Inhalation Injury

Symposium on Burns

Inhalation Injury Donald D. Trunkey, M.D.*

Pulmonary damage due to smoke inhalation and carbon monoxide intoxication is thought to be the leading cause of death in fire victims. Of 12,000 annual deaths in the United States due to fire, 50 to 60 per cent are secondary to inhalation injury. In two carefully done studies in Maryland and New York City, very few victims died from burns alone; the great majority died from carbon monoxide or a combination of smoke inhalation and burns. These figures become more staggering when it is realized that at least 50 per cent of these deaths could have been prevented by such devices as smoke detectors. The study of smoke inhalation and the recognition of its existence did not begin until after the Coconut Grove fire. Recently, many studies have contributed to our further understanding of the disease and yet the pathophysiology is not clear. This is partly due to the fact that severe inhalation injury in humans is not that common in the absence of thermal injury to the skin. It is well documented that thermal injury alone, particularly when combined with shock, will cause severe pulmonary sequelae. Pure inhalation injury in experimental animals has increased our understanding of the pathophysiology. In the next few pages an attempt will be made to synthesize the available information on smoke inhalation.

MECHANISMS OF INJURY There are two distinct mechanisms of pulmonary injury following inhalation: carbon monoxide and smoke toxicity. Smoke toxicity is further divided into direct injury and smoke poisoning. It was once thought that direct injury to the airway was uncommon, but recent studies would tend to refute this. Carbon monoxide, probably the most common cause of death in burn victims, is clearly a very distinct cause of inhalation injury and is quite different in its pathophysiology from either direct injury or smoke poisoning. Smoke poisoning is due to the noxious chemicals formed in the burning process and is particularly prevalent when organic compounds such as plastics undergo combustion. *Associate Professor of Surgery, University of California School of Medicine, San Francisco; Director, Burn Center, San Francisco General Hospital, San Francisco, California

Surgical Clinics of North America-Vol. 58, No.6, December 1978

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Table 1. Signs and Symptoms of Toxicity of Reduced Levels of Oxygen Due to Fire Conditions* PER CENT OF OXYGEN IN AIR

SIGN OR SYMPTOM

20 (or above) 12 to 15

Normal Muscular coordination for skilled movements lost Consciousness continues but judgment is faulty and muscular effort leads to rapid fatigue Collapse occurs quickly but rapid treatment would prevent fatal outcome Death in 6 to 8 minutes

10 to 14

6to8

6 (or below)

*From Underwriters Laboratories Inc., Bulletin of Research, No. 53, July 1963, p. 49. Information abstracted from National Fire Protection Association Quarterly: Fire gas research report. 45:3:280-306, 1952.

Carbon Monoxide Carbon monoxide is a colorless, odorless, tasteless, and nonirritating gas produced by the incomplete combustion of carbon containing materials. The biologic effects are due to tissue hypoxia. Carbon monoxide combines with hemoglobin to form carboxyhemoglobin and competes with oxygen for the available hemoglobin binding sites. The affinity of hemoglobin for carbon monoxide is 200 times greater than for oxygen, so that carboxyhemoglobin concentration is great even when the carbon monoxide concentration is less than 5 per cent in inhaled gas. Toxicity will be dependent on the concentration of the gas in the inspired air and the time of exposure. Factors that potentiate the effects of carbon monoxide include decrease in oxygen con tent in the burning room and the additional pulmonary effects of smoke poisoning. Direct Injuries Inhalation of hot dry air (300° F. or higher) does not seem to have much effect upon the lower respiratory tract. This hot air may lead to tissue damage in the upper airway and larynx by causing laryngeal spasm, edema, and possible suffocation, but since the heat capacity of air is small, most of the heat is dissipated in the nasopharynx. In the presence of water (steam), thermal damage to the more distal lung tissues can occur since steam has a much higher heat capacity than does dry air. Progression of a fire in a closed space consumes oxygen and the heat at the ceiling of a room may reach 1000° F. or greater. Combustion is incomplete and considerable soot and particulate matter is formed. Most of these particles, as they are inhaled, are filtered in the upper airway, but some reach the lower airway and cause direct damage to the mucosa since they are superheated. It is also highly likely that these particles contain some of the toxic agents responsible for smoke poisoning. Examples of these toxic agents include 80 2 and N0 2, which adhere to the soot. In the presence of H 20 they form corrosive acids and alkalis that are extremely toxic to the mucosa. The exact extent of the injury caused by this direct mechanism is not known, but is greater than was once appreciated.

