How should patients with burns be managed in the intensive care unit?

76 How Should Patients With Burns Be Managed in the Intensive Care Unit? Marc G. Jeschke

More than 500,000 burn injuries occur annually in the United States.1 Although most are minor, approximately 40,000–60,000 burn patients require admission to a hospital or major burn center for appropriate treatment.2 The devastating consequences of burns have resulted in the allocation of significant clinical and research resources. Indeed, preventive strategies and improved care have resulted in a 50% decline in burn-related deaths and hospital admissions in the United States during the past 20 years.3,4 Advances in therapy strategies, based on implementation of critical care bundles, improved understanding of resuscitation, enhanced wound coverage, better support of the hypermetabolic response to injury, more appropriate infection control, and better treatment of inhalation injury have improved the clinical outcome of this unique patient population. It is important to recognize that successful management of burn patients requires a diversified and multidisciplinary approach. This chapter gives an overview of the evidencebased management of severely burned patients in the intensive care unit (ICU).

INITIAL ASSESSMENT AND EMERGENCY TREATMENT All burned patients should initially be managed as trauma patients, following the guidelines of the American College of Surgeons Committee on Trauma and the Advanced Trauma Live Support Center.5 The algorithms for trauma evaluation should be diligently applied to the burn patient. In particular, any wheezing, stridor, hoarseness, or tachypnea may be a sign of airway compromise. Tracheal tugging, carbonaceous sputum, soot around the patient’s airway passages, and singed facial or nasal hair may suggest an airway burn or smoke inhalation. As in any trauma patient, progression to the next step in the primary survey is delayed until a proper airway is established and maintained. Cardiac performance may be difficult to evaluate in the burn victim. In particular, burned extremities may impede the ability to obtain a blood pressure reading. In these situations, arterial lines, particularly femoral lines, are useful to monitor continuous blood pressure readings. Use of a pulmonary artery catheter (PAC) may be beneficial in the assessment of cardiovascular performance in certain situations 548

(e.g., inadequate noninvasive monitoring, difficult-to-define end points of resuscitation),6 but the general practicability, risk-to-benefit ratio, and lack of mortality reduction when the PAC is used have been widely criticized. Currently, there are no studies in burn patients that provide evidence-based recommendations. Because of the disadvantages of PAC use, less-invasive techniques have been developed.7 None of these, however, is of specific value in burn patients. Several descriptive studies using PiCCO technology, in which cardiac performance is approximated with an arterial thermodilution catheter, have been conducted in burn patients.8,9 Prospective trials are underway.

FLUID RESUSCITATION Severe burns cause significant hemodynamic changes. These must be managed carefully to optimize intravascular volume, maintain end-organ tissue perfusion, and maximize oxygen delivery to the tissues.10 Massive fluid shifts after severe burn injury result in the sequestration of fluid in burned and unburned tissue.11 The result of this generalized edema may be burn shock, a leading cause of mortality in severely burned patients.12–14 Therefore, early and accurate fluid resuscitation of patients with major burns is critical.15 Calculations of fluid requirements are based on the amount of body surface involved in second- or third-degree (but not first-degree) burns. The “rule of nines” (Fig. 76.1A) has been used to estimate the area of burned body surface, but this rule has limitations, particularly in children, in whom the head accounts for a disproportionate fraction of body mass. In these cases, a more accurate assessment can be made by using the Lund and Browder chart, which takes into account changes associated with growth (Fig. 76.1B). Various resuscitation formulas have been used. These differ in the amount of crystalloid and colloid to be given and in fluid tonicity (Table 76.1).10,16 The modified Brooke and Parkland (Baxter) formulas are most commonly used for early resuscitation,17 but no formula will accurately predict the volume requirements of an individual patient. Recently, the American Burn Association recommended that the initial volume of resuscitative fluid be decreased from 4 to 2 cc/kg/% burn. It is currently not known whether decreased fluids are associated with improved outcomes. A recent study showed that resuscitation

