The Burned Patient Case File

The Burned Patient Case File

Lydia Conlay, MD, PhD, MBA, Julia Pollock, MD, Mary Ann Vann, MD, Sheela Pai, MD, Eugene C. Toy, MD

Case 43

A 27-year-old man who jumped from the second story of a burning building is brought to the emergency room with second- and thirddegree burns over 50% of his body. He also has an open fracture of the left tibia. He is moaning on arrival and somewhat obtunded. Though hoarse, he is eventually able to communicate that he has no medical problems and no allergies. On physical examination, the patient’s heart rate is 50 beats/minute (with frequent premature ventricular complexes); blood pressure, 85/55 mm Hg; respiratory rate, 22 breaths/minute; SpO2, 99%; and temperature, 34.5°C (94.1°F). Carbonaceous material is in his nares, and he has mild inspiratory and expiratory wheezes. Blood is oozing from the open tibial fracture. The patient’s hematocrit is 49%, potassium is 3.9 mEq/L, and carboxyhemoglobin level is 9%. Following the administration of 1 L of lactated Ringer solution, he is brought to the operating room for placement of an external fixation device for the tibial fracture.

➤ What is/are the most urgent priorities in caring for this patient?

➤ What is a secondary, albeit urgent issue?

➤ What would likely be seen at direct laryngoscopy?

ANSWERS TO CASE 43:

The Burned Patient

Summary: A 27-year-old man with severe burns and an orthopedic injury develops bleeding and dysrhythmias after undergoing emergency surgery.

➤ Most urgent priorities: Hypothermia. The patient’s hypothermia is life threatening, most likely causing the disturbance in cardiac rhythm, and perhaps, a coagulopathy. His high hematocrit is suggestive of dehydration. Warmed fluid for resuscitation, radiant-air warming, and maintaining a high environmental temperature are current critical priorities.

➤ Second priorities: Once the patient is stabilized, he should be taken promptly to the operating room for fixation of the open tibial injury. Although not immediately life-threatening as are the factors above, a delay in the fixation of the open injury risks loss of limb from infection.

➤ Laryngoscopic findings: Given the patient’s hoarseness and the carbonaceous material surrounding his nares, a difficult intubation should be anticipated due to swelling of the pharynx and vocal cords, potentially even obstructing the glottic opening.

ANALYSIS

Objectives

1. Become familiar with the major physiological changes after burn injuries.

2. Be able to identify the intraoperative anesthetic concerns in the burn patient.

3. Be able to recognize the potential for a difficult airway in burn patients.

Considerations

The initial 24-hour period following a significant burn is characterized by capillary leak, intravascular volume depletion, and a moderately decreased cardiac output. Fluid resuscitation using warmed crystalloid solutions is the mainstay of therapy during this period, in addition to the correction of any electrolyte abnormalities. Because of his rapidly changing fluid status, a largebore intravenous and central venous monitoring are probably warranted. Should frequent blood gas sampling be required because of a respiratory burn, an arterial catheter may also be warranted.

The patient should be warmed and resuscitated with warm fluids to increase his body temperature and restore his intravascular volume before proceeding to the operating room. The operating room temperature should be warm to hot. Warming blankets, fluid warmers, and heated humidification are indicated in attempt to maintain the patient’s body temperature.

The patient’s airway may be affected by the inhalation of heated, possibly toxic substances causing airway edema and lung injury, which can be worsened by fluid loading and capillary leak. In addition to swelling and erythema, a respiratory burn may be accompanied by friable tissue in the airway, perhaps with a propensity for bleeding. Intubation, if necessary, should be performed early before the airway becomes obstructed, and appropriate equipment available in case the patient cannot be intubated using direct laryngoscopy.

APPROACH TO

A Burned Patient

Major burns affect all organ systems in ways that are dynamic and sometimes contradictory. In the early phase of a burn injury, a loss of capillary integrity leads to a reduction in intravascular volume requiring fluid resuscitation, while extravascular fluid increases. The excess extravascular volume is subsequently reabsorbed, though this process is offset by evaporative losses. The net balance of these processes varies with the percentage and degree of the body burned, and from individual to individual. The later stage of a burn injury is characterized by a high cardiac output, a dramatically increased metabolic rate, and protein catabolism.

Fluid and Electrolyte Management

During the first 24 hours after a burn injury, capillary integrity to water, solutes, and plasma proteins is drastically impaired reducing intravascular volume, and increasing extravascular fluid volume. Intravascular volume is replenished with crystalloid fluid, typically lactated Ringer solution. Colloid solutions are not used because they have been linked to greater formation of pulmonary infiltrates and decreased urine output.

There are several formulas to guide early fluid requirements, the most established being the Parkland formula. This method calculates fluid requirements for the first 24 hours post burn as 4 mL/kg/% of total body surface area (TBSA) burned. Half of the calculated volume is given over the first 8 hours; the remainder, over the following 16 hours. More fluid can be given as necessary to maintain a urine output greater than 30 to 50 mL/kg/h. In certain circumstances, such as crush injuries or electric burns that produce myoglobinuria, a higher urine output may be desirable to prevent pigment nephropathy. If fluid intake is increased repeatedly without improvement in urine output, placement of a central venous catheter or pulmonary artery catheter may aid in evaluation of intravascular volume.

