Management of Pulmonary Failure after Burn Injury

This article highlights the challenges in managing pulmonary failure after burn injury. The authors review several different ventilator techniques, provide weaning parameters, and discuss complications.

Key points

  • Inhalation injury at the time of burn injury increases both morbidity and mortality.

  • Pulmonary failure after burn injury can be managed by airway pressure release ventilation (APRV), pressure regulated volume control (PRVC), volumetric diffuse respiratory (VDR) ventilation, or even extracorporeal membraneous oxygenation (ECMO).

  • Weaning respiratory support remains a critical component of providing oxygenation and ventilation for burn patients.

Introduction

In recent years, survival from burn injury has increased with effective fluid resuscitation, respiratory management, and early surgical excision of the burned tissue. The mortality from burn trauma, however, continues to be high, with progressive pulmonary failure being one of the major determinants of morbidity and mortality in burn patients, both from inhalation injury and from secondary complications after burn injury. In 1 study, pulmonary failure was demonstrated to be the cause of death in 29% of pediatric burn patients.

This article reviews the diagnostic and therapeutic interventions along with the recent advances in management of pulmonary failure in burn patients.

Inhalation Injury

Inhalation injury is generally defined as injury to the respiratory tract from inhalation of smoke and chemical products of combustion. It is, along with age and total body surface area (TBSA), one of the three most significant predictors of mortality after thermal injury. The incidence of inhalation injury varies from about 2.2% in patients with less than 20% TBSA burn to 14% in those with 80% to 99% TBSA burn injury. In addition, disasters such as the Station Nightclub Fire in Rhode Island in 2005, or the devastating terrorism attacks on the World Trade Center in New York and Pentagon have significantly higher incidence of inhalation injury. For example, out of the 790 injured survivors from the World Trade Center attack, 49% suffered from inhalation injury.

Combined with cutaneous burns, inhalation injury increases fluid resuscitation requirements, incidence of pulmonary complications like prolonged ventilator days, pneumonia and acute respiratory distress syndrome (ARDS), and mortality.

Inhalation injury can be classified into 3 types: thermal injury, chemical injury of the respiratory tract and systemic toxicity due to metabolic asphyxiants, or a combination of these insults. Thermal injury is primarily restricted to the upper airways, causing damage to the mouth, oropharynx, and supraglottic larynx. In the setting of steam, however, the injury is pervasive, causing damage to both upper airways and direct thermal injury to lung parenchyma. Chemical injury caused by particulate matter and chemical constituents of smoke like sulfur dioxide, nitrogen dioxide, ammonia, or toxic aldehydes damages the epithelial and capillary endothelial cells of lower airways and lung parenchyma leading to inflammatory changes, bronchiolar edema, and eventually airway obstruction. Increased capillary permeability amplifies the pulmonary edema. Systemic toxicity is most often caused by incomplete products of combustion, most commonly carbon monoxide and hydrogen cyanide. Carbon monoxide poisoning compromises the delivery of oxygen to tissues by reducing the oxygen carrying capacity of blood and less efficient dissociation at the tissue level. Hydrogen cyanide, produced most often by combustion of household materials, inhibits the cytochrome oxidase pathway, causing hypoxia, acidosis, and decreased cerebral oxygen consumption.

Introduction

In recent years, survival from burn injury has increased with effective fluid resuscitation, respiratory management, and early surgical excision of the burned tissue. The mortality from burn trauma, however, continues to be high, with progressive pulmonary failure being one of the major determinants of morbidity and mortality in burn patients, both from inhalation injury and from secondary complications after burn injury. In 1 study, pulmonary failure was demonstrated to be the cause of death in 29% of pediatric burn patients.

This article reviews the diagnostic and therapeutic interventions along with the recent advances in management of pulmonary failure in burn patients.

Inhalation Injury

Inhalation injury is generally defined as injury to the respiratory tract from inhalation of smoke and chemical products of combustion. It is, along with age and total body surface area (TBSA), one of the three most significant predictors of mortality after thermal injury. The incidence of inhalation injury varies from about 2.2% in patients with less than 20% TBSA burn to 14% in those with 80% to 99% TBSA burn injury. In addition, disasters such as the Station Nightclub Fire in Rhode Island in 2005, or the devastating terrorism attacks on the World Trade Center in New York and Pentagon have significantly higher incidence of inhalation injury. For example, out of the 790 injured survivors from the World Trade Center attack, 49% suffered from inhalation injury.

