CASE REPORT alveolar hemorrhage; pulmonary barotrauma
Alveolar Hemorrhage as a Manifestation of Pulmonary Barotrauma After Scuba Diving We present the case of a 46-year-old man who developed diffuse alveolar hemorrhage as a consequence of a scuba diving accident. The diagnosis and presumptive pathophysio]ogical mechanism of this previously unreported complication are discussed. [Balk M, Goldman JM: Alveolar hemorrhage as a manifestation of pulmonary barotrauma after scuba diving. Ann Emerg Med August 1990;19:930-934.]
INTRODUCTION More than 2 million Americans participate in scuba diving, for commercial and recreational purposes. The medical complications associated with this activity include decompression sickness ("bends"), pulmonary barotrauma (pneumothorax, pneumomediastinum, and subcutaneous emphysema), and arterial gas embolism. Hemoptysis has been noted in a few divers in association with pulmonary barotrauma or air embolism.l There is little in the literature about hemoptysis in scuba divers, and we could find no reference to pulmonary hemorrhage as the sole manifestation of pulmonary barotrauma in the diving, environmental, or medical literature since 1940. 2-6 We present the following case to alert emergency physicians to the risk of alveolar hemorrhage as a complication of scuba diving.
Michael Balk, MD Jay M Goldman, MD Philadelphia, Pennsylvania From the Emergency Department, Hospital of the University of Pennsylvania, Philadelphia. Received for publication April 5, 1989. Revision received September 28, 1989. Accepted for publication December 1, 1989. Address for reprints: Jay M Goldman, MD, Division of Emergency Medicine, Thomas Jefferson University Hospital, 11th and Walnut Street, Philadelphia, Pennsylvania 19107.
CASE REPORT A previously healthy 46-year-old man was transferred to our hospital with hemoptysis, severe hypoxemia, and bilateral alveolar infiltrates. He was well until four hours before admission when he suffered a scuba diving accident at a depth of 85 ft seawater (fsw) and an ambient water temperature of 10 C. His bottom time was 25 minutes when his regulator malfunctioned. During ascent, which lasted approximately 30 seconds, he attempted to exhale continuously. His mask and regulator remained in place during his ascent, and he denied aspiration of seawater. On surfacing, he coughed up approximately 15 mL of bright red blood, became short of breath, and noted pleuritic substernal chest pressure. He denied vertigo, otalgia, sinus pain, joint pain, skin rash, epistaxis, paresthesias, or other neuromuscular complaints. The patient was a commercial diver with more than 20 years of experience and training in the US Navy. His last dive, one week previously, was to a depth of 150 fsw and was without complication. He had no history of cardiopulmonary disease or systemic illness and did not smoke cigarettes. He was taken to a local hospital where he was found to be cyanotic and in moderate respiratory distress. His examination was reported to be otherwise normal. Hemoglobin was 17 g/dL; arterial blood gases while the patient was receiving 6 L of supplemental oxygen were pH 7.34; Pco2, 40 m m Hg; and Po2, 42 m m Hg. His ECG was normal. His chest radiograph (Figure 1) with inspiratory and expiratory views revealed bilateral alveolar infiltrates without cardiomegaly, cephalization of vessels, pneumothorax, or pneumomediastinum. He was transferred to our hospital for further Care.
On arrival, the patient was in moderate respiratory distress with a blood pressure of 130/70 m m Hg; pulse, 100; and respirations, 24. He was afebrile. He had diffusely diminished breath sounds, rhonchi that cleared with coughing, and rare expiratory wheezes. The remainder of his physical ex-
19:8 August 1990
Annals of Emergency Medicine
930/125
ALVEOLAR HEMORRHAGE Balk & Goldman
FIGURE 1. Chest radiograph taken one hour after surfacing. Note fluffy bilateral alveolar infiltrates. FIGURE 2. Chest radiograph on arrival at our hospital, four hours after accident. Infiltrates have progressed.
amination was normal. His hemoglobin was 16.7 g/dL with WBCs of 20,300 cells/mm 3. Electrolytes, p l a t e l e t count, coagulation panel, and c r e a t i n i n e kinase were normal. Arterial blood gases while the patient was breathing 70% oxygen by a nonrebreather face-mask were pH 7.37; Pco~, 41 m m Hg; and Po2, 92 m m Hg. His chest radiograph (Figure 2) revealed progression of the bilateral patchy alveolar infiltrates without cardiomegaly or pleural effusion; his ECG was normal. The p a t i e n t ' s chest pressure resolved two hours later. Evaluation by an otorhinolaryngologist revealed no bleeding sites or other abnormalities. A nuclear cardiology scan (MUGA) revealed a normal ejection fraction of 50% with normal wall motion. Two days after admission, when he had i m p r o v e d c l i n i c a l l y and r a d i o graphically (Figure 3), sputum cytology showed hemosiderin-laden macrophages. Pulmonary function tests performed w h e n the patient had a Po~ of 65 m m Hg and a hemoglobin of 15.4 g/dL revealed a diffusing capacity (DLco) of 101% of the predicted value. P u l m o n a r y f u n c t i o n tests were otherwise normal. The patient continued to improve; at discharge four days after admission, his chest radiograph was norm a l (Figure 4). On f o l l o w - u p six weeks later, his Po 2 on room air was 101 m m Hg.
