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Module 14--Current Emergency--Smoke Inhalation:
Terms in this set (17)
Essentials of Diagnosis:
--Look for evidence of thermal injury (airway edema)
--Consider signs of chemical injury to lung parenchyma
--Evaluate for carbon monoxide toxicity
--Patients who have been trapped in a fire in a confined space inhale superheated gases and may have thermal injury to the mouth, oropharynx, and larynx.
--Direct flame injury of the face and neck may also occur and are associated with development of marked upper airway edema and possible airway obstruction.
--Because of the efficient thermal exchange system of the upper airway, direct thermal injury to the lower respiratory tract is unusual.
--Rarely, exposure to water or steam in the heated gas mixture may produce thermal damage in the lower trachea and bronchi.
Thermal Injury--Clinical Findings:
--Upper airway thermal injury should be suspected in any patient exposed to a fire occurring in a confined location and in patients with obvious neck or facial burns.
--Soot around the nares, carbonaceous sputum, singed nasal vibrissae, and burned facial hairs are also indicators of thermal injury to the upper airway.
--Pt's may complain of dyspnea; there may be stridor, drooling, or dysphonia.
--Lack of these findings does not exclude injury.
--Thermal injury to cutaneous tissues leads to widespread generalized edema which can involve the airway.
--Diagnosis is confirmed by visualization of the larynx by direct or video-laryngoscopy, or by flexible fiberoptic scope.
--Chemical injury to the airways and lung parenchyma may be caused by noxious products from combustion of flammable materials.
--Some of these products are directly toxic to the airways and lung parenchyma.
Chemical Injury--Clinical Findings:
--Chemical injury to the airways and lung parenchyma is difficult to diagnose in the emergency department.
--Wheezes, rales, rhonchi, and voice changes may be noted or initially absent in these patients.
--Direct laryngoscopy or flexible fiberoptic bronchoscopy may reveal mucosal friability and edema of the airways.
--Fiberoptic bronchoscopy is the burn center standard but is limited to upper airway evaluation.
--Initially the chest X-ray is often normal and serves as a baseline; noncardiogenic pulmonary edema may develop hours after exposure.
--Xenon lung scans, pulmonary function tests, and nitrogen washout studies have all been used to document the extent of pulmonary involvement but are not commonly available in the ED.
Common Toxic Products of Combustion:
Material burned: Wood, paper, cotton
Toxic product: Acrolein, acetaldehyde, formaldehyde, acetic acid, formic acid, nitrogen dioxide, carbon monoxide
Material burned: Polyvinyl chloride
Toxic product: Hydrochloric acid, phosgene, chlorine
Material burned: Polyurethane
Toxic product: Hydrocyanic acid, isocyanates (eg, toluene diisocyanate), carbon monoxide.
Material burned: Petroleum products
Toxic product: Acrolein, acetic acid, formic acid
Material burned: Agricultural wastes, automobile exhaust Toxic product: Nitrogen dioxide and other oxides of nitrogen; acetic acid; formic acid; carbon monoxide
--Acrolein is a highly reactive aldehyde that results from combustion of wood and petroleum products.
--Rapidly reacts with lung and airway tissues, causing injury by protein denaturation.
--Prolonged inhalation or exposure to high concentrations (>150 parts per million) for short periods of time (minutes) can be fatal.
--Lesser exposure causes pulmonary edema due to alveolar capillary leakage, bronchorrhea and bronchospasm (which may be severe), and ventilation -perfusion disturbances that cause hypoxemia that may persist even after the person is no longer exposed to smoke.
--Also causes conjunctivitis and ocular tearing at low concentrations.
-One of the main products of combustion of polyvinyl chloride, a material commonly found in the structural components of houses and high-rise buildings as well as in furnishings and plastics.
--Hydrolysis occurs when hydrochloric acid comes in contact with the mucosa of the upper airway and tracheobronchial tree, causing protein denaturation and cell death.
--Even limited exposure may cause marked ocular irritation and tearing, although individuals with repeated or prolonged exposure may become desensitized to this effect.
--More severe exposure is associated with dyspnea, chest pain, and irritation of mucous membranes.
--Onset of pulmonary edema may be delayed for 2-12 hours after exposure, and the patient may appear asymptomatic in the interim.
--Toxic levels of hydrochloric acid gas may persist for as long as 1 hour after a fire has been extinguished.
--Patients exposed to products of combustion of polyvinyl chloride may also demonstrate premature ventricular contractions and may be at risk for development of lethal cardiac arrhythmias.
--A product of combustion of polyurethane, a synthetic material found in almost all homes and offices, where it is used in seat cushions, mattresses, and carpet backing.
--Also found in insulation material.
--May cause severe bronchospasm, especially in persons with underlying obstructive lung disease, and it is also an ocular irritant.
--Produced in fires involving automobiles or agricultural wastes.
--An uncommon though important toxin, because even brief exposures to high concentrations may cause severe bronchospasm, laryngospasm, and pulmonary edema.
--If the patient survives, late development of bronchiolitis fibrosa obliterans and chronic interstitial lung disease may occur.
Other noxious products:
--Particulate matter in smoke may stimulate irritant receptors in the large airways and cause bronchoconstriction.
Systemic Chemical Poisoning--Mechanism: Carbon monoxide
--The most widely recognized and most common complication of smoke inhalation is carbon monoxide poisoning.
--Carbon monoxide is a product of incomplete combustion and is produced in varying amounts in all fires.
--Binds to hemoglobin with an affinity that is 260 times greater than that of oxygen, forming carboxyhemoglobin. The presence of even small amounts of carboxyhemoglobin drastically alters the affinity of the remaining unbound hemoglobin. Thus, even small concentrations of carbon monoxide may markedly reduce the binding of oxygen to hemoglobin, and the carbon monoxide that is bound is not easily displaced by oxygen.