Combined with cutaneous burns, inhalation injury increases fluid resuscitation requirements, incidence of pulmonary complications like prolonged ventilator days, pneumonia and acute respiratory distress syndrome (ARDS), and mortality.

Inhalation injury can be classified into 3 types: thermal injury, chemical injury of the respiratory tract and systemic toxicity due to metabolic asphyxiants, or a combination of these insults. Thermal injury is primarily restricted to the upper airways, causing damage to the mouth, oropharynx, and supraglottic larynx. In the setting of steam, however, the injury is pervasive, causing damage to both upper airways and direct thermal injury to lung parenchyma. Chemical injury caused by particulate matter and chemical constituents of smoke like sulfur dioxide, nitrogen dioxide, ammonia, or toxic aldehydes damages the epithelial and capillary endothelial cells of lower airways and lung parenchyma leading to inflammatory changes, bronchiolar edema, and eventually airway obstruction. Increased capillary permeability amplifies the pulmonary edema. Systemic toxicity is most often caused by incomplete products of combustion, most commonly carbon monoxide and hydrogen cyanide. Carbon monoxide poisoning compromises the delivery of oxygen to tissues by reducing the oxygen carrying capacity of blood and less efficient dissociation at the tissue level. Hydrogen cyanide, produced most often by combustion of household materials, inhibits the cytochrome oxidase pathway, causing hypoxia, acidosis, and decreased cerebral oxygen consumption.

Diagnosis of inhalation injury

Before transferring the patient to a burn center, it is important to assess the patient’s risk for airway and respiratory problems and secure the airway, if required. Classically, the diagnosis of inhalation injury was subjective and made mainly on the basis of reported history and clinical findings. The physician should thoroughly review the history and the reported mechanism of burn injury. Pertinent information that provide clues to likelihood of an inhalation injury include exposure to smoke, flame, noxious fumes, and chemicals (household and industrial) at the scene of fire; duration of exposure; exposure in an enclosed space; loss of consciousness; and disability.

In addition, it should be determined if the patient has been exposed to an explosion, as this can cause lung barotrauma. Pertinent symptoms indicating inhalation injury include facial burns, singed nasal vibrissae, carbonaceous sputum, and changes in voice. Clark and colleagues retrospectively reviewed the presenting symptoms in patients with inhalation injury ( Table 1 ).

Table 1
Frequency of physical examination findings in patients who had inhalation injury
Findings Frequency (%)
Burns, face 65
Carbonaceous sputum 48
Soot, nose and mouth 44
Wheeze 31
Rales, rhonchi 23
Voice change 19
Corneal burn 19
Singed nasal vibrissae 11
Cough 9
Stridor 5
Dyspnea 3
Intraoral burn 2
Adapted from Clark WR, Bonaventura M, Myers W. Smoke inhalation and airway management at a regional burn unit: 1974-1983. Part I: diagnosis and consequences of smoke inhalation. J Burn Care Rehabil 1989;10:52–62.

Fiberoptic bronchoscopy (FOB) remains the gold standard to assess the presence and severity of smoke inhalation injury. The relative ease and availability allows FOB to be used for initial diagnosis ( Fig. 1 ) and to serially follow-up the changes. FOB is used to visualize the pathognomic mucosal hyperemia, edema, and the presence or absence of carbonaceous material (soot) in the airways. In addition, patients may have copious or no secretions and may progress from necrosis to sloughing of the airway. Repeat bronchoscopy within 24 to 48 hours may be more revealing.

Fig. 1
Bronchoscopic findings in a patient 18 hours after inhalation injury depicting severe edema and congestion of the bronchus along with carbonaceous soot deposition ( A ) and formation of pseudomembrane ( B ).
( Adapted from Bai C, Huang H, Yao X, et al. Application of flexible bronchoscopy in inhalation lung injury. Diagn Pathol 2013;8:174.)