DISCUSSION Our patient presented with dyspnea, hemoptysis, severe hypoxemia, and diffuse alveolar infiltrates after experiencing a rapid free ascent. The differential diagnosis initially included pulmonary hemorrhage, aspiration, cardiogenic or noncardiogenic pulmonary edema, hypersensitivity pneumonitis from an unidentified allergen, toxin exposure, and pulmonary embolism. The patient denied aspiration, and the DLco would be r e d u c e d in p u l m o n a r y e d e m a or pneumonia. There was no evidence of toxin or allergen exposure, and the 126/931
patient had no atopic history. In the setting of an acute central nervous system event such as a cerebral arterial gas embolus, neurogenic pulmonary edema with capillary leak could have produced this syndrome. Annals of Emergency Medicine
However, the patient had a normal neurologic examination and no evidence of arterial gas emboli. T h r o m b o e m b o l i c p u l m o n a r y embolism could account for the sudden onset of pleuritic pain, dyspnea, he19:8 August 1990
FIGURE 3. Chest radiograph two
days later, showing considerable resolution of infiltrates.
moptysis, and hypoxia. However, this degree of hypoxia would be expected to be associated with a massive clot burden and hemodynamic instability (which were not seen in our patient). Furthermore, it would be most unusual for a massive pulm o n a r y embolus to resolve completely in the absence of thrombolysis or anticoagulation. In addition, the patient was an active, healthy man with no risk factors for pulmonary embolism. Pulmonary venous congestion can also slow pulmonary blood flow and produce pulmonary infarction. In a diver, this syndrome is k n o w n as "chokes" and is attributed to precipitation of occlusive gas bubbles in the pulmonary venous circulation after an i n a d e q u a t e l y d e c o m p r e s s e d dive.5, 6 Our patient's dive profile, however, did not require any decompression according to US Navy diving tables,7 and he had no other symptoms referrable to decompression sickness. The initial chest radiographs showed diffuse alveolar infiltrates (Figures 1 and 2}. This radiographic appearance was c o m p a t i b l e w i t h both intra-alveolar hemorrhage and p u l m o n a r y edema, s The normal ECG, MUGA scan, and absence of coronary artery disease argued against cardiogenic pulmonary 19:8 August 1990
edema. Further, chest radiograph findings of pulmonary edema clear rapidly, usually within 24 hours. 9 With pulmonary hemorrhage, however, the resolution is s o m e w h a t slower, t°, 1~ as it was in our patient. In addition, the presence of hemosiderin-laden alveolar macrophages in sputum (whether collected by expectoration or bronchoalveolar lavage) is a sensitive indicator of pulmonary hemorrhage. ~2,13 It takes 24 to 48 hours for alveolar macrophages to i n c o r p o r a t e the digested RBC products and produce hemosiderinstaining cells that can be identified on cytologic examination. Our patient's sputum samples collected two and four days after the alveolar hemorrhage revealed these typical hemosiderin-laden macrophages. The measurement of DLco is an accepted adjunct in the diagnosis of p u l m o n a r y hemorrhage.llA4, Is In this setting, the presence of RBCs and free hemoglobin in the alveolar space increases the number of available binding sites for carbon monoxide and thus increases DLc:o. In contrast, the DLco is decreased below the predicted value when other alveolar space-filling processes (eg, pulmonary edema, pneumonia) produce hypoxia and pulmonary infiltrates. 16 Our patient's D~co was 101% Of the predicted value at a time when he Annals of Emergency Medicine