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CHAPTER 76

Adult body

% of total

Part

BSA

Arm

9%

Head

9%

Neck

1%

Leg

18%

Anterior trunk

18%

Posterior trunk

18%

9% 1% Front 18% Age 9%

9%

Back 18%

0–1

2–4

5–9

10–14

15

A: ½ of head

9½%

8½%

6½%

5½%

4½%

B: ½ of one thigh

9½%

8½%

6½%

5½%

4½%

C: ½ of one leg

9½%

8½%

6½%

5½%

4½%

18% 18% A

A 3½%

3½% 1%

1% 2%

2%

2%

2% 13%

13% 1½%

9%

Child body

9%

Back 18%

14%

1½%

1½% 2½%

18% Front 18%

1½%

14%

A

1%

% of total

Part

BSA

Arm

9%

Head and neck

18%

Leg

14%

Anterior trunk

18%

Posterior trunk

18%

2½%

1½%

1½% 4¾% B

B

1½%

1½%

4¾%

4¾% B

B

C

4¾% B C

C C 3½% 3½%

3½%

1¾% 1¾%

1¾% 1¾%

3½%

Fig. 76.1  ​(A) Estimation of burn size with the “rule of nines.” (B) Estimation of burn size with the Lund and Browder method. BSA, body surface area.

TABLE 76.1  Formulas for Estimating Adult Burn Patient Resuscitation Fluid Needs. Colloid Formula

Electrolyte

Colloid

Evans

Normal saline, 1.0 mL/kg/% burn

1.0 cc/kg/% burn

Brooke

Lactated Ringer solution, 1.5 mL/kg/% burn

0.5 mL/kg

Slater

Lactated Ringer solution, 2 L/24 h

Fresh-frozen plasma, 75 mL/kg/24 h

Parkland

Lactated Ringer solution

4 mL/kg/% burn

Modified

Lactated Ringer solution

2 mL/kg/% burn

Crystalloid formulas

Hypertonic saline solutions Monafo

Volume to maintain urine output at 30 mL/h; fluid contains 250 mEq Na/L.

Warden

Lactated Ringer solution 150 mEq NaHCO3 (180 mEq Na/L) for 8 hours to maintain urine output at 30-50 mL/h. Lactated Ringer solution to maintain urine output at 30-50 mL/h beginning 8 hours postburn.

Dextran formula (Demling)

Dextran 40 in saline, 2 mL/kg/h for 8 hours. Lactated Ringer solution, volume to maintain urine output at 30 mL/h. Fresh-frozen plasma, 0.5 mL/kg/h for 18 hours beginning 8 hours postburn.

Na, sodium; NaHCO3, sodium bicarbonate. From Warden GD. Burn shock resuscitation. World J Surg. 1992;16(1):16-23.

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TABLE 76.2  Formulas for Estimating Pediatric Resuscitation Needs. Cincinnati Shriners Burns Hospital

4 mL 3 kg 3 % total BSA burn 1 1500 mL 3 m2 BSA

1st 8 hours 2nd 8 hours 3rd 8 hours

Galveston Shriners Burns Hospital

5000 mL/m2 BSA burn 1 2000 mL/m2 BSA

Lactated Ringer’s solution 1 12.5 g albumin

Lactated Ringer’s solution 1 50 mg NaHCO3 Lactated Ringer’s solution Lactated Ringer’s solution 1 12.5 g albumin

BSA, body surface area; NaHCO3, sodium bicarbonate.

under 4 cc/kg per %burn was associated with a significantly greater incidence of renal failure and did not improve outcome.18 In children, maintenance requirements must be added to the resuscitation formula. The Galveston and Cincinnati Shriners Burns Hospitals have devised useful formulas (Table 76.2). Intravascular volume status must be reevaluated frequently during the acute phase. Fluid balance during burn shock resuscitation is typically measured by hourly urine output through an indwelling urethral catheter. It has been recommended that urine output be maintained at approximately 0.5 mL/kg per hour in adults19 and 0.5–1.0 mL/kg per hour in patients weighing less than 30 kg.20 However, no clinical studies have identified the hourly urine output that is truly required to maintain vital organ perfusion during burn shock resuscitation. Because large volumes of fluid and electrolytes are administered initially and throughout the course of resuscitation, it is important to obtain baseline laboratory measurements.21 Crystalloid, in particular lactated Ringer’s solution, is the most popular resuscitation fluid currently in use for burn patients.22 Other crystalloid solutions and colloids have been used. Despite extensive study no outcome differences between the two have been identified.23–26 Proponents of crystalloid solutions alone report that colloids offer no added value and are more expensive.27 Nonetheless, most burn surgeons agree that patients with low serum albumin during burn shock may benefit from albumin supplementation to maintain oncotic pressure.28

