Airway Management in Burn Patients

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Chapter 44 Airway Management in Burn Patients

Bettina U. Schmitz, John A. Griswold

I Introduction

The airway of the burn patient presents ongoing challenges and special considerations during the period of initial burn injury and throughout the patient’s hospital course. As a consequence of their injuries, some burn patients have airway difficulties throughout the remainder of their lives.

The National Burn Repository reports 181,000 hospital admissions for burn injury for 1998 through 2007 in 73 U.S. burn centers. The overall mortality rate during this period was 4.9%.¹ A 2006 report of the National Burn Repository indicated an incidence of inhalational trauma of 5.7% during the previous 10 years.² Inhalational burn trauma was associated with a 27.3% mortality rate, compared with a rate of 4.5% for burned patients without inhalational injury.² A review of 850 children admitted with inhalational injury during a 10-year period at the four Shriner’s Pediatric Burn Centers in the United States found a mortality rate of 16.4%.³ Consequently, inhalational burns contribute significantly to mortality among the burn population. Although the outcomes for survival after burns and the quality of life of burn victims have improved, respiratory complications are an ongoing source of burn morbidity and mortality.

II Airway Management in the Acutely Burned Patient

A Evaluation of the Patient after Acute Burn Injury and Indication for Airway Management

1 Assessment at the Scene

First responders have a crucial role in the early management of burn patients. In addition to the usual trauma assessments, emergency medical service (EMS) staff must determine whether the patient’s condition warrants immediate intubation in the field or the patient can be observed. Indications for intubation at the trauma scene include the following ^4,⁵:

• Unconsciousness and altered mental status (with incumbent aspiration risk)

• Respiratory distress (e.g., desaturation with supplemental oxygen [O₂], tachypnea)

• Thermal airway injury

• Hoarseness, stridor, dysphagia, or drooling

• Burn injury to the neck and face after fire or smoke exposure in a closed space or carbonated sputum

• Prolonged transport to the hospital of the patient with possible airway injury

• Extensive burn injury

• Additional traumatic injuries

Patients with a flame injury from a barbecue or fire in an open space may have burns to the neck and face but no airway involvement and therefore do not require early intubation.

In addition to initial medical management of the patient, EMS staff gathers information about the type of injury and the patient’s medical history. The information should be recorded for transport with the patient to a specialized burn center.

The practice of prehospital intubation of the burned patient has been questioned. Eastman and colleagues ⁶ reviewed the charts of 1272 patients admitted after field intubation over a period of 23 years and found that 69% of them survived. However, 30% of the survivors were extubated on admission or on the second day after the burn. None required reintubation. Klein and associates⁷ reviewed the charts of patients admitted to the Washington Burn Center after a transport of more than 90 miles for the period of 2000 through 2003. They examined parameters such as duration of transport, error in burn severity estimation, fluid management, appropriateness of intubation, and transport complications. Of 1877 patients, 424 were transported more than 90 miles to the burn center. No patient died during transport, and 111 patients arrived intubated, with only 61% having inhalational burns. More than 50% of patients were extubated within the first 24 hours after admission.

Failure to secure an airway was one of the most common complications occurring during patient transport. The fact that airway obstruction can develop very quickly in burn patients and that the experience and equipment of EMS are often limited supports intubation in the field before transport in the patient with a potential for respiratory compromise.

2 Assessment in the Hospital

Roughly 10% of burn patients also present with other traumatic injuries. All burn patients are considered trauma patients and consequently undergo a primary trauma survey (i.e., the ABCDE algorithm: airway, breathing, circulation, disability, and exposure).⁸ The extent and surface area of the burn are noted, other traumatic injuries identified and treated, and the airway secured if indicated. The incidence of inhalational trauma, length of hospital stay, and mortality rate are increased for patients presenting with burns and other traumatic nonburn injuries.⁹

On arrival of the patient at the burn center, the tube position is confirmed with carbon dioxide (CO₂) monitoring and auscultation of the lung fields. Uncertainty about endotracheal tube (ETT) placement should be remedied by direct laryngoscopy or fiberoptic bronchoscopy. The mouth, pharynx, and larynx are examined by laryngoscopy to assess edema and identify any burned mucosa and the presence of soot (Fig. 44-1). A radiograph is obtained to verify the ETT position and identify other potential injuries, such as a pneumothorax. Lung parenchymal injuries usually are not immediately detectable by radiography immediately after injury. Patients presenting with a supralaryngeal airway (SLA) on arrival at the hospital require endotracheal intubation or a surgical airway.

