Fleisher: Anesthesia and Uncommon Diseases, 5th ed.

CHAPTER 18 – Burns

Sanjay M. Bhananker, MD,
Bruce F. Cullen, MD

  

 

Pathophysiology

  

 

Mediators of Inflammation

  

 

Cardiovascular Changes

  

 

Metabolic Changes

  

 

Hematologic Changes

  

 

Renal Function

  

 

Pharmacologic Changes

  

 

Inhalation Injury

  

 

Preoperative Preparation

  

 

Fluid Resuscitation

  

 

Fasting Requirements

  

 

Intraoperative Consideration

  

 

Surgical Procedure

  

 

Anesthetic Technique

  

 

Special Considerations for Pediatric Burns

  

 

Procedural Sedation

  

 

Conclusion

Perioperative management of patients with severe burn injuries offers significant challenges to the anesthesiologist. It is estimated that every year approximately 1.25 million burn injuries are treated in the United States, up to 100,000 of which require hospitalization. Over 6,500 patients succumb to their thermal injuries.[1] A better understanding of the pathophysiology of burn injuries, coupled with advances in burn resuscitation, critical care, and surgical practice, has resulted in improved survival in severely burned patients over the past 3 decades. [2] [3] [4] [5]

An expert task force of the American Burn Association (ABA) has developed a set of evidence-based guidelines for the management of acute burn injury. These guidelines summarize the current scientific basis of the clinical practice for the management of acute burn injury and have been published as a special supplement to the May/June 2001 issue of Journal of Burn Care & Rehabilitation.6

Modern care for the severely burned patient can be divided into four overlapping phases: (1) initial evaluation and resuscitation, (2) initial excision and biologic closure, (3) definitive wound closure, and (4) rehabilitation and reconstruction.[7] The anesthesiologist's services may be called on for airway management, intravenous access, and fluid resuscitation, in addition to providing sedation and analgesia in the acute phase. Administration of analgesia and sedation for wound care and provision of anesthesia for excision and grafting are even more challenging tasks. Reconstructive surgery poses special challenges due to development of contractures, making airway management and positioning difficult.

PATHOPHYSIOLOGY

The primary determinants of severity of burn injury are the size and depth of the burn. However, patient age, body part burned, presence of preexisting disease, and associated non-burn injuries have an important impact on the outcome. [3] [4] [5] The size of the burn is most commonly estimated in adults by using the “rule of nines” and expressed as percentage of total body surface area (%TBSA) ( Fig. 18-1 ). [8] [9] The burn depth is classified into superficial, partial thickness, and full thickness ( Table 18-1 ). First-degree (superficial) burns affect only the epidermis and are characterized by erythema and edema of the burned areas without blistering or desquamation. These are treated with daily dressing and wound care until epithelialization occurs. Second-degree (partial-thickness) burns involve the epidermis and a portion of the dermis. In most cases, these wounds can be expected to spontaneously heal in 1 to 4 weeks, although surgical treatment may be necessary for extensive or deep second-degree burns. Pain is characteristic of partial-thickness burns. Third-degree (full-thickness) burns extend entirely through both the epidermis and dermis and will not heal spontaneously.[10]

 
 

FIGURE 18-1  Rule of nines to estimate the percentage of body surface area.

 

 


TABLE 18-1   -- Classification of Burn Depth

Classification

Burn Depth

Outcome

Superficial (first degree)

Epidermis only

Heal spontaneously

Partial thickness (second degree)

Epidermis and dermis

 

Full thickness

 

 

 Third degree

Destruction of epidermis and dermis

Wound excision and grafting necessary

 Fourth degree

Fascia, muscle, bone burned

Complete excision required, functional limitation likely

 


Mediators of Inflammation

Severe burn injury results in release of circulating mediators that evoke a physiologic response (systemic inflammatory response syndrome [SIRS]) throughout the body ( Fig. 18-2 ).[11] These mediators include histamine,[12] serotonin,[13] cytokines,[14] tumor necrosis factor-α,[15] endotoxin, [16] [17] [18] oxygen-derived free radicals, [19] [20] [21] nitric oxide,[22] and complement. [23] [24]

 
 

FIGURE 18-2  Pathophysiology of burns.

 

 

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Fleisher: Anesthesia and Uncommon Diseases, 5th ed.