INHALATION INJURY Inhalation injury is one of the most critical problems accompanying thermal insult, with mortality paralleling that for acute respiratory distress syndrome in patients requiring ventilator support for more than 1 week.29,30 Early diagnosis of bronchopulmonary injury is initiated by a history of closedspace exposure; facial burns; or carbonaceous debris in the mouth, pharynx, or sputum.31 There are few evidence-based data regarding inhalation injury. Therefore the standard diagnostic method is bronchoscopy. Endorf and Gamelli established a grading system for inhalation injury (0, 1, 2, 3, and 4) derived from findings at initial bronchoscopy and based on Abbreviated Injury Score criteria.32 Bronchoscopic criteria that are consistent with inhalation injury included airway edema, inflammation, mucosal necrosis, presence of soot and charring in the airway, tissue sloughing, or carbonaceous material in the airway. At this time, however, there are neither uniform diagnosis criteria nor standardized treatment

guidelines. Management of inhalation injury consists of ventilatory support, aggressive pulmonary toilet, bronchoscopic removal of casts, and nebulization therapy.10 The American Burn Association guidelines do not recommend the use of prophylactic antibiotics.

INFECTION/SEPSIS Severely burned patients are susceptible to various infectious complications.33 Because burns induce a systemic inflammatory response,34 specific guidelines for the diagnosis and treatment of wound infection and sepsis in burns have been formulated (Box 76.1). That said, the burn community realized that sepsis is very complex, and while an ideal definition of sepsis does not currently exist, studies are ongoing to develop a burn-specific definition of sepsis. BOX 76.1  Definition of Burn Sepsis. American Burn Association Consensus Definition on Burn Sepsis • At least 3 of the following parameters: • T .38.5° C or ,36.5° C • Progressive tachycardia .90 beats/min in adults or .2 SD above age-specific norms in children • Progressive tachypnea .30 breaths/min in adults or .2 SD above age-specific norms in children • WBC .12,000 or ,4000 in adults or .2 SD above age-specific norms in children • Refractory hypotension: SBP ,90 mm Hg, MAP ,70, or an SBP decrease .40 mm Hg in adults or , 2 SD below normal for age in children • Thrombocytopenia: Platelet count ,100,000/mL in adults, ,2 SD below norms in children • Hyperglycemia: Plasma glucose .110 mg/dL or 7.7 mM/L in the absence of diabetes • Enteral feeding intolerance (residual .150 mL/h in children or 2 times feeding rate in adults; diarrhea .2500 mL/day for adults or .400 mL/day in children) and Pathologic tissue source identified: .105 bacteria on quantitative wound tissue biopsy or microbial invasion on biopsy Bacteremia or fungemia Documented infection as defined by Centers for Disease Control. MAP, mean arterial pressure; SBP, systolic blood pressure; SD, standard deviation; T, temperature; WBC, white blood cell count. From Greenhalgh DG, Saffle JR, Holmes JH, et al. American Burn Association consensus conference to define sepsis and infection in burns. J Burn Care Res. 2007; 28:776-790.

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TABLE 76.4  Formulas for Estimating

BURN WOUND EXCISION Methods for handling burn wounds have changed in recent decades. Increasingly, aggressive early tangential excision of the burn tissue and early wound closure primarily by skin grafts have led to significant improvement in survival and have substantially lowered costs in this patient population.10,35–38 Early wound closure also has been associated with decreased severity of hypertrophic scarring, joint contractures and stiffness, and with quicker rehabilitation.10,35 Techniques of burn wound excision have evolved substantially over the past decade. Published estimates of bleeding associated with these operations range between 3.5% and 5% of the blood volume for every 1% of the body surface excised.39,40 Burn wound excision should occur in the operating room soon after the patient is admitted; however, sometimes excision in the ICU may be necessary.

Caloric Requirements in Pediatric Burn Patients. Formula

Sex/Age

WHO89

Males

The metabolic consequences of severe burn injury are profound, and their modulation constitutes an ongoing challenge. Metabolic rates of burn victims exceed those of most other critically ill patients and cause marked wasting of lean body mass within days of injury.41 Failure to meet the subsequent energy and protein requirements may result in impaired wound healing, organ dysfunction, increased susceptibility to infection, and death.42 Thus, adequate nutrition is imperative. Because of the significant increase in postburn energy expenditure, high-calorie nutritional support was thought to decrease muscle metabolism,43 but a randomized, double-blind, prospective study found that aggressive highcalorie feeding with a combination of enteral and parenteral nutrition was associated with increased mortality.44 Therefore most investigators recommend adequate calorie intake through early enteral feeding and avoidance of overfeeding.10,41 Different formulas have been developed to address the specific energy requirements of burned adult and pediatric patients45–47 (Tables 76.3 and 76.4). The caloric requirements in adult burn patients most often are calculated using the Curreri formula. This calls for 25 kcal/kg per day plus 40 kcal/%BSAB (percentage of total body surface area burned) per day.48 Recommendations suggest administration