Figure 44-1 Carbonaceous sputum, singed nasal hairs, and facial burns indicate possible upper airway thermal injury.

In the unintubated patient, the presence of soot in the sputum, dyspnea, tachypnea, hoarseness, and stridor are signs of impending airway obstruction. Fiberoptic endoscopy is the gold standard for the diagnosis of inhalational trauma.¹⁰^–¹⁷ In the awake patient, a nasal fiberoptic examination under local anesthesia can be performed to evaluate the larynx and confirm the presence or absence of edema and soot. Patients with altered mental status, dyspnea, hoarseness, or stridor require immediate intubation.

A relevant history for airway management after burn injury includes the following information:

• Location and type of injury (e.g., flame, steam, chemical, electrical, vehicular)

• Mental and physical condition at the scene of injury and changes during transport

• History of a difficult airway

• Circumstances of the burn (e.g., open space, closed space)

• Other traumatic injuries

• Other medical history ^10,^12,^18,¹⁹

Rarely, inhalation of hot steam and hot fluids can lead to a rapidly progressive upper airway edema. Chemical fires can have more complex sequelae because the chemicals themselves can injure tissues after extinction of the fire. The circumstances of the burn injury and its duration can help to discern the likelihood of carbon monoxide (CO), cyanide (CN), and other toxicities.

6 Extensive Burns

Patients with large body surface area burns frequently have airway burns as well (Fig. 44-3). Edema after resuscitative efforts can make intubation impossible. After massive burns, patients develop a hypermetabolic state leading to increased CO₂ production requiring ventilator support. Some physicians suggest prophylactic intubation for total body surface area burns greater than 30%.^10,^12,^17,²²

Figure 44-3 Extensive burns to the chest and neck can require immediate escharotomy to facilitate ventilation.

7 Additional Injuries

Burn injuries can occur in explosions. In this setting, blast injuries, including pneumothorax and eardrum perforation, must be addressed. To escape a fire, victims often jump from windows, sustaining fractures. Burns caused by vehicular trauma can be associated with other traumatic injuries. Electrical high-voltage contact can be accompanied by brain edema, cardiac dysrhythmias, myonecrosis, and rhabdomyolysis with renal injury. C-spine injury should be ruled out as expeditiously as possible in the course of patient management, depending on the nature of the primary injury.

B Inhalational Injury

Approximately 20% to 30% of patients admitted to regional burn centers have some degree of inhalational injury and are at risk from toxic gases.^19,²⁴ Edelman and colleagues²⁵ reviewed 829 patients admitted to a burn center between 2000 and 2004 and found that 28% had an inhalational injury. Although the mortality rate for patients with solely a thermal injury was 3% and was 12% for those with an isolated inhalational injury, patients with combined thermal and inhalational injuries had a mortality rate of 14.6%.²⁵ Box 44-1 summarizes smoke inhalational injuries.

Box 44-1 Smoke Inhalational Injuries

• Inhalation injury occurs in 20% to 30% of burn patients.

• Inhalation injury increases burn mortality.

• The leading cause of immediate death from burns is inhalational injury, not the burn itself.

• Heat injury is confined above the vocal cords.

• Inhalation damage is caused by toxic chemicals and thermal injury.

• Sequelae of inhalational burns include pulmonary edema, mismatch, atelectasis, airway obstruction, and pneumonia.

• Carbon monoxide (CO) and cyanide (CN) systemic toxicities should be suspected with burns in confined areas.

1 Injury to the Respiratory Tract

a Upper and Lower Airway Inhalation Smoke Injury

Inhalational injury of the airway can be caused by steam, carbenoids, chemicals, and the toxic products of combustion. In most patients, the entire airway is involved, and several toxic agents are inhaled. Inhalational injury results from thermal injury (heat) to the upper airway, toxic chemicals in the respiratory tract, and CO and CN toxicities.

Thermal injury and inhaled chemical toxins cause burn injuries by different mechanisms. In an enclosed environment, temperatures can exceed 800° C, with an O₂ concentration of just 10% and CO concentrations greater than 0.5%.^26,²⁷ Injuries are often described by the area of the tracheobronchial tree affected. The upper airway lies above the vocal cords, whereas the lower airway consists of the tracheobronchial tree, including the terminal bronchi and alveoli.

