Pulmonary Injury inBurn Patients

Bruce M. Potenza

The diagnosis and treatment of pulmonary problems encountered in patients with severe burn injuries may be challenging. Pulmonary injury may occur as a sole entity or in combination with cutaneous burn injury. Approximately 30% of patients with cutaneous burns will have an associated pulmonary injury. The presence of smoke inhalation with a cutaneous burn may increase mortality by 20% to 50% depending upon the size of the burn. Eighty percent of all burn fatalities result from smoke inhalation, with most occurring in house fires and at night. Care for patients with smoke inhalation ranges from supplemental oxygen and β-agonist nebulizers to advanced ventilator management and bronchoscopy. The course of pulmonary support in burn patients is different from that for general medical and surgical patients requiring respiratory assistance. This is, in part, due to the pathophysiology of inhalation injury compounded by the long hospital course associated with a large burn.

INHALATION INJURY

Exposure to smoke and flame in an enclosed area such as a home, automobile, industrial building, tank, or silo is the major risk factor for smoke inhalation injury. In a closed-space fire, the oxygen concentration of the atmosphere may be 10% or less depending upon the fire characteristics. The toxic byproducts of combustion are confined, resulting in high concentrations of carbon monoxide (CO), aldehydes, ammonia, hydrogen (chloride, cyanide, and sulfide), phosgene, and sulfur dioxide. Some of these gases, which are heavier than air, settle at the lower levels of the enclosed space increasing the exposure of a victim who is crawling to escape the fire or is lying unconscious. In addition, more particulates tend to be released during a fire in a closed space and act as a vehicle to deposit the toxic byproducts of combustion deep into the respiratory tract. Industrial inhalation injuries may occur without a fire when workers are exposed to noxious aerosolized chemicals in a confined space. Often, these patients become unconscious due to the prolonged exposure.

Clinical signs and symptoms of inhalation injury may include facial, neck, and upper torso cutaneous burns; singed eyebrows, nasal and scalp hair; and soot in the nares, mouth, or hypopharynx. The patient may exhibit a change in voice (hoarseness or high-pitched) or stridor. Additional findings may include tachypnea, hypoxemia, and the presence of carboxyhemoglobin. Bronchoscopic confirmation of airway injury includes soot deposition, respiratory epithelial edema, hyperemia, ulceration, sloughing, or hemorrhage.

Inhalation injury is composed of three separate pathophysiologic mechanisms: injury due to particulate matter, toxic byproducts of combustion, and direct thermal injury. Any one or all three mechanisms may be involved in any patient. Inhalation injury due to particulate matter (smoke and soot) depends upon the size of the particles that are deposited in different anatomic areas. Larger particles are deposited proximally in the nares, concha, and hypopharynx. Smaller particulates are transmitted into the trachea and bronchioles. These smaller particles adhere to the respiratory epithelium and tend to incite or exacerbate reactive airway problems best treated with β-agonists and supplemental oxygen. It is usually a self-limiting process, but, in patients with a long exposure time, intubation and bronchoscopy to evaluate the airways and facilitate airway clearance may be indicated. Particulate matter that is adherent to the lower respiratory epithelium may take 24 to 48 hours to fully clear in moderate cases and up to 3 days in severe smoke inhalation.

The classic model for inhalation injury due to toxic byproducts of combustion is CO poisoning. Other frequent byproducts include cyanide, hydrogen chloride or sulfide, ammonia, and formaldehyde. Cyanide poisoning is difficult to diagnose, since there is no readily available laboratory test to confirm the diagnosis in real time. The presence of a persistent anion gap acidosis and elevated serum lactate is supportive evidence of cyanide poisoning.

Treatment for CO poisoning is high-flow oxygen. CO has a 200- to 250-fold higher affinity to bind hemoglobin than oxygen. The half-life of CO is 320 minutes on room air (21% FIO₂), but can be reduced to 90 minutes at 100% FIO₂. Most hospital and paramedic pulse oximeters cannot differentiate oxyhemoglobin and carboxyhemoglobin. Therefore, a patient with a high CO level may still have a high oxygen saturation level measured by the pulse oximeter. The correct oxygen saturation can be determined from the arterial blood gas and is often significantly lower. The actual CO level can be measured from an arterial or venous blood sample. It is our policy (extrapolated to the prehospital area) to place all patients with a history of fire exposure in a closed-space environment on high-flow 100% oxygen until the oxygen saturation and CO levels are validated by a blood gas.

Patients with high CO levels may be candidates for hyperbaric oxygen therapy to reduce serum CO levels but, more importantly, reduce central nervous system levels of CO. Long-term cognitive deficits are seen in 10% of patients with CO poisoning; hyperbaric therapy may reduce this. Three “dives” in a hyperbaric chamber are typically completed within the first 24 hours of exposure in patients with CO levels greater than or equal to 25%. Care must be taken in the burn patients to ensure that they are sufficiently hemodynamically stable to undergo hyperbaric treatment. If unstable, the dive should not be attempted. Cyanide poisoning is treated with hydroxycobalamin (CYANOKIT^®) and, if this is not available, amyl nitrate.

Direct thermal injury is the least common form of smoke inhalation and represents an injury that occurs with a very intense heat source or with lesser heat and long exposure. These injuries result in airway edema; respiratory epithelial sloughing or ulceration; and copious production of thick, tenacious sputum. Intubation and bronchoscopic evaluation and aggressive pulmonary toilet are indicated in these patients. Secondary postobstructive pneumonia and acute respiratory disease syndrome (ARDS) is not uncommon in these individuals.

CHRONIC OBSTRUCTIVE PULMONARY DISEASE AND FACIAL BURNS

A special situation in the burn unit is the patient with chronic obstructive pulmonary disease (COPD) on supplemental oxygen who has been smoking and suffers a flash burn to the face and nares. This usually results in a small, 1% to 2% total body surface area (TBSA) partial thickness burn that does not require grafting. The mucosa of the nose, however, often is burned and results in edema and sloughing. This makes the act of breathing more difficult and uncomfortable requiring these patients to breathe predominantly through their mouth. They may develop severe rhinorrhea and epithelial sloughing and require aggressive external pulmonary toilet. Admission for 24 to 48 hours is usual and permits serial burn wound care to the face as well as good pulmonary toilet—intubation or mechanical ventilation usually is not required as the actual burn injury is small, superficial, and does not extend distal to the nasal or hypopharyngeal tissue. Nevertheless, they are prone to develop pneumonia as a late complication within a week of the burn injury, so it is very important to follow these patients carefully after discharge.

INTUBATION

The control and maintenance of the airway in a burn-injured patient is a high priority and may be quite challenging. Direct burn injury to the face and upper airway may create a critical situation where intubation and mechanical ventilation are lifesaving. Edematous oral, pharyngeal, and supraglottic tissue may complicate airway control. Traditional landmarks may be distorted and the ability to preoxygenate such patients tends to be limited. One must be prepared to secure an airway with direct laryngoscopy and an endotracheal tube or establish an airway surgically with an emergent cricothyroidotomy.

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