After 24 hours, the characteristics of the patient’s vascular system change as it begins to reabsorb extravascular fluid. At the same time, burns predispose to considerable evaporative losses. During the second 24-hour period, patients with substantial burns are generally given colloid solutions equal to 0.3 to 0.5 mL/kg/% TBSA burned, supplemented with 5% dextrose in water to maintain adequate urine output. Patients with smaller burned areas (<30% TBSA) may not require colloid and can often be given standard maintenance fluids. In the postresuscitation period, the goal of fluid management is to allow the patient to mobilize, excrete fluid, and return to normal preburn weight by postburn days 8 to 10. Thus, maintenance of fluid requirements after 48 hours is calculated to allow for daily losses of 2% to 3% of maximal body weight from insensate losses.

Electrolyte disturbances are common after burn resuscitation and should be carefully monitored perioperatively. After resuscitation, patients may be slightly hyponatremic from administration of high volumes of hypotonic fluids. Hyponatremia does not typically require treatment, and is usually corrected by postresuscitation diuresis. Patients may later become hypernatremic from excessive water losses and hyperglycemia-induced diuresis. Hyperkalemia, which also is common after large burns that destroy tissue, can be exacerbated by hypoventilation and acidosis. While ionized calcium is rarely affected by burn injuries, total calcium levels may be low because levels of serum-binding proteins are low.

Cardiovascular Management

Even within half an hour following a major burn, cardiac output can decrease substantially. The decrease is disproportionate to depletion of intravascular volume, and most likely reflects other neurohumoral mechanisms. Fluid resuscitation usually results in a return of cardiac output to normal levels. However, if oliguria persists even though pulmonary artery catheterization or echocardiography indicate fluid overload, inotropes such as dopamine or dobutamine may be required to increase cardiac output.

Shortly thereafter, fluid is reabsorbed and mobilized from the extravascular space. Cardiac output increases to supranormal levels, systemic vascular resistance is low, and there is an overall increase in metabolism. This response continues until burn wounds are grafted and fully healed.

Pulmonary and Airway Management

Multiple mechanisms contribute to the respiratory failure that occurs following a burn injury. Most commonly, toxins contained in smoke injure and inflame the airway. Upper airway edema may completely obstruct the airway, and lower airway edema may close small airways and lead to pneumonia. Patients at risk may have stridor, wheezing, hoarseness, facial burns, or carbonaceous sputum, but these signs are not always present. In many cases, fiberoptic bronchoscopy may be necessary to reveal inhalation injury.

If an inhalation injury is suspected, the airway should be secured promptly by endotracheal intubation since the development of edema is unpredictable and may worsen with fluid resuscitation. Patients are assumed to have a full stomach, indicating a rapid-sequence intubation in most cases. A small-sized endotracheal tube should be available, in case the glottis is swollen. For intubations which are predicted to be difficult because of airway swelling, atypical anatomy, or body habitus, the intubation is performed with the aid of a fiberoptic bronchoscope while the patient is breathing spontaneously. A supraglottic airway (eg, LMA) may not be useful in patients with glottic edema.

The inhalation of carbon monoxide is associated with a reduction in oxygen delivery even in the presence of normal gas exchange. Carbon monoxide binds to hemoglobin with 200 times the affinity of oxygen, shifting the oxyhemoglobin dissociation curve to the left and decreasing oxygen-carrying capacity. It is crucial to measure carboxyhemoglobin levels in patients with possible inhalation injury. Pulse oximetry and the measurement of simple arterial blood gases do not account for this effect, and may significantly overestimate oxygen delivery. Carbon monoxide poisoning should be suspected in any burn patient with confusion, loss of consciousness, or agitation, especially if the patient was burned in a closed space. A carboxyhemoglobin level greater than 10% confirms the diagnosis. Treatment consists of administration of 100% oxygen, using hyperbaric oxygen therapy if the patient is comatose or otherwise suffering from the more severe consequences of carbon monoxide poisoning.

Temperature Management

Burn patients are at high risk for hypothermia from loss of the protective barrier of the skin. This risk is proportional to the surface area burned. Hypothermia has multiple manifestations including coagulopathy, dysrhythmias, hypotension, and slow drug metabolism. The body’s primary responses to hypothermia (peripheral vasoconstriction and shivering) are inhibited by anesthetics. Shivering may increase myocardial oxygen consumption.

Maintenance of normothermia relies on heating intravenous fluids, humidifying inhaled gases, using forced-air heating blankets, and raising the environmental temperature. Although effective, forced-air heating blankets are used with caution in patients with extensive burns to avoid overheating devitalized tissue.