The upper airway consists of the nasal and oral cavities, the pharynx, and laryngeal structures such as the epiglottis, false vocal cords, and true vocal cords. Direct injury of the upper airway with steam, superheated air, or hot liquid is rare. The heat-conducting capacity of air is low, reducing the potential for injury. Reflex closure of the glottis usually protects the structures below the vocal cords from steam injury. Signs of upper airway injury by heated air and steam include erythema, edema, ischemia, and pharyngeal ulcerations. Although the initial presentation of injury may be unimpressive, these lesions can quickly lead to airway edema and obstruction.

The lower airway includes the tracheobronchial system and the lung parenchyma. Most injuries of the upper and lower airway result from the chemical toxins produced by combustion. Burned rubber and plastics release ammonia, chloride, sulfur, and nitrogen dioxides. Cotton and wool fires produce toxic aldehydes, including formaldehyde. Laminated structures produce cyanide.^16,^21,^22,²⁸^–³⁰

b Pathophysiology of Smoke Inhalational Injury

Different mechanisms contribute to the pulmonary changes after smoke inhalation. An increase in bronchial perfusion contributes to the development of pulmonary edema, as does the increased permeability of the pulmonary vasculature caused by an increase in nitric oxide (NO).

NO formed from arginine by nitrous oxide synthetase (NOS) has an important role in pulmonary changes after smoke injury. Smoke inhalation stimulates vasomotor and sensory nerve endings in the tracheobronchial tract, releasing neuropeptides with bronchoconstricting properties. Neutrophil activation produces reactive oxygen species (ROS), increasing the activity of NOS.³¹

Increased NO in the lung reduces hypoxic pulmonary vasoconstriction, leading to ventilation-perfusion ()) mismatch and edema formation. O₂ and NO react to form peroxynitrite. Peroxynitrite causes cellular injury and damage to cell membranes that results in increased pulmonary vascular permeability and pulmonary edema. Peroxynitrite, other reactive O₂ species, and reactive nitrogen (N₂) species damage DNA. In an effort to repair damaged DNA, poly(ADP-ribose) polymerase (PARP) is activated. PARP uses ATP energy reserves to repair damaged DNA. Depletion of ATP by PARP activity results in cell death.³²^–³⁵

The coagulation cascade is activated, leading to fibrin deposition in the airway. Airway casts are formed, often obstructing the airway and impairing gas exchange in the lungs. Inhibition of surfactant leads to alveolar collapse, atelectasis, and mismatch.^11,^16,^21,^28,^34,³⁶

d Diagnosis

The gold standard for the diagnosis of an inhalational injury is direct or fiberoptic inspection of the larynx and tracheobronchial tree. Initial evaluation should document the presence and extent of injury to establish a baseline of the airway injury. Recurrent examinations are needed to evaluate the course of injury and to remove necrotic tissue to prevent airway obstruction and atelectasis.¹⁰^–¹⁷

Flow-volume curves are difficult to obtain and depend on the patient’s effort, making them less useful for discerning airway obstruction and compromise in the acute burn patient.^10,¹⁶ The arterial blood gas determination may not demonstrate any abnormalities during the early stage of airway injury,^10,¹⁶ and the radiograph obtained at presentation may not reveal any pathologic changes caused by the burn. Previous changes and nonburn injuries, however, are evident. Radioisotope evaluation of the lungs can demonstrate injury to the lung parenchyma and small airways. After intravenous injection of xenon 133 or inhalation of technetium 99, the healthy lung can rapidly clear the isotopes, but injured parenchyma clears isotopes in a delayed and uneven manner. This type of testing is not practical in the acutely injured patient.^16,^17,²¹

2 Systemic Toxicity from Inhalational Injury

a Carbon Monoxide Poisoning

CO is a product of combustion. It is a colorless, odorless, tasteless gas. Burn victims injured in a confined space should always be evaluated for possible CO poisoning. CO has great avidity for the iron of hemoglobin and cytochrome oxidase. CO’s affinity for hemoglobin is 200 times greater than that of O₂. Moreover, carboxyhemoglobin shifts the O₂ dissociation curve to the left, impeding the delivery of O₂ to the tissues. CO binds to cytochrome oxidase in the mitochondria, impairing O₂ use on a cellular level and producing tissue hypoxia and acidosis.^6,^10,^13,^21,²⁸

CO poisoning is the leading cause of poisoning death in the United States.³⁷ It is often missed because the signs and symptoms are nonspecific, including fatigue, headache, weakness, dizziness, confusion, and loss of consciousness.^10,³⁸ A history, examination, and laboratory studies are required to make the diagnosis of CO poisoning and to plan treatment.³⁹^–⁴³

The history should elicit the circumstances of burn (e.g., closed-space fire), time of exposure, and source (e.g., internal combustion engines in closed space, smoke inhalation, stoves, furnaces). The examination should take into account the pathophysiology of burn injuries, including an affinity of CO for hemoglobin that is 240 times more than that of O₂, reduced hemoglobin O₂ carrying capacity, tissue hypoxia, and the leftward shift of the hemoglobin dissociation curve.