Equation (Daily Requirement in kcal)

0–3 years

(60.9 3 W) 2 54

3–10 years

(22.7 3 W) 1 495

10–18 years

(17.5 3 W) 1 651

Females

RDA90

METABOLIC RESPONSE AND NUTRITIONAL SUPPORT Curreri junior91

0–3 years

(61.0 3 W) 2 51

3–10 years

(22.5 3 W) 1 499

10–18 years

(12.2 3 W) 1 746

0–6 months

108 3 W

6 months to 1 year

98 3 W

1–3 years

102 3 W

4–10 years

90 3 W

11–14 years

55 3 W

,1 year

RDA 1 (15 3 %BSAB)

1–3 years

RDA 1 (25 3 %BSAB)

4–15 years

RDA 1 (40 3 %BSAB)

Galveston infant92

0–1 years

2100 kcal/m2 BSA 1 1000 kcal/m2 BSAB

Galveston revised47

1–11 years

1800 kcal/m2 BSA 1 1300 kcal/m2 BSAB

Galveston adolescent93

121

1500 kcal/m2 BSA 1 1500 kcal/m2 BSAB

BSA, body surface area; BSAB, body surface area burned; %BSAB, percentage of total body surface area burned; RDA, Recommended Dietary Allowance (US); W, weight (kg);WHO, World Health Organization.

of 1 to 2 g/kg per day of protein.42 Because of glucose intolerance and futile cycling in critical illness, most ICUs provide a significant amount of caloric requirements as fat.42,49 However, burn patients exhibit lipid intolerance that may result in hyperlipidemia and fatty liver infiltration. These complications are associated with a higher incidence of infection and higher postoperative mortality rates.50–53 Thus the extent to

TABLE 76.3  Formulas for Estimating Caloric Requirements in Adult Burn Patients. Formula Harris-Benedict

Age/Sex 88

Equation

Men

BEE (kcal/day) 5 66.5 1 (13.75 3 W) 1 (5.03 3 H) 2 (6.76 3 A)

Women

BEE (kcal/day) 5 655 1 (9.56 3 W) 1 (1.85 3 H) 2 (4.68 3 A)

Comment: Multiply BEE by stress factor of 1.222.0 (1.221.5 sufficient for most burns) to estimate caloric requirement. Curreri45

Age: 16–59 years

551

Calories (kcal/day) 5 (25 3 W) 1 (40 3 %BSAB)

Age: .60 years Calories 5 (20 3 W) 1 (65 3 %BSAB) Comment: Specific for burns, may significantly overestimate energy requirements, maximum 50% BSAB. A, age (year); BEE, basal energy expenditure; %BSAB, percentage of total body surface area burned; H, height (cm); W, weight (kg).

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which exogenous lipid can be used as an energy source is limited.49,54,55 Studies in a large cohort of severely burned children demonstrated that patients receiving a low-fat, highcarbohydrate diet had a significantly lower incidence of fatty liver on autopsy. Relative to historic controls, these patients had a significantly lower incidence of sepsis, prolonged survival, and significantly shorter stays in the ICU (grade C data). On the basis of these findings, nutritional regimens for treatment of burn patients which include a significantly reduced proportion of fat as the source of total caloric intake are recommended. Diminished gastrointestinal absorption, increased urinary losses, altered distribution, and altered carrier protein concentrations after severe burns may lead to micronutrient (trace elements and vitamins [such as Cu, Fe, Se, Zn, vitamins C and E]) deficiency in major burns.56–58 Such deficiencies may, in turn, lead to infectious complications, delayed wound healing, and stunting in children.59 Thus supplementation would seem appropriate, but evidence-based practice guidelines are not currently available. Enhancing trace element status and antioxidant defenses by supplementing selenium, zinc, and copper was shown to decrease the incidence of nosocomial pneumonia in critically ill, severely burned patients in two consecutive, randomized double-blind trials.60 Caution should be used to avoid toxic side effects.