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Smoke Poisoning In addition to carbon monoxide, the thermodegradation of both natural and man-made materials results in the production of noxious gases. In natural materials this includes the oxides of sulfur and nitrogen and aldehydes. One of these aldehydes, acrolein, in a concentration of 5. 5 parts per million (ppm) has been shown to cause irritation of the upper respiratory tract with pulmonary edema occurring at 10 ppm in exposure times of as little as a few seconds. Noxious gases from the pyrolysis of man-made polymers include hydrogen cyanide, hydrochloric acid, sulfuric acid, and halogens. Some of these plastics also produce large amounts of benzene. Since benzene acts as an anesthetic, it is possible that this allows the corrosive acids and alkalis to pass down the respiratory tract into the alveoli and be absorbed. More recently, it has been discovered that the addition of a phosphorus fire retardant to plastics may produce even more lethal noxious gases including phosgene and related substances. PATHOPHYSIOLOGY Carbon monoxide causes no pathological changes to the tracheal bronchial tree. The pathological picture following inhalation of soot particles and/or noxious gases is difficult to separate, since there is considerable overlap and the soot particles may actually be carrying the great majority of the toxic gases. For the purpose of this discussion no attempt will be made to separate these two entities. The immediate effect ofthe inhalation of smoke is loss of ciliary action and severe mucosal edema. Within seconds surfactant activity in the lung is severely compromised, resulting in congestion with micro- and sometimes macro-atelectasis. If the inhalation injury is severe there may be damage to alveolar and bronchiolar epithelium. This probably spares the capillaries. Within minutes there is a detectable bronchiolar and perivascular edema, which then may lead to wheezing due to bronchiolar obstruction. Expectoration of carbonaceous sputum is common during this time. After several hours, sloughing ofthe tracheobronchial mucosa begins and a mucopurulent membrane develops. At this time the patient may cough up mucosa and bronchial casts. Following pseudomembranous tracheobronchitis there is necrotizing bronchiolitis, hyaline membrane formation, intraalveolar hemorrhage, fibrin-thrombus formation, and finally alveolar pulmonary edema. A carefully done autopsy study in New York City of smoke and carbon monoxide poisoning victims showed that most victims died within 12 hours, and a surprisingly small number had respiratory tract pathology. Most died of asphyxia. Those patients without pathological findings pro bably died of carbon monoxide poisoning, whereas the few with pathological findings died from smoke poisoning. Conversely, those dying after 12 hours had more respiratory tract pathology including bronchopneumonia. This last finding is probably uncommon in pure inhalation injury and represents secondary pathological processes including sepsis and the effects of treatment interventions such as tracheostomy and ventilators.