Copyright © 2005 Saunders, An Imprint of Elsevier

Cardiovascular Changes

There is an increase in capillary permeability and “third spacing” of fluid in tissues surrounding the burn. Interstitial edema and organ dysfunction in distantorgans result from combination of the vasoactive mediators and hypoproteinemia in severe burns. [25] [26] Increased capillary permeability is seen in the burned tissue for more than 72 hours and in the non-burned tissue for up to 24 hours.[27] Tumor necrosis factor-α, oxygen free radicals, and endothelin-1 exert a negative inotropic effect and reduce the cardiac output acutely. The cardiovascular response to both endogenous and exogenous catecholamines is attenuated owing to decreased adrenergic receptor affinity and decreased production of second messenger. Systemic vascular resistance increases in the initial post-burn period.

Later, following successful resuscitation, in the hypermetabolic phase the cardiovascular response is an increased cardiac output and reduced systemic vascular resistance.

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Metabolic Changes

Up to a 10-fold increase in circulating levels of catecholamines has been demonstrated after severe burn injury. [28] [29] These, along with wound-released mediators, hormones, and bacterial products from the gut and wound result in SIRS, manifested as hyperdynamic circulation and large increases in basal energy expenditure (hypermetabolic response). [7] [27] [29] The secretion of glucagon and cortisol are increased and, together with post-injury insulin resistance, result in the use of amino acids to fuel production, with consequent muscle wasting and nitrogen imbalance.[25] The supraphysiologic thermogenesis is associated with resetting of the core temperature to higher levels, proportional to the size of the burns. [30] [31] Damaged skin is no longer able to retain heat and water, and the vasomotor thermoregulatory responses are impaired. Consequently, large evaporative losses ensue. [31] [32] Loss of barrier function of skin and blunting of immune response result in increased susceptibility to infection and bacterial overgrowth within the eschar. [26] [31] [33] [34] Adequate pain control, alleviation of anxiety, maintenance of a thermoneutral environment, and treatment of infection are important steps in limiting catecholamine secretion and thus hypermetabolism.

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Hematologic Changes

Hematologic and coagulation factor changes after burn injury depend on the magnitude of burn injury and time from injury. Hematocrit is typically maintained early in the post-burn period but drops during the weeks of care as erythrocyte half-life is reduced. [27] [35] Platelet count diminishes as a result of formation of microaggregates in the skin and smoke-damaged lung, although this is rarely a clinical problem. Both the thrombotic and fibrinolytic mechanisms are activated after major burns. [35] [36] Clinically, hypercoagulability may be a problem in late post-burn injury period and patients should receive thromboembolism prophylaxis.

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Renal Function

The incidence of acute renal failure in burn patients ranges from 0.5% to 38%, depending on the severity of burns. [37] [38] In the early post-burn period, the renal blood flow is reduced as a result of hypovolemia and decreased cardiac output. In addition, increased levels of catecholamines, angiotensin, vasopressin, and aldosterone contribute to renal vasoconstriction.[39] Myoglobinuria and sepsis can also aggravate renal dysfunction. Despite an increase in the renal blood flow during the hypermetabolic phase of burn injury, tubular function and creatinine clearance may be reduced and renal function may be variable.

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Pharmacologic Changes

Burn injury also affects the pharmacodynamic and pharmacokinetic properties of many drugs. A decreased level of serum albumin in these patients leads to increased free fraction of acidic drugs such as thiopental or diazepam, whereas an increased level of α-acid glycoprotein results in decreased free fraction of basic drugs (with pKa > 8) such as lidocaine or propranolol.[31] Renal and hepatic functions may be impaired in patients with large burns, and this may impair the elimination of some drugs, whereas increases in renal blood flow and glomerular filtration rate in the hyperdynamic phase of burns may enhance the renal excretion of drugs. It has been shown that some drugs such as gentamicin may be lost through the open wounds.[40] The response to muscle relaxants (other than mivacurium) is altered owing to proliferation of acetylcholine receptors away from the synaptic cleft of the neuromuscular junction (see later). Pharmacokinetics of morphine are unchanged after burn injury.[41] Although lorazepam has an increased volume of distribution, increased clearance, and a reduced half-life,[42] the elimination half-life of diazepam is significantly prolonged in burn patients.[43]

