55: The Burned Patient

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CHAPTER 55 The Burned Patient

Philip R. Levin, MD, Alma N. Juels, MD

1 Who gets burned?

Approximately 2 million fires are reported each year, which result in 1.2 million people with burn injuries. Approximately 45,000 people are hospitalized in the United States for thermal injury. There are about 5000 fire and burn deaths per year. The majority of burns are thermal injuries. Electrical burns usually cause tissue destruction by thermal and associated injuries. In chemical burns the degree of injury depends on the particular chemical, its concentration, and duration of exposure. Seventy percent of burn patients are men. Mean age for all cases is 35 years old. Scalds are the most common in those below 5 years of age, whereas fire injuries are more common in older patients.

2 What are the three main factors that correlate with increased mortality with burn injury?

Advanced age, burn size, and presence of inhalation injury correlate with increased mortality.

3 What are the consequences of skin damage?

The skin is the largest organ of the human body. It has three principal functions, all of which are disrupted by burn injury:

image The skin is an important sensory organ.
image It performs a major role in thermoregulation for the dissipation of metabolic heat.
image The skin acts as a barrier to protect the body against the entrance of microorganisms in the environment. A burn patient may have extensive evaporative heat and water loss, and loss of thermoregulation may lead to hypothermia. Burn patients have a profound risk of infection and sepsis.

4 How are burns classified?

The severity of the burn is graded by its depth, which depends on the extent of tissue destruction.

image Superficial burns involve the upper layers of the epidermis; the skin is painful and appears red and slightly edematous, much like a sunburn.
image Superficial partial-thickness burns occur when tissue damage extends into the superficial layer of the dermis, which is still lined with intact epithelium that proliferates and regenerates new skin. These burns develop blisters and have red or whitish areas that are very painful.
image Deep partial-thickness burns extend downward into the deeper layer of the dermis. Edema is marked, and sensation is altered.
image Full-thickness and subdermal burns affect every body system and organ. A full-thickness burn extends through the epidermis and dermis and into the subcutaneous tissue layer. A subdermal burn damages muscle, bone, and interstitial tissue. Some centers are now using laser Doppler imaging to better determine burn depth.

5 What systems are affected by burns?

All physiologic functions can be affected by burns, including the cardiovascular and respiratory systems; hepatic, renal, and endocrine function; the gastrointestinal tract; hematopoiesis; coagulation; and immunologic response.

6 How is the cardiovascular system affected?

A transient decrease in cardiac output, as much as 50% from baseline, is followed by a hyperdynamic response. In the acute phase organ and tissue perfusion decreases because of hypovolemia, depressed myocardial function, increased blood viscosity, and release of vasoactive substances. The acute phase starts immediately after injury; the second phase of burn injury, termed the metabolic phase, begins about 48 hours after injury and involves increased blood flow to organs and tissues. Geriatric patients may have a delayed or nonexisting second phase. Hypertension of unknown cause develops and may be quite extensive.

7 How is the respiratory system affected?

Pulmonary complications can be divided into three distinct syndromes based on clinical features and temporal relationship to the injury. Early complications, occurring 0 to 24 hours postburn, include carbon monoxide (CO) poisoning and direct inhalation injury and can lead to airway obstruction and pulmonary edema. Delayed injury, occurring 2 to 5 days after injury, includes adult respiratory distress syndrome. Late complications, occurring days to weeks after the injury, include pneumonia, atelectasis, and pulmonary emboli. The two most common complications of burn injury are pneumonia and respiratory failure.

8 What is inhalation injury?

Inhalation injury occurs when hot gases, toxic substances, and reactive smoke particles reach the tracheobronchial tree. These substances result in wheezing, bronchospasm, corrosion, and airway edema and should be suspected if the burn was sustained in a closed space. The presence of carbonaceous sputum, perioral soot, burns to the face and neck, stridor, dyspnea, or wheezing are indications for complete respiratory tract evaluation. Inhalation injury can cause damage to the upper airway (i.e., airway compromise, nasal obstruction, and acute laryngitis with varying degrees of laryngeal edema), damage to the conducting airway (i.e., tracheitis and bronchitis), and injury to the lower respiratory tract (i.e., pneumonitis, pulmonary edema, and adult respiratory distress syndrome). Chest radiographs during the initial phase usually underestimate the severity of lung damage because the injury is usually confined to the airways. Fiber-optic bronchoscopy has been quite useful in diagnosis of inhalation injury.