Laboratory tests include pulse oximetry and O₂ saturation, but O₂ partial pressure does not reflect CO poisoning.^10,^13,¹⁷ Carboxyhemoglobin is measured and normally is less than 2% in nonsmokers. The carboxyhemoglobin level is slightly higher in pregnant patients due to fetal CO. The concentration of carboxyhemoglobin is chronically 3% to 8% in smokers and more than 10% to 15% after smoking.

Symptoms of CO poisoning include headache, nausea, fatigue, and dizziness with carboxyhemoglobin levels between 10% and 20%. Few symptoms occur with levels lower than 10%. Disorientation may occur with carboxyhemoglobin levels between 20% and 40%; stupor or coma with levels between 40% and 60%; and death with levels greater than 60%. Pets exposed to CO can likewise be affected.

Treatment includes 100% O₂ administered to all burn victims. This level of O₂ accelerates the dissociation of CO from hemoglobin by 50% every 30 minutes. Patients with CO-hemoglobin levels between 20% and 25% should be intubated. Hyperbaric O₂ therapy increases the elimination of CO and can be considered for unconscious patients.^11,^13,^22,²⁸ No data suggest that hyperbaric O₂ therapy mitigates any long-term sequelae of CO poisoning. Limited availability of these chambers and difficulties accessing the patient while in the chamber impede the use of hyperbaric therapy for acute care of burned patients.

Sequelae include delayed neurologic symptoms such as ataxia, mental degradation, and incontinence, which are seen in 12.5% of patients with high initial CO-hemoglobin levels. Computed tomography (CT) can demonstrate decreased density of the globus pallidus.^10,^11,^13,^16,^17,²¹

b Cyanide Poisoning

CN is the product of burning plastics containing high amounts of nitrogen, such as polyurethane, polyacrylonitrile, and acrocyanate. CN causes asphyxia at the cellular level by inhibiting cytochrome oxidase and preventing mitochondrial respiration. O₂ consumption is reduced through interruption of the tricarboxylic acid cycle, and anaerobic metabolism occurs with the development of a lactic acidosis.^10,^11,^13,^16,⁴⁴

A history, examination, and diagnostic studies are required to determine CN poisoning and its treatment. Inhalational injury in a confined space makes CN poisoning more likely, as does an increased CO-hemoglobin concentration. Measurement of blood CN concentration can be made but may not be immediately available. Levels between 0.5 and 1 mg/L are considered toxic, and levels above 1 mg/L are thought to be lethal.^13,^44,⁴⁵

The symptoms, including headache and confusion, are similar to those of CO poisoning. Electrocardiographic changes may be seen, and seizures may occur. Loss of consciousness is often transitory in CO poisoning but is sustained in CN poisoning. Bradypnea occurs in CN poisoning but is not found in CO poisoning. Pupillary dilatation may occur in CN poisoning but is not frequently found in CO poisoning.

Therapy includes amyl nitrite and sodium nitrite to induce methemoglobinemia, which binds with CN. Thiosulfate is a substrate in the metabolism of CN into less toxic thiocyanate by hepatic rhodanese. Hydroxycobalamin also binds with CN, forming nontoxic cyanocobalamin. Hydroxycobalamin has minimal side effects, whereas methemoglobinemia reduces tissue O₂ delivery to patients with impaired use of O₂ at the cellular level.^44,⁴⁶^–⁵¹

C Airway Management Approaches

1 Airway Management in the Field

Intubation when indicated should be performed at the scene according to locally established management protocols. Video-assisted intubation can be performed if the equipment is available. Depending on the nature of the injury, C-spine precautions should be employed. All patients should have a rapid-sequence induction.