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Inhalation Injury

Most airway inhalation injuries are due to inhalation of smoke. A history of closed space exposure to hot gases, steam or smoke, singed nasal vibrissae, carbonaceous sputum, or elevated levels of carboxyhemoglobin or cyanide all point toward the clinical diagnosis. [6] [26] Inhalation injury is a predictor of increased morbidity and mortality in burn victims. [44] [45] [46]

Upper Airway Injury

Direct thermal injury to the subglottic airway is rare, unless superheated air or steam is inhaled. The severity of inhalation injury depends on the fuels burned, intensity of combustion, duration of exposure, and confinement. Unless steam is involved, heat injury to the airway is supraglottic, causing swelling of the posterior pharynx and supraglottic regions, leading to potential upper airway obstruction. The natural history of upper airway inhalation injury is edema formation that narrows the airway over the initial 12 to 48 hours. Early tracheal intubation is recommended in patients who present with stridor, wheeze, or voice changes. Burns to the face and neck can result in tight eschar formation, which when combined with pharyngeal edema can cause difficult airway management.

Lower Airway Injury (Smoke Inhalation Injury)

Lower airway or pulmonary parenchymal damage results from inhalation of the chemical constituents of smoke, usually becoming apparent 24 to 72 hours after the injury. Findings include dyspnea, rales, rhonchi, and wheezing. Gas phase constituents of smoke include carbon monoxide (CO), cyanide, hydrochloric acid, aldehyde gases, and oxidants. These can cause direct damage to mucociliary function and bronchial vessel permeability, as well as produce bronchospasm, alveolar destruction, and pulmonary edema. Small airway occlusion results from endobronchial sloughing and resultant debris, whereas alveolar, interstitial, and chest wall edema may cause intrapulmonary shunting and reduction in compliance. [26] [47] The risk of pulmonary infection and barotrauma is also increased. The clinical picture is identical to that of acute respiratory distress syndrome (ARDS). Delayed ARDS (6 to 10 days post burn) may also develop in the absence of inhalation injury in burn victims.[48] Bronchoscopy reveals carbonaceous endobronchial debris and/or mucosal ulceration. [49] [50] The usefulness of serial chest radiographs or of radioisotope scanning with xenon or technetium for diagnosis and predicting prognosis is questionable. [6] [51] [52] Meticulous pulmonary toilet is the cornerstone of early care. Tracheal secretions are often very viscous and may contain carbonaceous particles and pieces of mucous membrane.

Carbon Monoxide and Cyanide Poisoning

Carbon monoxide has a high affinity for hemoglobin (250 times more than oxygen) and can interfere with oxygen delivery to the tissues at higher concentrations. Administration of 100% oxygen reduces the half-life of carboxyhemoglobin from 2.5 hours to 40 minutes and facilitates the elimination of CO.[53] Hyperbaric oxygen therapy has limited indications owing to the logistical challenges presented by transport of patients with concomitant burns to such chambers. [54] [55] Cyanide causes tissue hypoxia by uncoupling oxidative phosphorylation in mitochondria. Treatment with sodium nitrite, sodium thiosulfate, hydroxocobalamin, or dicobalt edetate should be considered for cyanide poisoning in patients with unexplained severe metabolic acidosis associated with elevated central venous O2 (therefore patients are clinically not cyanotic), normal arterial O2content, and low carboxyhemoglobin.[56]

Signs such as hyperthermia, tachycardia, leukocytosis, and tachypnea cannot be used to diagnose sepsis in burn victims. Other identifiers, such as thrombocytopenia,[57] enteral feeding intolerance,[58] and hyperglycemia have been used instead.

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PREOPERATIVE PREPARATION

The preoperative evaluation of burn patients should take into account the continuum of pathophysiologic changes due to burns. Patient age, %TBSA burned, depth of burns, time after injury, sites and extent of planned excision and donor areas, presence of infection, other injuries (especially inhalation injury), and the presence and extent of comorbidities should all be assessed.

Careful assessment of airway should be made using the usual bedside tests. Mallampati class, thyromental distance, head, neck and jaw mobility, presence of facial or airway burns (or edema), and contractures of face and neck should be looked for and used to plan the perioperative airway management technique. When there is potential for airway complications, a difficult airway cart containing a range of various-sized endotracheal tubes, Eschmann stylet, laryngeal mask airways (LMAs), Fastrach LMA, fiberoptic bronchoscope, and fiberoptic stylets should be available.