9 What is the best way to treat inhalation injury?

Management is generally supportive. Oxygen should be provided as necessary to ensure adequate oxygenation. Bronchospasm usually responds to β-agonists. Patients with smoke inhalation can require greater fluid resuscitation than other patients with burns. Pulmonary toilet may be important if there is excessive carbonaceous material in the lungs. Intubation or tracheotomy may be necessary if there is significant upper airway compromise. Patients with heat and smoke injury plus extensive face and neck burns usually all require intubation. Patients with oral burns but no smoke injury should still be intubated early because these patients have significant edema and secretions and it may be nearly impossible to intubate at a later date. If intubation occurs, make sure to secure the endotracheal tube because it may be extremely difficult to replace it if it becomes dislodged. High-frequency percussive ventilation has also been shown to be effective in clearing secretions.

10 What are the features of carbon monoxide poisoning?

CO toxicity is one of the leading causes of death in fires. CO is produced by incomplete combustion associated with fires, exhaust from internal combustion engines, cooking stoves, and charcoal stoves. Its affinity for hemoglobin is 200 times that of oxygen. When CO combines with hemoglobin, forming carboxyhemoglobin (COHb), the pulse oximeter may overestimate hemoglobin saturation. Symptoms are caused by tissue hypoxia, shift in the oxygen-hemoglobin dissociation curve, direct cardiovascular depression, and cytochrome inhibition. The persistence of a metabolic acidosis in the patient with adequate volume resuscitation and cardiac output suggests the persistent CO impairment of oxygen delivery and use. Treatment is initiated with 100% oxygen, which decreases the serum half-life of COHb. Hyperbaric oxygen (2 to 3 ATM) produces an even more rapid displacement and is most useful in cases of prolonged exposure, when it is more difficult to displace CO from the cytochrome system. The drawback of hyperbaric oxygen use is the inability to get to the burn patient during the crucial period of hemodynamic and pulmonary instability. The vast majority of cases can be managed simply by using 100% oxygen.

11 How do burns affect the gastrointestinal tract?

Ileus may occur. Acute ulceration of the stomach or duodenum, referred to as Curling’s ulcer, may lead to gastrointestinal bleeding. The small and large intestine may develop acute necrotizing enterocolitis with abdominal distention, hypotension, and bloody diarrhea.

12 How is renal function affected?

Renal blood flow and glomerular filtration diminish immediately, activating the renin-angiotensin-aldosterone system. Antidiuretic hormone is released, resulting in retention of sodium and water and loss of potassium, calcium, and magnesium. The incidence of acute renal failure in burned patients varies from 0.5% to 38%, depending primarily on the severity of the burn. The associated mortality rate is very high (77% to 100%). Hemoglobinuria secondary to hemolysis and myoglobinuria secondary to muscle necrosis can lead to acute tubular necrosis and acute renal failure.

13 How is myoglobinuria treated?

Myoglobinuria is treated by vigorous fluid resuscitation, to the end point of a urine output of 2 ml/kg/hr. Administration of bicarbonate to alkalinize the urine may reduce the incidence of pigment-associated renal failure. Osmotic diuretics (i.e., mannitol) can be used in rare circumstances, except that its use obscures urine output as an indicator of circulating volume.

14 How is hepatic function affected?

Acute reduction of cardiac output, increased viscosity blood, and splanchnic vasoconstriction can cause hepatic hypoperfusion, which can result in decreased hepatic function.

15 Are drug responses altered?

Drugs administered acutely by any route other than intravenously have delayed absorption. After 48 hours the plasma albumin concentration is decreased, and albumin-bound drugs such as benzodiazepines and anticonvulsants have an increased free fraction and therefore a prolonged effect. The effect of drugs metabolized in the liver by oxidative metabolism (phase I reaction) is prolonged (e.g., diazepam). However, drugs metabolized in the liver by conjugation (phase II) are not affected (e.g., lorazepam). Opioid requirements are increased, most likely because of habituation and hypercatabolism. Ketamine may cause hypotension secondary to hypovolemia and depleted catecholamine stores, exerting its direct cardiodepressant effect. Propofol, thiopental, and etomidate may cause hypotension secondary to hypovolemia in the acute phase. Inhalational agents are likewise poorly tolerated in hypovolemic patients.

16 What is the endocrine response to a burn?

The endocrine response to a thermal burn involves massive release of catecholamines, glucagon, adrenocorticotropic hormone, antidiuretic hormone, renin, angiotensin, and aldosterone. Glucose levels are elevated, and patients are susceptible to nonketotic hyperosmolar coma. Patients with larger burns are more highly associated with development of adrenal insufficiency.

17 What are the hematologic complications that occur with burns?

Anemia is a common finding in severely burned patients. In the immediate postburn period erythrocytes are damaged or destroyed by heat and removed by the spleen in the first 72 hours. This decrease in red cell mass is not immediately apparent because of the loss of plasma fluid and hemoconcentration. With fluid resuscitation the deficit becomes more apparent. In the early postburn period more red cell loss occurs secondary to decreased erythropoiesis. In addition, ongoing infection can result in subacute activation of the coagulation cascade. Consumption of circulating procoagulants results in various degrees of coagulopathy. Platelet function is both qualitatively and quantitatively depressed. Antithrombin deficiency has been noted in severe burn patients, usually found in the first 5 days after injury. The incidence was higher with increasing burn size and the diagnosis of inhalation injury.