Several studies have demonstrated that inhalation injury is a graded phenomenon, with increasing severity correlating with worse outcomes. Many authors have described criteria to grade the severity of inhalation injury based on the findings of initial FOB. The Abbreviated Injury Score (AIS) ( Table 2 ) has been shown to correlate with increased mortality and impaired oxygenation and ventilation. Endorf and colleagues found that patients with higher grades of inhalation injury on initial presentation had worse survival rates than those with lower grades.

Table 2
Abbreviated injury score grading scale for inhalation injury on bronchoscopy
Grade Class Description
0 No injury Absence of carbonaceous deposits, erythema, edema, bronchorrhea, or obstruction
1 Mild injury Minor or patchy areas of erythema, carbonaceous deposits, bronchorrhea, or bronchial obstruction.
2 Moderate injury Moderate degree of erythema, carbonaceous deposits, bronchorrhea, or bronchial obstruction
3 Severe injury Severe inflammation with friability, copious carbonaceous deposits, bronchorrhea, or obstruction.
4 Massive injury Evidence of mucosal sloughing, necrosis, endoluminal obstruction
Adapted from Albright JM, Davis CS, Bird MD, et al. The acute pulmonary inflammatory response to the graded severity of smoke inhalation injury. Crit Care Med 2012;40:1113–21.

Several other modalities that have been described in the literature for diagnosis of inhalation injury include computed tomography (CT), carboxyhemoglobin measurement, and radionuclide imaging with 133 Xenon. Many of these modalities lack sensitivity, are invasive, vary significantly between institutions and hence are not routinely employed for initial diagnosis. Chest radiographs usually appear normal at admission, therefore are a poor indicator of inhalation injury; still, they are important for baseline evaluations. Late findings include alveolar or interstitial edema, diffuse or focal infiltrates, bronchial thickening, consolidation, and atelectasis.

Airway management

It is imperative for the physician to identify burn patients requiring early intubation. Patients with direct thermal injury to the upper airways (including mouth and oropharynx), higher grades of inhalation injury, and extensive facial and circumferential neck burns are at a high risk of rapid airway edema formation, which may lead to catastrophic obstruction. Prophylactic intubation in these scenarios is appropriate, as a rapidly developing airway edema may hinder intubation later on, thus requiring immediate cricothyroidotomy at that moment. Ideally, the clinician most experienced in airway management should perform the intubation with the largest available and age-appropriate endotracheal tube. Special consideration should be given to patients who require higher fluid resuscitation volumes as they can develop significant postburn airway edema. Patients with altered mental status due to suspected metabolic asphyxiation and patients with subglottic injury leading to pulmonary failure are also good candidates for early intubation to prevent hypoxic injury. It important to note that not all patients with smoke inhalation injury require intubation; patients with inhalation injury but no facial or neck burns can be carefully observed and later intubated, if neccessary.

After the patient is endotracheally intubated, the tube should be carefully secured. Accidental removal of the endotracheal tube can be severely damaging, if not fatal. A dislodged endotracheal tube may damage the vocal cords, necessitating tracheostomy to prevent further damage. It is important to note that adhesive tape will not stick to extensive burn areas. In that case, cotton ties or even umbilical ties can be used to safely secure the endotracheal tube.

Although endotracheal intubation is the preferred route for placement of an artificial airway in the immediate postburn period, early tracheostomy may be required as an adjunct to the care of patients with indications of prolonged respiratory failure or acute loss of airway. In a retrospective analysis, it was demonstrated that tracheostomies were more likely to be performed on patients with TBSA greater than 60%, full-thickness burns to the face requiring reconstruction, and patients with pre-existing pulmonary disease. The patient population requiring late tracheostomy includes those with ventilation weaning problems or failed extubation. The complications associated with tracheostomies include chest infection, tracheal stenosis (TS), tracheoesophageal fistula (TEF), tracheoarterial fistula (TAF), and speech problems.

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Nov 21, 2017 | Posted by in Dental Materials | Comments Off on Management of Pulmonary Failure after Burn Injury
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