Fluid Resuscitation

The widely quoted Baxter (Parkland) formula for initial fluid resuscitation of burn victims is 4 mL of Ringer's lactate per kilogram of body weight per %TBSA burned, with one half to be given during the first 8 hours after injury and the rest in the next 16 hours.[59] Hypertonic saline may be useful in early shock, [60] [61] and colloids are most effective when used in the 12- to 24-hour period of resuscitation.[6] [62] It is widely believed that the Parkland formula underestimates resuscitation volumes, particularly when concomitant smoke inhalation is present. [59] [63] Repeated bedside observations and clinical evaluations are useful to judge the adequacy of resuscitation. Normal mentation, stable vital signs, and urine output of 30 to 50 mL/hr can be used as end points,[6] whereas use of core-periphery temperature gradient may be unreliable.[64] However, several studies have shown advantages to invasive hemodynamic monitoring (with pulmonary artery catheter) in adults with serious burns who do not respond as expected to fluid resuscitation. [65] [66] Serial lactate levels,[67] monitoring the base deficit, [68] [69] and optimization of intrathoracic blood volumes (ITBV)[70] have also been shown to be useful guides to successful resuscitation ( Table 18-2 ).

TABLE 18-2   -- Critical Questions to Ask Patients and/or Primary Medical Doctor

  

 

Mechanism of injury, % body surface area burned and depth of burns

  

 

Closed space confinement, black sputum

  

 

Elapsed time from injury

  

 

Adequacy of resuscitation

  

 

Extent of planned excision, location of burn areas to be excised and donor areas

  

 

Surgical position, need for intraoperative change of positions

  

 

Pain scores, 24-hour analgesic requirements

  

 

Associated injuries

  

 

Coexisting diseases

 

 

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Fasting Requirements

Metabolic complications in burn patients are directly related to extent of burn. Thermal injury leads to hypermetabolism and protein hypercatabolic state. Early postpyloric enteral feeding, which can be continued in the perioperative period, is recommended by the evidence-based guidelines of the ABA.[6] Early institution of enteral feeding in these patients decreases infections and sepsis,[71] improves wound healing and nitrogen balance, [72] [73] and reduces stress ulceration and duration of hospitalization. [74] [75] Gastric emptying may not be delayed in burn patients,[76] and gastric acid production may actually be reduced in the early post-burn period.[77] The safety and advantages of perioperative enteral feedings have been reported by Jenkins and colleagues.[78] At our institution, we continue enteral feedings throughout the perioperative period in patients who come to the operating room intubated. In nonintubated patients, shorter fasting times (typically 2 to 4 hours) may be acceptable. [27] [79]

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INTRAOPERATIVE CONSIDERATIONS

Burn patients could present for five types of surgical procedures: (1) decompression procedures such as escharotomy or laparotomy, (2) excision and biologic closure of burn wounds, (3) definitive closure procedures, (4) burn reconstructive procedures, or (5) general supportive procedures such as gastrostomy or line placement.[80]

Surgical Procedure

The need and timing for surgery is determined primarily by the size of injury. The objective is to identify, excise, and achieve biologic closure of all full-thickness burns. The advantages of early excision and grafting (within 1 to 5 days after burn injury) include reduction in incidence of septic episodes, reduced hospital stay, and increased survival rates. [81] [82] [83] [84] [85] [86] Extensive burns may need staged excision to limit the physiologic insult of one massive surgery and to allow autologous skin grafts to be available. Excision and grafting involves “tangential excision” of the second-degree burn wound, in which the eschar is shaved off from the burn until a plane of viable tissue is reached, followed by covering the excised wound with a split-thickness skin graft, allogeneic skin from cadavers, or skin substitutes such as Integra.[87] Excision of third-degree burns requires “fascial excision,” where the overlying burned skin and subcutaneous fat are excised down to muscle fascia.