MODULATION OF THE HORMONAL AND ENDOCRINE RESPONSE Modification of adverse components of the hypermetabolic response to burn injury, particularly protein catabolism, would seem to be desirable. b-adrenergic blockade, b-adrenergic supplementation, anabolic steroids, recombinant growth hormone, and insulin-like growth factor (IGF) are under active investigation. Various studies have demonstrated the potential beneficial effect of b blockers in burn patients. In a single-center study, administration of propranolol in doses that decrease the heart rate by approximately 15% to 20% from baseline reduced the release of free fatty acids from adipose tissue, decreased hepatic triacylglycerol storage and fat accumulation, and reversed muscle protein catabolism.61–63 In a retrospective study of adult burn patients, use of b blockers was associated with decreased mortality, wound infection rate, and wound healing time.64 Therefore b blockers appear to have high potential as an anticatabolic treatment in severely burned patients. Treatment with anabolic agents, such as oxandrolone, a testosterone analog, improved muscle protein catabolism through enhanced protein synthesis efficiency,65 reduced weight loss, and increased donor site wound healing.66 In a prospective randomized study, Wolf and colleagues demonstrated that administration of 10 mg of oxandrolone every 12 hours decreased hospital length of stay.67 In a large prospective, double-blind, randomized single-center study, oxandrolone given at a dose of 0.1 mg/kg every 12 hours shortened acute hospital length of stay, maintained lean body mass, and improved body composition and hepatic protein synthesis.68

The use of recombinant human growth hormone in daily subcutaneous doses has been reported to accelerate donor site healing and restore earlier positive nitrogen balance.69–71 Indeed, administration of 0.05 mg/kg of recombinant human growth hormone given over a 12-month period after burn injury significantly improved height, weight, lean body mass, bone mineral content, cardiac function, and muscle strength.72 These findings are in contrast to those of Takala and colleagues in adults with critical illness from multiple etiologies73 and with studies showing that growth hormone treatment induced hyperglycemia and insulin resistance.71,74 It is likely that the prolonged catabolic nature of burn injury and perhaps the dose account for these discrepant results. IGF-1 has been shown to decrease the metabolic rate after burn injury and to increase whole-body anabolic activity without hyperglycemia or insulin resistance.75 Studies by Van den Berghe and colleagues indicate that the use of IGF-1 alone is not effective in critically ill patients without burns.76 Again, the prolonged catabolic nature of burn injury may explain the difference.

GLUCOSE CONTROL A prominent component of the hypermetabolic response after burn injury is hyperglycemia and insulin resistance.77 These result from both an increase in hepatic gluconeogenesis and impaired insulin-mediated glucose transport into skeletal muscle, cardiac muscle and adipose tissue.78–81 Hyperglycemia and elevations in circulating insulin concentration are of serious clinical concern. Hyperglycemia has been linked to impaired wound healing, increased infectious complications, and increased mortality.82–85 A randomized controlled trial in severely burned pediatric patients indicated superiority for glucose control using insulin.86 Care providers need to be vigilant of an increased incidence of hypoglycemia that is associated with a 4- to 9-fold increase in morbidity and mortality. A recent Phase I/II prospective trial in burn patients showed safety, significantly less hypoglycemia when compared to insulin, and efficacy of metformin in burn patients and currently, larger trials are being designed to test metformin as a glucose modulating agent in the setting of burn patients.87

AUTHOR’S RECOMMENDATIONS • Burn patients should be managed initially as trauma patients. Algorithms for trauma evaluation should be diligently applied to the burn patient. • Early and accurate fluid resuscitation of patients with major burns is critical for survival, but overaggressive resuscitation should be avoided, particularly in small children younger than 4 years. • Early diagnosis of bronchopulmonary injury is critical. Management of inhalation injury consists of ventilatory support, aggressive pulmonary toilet, bronchoscopic removal of casts, and nebulization therapy.

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• Adequate nutritional intake through enteral tube feeding will aid in the control of stress ulceration, preserve intestinal mucosal integrity, and provide fuel for the resulting hypermetabolic state. Nutritional regimes for the treatment of burn patients include a significantly reduced proportion of fat as the source of total caloric intake. • Modulation of the hypermetabolic response improves outcomes. • Hyperglycemia in burn patients is associated with increased complications and needs to be controlled to a target level of 130 mg/dL. Hypoglycemia needs to be avoided because it leads to increased mortality after burn. • Hyperlipidemia should be treated to avoid fatty infiltration of organs.

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e1 Abstract: Burns are a complex and severe trauma requiring specialized burn and intensive care. This chapter discusses the evidence in current developments of critical burn care.

Keywords: anabolic agents, burns, hypermetabolism, infection, nutrition, resuscitation, sepsis.