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Resident Orientation Manual

Produced by Galveston Shriners Burn Hospital and
The University of Texas Medical Branch Blocker Burn Unit.
Contributors:  Sally Abston MD, Patricia Blakeney PhD, Manubhai Desai MD,
Patricia Edgar RN, CIC,John P Heggers PhD, David N Herndon MD,
Marsha Hildreth RD, Ray J Nichols Jr. MD



   Inhalation injury is evident in over 30% of hospitalized burn patients and in 20-84% of burn-related mortalities.  Heat can result in damage and edema to the upper airway, but uncommonly produces injury below the vocal cords except with steam burns.  Acute asphyxia can occur due to environmental oxygen consumption by the fire or by reduction in oxygen transport from carbon monoxide poisoning.  Smoke inhalation induces a multitude of physiologic changes.  Lung vascular permeability is increased, promoting pulmonary edema.  De-activation of surfactant in the pulmonary alveoli reduces pulmonary compliance, increases ventilatory work, and adds to metabolic demands.  The majority of tissue damage attributed to inhalation injury is mediated by a chemical injury from incomplete combustion products carried by smoke, including aldehydes, oxides, sulfur, nitrogen compounds, and hydrochloric gases.  This chemical damage to the lower airways and parenchyma is propagated by polymorphic neutrophils (PMN's) and leukokinesis.  In severe injuries, desquamation of small airways along with inflammation produces airway costs.  Areas of atelectatic lung tissue alternating with compensatory emphysematous regions leads to acute pulmonary insufficiency and bronchopneumonia.

   Diagnosis of inhalation injury should be suspected in patients with facial burns, singed nasal hair, cough, carbonaceous sputum, or evidence of upper airway edema, including hoarseness, stridor, or wheezing.  Pulmonary injury should be considered in any patient with history of burn in a closed space, loss of consciousness, or altered mental status.  In unconsciousness, protective reflexive laryngospasm to pulmonary irritants is lost and lung parenchymal injuries tend to be more severe.  Arterial blood gases and carboxyhemoglobin content should be determined, but may be misleading if initially normal.  Diagnosis of inhalation injury is best confirmed by fiberoptic bronchoscopy which detects airway edema, mucosal sloughing, or charring or soot in the upper airways.  Chest x-ray is an insensitive initial test, as parenchymal changes may not be evident for 48-72 hours.  Currently, fiberoptic bronchoscopy is the gold standard for evaluation of inhalation injuries, providing more frequent and earlier diagnosis.  In addition, there are xenon lung scopes which evaluate alveolar air trapping from obstruction, and extravascular lung water determinations which assess parenchymal fluid levels.  Each can identify parenchymal lung injury and help differentiate upper airway and parenchymal inhalation damage.  However, no studies accurately quantify the extent of inhalational damage, or prognosticate for parenchymal injuries.

   Inhalation injury can be divided into three clinical phases:  acute pulmonary insufficiency, pulmonary edema, and bronchopneumonia.  Acute pulmonary insufficiency occurs between 0 and 36 hours post-burn due to acute asphyxia, carbon monoxide poisoning, bronchospasm, upper airway obstruction, and/or severe parenchymal damage.  Pulmonary edema is seem 6-72 hours post-burn.  Bronchopneumonia occurs most commonly 3-10 days post-injury.

   Treatment of inhalation injury should begin at the scene with immediate administration of 100% oxygen.  Carbon monoxide poisoning produces asphyxia by binding competitively to hemoglobin and reducing oxygen carrying capacity.  Hemoglobin has a 210 times greater affinity for carbon monoxide than oxygen.  On room air, carboxyhemoglobin (CO-Hgb) has a half-life of about 4 hours in the bloodstream.  The half-life is reduced to 20 minutes when breathing 100% oxygen.  If oxygen supplementation is started promptly, anoxic cerebral injuries are reduced.  Levels of CO-Hgb greater than 15% are clinically significant, and levels above 40% can produce coma.

   Maintenance of the airway is critical.  If early evidence of upper airway edema is present, then intubate early.  Airway edema increases over 12-18 hours.  Prophylactic intubation without good indications should not be done, as intubation may otherwise increase pulmonary complications in burn patients.  Fluid resuscitation should not be restricted.  Although over-hydration can increase pulmonary edema, inadequate hydration increases the severity of pulmonary injury by sequestration of PMN's.  Bronchodilators are used to reduce lower airway bronchospasm.  Many patients who require intubation due to airway edema will also need mechanical venilatory support for parenchymal damage, as indicated by criteria similar for other critically ill patients.  Treatment for pulmonary edema generally necessitates ventilatory support with increases in tidal volume, oxygen supplementation, and positive end-expiratory pressure (PEEP).  Adequate oxygenation is assured by serial ABG's.  Chest x-rays help document pulmonary progression.  Chest physiotherapy, early ambulation, and appropriate use of PEEP help to reduce post-injury atelectasia, consolidation, and pneumonia.  Serial bronchoscopies with lavage can be useful for clearing of mucus plugs.  Prophylactic antibiotics for inhalation injury are not indicated.

   The nebulization of various substances has been demonstrated to allocate some of the adverse symptomatology following inhalation injury.  In addition to bronchodilators, heparin is indicated for patients with abnormal ABG's or inspissated mucous secretions.  Heparin (10,000 units) in 3 ml of normal saline may be administered every 4 hours via endotracheal or tracheostomy tube.  In severe cases, the heparin can be augmented with Mucomyst (n-acetyl-cysteine) treatment (3-5 ml 20% soln.) every 4 hours, timed so that either heparin or Mucomyst is administered every 2 hours.  Bronchopneumonia is the most common cause of sepsis in the burn patient.  Pneumonias that develop within the first week are most commonly aureus.  Pneumonias occurring after one week are more likely due to resistant gram negative bacteria, e.g. Pseudomonas or Klebsiella.  Systemic antibiotic regimens are based on serially monitored sputum cultures, bronchial washings or transtracheal aspirates.  Chest physiotherapy is an important adjuvant treatment for bronchopneumonia.  We do not use hyperbaric oxygen therapy as has been suggested and corticosteroids are strictly contraindicated.


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