--The presence of carboxyhemoglobin shifts the oxy-hemoglobin dissociation curve to the left, making it more difficult for hemoglobin to release bound oxygen to the tissues. The net result is tissue hypoxia and lactic acidosis due to cellular anaerobic metabolism.
--Also inhibits mitochondrial function.
--Brain damage due to excitatory amino acids, inflammation, and oxidative stress may occur.
--In high concentrations, carbon monoxide is also bound to myoglobin, and may lead to rhabdomyolysis with myoglobinuria and renal failure.
--The half-life of carboxyhemoglobin is about 4-5 hours, which can be reduced to 60 minutes by administration of 100% oxygen.
Systemic Chemical Poisoning--Mechanism: Cyanide
--Reports have documented the presence of cyanide in the smoke of residential fires.
--Because of the difficulties in measuring cyanide levels in patients and because of the difficulty in recognizing smoke-related cyanide poisoning, the clinical relevance of cyanide poisoning in smoke inhalation is uncertain.
--Due to the risks associated with traditional treatments of cyanide poisoning—which involves the production of methemoglobin by infusion of sodium nitrite—in a patient who also demonstrates carboxyhemoglobinemia, this empiric therapy for cyanide poisoning is not recommended.
--More recent evaluation of newer cyanide antidotes continues to develop.
--Sodium thiosulfate and hydroxocobalamin have potential as empiric treatments in suspected cyanide poisoning.
Systemic Chemical Poisoning--Clinical Findings--carbon monoxide:
--Systemic chemical poisoning due to carbon monoxide should be suspected in every victim of fire and may be confirmed by measuring the serum carboxy-hemoglobin level.
--The often-described cherry-red skin color is not a frequent or reliable finding in patients with carbon monoxide poisoning. Similarly, arterial blood gas measurements are not reliable determinants of carbon monoxide poisoning, because PaO2 and the calculated percentage of oxygen saturation of hemoglobin (the value that is routinely reported by clinical laboratories) are not affected by carboxyhemoglobin. The oxygen saturation measured by pulse oximetry does not distinguish oxyhemoglobin from carboxyhemoglobin. Hence, the actual saturation is obtained by subtracting the percent of carboxyhemoglobin from the measured saturation obtained from the pulse oximeter.
--Typical nonexposed, nonsmoking individuals may have serum carboxyhemoglobin levels of up to 1%; smokers usually have levels of 4-6%. Levels above 10% signify significant exposure.
--Patients may be asymptomatic when carboxyhemoglobin levels are below 10-15%. Levels higher than 50-60% are associated with a high incidence of coma and seizures, and levels higher than 70% are frequently fatal.
--Myocardial ischemia or infarction and cardiac arrhythmias occur frequently, especially in patients with underlying atherosclerotic heart disease.
--Some patients who initially appear to have recovered may experience delayed onset of a neurologic syndrome characterized by dementia, ataxia, and other sensory and motor abnormalities. This syndrome may be due to infarcts in the globus pallidus. Loss of consciousness may be transitory.
Systemic Chemical Poisoning--Clinical Findings-Cyanide:
--Sustained loss of consciousness, dilated pupils, seizures, and hypotension are findings that are more likely in cyanide poisoning.
--Tachypnea may be followed by central apnea. Lactate levels correlate strongly with toxin levels.
--If there are signs of thermal injury to the airway, endotracheal intubation is indicated.
--In patients with major burns (particularly greater than 40-60% total body surface area), even if the airway is patent initially, edema frequently occurs minutes or hours later. Prophylactic intubation prevents a subsequent difficult intubation or surgical airway.
--Obtain arterial blood gas and carboxyhemoglobin determinations in all patients with possible smoke inhalation.
--While waiting for the results, give 100% oxygen by tight-fitting reservoir mask or, if indicated, by endotracheal tube.
--Avoid alkalosis and hypothermia, which decrease the dissociation of carbon monoxide from hemoglobin. Indications for hyperbaric oxygen therapy have been described as a carboxyhemoglobin level greater than 25%, neurologic symptoms, seizures, pregnancy, or depressed consciousness. The efficacy of hyperbaric oxygen in clinical management remains unproved and its use cannot be mandated.
--Although therapy shortens the half-life of carboxyhemoglobin to roughly 20 minutes, the hazards and the length of time involved in transporting a critically ill patient to the nearest hyperbaric oxygen facility and the limited resuscitative environment of the chamber may outweigh the benefits of treatment.
--Hyperbaric oxygenation may be useful in the severely poisoned patient who fails to respond to therapy with 100% oxygen. If carboxyhemoglobin levels are under 2% and if oxygenation is adequate, the inspired oxygen content can be decreased.
--In stable patients with suspected thermal or chemical injury of the airway, evaluate mucosa injury using direct laryngoscopy.
--Obtain an ECG, and monitor cardiac rhythm. Carbon monoxide poisoning is associated with myocardial ischemia and cardiac arrhythmias.
--Obtain a chest X-ray to look for signs of lung injury if smoke inhalation has occurred and to serve as a baseline for further changes. Give inhaled and parenteral bronchodilators to patients with clinical evidence of bronchospasm.
--Obtain a urine specimen for assessment of myoglobinuria.
--No evidence supports the use of prophylactic antibiotics or systemic corticosteroids in the treatment of inhalation injuries.
--Because victims of smoke inhalation may develop late respiratory failure, these patients should be hospitalized for 24 hours for observation.
--All patients with carboxyhemoglobin levels higher than 25% should be hospitalized.
--Patients who present to the emergency department with respiratory compromise or respiratory failure should be hospitalized in an intensive care unit.
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