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The above picture is complicated if the patient has also sustained thermal injury to the skin. This will lead to damage on the vascular side of the ventilation perfusion pathway. The combination of resuscitation, disseminated intravascular clotting, micro emboli , and probable burn toxins may lead to increased capillary permeability, interstitial edema, and alveolar flooding. It is also known that skin burns depress the immune system, particularly A cell or accessory cell (macrophage) and T cell (cell-mediated) function. This undoubtedly sets the stage for the development of bronchopneumonia and sepsis. It has been possible by studying smoke inhalation victims and using experimental models to develop stages of inhalation injury. These four stages are based on clinical and laboratory measurements. During smoke inhalation, stage, I, profound hypoxemia and hypercapnia are associated with acidosis. Cardiac output is low and this is probably related to carbon monoxide. Initially there is hyperventilation, but as the patient is overcome, apnea may occur. This is secondary to the carbon monoxide, a decrease in ambient air oxygen, and other noxious gases such as methane. During the second stage (0 to 30 minutes) immediately following inhalation, hypercapnia as well as a mild hypoxemia continues. Cardiac output becomes more severely depressed, possibly reflecting an increase in pulmonary vascular resistance which in turn is caused by cerebral hypoxia. There is a concomitant increase in peripheral vascular resistance, an increase in the physiologic dead space, and a slight decrease in compliance. Carboxyhemoglobin levels in the blood are measurable. Stage III (2 to 24 hours) is associated with the clearing of carbon monoxide. There is, however, increasing hypoxemia as injured alveoli close off and interstitial edema develops. This is also reflected in a decreasing compliance and altered ventilation:perfusion ratios. Cardiac output may vary and depression is more likely due to burn shock or burn toxins. Most patients who survive to this stage will do well if they have no other injuries. Following the first 24 hours (stage IV) the clinical manifestations are primarily based on the development of bronchopneumonia, adult respiratory distress syndrome, or pulmonary edema. These are most often complications of skin burns, resuscitation, and other treatment.

DIAGNOSIS The history and physical examination are essential in making the diagnosis of smoke inhalation. If the victim has been burned in a closed space this should immediately cause the clinician to have a high index of suspicion that smoke inhalation has occurred. The physician should ask the patient about the types of things that were burning in the room at the time of exposure, such as type of carpet, the presence of vinyl furniture, flooring, and the type of clothing the victim was wearing. Physical findings that support the diagnosis ofinhalation injury include upper body burns, singed hairs in the nares, soot in the oropharynx, and carbonaceous

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Table 2. Carbon Monoxide Poisoning CARBOXYHEMOGLOBIN LEVEL

SEVERITY

20 per cent

Mild

20 to 40 per cent

Moderate

40 to 60 per cent

Severe

60 per cent

Fatal

SYMPTOMS

Headache, mild dyspnea, visual changes, confusion Irritability, diminished judgment, dim vision, nausea, easy fatigability Hallucinations, confusion, ataxia, collapse, coma

sputum_ Cyanosis, hoarseness, and rales may develop as the patient is resuscitated. Confirmation of the diagnosis of smoke inhalation is possible with certain laboratory tests. The easiest tests to perform early in the course of illness are blood gases and carboxyhemoglobin levels (Table 2). Hypoxemia, hypercapnia, and increased carboxyhemoglobin levels are the hallmarks of smoke inhalation. As resuscitation is ongoing there is a widening of the A-a02 difference. Initially the chest x-ray is not very useful unless severe injury has occurred and there is obvious atelectasis. The most reliable laboratory test that can be performed to diagnose smoke inhalation is bronchoscopy. Mucosal erythema, hemorrhage, ulceration, edema, and carbonaceous particles are common findings. In a recent study comparing fiberoptic bronchoscopy with xenon clearance, bronchoscopy was clearly more accurate. Radioactive xenon has been used also to diagnose smoke inhalation. Failure to clear 133xenon from the lung by 90 seconds or segmental retention is considered to be an abnormal result. False positive results may be seen in patients with antecedent chronic obstructive pulmonary disease or other bronchospastic disorders. Another deterrent to its widespread use is that many patients are too critical to be transported to nuclear medicine laboratories. Other laboratory investigations include pressure volume loops and exfoliative cytology. Although these may be helpful, they are not as simple or as reliable as bronchoscopy.

TREATMENT The initial treatment is the same as for any other individual who has been seriously injured. An airway must be established that may consist simply of oropharyngeal suction, removing debris, and maintaining an unobstructed flow of air. Ideally, 100 per cent oxygen should be started as soon as possible. This is often impossible in field conditions where mask and nasal prongs can only achieve an inspired oxygen concentration of 35 to 40 per cent. The half-life of carbon monoxide on the hemoglobin molecule is approximately four hours while breathing room air, but decreases to % hour when 100 per cent oxygen is breathed. If measurement of carboxyhemoglobin levels in the hospital confirms high values, it may

