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464
J. L. Sparling and J. A. J. Martyn
ting of volume resuscitation), or cytokine-related
neuroinflammation [52].
Coma, delirium, seizure, or focal neurologic deficits may
develop because of these injuries. Brain imaging upon presentation may be useful to diagnose the presence of cerebral
edema and signs of elevated intracranial pressure, due to
either concomitant injuries or hypoxic damage during the
initial phase. Imaging can prompt neurologic or neurosurgical
consultation as indicated. It is further helpful to establish a
preanesthetic baseline neurologic status, when able, but this is
proven difficult for patients who present from the ICU
already receiving several sedative or analgesic infusions.
Hematologic
Following initial burn injury, prior to adequate fluid
resuscitation, patients may experience hemoconcentration,
which together with elevated plasma proteins as a component
of acute phase reactants, increase blood viscosity. The anemia
of thermal injury begins to develop approximately 2 days
following injury and is multifactorial due to a combination of
hemorrhage, hemolysis, and a decline in erythropoiesis [53].
Serial phlebotomy may also contribute. Some studies of
recombinant erythropoietin in severely burned patients have
shown a mortality benefit, while others have shown to have
impact on mortality, blood transfusion requirements, or rate
of thromboembolic complications [54]. Erythropoietin is also
posited to mitigate burn-induced muscle wasting and secondary burn progression in animal models [55, 56].
Following major burn, platelets exhibit a biphasic response.
Initially, thrombocytopenia occurs due to platelet aggregation and trapping in the lungs. Lower platelet nadirs and a
longer duration of thrombocytopenia correlate with increased
mortality. Additionally, patients are at higher risk of disseminated intravascular coagulopathy (DIC) in the first 3–5days.
Approximately 10–14days following injury, thrombocytosis
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465
occurs due to inflammation. Later fluctuations in platelet
count may be attributed to medication effect, sepsis, and dilutional effects [57].
Gastrointestinal
Acutely following burn injury, patients develop delayed
gastric emptying and ileus. Because of this, all acute burns
should be considered to have a full stomach prompting rapid
sequence intubation (RSI). Additionally, prompt
decompression of the stomach should occur, and appropriate
gastric ulcer prophylaxis should be initiated. Bowel edema
begins to resolve 2–3days following injury, and early enteral
feeding should be established to improve caloric intake,
prevent stress ulcer formation, limit the requirement for
gluconeogenesis, diminish muscle catabolism, and reduce
bacterial translocation from the gut. Early enteral feeding is
associated with reduced mortality and shorter hospitalizations
[58]. Post-pyloric (e.g., nasoduodenal or nasojejunal) feeding
tubes may be helpful in patients who do not tolerate gastric
feeds due to impaired gastric emptying from edema or opioids
[59].
Endocrine
Several endocrinologic alterations occur in patients with
severe burn. Vasopressin is highest at the time of ICU admission and correlates with the percentage TBSA affected. Atrial
natriuretic peptide (ANP) peaks around the fifth to sixth
postburn day and plays an important role in restoring intravascular fluid homeostasis. Catecholamines remain elevated
through at least the first week following injury [60].
Testosterone levels decline in the acute phase of burn, but
replacement with the testosterone analogue oxandrolone has
been demonstrated to shorten hospital length of stay, main-
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J. L. Sparling and J. A. J. Martyn
tain lean body mass, improve body composition, and increase
hepatic protein synthesis [61].
Alterations in the insulin signaling pathway occur following
severe burn, resulting in insulin resistance, altered glucose
metabolism, and hyperglycemia. These changes occur due to
increased cortisol, proinflammatory cytokines, and free radical formation [62]. Patients with larger burns, older age, and
increased body fat percentage are at higher risk for the development of insulin resistance [63].
Hypocalcemia develops in many patients with large burns
due to altered calcium and magnesium metabolism, reduced
secretion of PTH, and citrate toxicity due to blood product
administration [64]. Aggressive calcium repletion is necessary
to avoid the impaired cardiovascular function associated with
ionized hypocalcemia.
Skin
Large TBSA burns impair temperature regulation, fluid and
electrolyte maintenance and create a breakdown in the ability to physically block bacterial entry, with increased depth
of burns correlating with the degree of permeability. Body
heat may be preserved by elevating ambient temperature
and utilizing radiant and forced air warmers, plastic coverings around the extremities, reflective insulated barriers,
heat- and- moisture exchangers (HMEs) in ventilator circuits, and fluid warmers. In the chronic phase of burn injury,
contractures may occur and limit respiratory excursion,
reduce mouth opening, and make vascular access difficult.