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Anesthetic Technique

General anesthesia, with the combination of an opioid, muscle relaxant, and a volatile agent, is the most widely used technique for burn excision and grafting.[27] Succinylcholine administration to patients more than 24 hours after burn injury is unsafe, owing to the risk of hyperkalemic ventricular dysrhythmias.[88] The time frame during which succinylcholine must be avoided after a burn begins 48 hours after the event.[89] Patients who have been bedridden because of severity of illness or concomitant disease or injury, or those receiving prolonged muscle relaxant therapy to facilitate mechanical ventilation, may be particularly vulnerable.[90] The exact period of risk is unknown, but a duration of 6 months can be considered the absolute minimum.[91] This is because of proliferation and spread of acetylcholine receptors (AChR) throughout the skeletal muscle membrane under the burn and at sites distant from the burn injury.[92] The upregulation of acetylcholine receptors, along with altered protein binding, especially to α1-glycoprotein, makes patients with thermal injury resistant to the action of nondepolarizing muscle relaxants. [93] [94] [95] In these patients, larger doses of nondepolarizing muscle relaxants may be required to achieve a given degree of neuromuscular blockade, the onset of paralysis may take longer, and the duration of paralysis may be shorter. The resistance is usually seen in patients with greater than 30% TBSA burns; it develops after the first week of injury and peaks at 5 to 6 weeks post injury. [94] [96] Mivacurium may be immune to this resistance, possibly as a result of decreased metabolism of the drug from depressed pseudocholinesterase activity in burn patients. [97] [98]

Airway Management

Airway management in burn patients can be challenging. Mask ventilation may be a problem with facial burns. Successful use of an LMA for burn surgery has been reported. [99] [100] However, major procedures in critically ill patients, with frequent intraoperative changes in patient position, are best done with endotracheal intubation. Awake fiberoptic intubation may be indicated if difficulties for intubation and/or ventilation are identified preoperatively. Inhalation induction, maintenance of spontaneous respirations, and intubation with fiberoptic guidance or Fastrach LMA may be advocated in uncooperative patients.

Location of burns and donor skin sites indicate the need for special positioning, for repositioning the patient during operation, or both. Fixing the endotracheal tube for prone positioning in the presence of facial burns is best achieved by wiring it to the teeth or stitching it to the nares.[101] We commonly use dental floss to tie the tube to the teeth or tie the tube to an oronasal loop of rubber catheter. A combination of prolonged prone positioning and relatively high fluid volume administration may cause significant airway swelling. It is best to wait until an air leak is present around the endotracheal tube before tracheal extubation, because this indicates resolution of edema, especially in older children. [102] [103] If there is still no air leak and the patient is deemed ready for tracheal extubation, direct laryngoscopy may be necessary to determine the extent of residual edema. Once extubated, the patient should be closely monitored for progressive airway obstruction during the subsequent 24 to 48 hour.

Depending on the age of the burns, edema, scarring, or contractures may narrow the mouth opening and limit the neck movements. Surgical release of neck contractures to facilitate intubation has been described in both elective and emergency settings. [104] [105]

Analgesia

Severe pain is an inevitable consequence of a major burn injury, and perioperative analgesic requirements are frequently underestimated. [106] [107] Anxiety and depression are common components in a major burn and can further decrease the pain threshold. Perioperative pain management should be based on an understanding of the types of burn pain (acute or procedure-related pain versus background or baseline pain), frequent patient assessment by an acute pain service team, and the development of protocols to address problems such as breakthrough pain.

High-dose opioids are needed to manage pain associated with burn procedures, and morphine is currently the most widely used drug.[108] The pharmacokinetics of morphine are similar in burned patients and control subjects.[41] It has been shown that provision of adequate analgesia using morphine reduces the risk of post-traumatic stress syndrome.[109] Most burned patients rapidly develop tolerance to opioids. There is an interindividual variation in response to morphine, so “titration to effect” and frequent reassessment are important.

Fentanyl is also a useful analgesic perioperatively. Continuous infusion of fentanyl in the preoperative period may induce a rapid tolerance in burn patients.[110]

Methadone has the advantage of N-methyl-d-aspartate (NMDA) receptor antagonist activity, which helps in preventing the development of central sensitization, secondary hyperalgesia, and neuropathic pain.[10] In addition, the long duration of action helps in achieving postoperative analgesia and it can be administered orally in the postoperative period.

Nonsteroidal anti-inflammatory agents reduce pain perception and modify the systemic inflammatory response through inhibition of cyclooxygenase. The incidence of gastric ulceration, increased operative blood loss, and exacerbation of asthma is reduced with the use of selective cyclooxygenase-2 inhibitors. However, potential for renal tubular dysfunction does exist. These drugs have not yet been systematically evaluated in burn patients.