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be prudent to sedate and intubate the patient so that 100 per cent oxygen can be administered. As blood carboxyhemoglobin levels fall and hypoxemia decreases, as determined by blood gases, the inspired oxygen concentration is reduced proportionately. Smoke inhalation represents a spectrum of severity and treatment that must be appropriately graduated. In mild cases, humidification of inspired air, encouragement of coughing, and occasional bronchial suctioning may be all that is required. In moderate to severe cases, more frequent bronchial suctioning will be required and judicious use ofbronchodilators such as aminophylline or terbutaline may be beneficial. Mucolytic agents have been employed with some success. If atelectasis is shown on x-ray films and the patient develops respiratory symptoms, intubation and mechanical ventilation with the use of PEEP should be initiated. In more severe forms of the illness characterized by facial burns and oropharyngeal edema, intubation is mandatory. If there is any doubt as to the patency ofthe airway, or if there is impending obstruction, intubation should be performed. In our experience, it has been far better to insert a nasotracheal or endotracheal tube rather than to wait until an emergency tracheostomy has to be performed. We have almost entirely abandoned tracheostomy in favor of the soft cuff, high compliance endotracheal tubes with external pressure regulating pilot balloons (Lanz). Complications such as tracheoesophageal fistulae and tracheal stenosis have been essentially eliminated with this regimen. Specific indications for intubation and ventilator management based on physiologic parameters are: Parenchymal lung failure Chest x-ray (moderate to severe infiltrates) Tachypnea rate> 35 A-a DO z > 300 torr Compliance < 30 ml per cm of water Shunt fraction of 15 per cent or greater The same indications in reverse order may be used as criteria for discontinuing ventilator treatment. In patients with combined thermal injury and inhalation injury, we have found it useful to carefully titrate fluid balance during the initial resuscitation so as to minimize pulmonary and renal complications. In this regard, use of the Swan-Ganz catheter to monitor pulmonary artery wedge pressure has been extremely helpful. We would prefer to keep the atrial filling pressures at or near normal (3 to 8 torr). Urine output should be maintained at greater than 0.5 ml per kg per hour. Oftentimes the clinician is faced with a situation in which pulmonary artery wedge pressure (PAWP) is rising and urine output is falling. It is at this time that measurements of cardiac ou tput may be most useful. If P AWP is increasing and urine output is decreasing and cardiac output is also depressed, the use of a cardiotropic drug such as isoproterenol (Isuprel) or dopamine is indicated. If, on the other hand, the PAWP is increasing and urine output decreasing as cardiac output remains normal or above normal,

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judicious use of diuretics is indicated. An osmotic diuretic such as mannitol is preferable initially. If it is ineffective, loop diuretics such as ethacrynic acid or furosemide may be used. We do not use prophylactic antibiotics, as we do not believe (as opposed to others) that they will decrease the late complications of smoke inhalation such as bronchopneumonia and tracheobronchitis. In fact, they are probably detrimental in that they will select out resistant organisms. Daily Gram stains of the sputum should be performed to guide the clinician in antibiotic treatment. If the sputum shows sheets of organisms and large numbers of neutrophils, infection is imminent. If the organism is gram-positive, penicillin or one of the penicillinase-resistant antibiotics should be used. If the organism is gram-negative, high dose penicillin and an aminoglycoside are useful until specific cultures and sensitivities can be obtained. Steroids have also been advocated as useful in preventing some ofthe late sequelae of smoke inhalation. The rationale is that corticosteroids have been shown to suppress the inflammatory response. This suppression is manifest positively in three ways: (1) by blocking the increased endothelial capillary permeability induced by acute inflammation; (2) by preserving plasma membrane integrity and preventing swelling and destruction of cells; and (3) by stabilizing lysosome membranes, thus preventing rupture and secondary tissue damage. Unfortunately, corticosteroids also have undesirable effects, including salt and water retention and delayed wound healing. Additionally, the corticosteroids inhibit antigen processing by macrophages, cell-mediated immunity, and the inflammatory response after antigen antibody union. Thus the advantages of steroid treatment of inhalation injury are outweighed by the disadvantages. Two recent studies support this, one showing no benefit in steroid-treated patients and the other showing increased late infection in the steroid-treated group.

