirements. Concerns have been
available. raised that it may overestimate the volume needed, prompt-
ing bodies such as the American Burn Association to recom-
mend less than 4 ml kg1 TBSA1.8 However, we advocate
Intraoperative management
using 4 ml kg1 TBSA1 for initial calculations and then per-
Monitoring can prove challenging. Electrocardiogram elec- forming regular clinical reviews to permit escalation or de-
trodes sometimes require sutures or skin clips for reliable escalation of fluid input based on individual patient physi-
contact. Pulse oximetry and blood pressure cuff positioning ology, as opposed to rigidly adhering to any one formula.
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Major burns, part 2
CHECK
HOURLY 0.5-1 ml kg–1 h–1 Continue current fluid rate
URINE
VOLUMES
Use ml kg–1 of
IDEAL body 1-2 ml kg–1 h–1 REDUCE fluid rate by 10%
weight
*Persisting low urine output may be due to problem other than under-resuscitation.
Reassess patient using:
• Peripheral perfusion, mean arterial pressure, pulse pressure variation
• Blood lactate, haematocrit, base excess
• Cardiac output monitor
• Measure intra-abdominal pressures
Fig 1 Resuscitation protocol for resuscitation with i.v. fluids in the adult patient with burns (adapted with permission from Care of burns in Scotland [COBIS]).
Goal-directed fluid therapy therapy. The additional use of cardiac output monitoring to
The most common and easy method of ensuring appropriate guide fluid delivery in patients with major burns has
fluid resuscitation is by targeting an hourly urine output of demonstrated improvements in cardiac output, oxygen de-
0.5e1 ml kg1 ideal body weight. Failure to meet this target livery and organ dysfunction, but a mortality benefit has not
should prompt reassessment and adjustment of fluid delivery been identified.9
as detailed in Figure 1.
However, an inadequate urine output is not always caused
Choice of fluid
by volume depletion. Renal failure from acute tubular necrosis
or rhabdomyolysis can result in oliguria, as can increased Balanced crystalloids such as Hartmann’s solution are the
anti-diuretic hormone release in response to injury. Other mainstay of fluid resuscitation in major burn injuries. Their
causes such as vasoplegia, low cardiac output and abdominal use, when compared with 0.9% saline, has been demonstrated
compartment syndrome should also be considered. to reduce the incidence of significant electrolyte disturbances
Conversely, urine volumes in excess of targeted values should such as hyperchloraemic metabolic acidosis.10 The use of
prompt a reduction in the volumes of fluids given, mitigating colloids such as human albumin solution in combination with
against the phenomenon of ‘fluid creep’, whereby more fluid crystalloids may reduce overall fluid volume requirements,
than required is given. mitigate against ‘fluid creep’ and lessen increases in intra-
Peripheral perfusion, serum lactate, acidebase balance abdominal pressures compared with crystalloids alone.9 We
and haematocrit should also be used to help guide fluid recommend the addition of 4.5% human albumin solution if
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Major burns, part 2
Table 1 Formulae to calculate daily caloric requirements (kcal day1) in patients with burn injuries. TBSA, total body surface area.
HarriseBenedict Men: 66.5 þ 13.75 (weight in kg) þ 5 Multiplied by factor determined by burn
(height in cm) e 6.76 (age in yrs) size:
Women: 66 þ 9.56 (weight in kg) þ 1.85 <20% TBSA 1.5
(height in cm) e 4.68 (age in yrs) 20e40% TBSA 1.6
>40% TBSA 1.7
Toronto e4343 þ 10.5 (%TBSA) þ 0.23 (caloric Can be adjusted by activity factor:
intake in last 24 h) þ 0.84 (Harris Confined to bed: 1.2
eBenedict unadjusted) þ 114 (temp in C) Minimal ambulation: 1.3
e 4.5 (days after injury) Moderate activity: 1.4
Hangang 867.542e5.546 (age in yrs) þ 13.297 Adjusted for each post-burn day (PBD)
(weight in kg) þ 4.879 (% TBSA) e 9.844 and if mechanically ventilated (V¼1 if
(PBD) þ 500.612 (V) ventilated, V¼0 if not)
fluid resuscitation volumes in the first 24 h are projected to be of stay, improve wound healing and reduce wound in-
greater than 6 ml kg1 %TBSA1 (Fig. 1). This technique of fections.14 The British Burn Association (BBA) national stan-
‘colloid rescue’ should be continued until 48 h after the burn dards state15:
injury.