Acetaminophen is a useful adjunctive analgesic in combination with opioids. Its antipyretic action is particularly useful in burn patients. Doses of 15 mg/kg can be given orally or rectally every 6 hours to a maximum of 4 g/day. Liver function tests and acetaminophen levels should be checked weekly in patients receiving long-term therapy.

Tumescent local anesthesia with maximal dose of 7 mg/kg lidocaine has been shown to be safe and to be the sole possible effective locoregional anesthesia technique for the surgical treatment of pediatric burns.[111] Postoperative pain from split-skin donor sites is often more intense than the pain at the grafted site. Addition of bupivacaine or lidocaine to the “Pitkin solution” (subcutaneous crystalloid injection) can provide analgesia for pain originating from the donor areas. [112] [113] A continuous fascia iliaca compartment block can also be used to reduce the pain at the thigh donor site.[114] Intravenous lidocaine (1 mg/kg) has been reported to provide significant postoperative analgesia for up to 3 days.[115]

Ventilation

Mechanical ventilation is necessary for patients with respiratory complications, inhalation injury, or large burns. Hypermetabolic state after burn injury increases the carbon dioxide production, and these patients need higher minute ventilation to maintain normocapnia. In patients who have acute lung injury and need high levels of positive end-expiratory pressure (PEEP > 15 cm H2O) or peak inspiratory pressure (PIP > 50 cm H2O) to maintain gas exchange, use of sophisticated intensive care ventilator and anesthesia maintenance using total intravenous anesthesia technique (TIVA) may be warranted.

Regional Anesthesia

Regional anesthesia alone or in combination with general anesthesia can be used in patients with small burns or for reconstructive procedures. For procedures on lower extremities, lumbar epidural or caudal catheters can be used to provide intraoperative and postoperative analgesia. The greatest limitation to the use of regional techniques is the extent of surgical field; most patients with major burns have a wide distribution of injuries and/or need skin harvesting from areas too large to be blocked by a regional technique. The presence of a coagulopathy or systemic or local infection may also contraindicate regional anesthetic techniques in these patients.

Monitoring

Monitoring for burn surgery should be based on knowledge of the patient's medical condition and the extent of surgery. Standard electrocardiographic electrodes may not adhere to burned surfaces. Needle electrodes or alligator clips attached to skin staples may be effective alternatives. If skin sites for pulse oximetry monitoring are limited, the ear, nose, tongue, or penis can be used with standard probes.[116]The alternative is to use reflectance pulse oximetry.

Arterial line placement allows repeated blood sampling for estimation of gas tensions, hematocrit, electrolytes, lactate, and coagulation profiles, in addition to continuous blood pressure monitoring. The decision to use invasive monitoring such as a central venous or pulmonary artery catheter should be based on coexisting medical conditions or burn-related complications. Core temperature (bladder or esophageal), urine output, and degree of neuromuscular blockade should be routinely monitored.

Hypothermia is a common complication of excision and grafting and often delays extubation. Body temperature is best maintained by a thermoneutral environment (room temperature of 28° to 32°C) with the additional use of an over-bed warming shield and warming of intravenous fluids.[85] Dry-air warmers used directly over the burn wound can cause tissue desiccation. Forced air warming devices are less effective in these patients because of the significant area of burned and donor skin sites that must remain exposed. Use of “space blankets” (aluminum foil coverings on nonexposed areas), plastic sheets over the head and face, heat and moisture exchangers in the breathing system, and low fresh gas flow with circle absorber can also help to reduce the heat loss.[31]

Blood Loss and Transfusion Requirements

Burn excision can result in massive and sudden blood loss[117] that increases with delay to primary burn excision, with a peak at 5 to 12 days after burn injury. [118] [119] Other factors that correlate with increased blood loss include older age, male sex, and larger body size; area of full-thickness (third-degree) burn; high wound bacteria counts (derived from quantitative tissue cultures); total wound area excised; and operative time.[118] A mean blood loss of 2.6% to 3.4% of a patient's blood volume for each %TBSA excised has been reported in the literature. [120] [121]

