Chapter 42 Burns

Deaths from fires and burns are the fifth most common cause of unintentional injury deaths in the United States and the third leading cause of fatal home injury.^1,2 In 2008 someone in the United States died in a fire approximately every 158 minutes and was injured in a fire every 31 minutes.³ Burn injuries account for an estimated 700,000 visits to the emergency department (ED) annually; of these, 45,000 require hospitalization in a burn center.⁴ The high-risk, low-frequency exposure to burn-injured patients continues to be anxiety provoking to many emergency personnel. However, proper management in the ED is an essential first step in appropriately managing burn care and can have a significant impact on patient outcomes.

Pathophysiology

The body’s response to burn injury varies with the degree of tissue damage, cellular impairment, and fluid shifts. Damage to burned tissue causes the release of mediators that initiate an inflammatory response. The release of these mediators is associated with vasodilation and increased capillary permeability, resulting in intravascular fluid loss and tissue edema.⁶

Burn injury results in:

• Vasodilation

• Increased capillary permeability

• Intravascular fluid loss

• Tissue edema

Burn shock is the most significant component of burn pathophysiology. Direct thermal injury can result in dramatic changes in the microcirculation, particularly the increase in capillary permeability throughout the body. Burn shock is both hypovolemic shock and cellular shock.⁵ Table 42-2 summarizes the pathophysiology of hypovolemic burn shock. Table 42-3 describes the extensive effects of burn injury on the body.

TABLE 42-2 PATHOPHYSIOLOGY OF BURNS

TABLE 42-3 IMPACT OF BURN INJURY ON BODY SYSTEMS

Cellular Response • Direct thermal injury to endothelial cells with increased burn tissue osmolarity • Decreased tissue oxygen tension • Sodium and water shift into cell—intracellular swelling • Possible cell death • Shifting of potassium out of the cell resulting in increased serum potassium • Decreased oxygen level • Anaerobic metabolism begins • Increased lactic acid levels • Increased lactic acid levels lead to metabolic acidosis Cardiovascular System—First 24 Hours • Activation of the sympathetic nervous system and catecholamine release • Tachycardia • Vasoconstriction • During early phase: • Classic signs and symptoms of compensated shock • Dramatic decrease in cardiac output • Volume loss and decreased venous return • Decreased preload • Decreased cardiac filling pressure • Decreased central venous pressure and pulmonary artery occlusion pressure (PAOP) Respiratory System • Upper airway and parenchymal injury • Involves all airways to level of true vocal cords • Initially because of inflammation from heat of inspired smoke • Exacerbated by accumulation of excess interstitial fluid Neurologic System • Decreased cerebral perfusion • Cerebral edema as a result of sodium shifts • Carbon monoxide poisoning or associated head injury may cause neurologic changes Gastrointestinal System • Slowed peristalsis and possible ileus • Increased hydrochloric acid production from stress response • Narcotics for pain management further impair gastrointestinal function Immune System • Alters function of immune cells • Decreases “killing power” of neutrophils • Macrophages and lymphocytes ineffective Hematologic System • Destruction of red blood cells • Hemoglobinuria • Increased hemoglobin level and hemoconcentration • Increased white blood cells • Altered coagulation

Primary Assessment

Airway and Breathing

Airway, Airway, Airway!

• Assess it first, assess it often.

• When in doubt, intubate early.

All burn patients should receive supplemental oxygen by EMS personnel en route to the ED; its administration should be continued until deemed unnecessary. Intubation must be considered immediately in any patient with symptoms of a compromised airway.

Inhalation Injury

Assessment for inhalation injury should be completed on every burn patient on arrival at the ED. An inhalation injury cannot be ruled out until the components of the Inhalation Injury Triad have been considered (Fig. 42-1).

Fig. 42-1 Inhalation Injury Triad.

Mechanism of Injury

• Assess for burns that occurred in an enclosed space with heat or smoke exposure for an extended period of time. The likelihood of airway injury is greater in an enclosed space than it is outdoors.