(i) Enteral nutrition should be started as soon as possible in
major burns, ideally within 6e12 h after the injury.
Thermoregulation (ii) Total body weight loss should not exceed 10% of the pa-
tient’s weight at admission.
Major burn injuries are associated with thermodysregulation,
with an initial propensity to hypothermia driven by heat and
fluid loss from the burn wounds themselves. Steps to reduce Route of nutrition
heat loss during the initial stages of resuscitation are detailed As with most critically ill patients, the enteral route is
in Part 1.2 The principles of maintaining an adequate core preferred. Postpyloric feeding may be required if gastric stasis
temperature in the operating theatre also apply to the inten- is present and impairing calorie delivery. Postpyloric feeding
sive care environment. may also help reduce the risk of aspiration, especially in pa-
Most patients with major burns will subsequently develop tients requiring multiple interventions under general anaes-
a raised core temperature. This reflects altering of the hypo- thesia. Parenteral nutrition is rarely required, but when used,
thalamic setpoint for thermoregulation by pyrogens such as caution should be exercised because of the associated risks
interleukin-1 (IL-1) and tumour necrosis factor.11,12 More including infection, overfeeding and erratic blood glucose
profound hyperthermia, with temperatures exceeding 40 C, control.
can occasionally occur and may lead to multiorgan failure.
Steps to address potentially harmful hyperthermia should be Caloric requirements
taken in patients with a core temperature above 39.5 C. The aim of nutritional support in patients with major burns is
Techniques include debulking dressings, giving antipyretics to meet the substantially increased caloric requirements in
such as paracetamol, applying ice to non-burned areas, infu- these patients while avoiding harmful overfeeding. The
sion of cooled i.v. fluids, and irrigating the bladder and complications of overfeeding include hyperglycaemia,
stomach with cold fluids. More invasive approaches such as hypertriglyceridaemia, hepatic steatosis, hypercapnoea and
intravascular heat exchange catheters or extracorporeal cir- prolonged duration of mechanical ventilation.14 Various
cuits may also need to be considered. methods have been used to assess caloric needs. The most
accurate method is indirect calorimetry, but this remains
mainly a research tool. In lieu of this, various formulae have
Nutrition
been devised to guide clinicians (Table 1).14,16 Such formulae
Basal metabolic rate can increase significantly after a burn may under- or overestimate requirements at different times
injury, more than doubling in patients with burns >40% during a patient’s admission. Given the complexities of
TBSA.13 If not addressed, this can result in loss of lean body providing optimum nutritional support, specialist input from
mass, immune compromise and impaired healing. There is a a dietician within the burns team is essential.