Several techniques have been used to reduce blood loss during primary burn excision. Intraoperative tourniquet use on burned extremities reduces overall blood loss. [122] [123] [124] Postexcision compression dressings and topical epinephrine have been used to reduce blood loss during excision and grafting procedures. Application of bandages soaked in 1:10,000 epinephrine after excision of burned skin and/or use of thrombin spray, fibrin sealant, or platelet gel is effective in producing a bloodless surface for placement of skin grafts. [85] [125] [126] Extremely high levels of catecholamines in the blood have been measured after the use of this technique. Sinus tachycardia and/or hypertension are common, and hence heart rate and blood pressure cannot be used to reliably titrate anesthetic or analgesic agents. Serious dysrhythmias are fortunately rare. [127] [128]

Subcutaneous crystalloid is injected in generous amounts using pressure-bags and Pitkin syringes (tumescent technique) to facilitate donor skin harvesting and reduce blood loss. Epinephrine and/or local anesthetics such as bupivacaine or lidocaine may be added to this. [112] [126] [129] [130]

Quantifying blood loss is typically difficult in burn patients,[121] and transfusion is best guided by serial hematocrit estimations. Adequate venous access is a prerequisite to burn excision and grafting procedures. At least two intravenous access routes should be established (peripheral or central), and these lines should be sutured securely to prevent accidental dislodgment while positioning. Blood products should be readily available before excision begins. Femoral venous catheters placed through burned skin have been shown to be safe,[131] although this issue has been questioned.[132] The decision to transfuse blood products should be individualized by carefully weighing the risks of transfusion, including immunosuppression, versus the benefits of correcting anemia in the setting of hypermetabolism and increased oxygen demands. If blood loss is excessive, it is prudent to rule out coagulation abnormalities. Burned patients have a consumption coagulopathy that, in combination with hemodilution during operation, results in a clinically significant deficiency of coagulation factors II, VII, and X, in spite of reactive elevation of coagulation factor VIII and fibrinogen.[133] Platelets or coagulation factors may need to be replaced, guided by the coagulation profile.

Although infrequently used in current clinical practice, intraoperative blood salvage in excisional burn surgery, using a cell saver, has been shown to recover more than 40% of shed red blood cells with acceptable levels of bacterial contamination and inflammatory mediators. [134] [135]

A list of things to prepare for burn excision and grafting is presented in Table 18-3 . The agent suxamethonium is contraindicated in a patient with burns.

TABLE 18-3   -- Things to Prepare for Burn Excision and Grafting

  

 

Difficult airway cart, umbilical tape, dental floss, wire for suturing tube

  

 

Operating room warmed to 28° to 32°C, fluid warmer, radiant heat warmer

  

 

Availability of blood products

  

 

Adequate intravenous access; consider invasive monitorings

 

 

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SPECIAL CONSIDERATIONS FOR PEDIATRIC BURNS

Nearly one third of burn admissions and burn deaths occur in children below 15 years of age. Burns are second only to motor vehicle crashes as the leading cause of death in children older than 1 year. Flame burns account for about a third of pediatric burns, are often more severe, and frequently involve concomitant inhalation injury. Children younger than 2 years of age have high surface area to body mass ratios, extremely thin skin, and minimal physiologic reserves, causing higher morbidities and mortalities than in the older age groups. The possibility of child abuse must always be considered in this age group.

The disproportionate ratio of head to body size makes the rule of nines (to estimate TBSA) not applicable in small children. Lund-Browder or Berkow charts divide TBSA into smaller units and make age-appropriate corrections ( Table 18-4 ). [9] [26] When calculating fluid resuscitation volumes, allowances should be made for daily maintenance fluids in infants and toddlers. Adequate resuscitation is reflected by normal mentation, stable vital signs, and a urine output of 1 to 2 mL/kg/hr. Infants should be monitored for signs of fluid overload and hyponatremia/hypernatremia, because their immature kidneys may not be able to handle excessive fluid and electrolyte load. Blood glucose levels should be monitored, and glucose-containing solutions added as necessary, in infants.