18 What are the immunologic complications that occur with burns?

Infection in the burn patient is a leading cause of morbidity and mortality and remains one of the most demanding concerns for the burn team. Initially the burn wound is colonized principally with gram-positive organisms. Within a week they usually are replaced by antibiotic-susceptible gram-negative organisms. If wound closure is delayed and the patient becomes infected, requiring treatment with broad-spectrum antibiotics, these flora may be replaced by yeasts, fungi, and antibiotic-resistant bacteria. As burn wound size increases, bloodstream infection increases dramatically secondary to increased exposure to intravascular catheters and burn wound manipulation-induced bacteremia. Systemic antimicrobials are indicated to treat only documented infections such as pneumonia, bacteremia, wound infection, and urinary tract infection. Prophylactic antimicrobial therapy is only recommended if the burn wound must be excised or grafted in the operating room. It should be used only for coverage of the immediate perioperative period. Fifty percent or more of patients with both a major burn and an inhalation injury develop pneumonia. One of the major concerns is the worldwide emergence of antimicrobial resistance among a wide variety of nosocomial bacterial and fungal burn wound pathogens, which seriously limits the available effective treatment of burn wound infections.

19 How are patients with burns resuscitated?

The goal of fluid resuscitation is to correct hypovolemia and optimize organ perfusion. Adequate fluid administration is critical to the prevention of burn shock and other complications of thermal injury. Burns cause a generalized increase in capillary permeability, with loss of fluid and protein into interstitial tissue; this loss is greatest in the first 12 hours. A perfect formula for predicting fluid requirements remains elusive despite decades of research and debate. Two general principles most agree on are to give only what is needed and continuously reassess fluid requirements to prevent underresuscitation or overresuscitation. The goal of fluid resuscitation is to maintain a urinary output of 0.5 ml/kg/hr, which is thought to indicate adequate renal perfusion. The most common formula used today is the Parkland formula. The Parkland formula involves giving 4 ml of lactated Ringer’s (LR) solution per kilogram of body weight per percent of total body surface area (TBSA) burned (4 ml/kg/% TBSA). One half of the calculated amount is given during the first 8 hours, and the remainder is given over the next 16 hours, in addition to daily maintenance fluid. Most burn centers use crystalloid as the primary fluid for burn resuscitation. Another formula that some use is the modified Brooke formula: 2 ml/kg/% TBSA LR administered as noted previously. The administration of colloid has been associated with increased risk of lung injury. In the United States most believe that colloid solutions should not be used in the first 24 hours. On the second day after injury capillary integrity is restored, and the amount of required fluid is decreased. Infusion of crystalloid is decreased after the first day, and colloids are administered:

image 0% to 30% TBSA burned: no colloid required
image 30% to 50% TBSA burned: 0.3 ml/kg/%burn/24 hr of colloid required
image 50% to 70% TBSA burned: 0.4 ml/kg/%burn/24 hr of colloid required
image 70% to 100% TBSA burned: 0.5 ml/kg/%burn/24 hr of colloid required

20 How do you calculate the percent of total body surface burned?

The severity of a burn injury is based on the amount of surface area covered in deep partial-thickness, full-thickness, and subdermal burns. The rule of nines method allows reasonable estimation (Table 55-1). Because of the difference in body habitus (particularly head and neck), the rule of nines must be altered in children (Table 55-2).

TABLE 55-1 Rule of Nines for Adults

Head and neck 9%
Upper extremities 9% each
Chest (anterior and posterior) 9% each
Abdomen 9%
Lower back 9%
Lower extremities 18%
Perineum 1%

TABLE 55-2 Rule of Nines for Children: Percent of Body Surface according to Age

image

21 Early surgical burn wound intervention has recently been shown to be one of the major reasons for the improved outcome in burn patients. What are the four categories of operations that are common for the burn-injured patient?

image Decompression procedures (escharotomies and fasciotomies)
image Excision and closure operations
image Reconstruction operations
image Supportive general surgical procedures (tracheostomy, gastrostomy, cholecystectomy, bronchoscopy, vascular access procedures)

22 What is important in the preoperative history?

It is important to know at what time the burn occurred for fluid replacement. The type of burn is also important to assess airway damage, associated injuries, and the possibility of more extensive tissue damage than initially appreciated (electrical burns). A standard preoperative anesthetic history also must be taken, including past coexisting medical conditions, medications, allergies, and anesthetic history.