If intubation is difficult in the upper airway patent, an SLA (e.g., laryngeal mask airway [LMA], King LT, Easytube, Combitube) can be employed as needed. Unfortunately, none of these devices protects the airway from aspiration. Moreover, with time, airway and laryngeal edema make ventilation with an SLA progressively difficult, and when necessary, a surgical airway should be employed.³⁰

2 Airway Management in the Hospital

Airway assessment is performed as previously described using fiberoptic bronchoscopy. Signs of airway injury include the following:

• Airway soot

• Erythema, edema, or ulceration

• Mucosal fragility

• Increased secretions

• Loss of cough reflex (indicates greater depth of mucosal injury)

• Mucosal necrosis

Evaluation of the lower airway requires airway topicalization and sedation. Evaluation of the upper airway can determine the need for intubation. After intubation, fiberoptic evaluation of the tracheobronchial tree can proceed. Patients with significant soot, hyperemia, and edema are intubated immediately. Patients without such symptoms can be observed and undergo serial airway examinations. Anesthetic agents to facilitate intubation must be selected on an individual basis. Combined propofol and ketamine may be useful to facilitate intubation with minimal perturbations of the patient’s hemodynamics.

Rapid-sequence intubation techniques should be employed because the patients are unlikely to have been fasted before their burn. Succinylcholine is considered safe to administer in the first 24 hours after a burn. After this 24-hour window, succinylcholine use is contraindicated due to the development of immature nicotinic receptors over the muscle membrane, which can lead to hyperkalemia after succinylcholine administration.⁵² These receptors occur at the neuromuscular junction and over the entire muscle membrane. Moreover, the prolonged channel opening time of these receptors contributes to the release of potassium from the myocyte. Over time, the number of receptors returns to baseline as the burn heals; however, the patient may be at risk for hyperkalemia for up to 2 years.^53,⁵⁴

In patients with severe neck burns, laryngoscopy can be impossible, necessitating a surgical airway. The precise airway tools to employ depend on the individual practitioner’s preference. Fiberoptic intubation limits movement of the head and neck but may be impossible in the sooty, bloody airway of the burn patient with a smoke inhalation injury. Various video laryngoscopes can be used to provide airway visualization, especially when in-line stabilization is employed for patients at risk for C-spine injury. Surgical airway approaches should always be considered and employed when needed.

In patients presenting with a LMA in place, fiberoptic intubation through the LMA can be performed. The Aintree intubation catheter can be placed with fiberoptic endoscopy into the trachea, the LMA removed, and an ETT passed into the trachea. Chapter 50 further explains this technique.

In patients arriving with an Easytube, Combitube, or VBM Laryngeal Tube in place, an Airtraq intubation device can be inserted between the tongue and the laryngeal tube, and after partial deflation of the laryngeal tube cuff, the Airtraq can be advanced until the cords are visualized. Other devices, such as any of the video laryngoscopes, flexible fiberoptic laryngoscopes, or fiberoptic stylets can be used in the same fashion. Leaving the SLA in place permits O₂ delivery while intubation is attempted. Direct laryngoscopy with in-line stabilization when indicated can also be employed. Surgical airways should be performed when intubation appears doubtful and is needed. Surgical airways should not be delayed for multiple attempts at direct or video laryngoscopy. The same considerations that complicate intubation also complicate the performance of a surgical airway in the burn patient. An SLA often can be employed to provide ventilation while a definitive surgical airway is obtained. A cart for the management of a difficult airway should be available with a variety of devices, catheters, video laryngoscopes, and a surgical airway tray when inhalation burn patients are treated.

3 Airway Management in Burned Children

Because of their small airway diameters, even a modest degree of airway edema in pediatric patients can lead to airway collapse. Because the resistance to flow is inversely proportional to the fourth power of the radius of the tube, decreasing the radius by one half increases resistance 16-fold.

Loss of airway and aspiration is the fourth most common cause of death cited in a study of pediatric burn patients.^55,⁵⁶ Intubation may be indicated when the amount of resuscitative fluid is predicted to be more than 180 mL/kg.⁵⁷ Intubation with a Miller blade is often successful in children because the high position of the larynx requires lifting of the epiglottis. Cuffed ETTs are preferred because they allow the delivery of higher ventilator pressures and eliminate the need for repeated laryngoscopy and exchanges of the endotracheal tube if the leak is too great.^56,⁵⁸