TABLE 18-4   -- Berkow Chart for Estimating TBSA Burned in Various Age Groups

Area

1 Yr

1-4 Yr

5-9 Yr

10-14 Yr

15 Yr

Adult

Head

19

17

13

11

9

7

Neck

2

2

2

2

2

2

Anterior trunk

13

13

13

13

13

13

Posterior trunk

13

13

13

13

13

13

Right buttock

2.5

2.5

2.5

2.5

2.5

2.5

Left buttock

2.5

2.5

2.5

2.5

2.5

2.5

Genitalia

1

1

1

1

1

1

Right upper arm

4

4

4

4

4

4

Left upper arm

4

4

4

4

4

4

Right lower arm

3

3

3

3

3

3

Left lower arm

3

3

3

3

3

3

Right hand

2.5

2.5

2.5

2.5

2.5

2.5

Left hand

2.5

2.5

2.5

2.5

2.5

2.5

Right thigh

5.5

6.5

8

8.5

9

9.5

Left thigh

5.5

6.5

8

8.5

9

9.5

Right leg

5

5

5.5

6

6.5

7

Left leg

5

5

5.5

6

6.5

7

Right foot

3.5

3.5

3.5

3.5

3.5

3.5

Left foot

3.5

3.5

3.5

3.5

3.5

3.5

Total

100

100

100

100

100

100

 

 

In children requiring high inspiratory pressures during mechanical ventilation, a cuffed endotracheal tube may be a better choice. The small internal diameter of pediatric airway and endotracheal tubes increases the risk of obstruction by the thick secretions or edema, especiallyin the presence of inhalation injury. Frequent suctioning helps in clearing the mucus and debris from the tracheal tree, and a high index of suspicion should be maintained for plugging of the tracheal tube. A substantial portion of subcutaneous crystalloid fluid injected for tumescent technique to harvest skin graft may be absorbed into the circulation and may cause hypervolemia in small children. Thermal maintenance is critical in young children, especially those with burns of more than 10% TBSA.

Procedural Sedation

Procedures such as dressing changes, wound care, and physical therapy frequently require sedation and analgesia in pediatric burn patients. These procedures are often performed on a daily basis on the burn ward, making involvement of an anesthesiologist impractical.

Nurse-administered opioids (intravenous, oral, or transmucosal), alone or in combination with benzodiazepine anxiolysis, is the typical regimen. However, when wound care procedures are extensive, particularly in children, more potent anesthetic agents may be of benefit. Patient monitoring must be appropriate to the level of sedation, as required by the Joint Commission on the Accreditation of Healthcare Organizations and described by the American Society of Anesthesiologists guidelines for sedation monitoring.

Oral transmucosal fentanyl citrate lozenges have been shown to be safe and effective for pediatric burn wound care.[136] The starting dose for fentanyl lozenges is 10 μg/kg. Peak effect occurs after 20 to 30 minutes. About 25% of the total dose is systemically available after buccal absorption. The remaining 75% is swallowed and is slowly absorbed from the gastrointestinal tract. Up to a third of this (25% of total dose) avoids hepatic first-pass metabolism and is systemically available.[137]

Ketamine offers the advantage of stable hemodynamics and analgesia and has been used extensively as the primary agent for both general anesthesia and analgesia for burn dressing changes. [138] [139] [140]Nitrous oxide with oxygen has been used effectively for analgesia during burn wound dressing changes. [140] [141] However, scavenging of the gas when administered outside of an operating room is problematic. Combination of nitrous oxide with opioids may induce a state of general anesthesia with profound respiratory depression. The efficacy of general anesthesia administered by an anesthesiologist for procedures on a burn intensive care unit has been well documented.[142]

Analgesics such as acetaminophen can be used for their opioid-sparing effect and are combined with generous administration of oral opioids. [106] [143] Nonsteroidal anti-inflammatory drugs have antiplatelet effects and may not be appropriate for patients who require extensive excision and grafting procedures. In addition, burn patients can also manifest the nephrotoxic effects of nonsteroidal anti-inflammatory drugs. Music therapy,[144] hypnotherapy, [145] [146] [147] massage, a number of cognitive and behavioral techniques,[106] and, more recently, virtual reality techniques [148] [149] [150] have been successfully used to reduce pain during débridement and wound care.

Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com

Fleisher: Anesthesia and Uncommon Diseases, 5th ed.

Copyright © 2005 Saunders, An Imprint of Elsevier

CONCLUSION

Patients with severe burn injury are a challenge for the anesthesiologist. Recent advances in burn care and burn surgery have led to an improved survival of these patients. Early excision and grafting is becoming a standard practice. Effective anesthetic management of these patients requires knowledge of the continuum of pathophysiologic changes, proper planning, and a team effort.

Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com

Fleisher: Anesthesia and Uncommon Diseases, 5th ed.

Copyright © 2005 Saunders, An Imprint of Elsevier

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