PREVENTION A discussion of inhalation injury would be incomplete without mentioning prevention, particularly since 50 per cent of inhalation injuries are preventable. There are 750,000 residential fires each year in the United States, which account for 57 per cent of all fire deaths. Most ofthese occur at night during sleeping hours. Since carbon monoxide is odorless and tasteless, many victims are overcome by smoke without any warning. Smoke detectors can be life-saving. There are two types of smoke detectors commonly used in the home. Ionization detectors use a radioactive source (Americum) to ionize the air in their detection chambers. Smoke impedes the flow of current produced by the ionization and sets off the alarm. Photoelectric detectors have a photo source that passes through a chamber. Smoke particles scatter the light beam which is then picked up by a photo cell, sounding the alarm. Finally, if a person is trapped in a smoke-filled room, protection of the nares and mouth by a damp cloth would be advantageous. This would

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markedly reduce the inoculum of particulate matter to the airway and thus reduce the likelihood of smoke poisoning.

REFERENCES 1. Agee. R. N., Long, J. M., Ill, Hunt, J. L., et al.: Use of ""'xenon in early diagnosis ofinhalation injury. J. Trauma, 16:218, 1976. 2. Ambiavagar, M., Chalon, J., and Zargham, 1.: Tracheobronchial cytologic changes following lower airway thermal injury. J. Trauma, 14:280, 1976. 3. Dressler, D. P., and Skornik, W. A.: Effect of antimicrobial therapy on lung bacterial clearance in the burned rat. Ann. Surg. 75:241, 1972. 4. Garzon, A. A., Seltzer, B., Song, 1. C., et al.: Respiratory mechanics in patients with inhalation burns. J. Trauma, 10:57, 1970. 5. Hunt, J. L., Agee, R. N., and Pruitt, B. A., Jr.: Fiberoptic bronchoscopy in acute inhalation injury. J. Trauma, 15 :641, 1975. 6. International Symposium on Toxicity and Physiology of Combustion Products, University of Utah, March 1976. 7. Mellins, R. B., and Park, S.: Respiratory complications of smoke inhalation in victims of fires. J. Pediat., 87:1, 1975. 8. Moylan, J. A., Jr., Wilmore, D. W., Mouton, D. E., et al.: Earlydiagnosisofinhalationinjury using 13"xenon lung scan. Ann. Surg., 477, 1973. 9. Physiological and Toxicological Aspects of Combustion Products: International Symposium. Washington, D.C., National Academy of Sciences, 1976. 10. Pruitt, B. A., Jr., Erickson, D. R., and Morris, A.: Progressive pulmonary insufficiency and other pulmonary complication of thermal injury. J. Trauma, 15 :369, 1975. 11. Skornik, W. A., and Dressler, D. P.: The effects of short-term steroid therapy on lung bacterial clearance and survival in rats. Ann. Surg., 179:415, 1974. 12. Stephenson, S. F., Esrig, B. C., Polk, H. C., et al.: The pathophysiology of smoke inhalation injury. Ann. Surg., 182:652, 1975. 13. Stone, H. H., and Martin, J. D., Jr.: Pulmonary injury associated with thermal burns. Surg. Gynecol. Obstet. 129:1242, 1969. 14. Zawacki, B. E., Jung, R. C., Joyce, J., et al.: Smoke, burns and the natural history of inhalation injury in fire victims. Ann. Surg., 185 :1, 1977. 15. Zikria, B. A., Ferrer, J. M., and Floch, H. F.: The chemical factors contributing to pulmonary damage in smoke poisoning. 71 :704, 1972. 16. Zikria, B. A., Weston, G. C., Chodoff, M., et al.: Smoke and carbon monoxide poisoning in fire victims. J. Trauma, 12:641, 1972. Department of Surgery University of California School of Medicine San Francisco General Hospital San Francisco, California 94110