4 Tracheotomy

Tracheotomy is performed in burn patients when laryngoscopy and intubation attempts fail. Elective tracheotomy for burn patients who need prolonged periods of positive-pressure ventilator support has been associated with airway strictures and stenosis after recovery.^10,^13,^37,⁵⁹ However, most studies do not identify an increased risk of tracheotomies in burn patients compared with other populations.⁶⁰^–⁶³ In a retrospective study, Namdar and colleagues⁶⁴ demonstrated that tracheotomy permitted the use of lung-protective ventilation strategies in burn patients. However, Saffle and assocates⁶⁵ found no benefit for early tracheotomy as far as duration of ventilator support, length of stay, infection complications, or survival. In the pediatric population, tracheotomy caused no increased risk of complications.^38,^66,⁶⁷ The potential loss of the airway is less in children with a tracheotomy than those with an ETT in place. Some studies have found that percutaneous tracheotomy has reduced mechanical ventilation, hospital stay, and cost compared with traditional surgical tracheotomy.^61,⁶⁸^–⁷¹

5 Securing the Artificial Airway

Securing the ETT of the burned patient can be challenging. Ideally, the ETT should be fixed without producing additional facial injuries and adjust to facial swelling. Taping usually is ineffective in securing the ETT. Suturing the tube to the gums, wiring it to a tooth, wiring it to brackets anchored to the enamel of the incisors, and circumferential fixation devices have all been employed.⁷² Tying the tube with sling ribbon (umbilical tape) or even use of a disposable surgical free mask can secure it to the head. Care must be taken so that the items tied about the head do not lacerate the corners of the mouth or the ears. The tape stops must be checked routinely because facial edema can expand and pull the tube out of the trachea. If a leak develops, fiberoptic laryngoscopy can be used to guide the ETT back into the trachea. The ETT’s position and taping should be checked frequently, especially during changes in patient position and after patient transport.

6 Extubation of the Burn Patient

a Extubation of the Burned Patient after 12 Hours of Intubation

After a burn injury, patients are at risk for strictures, granulomas, and airway stenosis. Patients can be symptomatic immediately after ETT removal, or strictures can develop over time, leading to progressive airway stenosis.

Before extubation, the upper airway should be assessed for patency. Fiberoptic inspection of the larynx and airway is useful to identify potential sources of immediate extubation airway loss. The patient’s other critical illnesses also should be corrected before considering extubation. Any gastric feedings should be discontinued at least 4 hours before extubation, and the patient should be free of ileus and gastrointestinal bleeding. All burn patients should pass a CPAP trial, fulfill routine extubation criteria, and have a leak around the deflated ETT cuff.⁷³

Extubation should be delayed if the patient requires an increased fraction of inspired oxygen (FIO₂) of more than 40%, pressure support of more than 10 cm H₂O, high minute ventilation, or a positive end-expiratory pressure (PEEP) greater than 5 cm H₂O to maintain an arterial oxygen saturation (SaO₂) of 94%. Routine intensive care unit ventilatory management parameters must always be considered.

In patients at high risk for airway compromise after extubation, the anesthesiologist and surgeon can be at the bedside to reintubate or provide a surgical airway if the extubation effort fails. A Cook catheter can be placed in the airway and left in position after extubation to serve as a reintubation guide.

After extubation, speech and swallowing consultants can help to restore the voice and assist in preventing aspiration. Because airway stenosis can occur, prolonged extubation follow-up and fiberoptic evaluation is indicated.^14,^16,^20,^28,^60,^69,⁷⁴^–⁷⁶ Video stroboscopic vocal cord evaluation can be used as a screening tool to decide whether further airway evaluation by an ear, nose, and throat specialist is required.

Extubation failure occurs with a higher incidence in the burn population than among other critically ill patients (30% versus 23%).⁷⁷ Usually, the cause of failure is poor pulmonary toilet. Extubation failure is associated with burn size, inhalational trauma, and age of the patient.

b Extubation after Burn Surgery

Patients without airway injuries can be managed according to usual anesthesia practices. If significant edema exists in the face or airway, extubation after surgery is delayed until it subsides. If other airway difficulties occur, extubation in a controlled manner is undertaken as described earlier.^13,^16,⁷⁸

III Airway Management during the Later Stages of Burn Management

Burn patients require multiple procedures after their initial intensive care course. Close airway evaluation is required in this population. SLAs and regional anesthetics can be employed when indicated.⁷⁹^–⁸¹ As always, the patient’s airway history is reviewed and an examination completed. Even weeks after extubation following a prolonged intubation, a patient can develop strictures and granulomas, which can complicate airway management.⁷¹ Availability of adjuvant airway management devices should be considered when the recovering burn patient is brought to surgery during a long-term convalescence (Fig. 44-4).