direct correlation between loss of lean body mass and adverse
events, including infectious complications and death.14 Macronutrients
The three main macronutrients e carbohydrates, proteins and
Timing of nutritional support lipids e provide substrates for adenosine triphosphate (ATP)
Starting enteral nutrition in the hours immediately after biosynthesis, wound repair, immune function and mainte-
injury has been shown to have beneficial effects on stress nance of lean body mass. Carbohydrates are generally the
hormones, improve gut integrity, reduce intensive care length preferred energy source, preventing a reliance on muscle
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Major burns, part 2
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Major burns, part 2
coli and Klebsiella can also cause invasive infections. Multi- for use in women and children. Oxandrolone has been used
resistant strains of pathogens including P. aeruginosa, Acine- from around Day 5 after burns, at a dose of 10 mg enterally
tobacter species and vancomycin-resistant Enterococcus (VRE) twice daily in patients with 30% TBSA burns, to minimise
are an increasing concern. Recognised risk factors include the weight loss, improve urinary nitrogen balance, increase
use of broad-spectrum antibiotics, colonisation at hospital muscle strength and reduce healing time. Some studies have
admission, need for escharotomy, prolonged hospital or shown benefits such as reduced ICU and hospital duration of
intensive care stay and multiple surgical procedures.22 Fungal stay, maintained lean body mass and improved whole body
colonisation and invasive fungal infections are also significant mass.29 Adverse events include hepatic injury with increased
problems. Fungal wound infection is independently associ- liver transaminases, renal injury and skin complications such
ated with increased mortality.23 Candida albicans is the most as cellulitis.
common pathogen, although Aspergillus and non-albicans
Candida such as Candida tropicalis and Candida krusei are
becoming more common.22 Regular clinical review and sam-
Pain management
pling of wounds and other potential sources of colonisation The pain experienced from a burn injury can be excruciating
and infection should guide antimicrobial therapy. and is often difficult to manage. Some studies suggest higher
pain scores during hospital admission are associated with
Toxic shock syndromes poorer long-term outcomes such as increased mental health
Toxin-producing strains of S. aureus can cause toxic shock problems.30 Given the complexities and challenges of effective
syndrome (TSS). Streptococcal toxic shock syndrome (STSS), pain management, a specialist pain service should be an in-
caused by group A Streptococcus, has a similar presentation. In tegral part of the burns team.15
addition to the non-specific clinical signs suggestive of
infection described previously, patients with TSS or STSS may Types of pain
also exhibit a diffuse macular rash, vomiting and diarrhoea,
thrombocytopenia, lymphopenia and deranged liver function Although the burn injury is usually the most significant source
tests. In addition to standard management of infections, an- of pain, there are many other causes. These include pain from
tibiotics that directly reduce exotoxin production, such as associated injuries, tracheal tubes, invasive lines and cathe-
clindamycin and linezolid, should be considered. The use of ters, skin autograft donor sites, pressure areas and in-
i.v. immunoglobulin has also been reported.24 terventions including position changes. Clinicians should
adopt a structured approach to management of acute burns
pain, addressing the three main types of pain: background,
Hypermetabolic and inflammatory response breakthrough and procedural pain.
Although changes in the metabolic and inflammatory
response are most pronounced in the acute phase, some Background pain
changes can persist for several years after a burn injury has Patients will experience a degree of persistent pain after a
healed.25 Changes include: burn injury and multimodal analgesia should be prescribed to
maintain adequate control. Infusions should be titrated to a
(i) Increased resting energy expenditure
targeted effect, maximising clinical benefit while avoiding
(ii) Increased serum and urine cortisol and catecholamines
unwanted adverse effects. Multiple methods for pain assess-
(iii) Increased cytokines including IL-6, IL-8 and granulocyte
ment exist including the VAS, designed for cooperative and
colony-stimulating factor (G-CSF)
communicative patients, and the Critical Care Pain Observa-
These persisting metabolic, inflammatory and immune tion Tool (CPOT) for use in the ICU.31 Non-pharmacological
changes can result in an increased risk of developing later measures such as appropriate dressings, comfortable posi-
problems (Table 2).26 Appropriate skin closure, nutritional tioning, cutaneous stimulation, acupuncture and techniques
support and analgesia are fundamental to mitigating this such as cognitive behavioural therapy and music therapy may
response. Several therapies have been proposed, some of also help alleviate this form of pain.
which are discussed further.