Pharmacologic Considerations

In burn patients, the responses to medications reflect alterations in drug metabolism and receptor physiology. In the immediate postburn period, drug clearance is impaired by decreases in intravascular volume, cardiac output, and hepatic and renal blood flow. In contrast, during the hypermetabolic postresuscitation period, the clearance of drugs is typically accelerated. Drugs which are administered either intramuscularly or enterally are variably and/or poorly absorbed when cardiac output is low. Decreases in the level of plasma proteins such as albumin and increases in levels of α1-acid glycoprotein alter drug metabolism.

Neuromuscular blocking drugs are a special concern in the burn patient. Succinylcholine can produce an exaggerated hyperkalemic response, leading to ventricular arrhythmias and cardiac arrest from the proliferation of immature extrajunctional acetylcholine receptors. The hyperkalemic response typically takes 24 to 48 hours to develop after the initial burn; its duration varies and can last years after burns have healed. Similar mechanisms may cause resistance to nondepolarizing neuromuscular blockers in burn patients. Incremental dosing with close monitoring of Train-of-Four is essential when using nondepolarizing neuromuscular blockers in this patient population. Succinylcholine is typically avoided.

The later stage of a burn injury is characterized by a high cardiac output, a dramatically increased metabolic rate, and protein catabolism. Levels of plasma proteins may be altered drastically, thus affecting plasma levels of free (not protein bound) drugs. Burn patients undergo changes in their neuromuscular junctions, which increase the requirement for nondepolarizing neuromuscular blocking agents. Depolarizing neuromuscular blockers can produce severe hyperkalemia. Management of this stage of a burn injury is multifaceted, and requires attention to nutrition, infection control, and the planning of reconstructive surgery (see Table 43–1). The surgical treatment of the burn wound is usually not the first priority, and is usually performed after the patient is stabilized and resuscitated. However, burn patients, as in the case above, may have other traumatic injuries, and these must be treated concurrently as the patient is resuscitated and stabilized.

Table 43–1
PHASE OF INJURY	CARDIAC OUTPUT	VASCULAR PERMEABILITY	METABOLISM
Early (first 48 hour)	Decreased	Increased	Normal to decreased
Late	Increased	Normal	Increased

Martyn JAJ, Abernethy DR, Greenblatt DJ. Plasma protein binding of drugs after severe burn injury.

Clin Pharmacol and Ther. 1984;35:534-536.

Comprehension Questions

43.1. A 34-year-old woman is admitted to the intensive care unit within 24 hours after sustaining burns over 80% of her body surface area. Which of the following is most likely increased in this 24-hour period?

A. Metabolism

B. Vascular permeability

C. Oxygen tension

D. Urine output

43.2. A 67-year-old man is scheduled for surgical debridement of a leg burn suffered 5 days ago. In the preoperative holding area, he receives midazolam and fentanyl. After induction with propofol and succinylcholine, the patient’s continuous electrocardiogram shows peaked T waves. Which of the following agents most likely caused the electrocardiogram changes?

A. Midazolam

B. Fentanyl

C. Propofol

D. Succinylcholine

43.3. A 19-year-old man in the emergency room has facial burns, carbonaceous sputum, and bilateral wheezing. He is agitated and confused. Abnormalities in which of the following most likely explain his neurological dysfunction?

A. Platelet count

B. Hemoglobin level

C. Carboxyhemoglobin level

D. Prothrombin time

ANSWERS

43.1. B. Vascular permeability increases in the initial phase after a burn injury.

43.2. D. The peaked T waves on ECG are suggestive of an elevated potassium level. Succinylcholine can produce an exaggerated hyperkalemic response in burn-injured patients.

43.3. C. Agitation and confusion are associated with carbon monoxide poisoning. Carboxyhemoglobin levels should be measured.

Clinical Pearls

➤ Burn injuries result in complex physiologic alterations that change over the course of the patient’s recovery.

➤ Although most surgeries on burn patients take place after resuscitation, patients may have additional injuries that require management in the early stages of the postburn period.

➤ Temperature control is of paramount importance, and requires the use of warming blankets, a warm ambient room temperature, and warm fluids.

➤ Succinylcholine is avoided except within the first 24 to 48 hours post burn.

➤ Early intervention is imperative in patients with an anticipated inhalation injury.

➤ Carbon monoxide poisoning is not accurately reflected in the patient’s SaO2 or PaCO2.

References

Goodwin CW Jr, Dorethy J, Lam V, et al. Randomized trial of efficacy of crystalloid and colloid resuscitation on hemodynamic response and lung water following thermal injury. Ann Surg. 1983;197:520. 

Martyn JAJ, Abernethy DR, Greenblatt DJ. Plasma protein binding of drugs after severe burn injury. Clinical Pharmacol Ther. 1984;35:534-536. 

Martyn JAJ, Richtsfeld M. Succinylcholine-induced hyperkalemia in acquired pathologic states: etiologic factors and molecular mechanisms. Anesthesiology. 2006;104:158-169.

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