Wound infection rates may be reduced by topical antimicrobial therapies [65].
Metabolic
Interleukin-1 (IL-1), tumor necrosis factor (TNF),
catecholamines, and stress hormones mediate the development
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of hypermetabolism in burn injury. Increased glucose, fat, and
protein metabolism lead to increased oxygen demand and
carbon dioxide production, which can be further exacerbated
by fever or neurogenic hyperthermia. Nutritional demands
are increased in burn patients, but carbohydrate-rich parenteral or enteral nutrition will further increase carbon dioxide
production and require a higher minute ventilation to maintain normal carbon dioxide balance [66]. Energy expenditure
is further increased by postoperative shivering, which may be
mitigated by meperidine or dexmedetomidine [67].
467
Psychiatric
Anesthesia clinicians should be cognizant of the psychological
trauma faced by many burn patients from both their initial
injuries and sequelae. Burn patients and their caregivers
commonly face depression, anxiety, acute stress disorder, and
post-traumatic stress disorder (PTSD) [68, 69]. These issues
should be anticipated and planned for by the anesthesia team
caring for a patient through measures such as attention to
such issues during informed consent, pharmacologic preoperative anxiolysis, and parental presence for pediatric patients
where appropriate.
Special Populations
Pediatric
Children under 16years represent 26% of admission to the
United States burn centers. They are at increased risk for
burns due to their immature motor and cognitive abilities,
inability to self-rescue, and dependence on others for supervision. Young children also have thinner dermal layers leading to deeper injury at the same temperature and exposure
duration, and the same quantity of hot liquid will affect a
larger TBSA in children due to their smaller size [70].
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J. L. Sparling and J. A. J. Martyn
Children are more susceptible to hypothermia due to the
heat loss from altered skin integrity, as they have a greater
ratio of surface area to mass. Further, the effects of hypermetabolism are accentuated due to children’s baseline
higher oxygen consumption on a weight basis. Children
have even less respiratory reserve during airway management for this reason. Difficult intravenous access in small
children is compounded in burn injury. Children may also
require general anesthesia for procedures which may be
done in the awake or less sedated adult, including dressing
changes and line changes.
Children with burn may require multiple general
anesthetics in both their acute injuries and the chronic phase
of injury, raising concern for the neurocognitive effects of
anesthetics on the developing brain [71]. Further prospective
research is needed for children with repeat exposures,
prolonged exposures, and in vulnerable populations.
Geriatric
Physical and cognitive limitations place elderly patients at
increased risk for burn and make more difficult to manage
due to the presence of medical comorbidities. In these
patients, the hypermetabolic phase of burn injury may be
delayed or absent. The increase in cardiac output may be
poorly tolerated in patients with ischemic heart disease due
to increased myocardial oxygen demand. Likewise, patients
with diastolic dysfunction may develop pulmonary edema
due to fluid resuscitation and peri-capillary leak. Medication
clearance of anesthetics, analgesics, and sedatives may also be
altered by impaired renal or hepatic function, and elderly
patients are at increased risk of delirium perioperatively. The
American Geriatrics Society recommends electroencephalographic (EEG) use during general anesthesia, regional analgesia when feasible, and optimization of non-opioid pain
medications to prevent delirium in high risk elders [72].
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Pharmacologic Considerations
Pharmacodynamics and pharmacokinetics are both affected
following major burn, i.e., those exceeding 40% TBSA.In the
initial resuscitative phase of burn injury, hypovolemia, myocardial impairment, reduced SVR, and increased blood viscosity compromise cardiac output and therefore organ
perfusion, resulting in reduced clearance [51]. However, once
the patient enters the hypermetabolic phase, usually around
48 hours after injury, provided resuscitation has been adequate, clearance may be enhanced by hepatic enzyme induction and increases in hepatic and renal blood flow depending
on the drug [51]. Edema may result in increased volume of
distribution, necessitating increased bolus doses and higher
maintenance rates of infusions. Additionally, plasma protein
concentrations are altered during both the acute and hypermetabolic phases, with a reduction in serum albumin and an
increase in α1-acid glycoprotein (AAG, an acute phase reactant). The activity of plasma protein bound drugs depends on
the unbound portion, so small changes in plasma protein
concentrations may result in large changes in the clinical
effect of a given dose. The effective (unbound) concentration
of drugs that bind albumin, such as benzodiazepines, is
increased. On the contrary, the effective (unbound) concentration of drugs that bind AAG (e.g., tricyclic antidepressants,
beta blockers, and local anesthetics) is reduced [73].