Breakthrough pain
Beta-blockers Breakthrough pain occurs on top of well-controlled back-
Beta-adrenergic blockade with drugs, such as propranolol, ground pain, either as an exacerbation of background pain or
suppress the catabolic effects of a burn by reducing energy originating from another source. This can be evoked, spon-
expenditure, limiting insulin resistance, preventing muscle taneous, predictable or unpredictable. It can be managed with
wasting and acting as anti-inflammatory agents. However, boluses of rapid-acting agents, increases in the rate of opioid
they must be used with caution in intensive care because of infusions or, if predictable, anticipatory doses of longer-acting
the risk of cardiovascular instability. A recent systematic re- agents.
view of the use of beta-blockers in patients with major burns
showed no benefit in terms of mortality, length of hospital Procedural pain
stay or incidence of sepsis.27 However, other studies have Procedural interventions include dressing changes and mobi-
demonstrated improved wound healing and reduced muscle lisation. Analgesic interventions should be timed appropri-
catabolism.28 ately to gain the maximum benefit from the agent being used.
Appropriate agents include opioid boluses, inhaled agents
Oxandrolone including nitrous oxide and methoxyflurane or analgosedative
Oxandrolone is an androgen receptor agonist, which stimu- agents such as ketamine. Other non-pharmacological
lates protein synthesis and muscle growth with much less methods may be beneficial, including hypnosis, virtual reality
virilising activity than testosterone, making it more suitable systems and other distraction techniques.
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Major burns, part 2
Dexmedetomidine
Dexmedetomidine is a highly selective a2 receptor agonist Declaration of interests
with both analgesic and sedative effects. It can be used in the
The authors declare that they have no conflicts of interest.
ICU as part of an analgosedative regimen, in combination
general anaesthesia, as a sedative for painful procedures and
also as an adjunct in PCA. Common adverse effects of dex- MCQs
medetomidine are bradycardia and hypotension. As recent
studies have highlighted the risk of pyrexia associated with The associated MCQs (to support CME/CPD activity) will be
dexmedetomidine use, caution is advised in the context of accessible at www.bjaed.org/cme/home by subscribers to BJA
hypermetabolism after burns.35 Education.
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Major burns, part 2
4. Gill P, Martin RV. Smoke inhalation injury. BJA Educ 2015; 21. Mun ~ oz B, Sua rez-Sa
nchez R, Herna ndez-Herna ndez O,
15: 143e8 Franco-Cendejas R, Corte s H, Magan
~ a JJ. From traditional
5. Cope O, Langohr JL. Expeditious care of full-thickness biochemical signals to molecular markers for detection of
burn wounds by surgical excision and grafting. Ann Surg sepsis after burn injuries. Burns 2019; 45: 16e31
1947; 125: 1e22 22. Norbury W, Herndon DN, Tanksley J, Jeschke MG,
6. Bhananker SM, Cullen BF, Burns, Fleisher LA, editors. Finnerty CC. Infection in burns. Surg Infect (Larchmt) 2016;
Anesthesia and uncommon diseases. 6th Edn. Philadelphia: 17: 250e5
Saunders; 2012. p. 526e36 23. Horvath EE, Murray CK, Vaughan GM et al. Fungal wound
7. Marsden NJ, Van M, Dean S et al. Measuring coagulation in infection (not colonization) is independently associated
burns: an evidence-based systematic review. Scars Burn with mortality in burn patients. Ann Surg 2007; 245: 978e85
Heal 2017; 3. 205951311772820 24. Raithatha AH, Bryden DC. Use of intravenous immuno-
8. Pham TN, Bettencourt AP, Bozinko GM et al. 2018 ABLS globulin therapy in the treatment of septic shock, in
provider manual 1. Chicago: American Burn Association; particular severe invasive group A streptococcal disease.