• Consideration should be given to the toxins that can be produced when objects are burning in an enclosed space.

• Damaged cilia in the airway result in an inability to clear secretions and bacteria manifested by a tracheal bronchitis.⁷

Progressive airway edema should be expected in the first 24 hours in a patient with inhalation injury.

Assessment Data.

Any of the following may be evident with an inhalation injury:

• Dyspnea

• Hoarse voice

• Cough

• Anxiety or agitation

• Stridor

• Wheezing

• Facial burns, singed nasal hairs^5,8

• Presence of carbonaceous sputum

Elevated Carboxyhemoglobin.

Carboxyhemoglobin level may be as high as 50% to 70%. See Table 42-4 for signs and symptoms of elevated carboxyhemoglobin level.

TABLE 42-4 SIGNS AND SYMPTOMS OF ELEVATED CARBOXYHEMOGLOBIN

Carboxyhemoglobin Saturation Percentage and Symptoms
5–10	Mild headache and confusion
11–20	Severe headache, flushing, dilation of skin vessels
21–30	Disorientation, nausea
31–40	Irritability, dizziness, vomiting, prostration
41–50	Tachypnea, tachycardia, prostration
51–69	Coma, seizures, convulsions, Cheyne-Stokes respiration. Death is possible
70–80	Slowing/stopping of breathing, death within hours
80–90	Death in less than 1 hour
90–100	Death within a few minutes

Data from Essig, M. G. (2008, March 18). Carbon monoxide (CO). Retrieved from http://firstaid.webmd.com/carbon-monoxide-co

Carbon Monoxide Poisoning

The majority of fatalities that occur at the scene of a fire are the result of asphyxiation or carbon monoxide poisoning. Carbon monoxide poisoning is also the most immediate threat to life in survivors of inhalation injury.

• Carbon monoxide binds to hemoglobin 200 times more effectively than oxygen does; tissue hypoxia occurs if sufficient hemoglobin is bound to carbon monoxide.⁹

• The skin of a patient with high carbon monoxide levels may appear cherry red in color, but this has been observed in only 50% of patients with severe carbon monoxide poisoning.

• Although the oxygen content of the blood is diminished, the amount of oxygen dissolved in the plasma (PaO₂) is unaffected by carbon monoxide poisoning; the arterial blood gas will appear normal.

• Pulse oximetry detects saturated hemoglobin and does not measure carbon monoxide, so the oxygen saturation usually appears normal.

• A serum carboxyhemoglobin level must be determined in any patient with potential exposure to carbon monoxide during a fire.

Management of Carbon Monoxide Poisoning or Inhalation Injury

• Immediately administer 100% oxygen if this has not been accomplished by EMS personnel prior to arrival at the ED.

• If the airway is compromised in any way, endotracheal intubation should be performed and difficult airway supplies should be available. See Table 42-5 for considerations for early intubation.

• Intubation can often be difficult in this patient population because of swelling of the face and hypopharynx.⁹

TABLE 42-5 CONSIDERATIONS FOR EARLY INTUBATION

• Agitation resulting from hypoxia, decreased level of consciousness • Carbonaceous sputum • Hoarseness, stridor • Progressive edema • Oral or nasal erythema • Inability to handle secretions • Crackles, rhonchi, diminished breath sounds • Facial burns, singed nasal hairs Only gold members can continue reading. Log In or Register to continue Share this: Click to share on Twitter (Opens in new window) Click to share on Facebook (Opens in new window) Related Related posts: Workplace Violence and Disruptive Behavior Alcohol Abuse Hematologic and Immunologic Emergencies Sepsis Triage Spinal Cord and Neck Trauma Stay updated, free articles. Join our Telegram channel Join Tags: Sheehys Manual of Emergency Care Aug 9, 2016 | Posted by admin in EMERGENCY MEDICINE | Comments Off on Burns Full access? Get Clinical Tree Get Clinical Tree app for offline access Get Clinical Tree app for offline access