Tolerance
Receptor-mediated drug effects are altered in acute burn
injury due to the up- or down-regulation of the corresponding receptors. For instance, extrajunctional acetylcholine
receptors, specifically the α-7 acetylcholine receptors, emerge
throughout the muscle membrane following large burn.
Thus, 48–72 h following burn, patients demonstrate an
increased sensitivity to depolarizing neuromuscular relaxants and a propensity for the development of succinylcho-
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J. L. Sparling and J. A. J. Martyn
line-induced hyperkalemia. Risk factors for development of
this hyperkalemic response include the dose of succinylcholine, time since burn injury, and severity of burn [51].
Conversely, the presence of extrajunctional acetylcholine
receptors results in tolerance to the non-depolarizing neuromuscular relaxants.
Tolerance in burn patients may also develop to β-adrenergic
antagonists, such as propranolol. This tolerance is hypothesized to be related to both high levels of circulating catecholamines and increased binding to plasma AAG, as above [74].
Antibiotic clearance is often augmented in burn patients, due
to the enhanced glomerular filtration rate; this results in subtherapeutic serum levels unless larger and more frequent
doses are administered. Similarly, renal clearance of
H2-receptor antagonists is increased in the hypermetabolic
phase, requiring increased doses for prophylaxis against gastric and duodenal ulcers [51]. Both tolerance and the potential for opioid-induced hyperalgesia occur in burn patients
receiving narcotics for analgesia, yet these agents remain the
cornerstone of pain control [75]. Finally, increased doses of
intravenous anesthetics such as propofol are necessary due to
both the increased volume of distribution and increased
hepatic clearance. Caution should be exercised due to the
potential for hypotension associated with large doses, particularly in hypovolemic patients.
Multimodal Analgesia
A multimodal approach to analgesia is necessary to address
pain and anxiety in critically ill burned patients and to mitigate the risk for developing opioid-induced hyperalgesia.
This approach will require modulation over time due to
changes in sensitivity and the development of tolerance.
Opioid-induced hyperalgesia and tolerance both occur with
continuous opioid infusions and potentiate the need for
further opioids. Opioid rotation, that is substitution of one
opioid agent for alternative, can reduce opioid tolerance
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471
and is usually achievable with a ~25–50% decrease in
equivalent dose [76].
As discussed above, adjunctive acetaminophen, NMDAantagonists (e.g., ketamine), α2-antagonists (i.e., dexmedetomidine, clonidine), gabapentinoids (i.e., gabapentin,
pregabalin), and/or local anesthetics reduce overall opioid
requirements and improve pain control. Additionally, selection of methadone as an agent with both opioid and
NMDA- antagonism activity offers theoretical advantages,
but its pharmacokinetics is highly variable and has not yet
been studied in burn patients. Observational studies have
shown that early methadone initiation may reduce duration
of mechanical ventilation [77]. A meta-analysis of four
studies in burn patients concluded that dexmedetomidine,
a selective α2-antagonist, may provide deeper sedation and
prevent hypertension in burn patients [78]. With each of
these agents, pharmacokinetics depend on the phase of
burn injury and individual heterogeneity, and thus they
should be titrated based on clinical criteria and laboratory
analysis of serum concentrations, when available.
Conclusion
Anesthesia care of severely burned patients must address the
complex pathophysiologic changes affecting every organ system in burn injury. Careful attention to the pharmacologic
changes in burn is necessary to choose and dose medications
optimally for burn patients, depending on their phase of injury.
Preparation and planning for the challenges of airway management, vascular access, and analgesia will afford the best opportunity for successful closure and subsequent care of severely
burned patients. Through these efforts, anesthesia clinicians
play an essential role in the multidisciplinary burn care team.
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References
1. Woo CH, Kim SH, Park JY, Bae JY, Kwak IS, Mun SH, etal.
Macintosh laryngoscope vs. Pentax-AWS video laryngoscope:
comparison of efcacy and cardiovascular responses to tracheal
intubation in major burn patients. Korean J Anesthesiol.
2012;62(2):119–24.
2. Apfelbaum JL, Hagberg CA, Connis RT, Abdelmalak BB, Agarkar
M, Dutton RP, etal. 2022 American Society of Anesthesiologists
practice guidelines for management of the difcult airway*.
Anesthesiology. 2022;136(1):31–81.
3. Davlantes C, Puga T, Montez D, Philbeck T, Miller L, DeNoia
E. 253: 48 hours dwell time for intraosseous access: a longer-
term infusion using a temporary solution. Crit Care Med.
2016;44(12):140.