23 What should the anesthesiologist look for on the preoperative physical examination?

In addition to the conventional concerns of any patient about to undergo surgery, the status of the patient’s airway should be the number one priority. A complete airway examination is a must. Excessive sputum, wheezing, and diminished breath sounds may suggest inhalation injury to the lungs. The cardiovascular system should also be evaluated, noting pulse rate and rhythm, blood pressure, cardiac filling pressures (if available), and urine output. Special attention should be given to the neurologic examination. It is important to assess the patient’s level of consciousness and orientation.

24 What preoperative tests are required before induction?

Special emphasis should be placed on correcting the acid-base and electrolyte imbalance during the acute phase. Therefore an arterial blood gas analysis and a chemistry panel are suggested. In the presence of CO poisoning, the pulse oximeter may overestimate the saturation of hemoglobin; therefore a COHb level, determined by co-oximetry, may be helpful to assess the degree of the CO poisoning and to guide treatment. Coagulation tests are also helpful, because such patients often have bleeding diathesis. A urine myoglobin should be done in patients with a history of electrical injury or pigmented urine.

25 What monitors are needed to give a safe anesthetic?

Access for monitoring may be difficult. Needle electrodes or electrocardiogram (ECG) pads sewn on the patient may be required for the ECG monitor and nerve stimulator. A blood pressure cuff may be placed on a burned area, but an arterial catheter may be better and allows frequent blood analysis. Temperature measurement is a must because of exaggerated decreases in body temperature. Invasive monitors are placed as deemed necessary, taking into account the patient’s previous baseline medical condition. If the procedure involves a large amount of blood loss, central venous pressure (right atrial pressure) should be monitored through an introducer sheath. If myocardial dysfunction is likely, a pulmonary artery catheter may be necessary, although authorities disagree on this point.

26 How must the use of muscle relaxants be modified for a burned patient?

From about 24 hours after injury until the burn has healed, succinylcholine may cause hyperkalemia because of proliferation of extrajunctional neuromuscular receptors. On the other hand, burned patients tend to be resistant to the effects of nondepolarizing muscle relaxants and may need two to five times the normal dose.

27 What techniques have been used to markedly reduce blood loss in excisional burn surgery?

Subeschar and subcutaneous epinephrine clysis, extremity exsanguinations, pneumatic tourniquet use, and maintenance of intraoperative euthermia are all simple surgical techniques that have been found to significantly decrease blood loss.

28 What induction drugs are good for burn patients?

Various medications have been given successfully to burn patients. In patients who are adequately volume resuscitated and not septic, propofol is an acceptable induction agent. Ketamine offers the advantage of stable hemodynamics and analgesia and has been used extensively for both general anesthesia and analgesia for burn dressing changes. Unfortunately it tends to produce dysphoric reactions. If the patient is hemodynamically unstable, etomidate is a reasonable induction alternative.

KEY POINTS: The Burned Patient image

1. The initial goal of resuscitation in burn patients is to correct hypovolemia. Burns cause a generalized increase in capillary permeability with loss of significant fluid and protein into interstitial tissue.
2. There should be a low threshold for elective intubation in patients suspected of having inhalation injury.
3. From about 24 hours after injury until the burn has healed, succinylcholine may cause hyperkalemia, because of proliferation of extrajunctional neuromuscular receptors.
4. Burned patients tend to be resistant to the effects of nondepolarizing muscle relaxants and may need two to five times the normal dose.

29 Describe specific features of electrical burns

Care of electrical burns is similar to care of thermal burns, except that the extent of injury may be misleading. Areas of devitalized tissue may be present under normal-appearing skin. The extent of superficial tissue injury may result in underestimation of initial fluid requirements. Myoglobinuria is common, and urine output must be kept high to avoid renal damage. The development of neurologic complications after electrical burns is common, including peripheral neuropathies or spinal cord deficits. Many believe that regional anesthesia is contraindicated. Cataract formation may be another late sequela of burn injury. Cardiac dysrhythmias and ventricular fibrillation or asystole may occur up to 48 hours after injury. Apnea may result from titanic contraction of respiratory muscles or cerebral medullary injury.

Website image

American Burn Association

www.ameriburn.org

SUGGESTED READINGS

1. Cone J.B. What’s new in general surgery: burns and metabolism. J Am Coll Surg. 2005;200:607-615.

2. Johnson A. Hyperbaric oxygen for carbon monoxide poisoning: a systematic review and critical analysis of the evidence. Toxicol Rev. 2005;24:75-92.

3. Klein M.B., Hayden D., Elson C., et al. The association between fluid administration and outcome following major burn: a multicenter study. Ann Surg. 2007;245:622-628.

4. Pham T.N., Cancio L.C., Gibran N.S. American Burn Association practice guidelines for burn shock resuscitation. J Burn Care Res. 2008;29:257-266.

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