was markedly hypoxic and had diffuse alveolar infiltrates; this lends further support to the diagnosis of pulmonary hemorrhage. We could locate only one report of p u l m o n a r y hemorrhage in a diver, which probably resulted from "thoracic squeeze" during an unconscious descent.17 This rare syndrome occurs when air in the lungs is compressed below the residual volume during a breath-hold descent. At a depth of 80 to 100 fsw, the ambient pressure squeezes the lung to the diver's residual volume, and alveoli are compressed to their smallest noncollapsible volume. On further descent, the pressure in the thoracic vasculature exceeds intra-alveolar pressure, and there is a tendency for distension ot alveolar capillaries and movement oi fluid into the alveoli. If the pressure differential is sufficient, the alveolar capillaries rupture and bleed into the interstitium and the alveolar space. This m e c h a n i s m of p u l m o n a r y hemorrhage, occurring only on descent, is the physiological opposite of the mechanism responsible for pulmonary barotrauma. Because our patient surfaced immediately on noticing malfunction of his regulator, he could not have developed "thoracic squeeze." Unless a diver exhales throughout ascent, the lungs will be exposed to an expanding volume of gas (Boyle's law). As ascent continues, alveoli increase in volume to the limit of distensibility and eventually rupture. This allows air to escape into the interstitium, pleural cavity, or pulmonary circulation is and results in pulmonary barotrauma. Manifestations of p u l m o n a r y b a r o t r a u m a include subcutaneous emphysema, pneumothor0x, pneumomediastinum, and arterial gas embolism. Diving accidents resulting in pulm o n a r y b a r o t r a u m a are rare. In a study of 50,000 ascents made in 100 fsw during submarine escape training, o n l y 25 a c c i d e n t s were reported. 19 The majority of these were cerebral gas embolism; there were four cases of mediastinal emphysema and one pneumothorax. Elliot et al 2° recently reported more than 200,000 trainee ascents during the past 20 932/127
ALVEOLAR HEMORRHAGE Balk & Goldman
FIGURE 4. Normal chest radiograph on discharge, four days after accident. years in which there were only 88 cases of p u l m o n a r y b a r o t r a u m a . Again, most patients had central nervous system findings, usually manifested by confusion, poor coordination, or loss of consciousness. There were ten cases of subcutaneous emphysema and several cases of pneumomediastinum and pneumothorax. Leitch and Gieen 1 reviewed civilian and naval diving accidents reported to the British Institute of Naval Medicine from 1965 t h r o u g h 1985. One hundred forty cases of pulmonary barotrauma were identified during this 20-year period with hemoptysis noted in 27 patients. No mention of major hemoptysis or pulmonary hemorrhage was made. However, this retrospective case review did not indicate the number of patients who had chest radiographs or give details about the subgroup with hemoptysis. It is probably the overdistension and stretching of lungs and not the elevated intrapuhnonary pressure per se that causes the pathology seen in p u l m o n a r y b a r o t r a u m a . This has been shown in a group of elegant yet simple experiments with rabbits, dogs, and fresh human cadavers. ~1-~3 A n i m a l s with o c c l u d e d tracheas were decompressed from significant depths and suffered air embolism and puhnonary interstitial emphysema as their lungs became distended with entrapped air. However, the air emboli and emphysema were prevented by the application of thoracoabdominal binders. These prevented overdistension of the lung despite a significant rise in transtracheal pressure with decompression. Similarly, the transtracheal pressure required to produce p u l m o n a r y barotrauma in fresh c a d a v e r s was s i g n i f i c a n t l y higher when both the chest and abdomen were bound, z2 If, during ascent, the diver's exhalation flow rate is insufficient to prcvent alveolar overdistention, pulmonary hemorrhage may result from rupture of alveolar walls. This has been demonstrated in rabbits decompressed very rapidly from 1 to 0.053 atm. a3 Alveolar hemorrhage occurred in 89% of animals. The change in ambient pressure produced in this 128/933
experiment was much greater than the change in ambient pressure imposed on our patient, but the mechanism of injury was similar.