4. Guerin L, Monnet X, Teboul JL. Monitoring volume and uid
responsiveness: from static to dynamic indicators. Best Pract Res
Clin Anaesthesiol. 2013;27(2):177–85.
5. Gavelli F, Teboul J-L, Monnet X. The end-expiratory occlusion
test: please, let me hold your breath! Crit Care. 2019;23(1):274.
6. Monnet X, Marik PE, Teboul JL. Prediction of fluid
responsiveness: an update. Ann Intensive Care. 2016;6(1):111.
7. Lawrence A, Faraklas I, Watkins H, Allen A, Cochran A, Morris
S, etal. Colloid administration normalizes resuscitation ratio and
ameliorates “fluid creep”. J Burn Care Res. 2010;31(1):40–7.
8. Navickis RJ, Greenhalgh DG, Wilkes MM. Albumin in burn
shock resuscitation: a meta-analysis of controlled clinical studies.
J Burn Care Res. 2016;37(3):e268–78.
9. Palmieri TL, Greenhalgh DG.Blood transfusion in burns: what
do we do? J Burn Care Rehabil. 2004;25(1):71–5.
10. Polderman KH. Hypothermia and coagulation. Crit Care.
2012;16(Suppl 2):A20–A.
11. Oda J, Kasai K, Noborio M, Ueyama M, Yukioka T.Hypothermia
during burn surgery and postoperative acute lung injury in
extensively burned patients. J Trauma. 2009;66(6):1525–9;
discussion 9–30.
12. Hofbauer R, Moser D, Hammerschmidt V, Kapiotis S, Frass
M. Ketamine significantly reduces the migration of leukocytes
through endothelial cell monolayers. Crit Care Med.
1998;26(9):1545–9.
Chapter 22. Anesthesia forBurn Patients
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
473
13. Kharasch ED.Current concepts in methadone metabolism and
transport. Clin Pharmacol Drug Dev. 2017;6(2):125–34.
14. Unlugenc H, Gunduz M, Guler T, Yagmur O, Isik G.The effect of
pre-anaesthetic administration of intravenous dexmedetomidine
on postoperative pain in patients receiving patient-controlled
morphine. Eur J Anaesthesiol. 2005;22(5):386–91.
15. Frestadius A, Grehn F, Kildal M, Huss F, Fredén F. Intranasal
dexmedetomidine and rectal ketamine for young children
undergoing burn wound procedures. Burns. 2022;48(6):1445–51.
16. Shank ES, Sheridan RL, Ryan CM, Keaney TJ, Martyn
JA.Hemodynamic responses to dexmedetomidine in critically
injured intubated pediatric burned patients: a preliminary study.
J Burn Care Res. 2013;34(3):311–7.
1 7. Verret M, Lauzier F, Zarychanski R, Perron C, Savard X,
Pinard A-M, etal. Perioperative use of gabapentinoids for the
management of postoperative acute pain: a systematic review
and meta- analysis. Anesthesiology. 2020;133(2):265–79.
18. Cavalcante AN, Sprung J, Schroeder DR, Weingarten
TN. Multimodal analgesic therapy with gabapentin and its
association with postoperative respiratory depression. Anesth
Analg. 2017;125(1):141–6.
19. Myhre M, Diep LM, Stubhaug A. Pregabalin has analgesic,
ventilatory, and cognitive effects in combination with
remifentanil. Anesthesiology. 2016;124(1):141–9.
20. Bussolin L, Busoni P, Giorgi L, Crescioli M, Messeri A.Tumescent
local anesthesia for the surgical treatment of burns and postburn
sequelae in pediatric patients. Anesthesiology. 2003;99(6):1371–5.
21. Horlocker TT, Vandermeuelen E, Kopp SL, Gogarten W,
Leffert LR, Benzon HT. Regional anesthesia in the patient
receiving antithrombotic or thrombolytic therapy: American
Society of Regional Anesthesia and Pain Medicine evidencebased guidelines (Fourth Edition). Reg Anesth Pain Med.
2018;43(3):263–309.
22. Maybauer MO, Asmussen S, Platts DG, Fraser JF, Sanfilippo
F, Maybauer DM. Transesophageal echocardiography in the
management of burn patients. Burns. 2014;40(4):630–5.
23. Etherington L, Saffle J, Cochran A. Use of transesophageal
echocardiography in burns: a retrospective review. J Burn Care
Res. 2010;31(1):36–9.
24. Haskins SC, Bronshteyn Y, Perlas A, El-Boghdadly K,
Zimmerman J, Silva M, et al. American Society of Regional
Anesthesia and Pain Medicine expert panel recommendations
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