Respiratory failure commonly occurs in patients with major cutaneous burns. Such patients often have associated inhalation injury, and the presence of inhalation injury significantly increases the mortality related with cutaneous burns. However, respiratory failure and the need for mechanical ventilation may occur in the absence of inhalation injury. There are recognized interactions between smoke inhalation and cutaneous burns (Figure 24-1). Pain management is an important aspect of the care of patients with burns, and may be associated with respiratory depression. Appropriate fluid management is difficult in patients with cutaneous burns, and fluid overload with associated hypoxemia and decreased lung compliance may occur. Sepsis can also occur, resulting in respiratory failure due to acute respiratory distress syndrome (ARDS). Burn patients may be hypermetabolic, which increases the ventilation requirement and may result in respiratory failure due to fatigue.
Respiratory dysfunction is central to the effects of smoke inhalation and cutaneous burns.
If full thickness circumferential burns of the thorax are present, severe chest wall restriction can occur. This will typically produce respiratory failure, and can make mechanical ventilation difficult. High ventilating pressures may be required, but may not place the patient at risk for overdistention lung injury because the transalveolar pressure may not be high due to the decreased chest wall compliance (Figure 24-2). Severe scarring and eschar formation can also restrict chest wall movement, and can result in difficulty weaning from mechanical ventilation. However, early surgical excision of the burn is commonly practiced, and this has reduced the need for escharotomies to improve chest wall compliance.
Effect of a stiff chest wall on transalveolar pressure. If the chest wall is stiff, there will be a greater increase in pleural pressure. Transalveolar pressure (the difference between the pressure inside and outside the alveolus) will be lower if the pleural pressure is increased. The amount of alveolar distention, and thus the risk of ventilator-induced lung injury, is decreased with a stiff chest wall. This is a setting where esophageal pressure monitoring is useful.
Inhalation injury is associated with increased morbidity and mortality. The effects of inhalation injury can be grouped by those related to thermal injury, parenchymal injury, and systemic toxins. Clinical predictors of inhalation injury are listed in Table 24-2.
Table 24-2Clinical Predictors of Inhalation Injury ||Download (.pdf) Table 24-2 Clinical Predictors of Inhalation Injury
• Exposure characteristics: closed space or entrapment, unconscious, inhaled toxin known
• Burns to the face and neck
• Carbonaceous sputum
• Respiratory symptoms: hoarseness, sore throat, cough, dyspnea, chest pain, hemoptysis
• Respiratory signs: pharyngeal inflammation and burns, stridor, tachypnea, cyanosis, abnormal breathing sounds (wheezes, rhonchi, stridor)
Because dry air has a low heat capacity, thermal injury to the lower respiratory tract is rare. However, inhalation of steam and explosive gases such as ether and propane can produce thermal injury to the lower respiratory tract. Thermal injury is almost always confined to the upper airway, which effectively cools hot gas before it reaches the lower respiratory tract. Thermal injury to the upper airway results in laryngeal edema, laryngospasm, swollen vocal cords, and increased mucus production. The diagnosis is made by examination of the upper airway, often using bronchoscopy.
Problems related to thermal injury to the upper airway usually occur within the first 24 to 48 hours. Due to the risk of complete obstruction of the upper airway, the symptomatic patient should be intubated. Many of these patients also require mechanical ventilation due to other severe associated injuries. However, some patients do not require mechanical ventilation, and can breathe adequately once the endotracheal tube bypasses the upper airway obstruction. If respiratory failure does not occur, these patients can often be extubated after several days, provided the upper airway swelling has improved. Bronchoscopic examination of the upper airway may be necessary before extubation, to assess the potential for obstruction if the patient is extubated. Due to the potential of complete upper airway obstruction with extubation, maintenance of a patent airway is paramount and vigilance is necessary to assure the security of the endotracheal tube. Securing the endotracheal tube can be difficult in patients with facial burns, and creative approaches for securing the airway are often necessary to prevent unplanned extubations.
Although thermal injury to the lower respiratory tract is unusual, injury due to the toxic chemical composition of smoke is common. Smoke inhalation can be harmful to both the airways and lower respiratory tract. Smoke inhibits mucociliary transport and induces bronchospasm. Airway obstruction due to retained secretions is particularly problematic in patients with preexisting lung disease, and severe bronchospasm can occur in patients with preexisting asthma.
ARDS commonly occurs in patients with smoke inhalation. The management of ARDS in this setting is similar to the management of ARDS in other settings, and includes oxygen administration, positive end-expiratory pressure (PEEP), and mechanical ventilation. The management of ARDS resulting from smoke inhalation may be complicated by sepsis, pneumonia, and fluid overload.
Systemic toxins include carbon monoxide (CO), cyanides, and a variety of nitrogen oxides. CO poisoning is the most important and the most common cause of death in fires. The toxicity of CO relates to the very high affinity of hemoglobin for CO, producing carboxyhemoglobin (HbCO). HbCO does not carry oxygen, and inhibits oxygen release from oxyhemoglobin (left-shifted oxyhemoglobin dissociation curve). Clinical effects of HbCO are related to hypoxia (Table 24-3). The diagnosis is made based upon symptoms and measurement of blood HbCO levels. Oxygen saturation and HbCO levels must be measured using CO oximetry. Arterial blood gases frequently demonstrate normal or increased Pao2, hyperventilation, and metabolic acidosis. The lethal effects of HbCO usually occur early after exposure. In patients who survive CO poisoning, symptoms may persist and occasionally get better and then worse.
Table 24-3Clinical Effects of Carbon Monoxide Poisoning ||Download (.pdf) Table 24-3 Clinical Effects of Carbon Monoxide Poisoning
|Carboxyhemoglobin level ||Physiologic effect |
|< 1% ||No effect |
|1%-5% ||Increase in blood flow to vital organs |
|5%-10% ||Increased visual light threshold, dyspnea on exertion, cutaneous blood vessel dilation |
|10%-20% ||Abnormal vision evoked response, throbbing headache |
|20%-30% ||Fatigue, irritability, poor judgment, diminished vision, diminished manual dexterity, nausea, and vomiting |
|30%-40% ||Severe headache, confusion, syncope on exertion |
|40%-60% ||Convulsions, respiratory failure, coma and death with prolonged exposure |
|> 60% ||Coma; rapid death |
The treatment for CO poisoning is oxygen administration. The half-life of HbCO is 4 to 5 hours breathing room air, 45 to 60 minutes breathing 100% oxygen, and 20 to 30 minutes breathing 100% oxygen at three atmospheres (hyperbaric oxygen). Use of 100% oxygen, and hyperbaric oxygen if available, is thus mandatory in the treatment of HbCO. Hyperbaric oxygen is useful even in patients with low HbCO levels who have prolonged neurological symptoms. Airway management and mechanical ventilation may be necessary due to depressed neurological status.