2017 Indian J Crit Care Med 2012; 16: 37e40
9. Guilabert P, Usúa G, Martı́n N, Abarca L, Barret JP, 25. Jeschke MG, Gauglitz GG, Kulp GA et al. Long-term
Colomina MJ. Fluid resuscitation management in patients persistence of the pathophysiologic response to severe
with burns: update. Br J Anaesth 2016; 117: 284e96 burn injury. PLoS One 2011; 6: e21245
10. Powell-Tuck J, Gosling P, Lobo DN et al. British consensus 26. Barrett LW, Fear VS, Waithman JC, Wood FM, Fear MW.
guidelines on intravenous fluid therapy for adult surgical Understanding acute burn injury as a chronic disease.
patients (GIFTASUP). BMJ 2009; 338: b2418 Burn Trauma 2019; 7: 23
11. Jeschke MG, Mlcak RP, Finnerty CC et al. Burn size de- 27. Hassoun-Kheir N, Henig O, Avni T, Leibovici L, Paul M.
termines the inflammatory and hypermetabolic The effect of b-blockers for burn patients on clinical
response. Crit Care 2007; 11: R90 outcomes: systematic review and meta-analysis.
12. Herndon DN, Tompkins RG. Support of the metabolic J Intensive Care Med 2021; 36: 945e53
response to burn injury. Lancet 2004; 363: 1895e902 28. Herndon DN, Hart DW, Wolf SE, Chinkes DL, Wolfe RR.
13. Williams FN, Herndon DN, Jeschke MG. The hypermeta- Reversal of catabolism by beta-blockade after severe
bolic response to burn injury and interventions to modify burns. N Engl J Med 2001; 345: 1223e9
this response. Clin Plast Surg 2009; 36: 583e96 29. Wolf SE, Edelman LS, Kemalyan N et al. Effects of oxan-
14. Clark A, Imran J, Madni T, Wolf SE. Nutrition and meta- drolone on outcome measures in the severely burned: a
bolism in burn patients. Burn Trauma 2017; 5: 11 multicenter prospective randomized double-blind trial.
15. British Burn Association. National standards for provision J Burn Care Res 2006; 27: 131e9
and outcomes in adult and paediatric burn care. British Burn 30. Patterson DR, Tininenko J, Ptacek JT. Pain during burn
Association; 2018. p. 1e83 (November) hospitalization predicts long-term outcome. J Burn Care
16. Rousseau AF, Losser MR, Ichai C, Berger MM. ESPEN Res 2006; 27: 719e26
endorsed recommendations: nutritional therapy in major 31. Buttes P, Keal G, Cronin SN, Stocks L, Stout C. Validation
burns. Clin Nutr 2013; 32: 497e502 of the critical-care pain observation tool in adult critically
17. Nordlund MJ, Pham TN, Gibran NS. Micronutrients after ill patients. Dimens Crit Care Nurs 2014; 33: 78e81
burn injury: a review. J Burn Care Res 2014; 35: 121e33 32. Mcguinness SK, Wasiak J, Cleland H et al. A systematic
18. Lachiewicz AM, Hauck CG, Weber DJ, Cairns BA, van review of ketamine as an analgesic agent in adult burn
Duin D. Bacterial infections after burn injuries: impact of injuries. Pain Med 2011; 12: 1551e8
multidrug resistance. Clin Infect Dis 2017; 65: 2130e6 33. Cuignet O, Pirson J, Soudon O, Zizi M. Effects of gaba-
19. Greenhalgh DG, Saffle JR, Holmes JH et al. American Burn pentin on morphine consumption and pain in severely
Association consensus conference to define sepsis and burned patients. Burns 2007; 33: 81e6
infection in burns. J Burn Care Res 2007; 28: 776e90 34. Evoy KE, Morrison MD, Saklad SR. Abuse and misuse of
20. Egea-Guerrero JJ, Martı́nez-Ferna ndez C, Rodrı́guez- pregabalin and gabapentin. Drugs 2017; 77: 403e26
Rodrı́guez A et al. The utility of C-reactive protein and 35. Grayson KE, Bailey M, Balachandran M et al. The effect
procalcitonin for sepsis diagnosis in critically burned of early sedation with dexmedetomidine on body tem-
patients: a preliminary study. Plast Surg (Oakv) 2015; 23: perature in critically ill patients. Crit Care Med 2021; 49:
239e43 1118e28
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