SUMMARY The presence of hemoptysis, alveolar infiltrates, hemosiderin-laden macrophages, and DLco of 101% of predicted in the prescnce of hypoxemia made the diagnosis of pulmonary hemorrhage likely in our patient. The absence of prior cardiac disease or concurrent infection and the mechanism of injury supported this diagnosis, as did the rate of resolution of clinical symptoms and radiographic abnormalities. The most likely alternative explanation for our patient's symptoms, aspiration of water, was denied by the patient and would have resulted in an abnormally low DLco. The cause for the alveolar hemorrhage in the absence of any other signs of pulmonary barotrauma is unclear; it may have been Annals of Emergency Medicine
secondary to inadequate exhalation of the rapidly expanding gas within the diver's lungs during emergency ascent. Even with frec ascent from a sign i f i c a n t depth, p u l m o n a r y overpressure accidents are rare. Most of these accidents occur during inadvertent breath-holding by inexperienced divers; thus, the best prevention is proper training in the technique of ascent. Pulmonary barotrauma may also occur during normal ascent in patients with obstructive lung diseases. Arterial gas embolism and mediastihal emphysema are the most common manifestations of pulmonary barotrauma; p n e u m o t h o r a x , pneumopericardium, and p n e u m o p e r i toneum can also occur. Alveolar h e m o r r h a g e should be added to the list of rare complications of diving accidents associated with barotrauma. Pulmonary barotrauma can occur in shallow water 19:8 August 1990
such as in swimming pools, for it is near the surface that the air in the lungs expands at the greatest rate during ascent. 3 Thus, e m e r g e n c y physicians, regardless of practice location, may encounter patients with pulmonary barotrauma and should be familiar with its many manifestations. REFERENCES 1. Leiteh DR, Green RD: Pulmonary barotrauma in divers and the treatment of cerebral arterial gas embolism. Aviat Space Environ Med 1986;57:931-938. 2. Boettger ML: Scuba diving emergencies: Pulmonary overpressure accidents and decompression sickness. Ann Emerg Med 1983;12:563-567. 3. Arthur DC, Margulies KA: A short course in diving medicine. Ann Emerg Med 1987;16: 689-701. 4. Kizer KW: Management of dysbaric diving casualities. Emerg Med Clin North A m 1983; 1:659-670. 5. Calder IM: Dysbarism: A review. Forensic Sci Int 1986;30:237-266.
NAV SEA 0994-LP-001-9010. Washington, DC, US Government Printing Office, vol 1, 1988. 8. Hyde I: Miscellaneous lung conditions, in Sutton D (ed): A Textbook of Radiology and Imaging, ed 4. Edinburgh, Churchill Livingstone, 1987, p 479-507. 9. Fraser RG, Pare JA: Pulmonary hypertension and edema, in Fraser RG, Pare JA leds): Diagnosis of Diseases of the Chest, ed 2. Philadelphia, WB Saunders Co, 1978, p 1201-1296. 10. Bowley N]~, Steiner RB, Chin WS: The chest x-ray antoglomerular basement membrane antibody disease (Goodpasture's syndrome). Clin Radiol 1979;30:419-429. 1]. Bowley NB, Hughes JMB, 8teiner RE: The ehest x-ray in pulmonary capillary haemorrhage: Correlation with carbon monoxide uptake. Clin Radiol t979;30:413-417. 12. Melamed MR, Zaman MB: Sputum cytology, in Fishman AP (ed): Pulmonary Diseases and Disorders, ed 1. New York, McGraw-Hill Book Co, 1980, p 111-121. 13. Finley TN, Aronow A, Cosentino AM, et ah Occult pulmonary hemorrhage in anticoagulated patients. A m Rev Respir Dis 1975; 112:23-29.
6. Strauss RH: Diving medicine. Am Rev Respir Dis 1979;119:1001-1023.
14. Ewan PW, Jones HA, Rhodes CG, et ah Detection of intrapulmonary hemorrhage with carbon monoxide uptake. N Engl J Med 1976; 295:1391-1396 .
7. US Navy Diving Manual. Publication No
15. Greening AP, Hughes JMB: Serial estima-
19:8 August 1990
Annals of Emergency Medicine
tions of carbon monoxide diffusing capacity in intrapulmonary hemorrhage. Clin Sci 1981; 60:507-512. 16. Conrad SA: Gas diffusion, in Conrad SA, Kinasewitz GT~ George RB (eds): Pulmonary Function Testing, Principles and Practice. New York, Churchill Livingstone, 1984, p 185-201. 17. Strauss MB, Wright PW: Thoracic squeeze diving casualty. Clin Aviat Aerospace Med 1971;42:673-675. 18. Macklin CC: Transport of air along sheaths of pulmonic blood vessels from alveoli to mediastinum. Arch Intern Med 1939;64:913-926. 19. Miles S: Underwater Medicine, ed 3. London, Staples Press, 1969, p 340. 20. Elliot DH, Harrison JAB, Barnard EEP: Clinical and radiologic features of 88 cases of decompression barotrauma. Proceedings of the Sixth Symposium on Underwater Physiology. Bethesda, Maryland, 1978, p 527-535. 21. Schaefer KE, et ah Mechanisms in development of interstitial emphysema and air embolism on decompression from depth. J Appl Physiol 1958;13:15~29. 22. Miles S: Underwater Medicine, ed 3. London, Staples Press, 1969, p 83-85. 23. Fang HS, Hsu WT: The appearance of pulmonary hemorrhage following explosive decompression in rabbits. J Formos Med Assoc 1982; 81:843-847.
934/129
Alveolar Hemorrhage as a Manifestation of Pulmonary Barotrauma After Scuba Diving We present the case of a 46-year-old man who developed diffuse alveolar hemorrhage as a consequence of a scuba diving accident. The diagnosis and presumptive pathophysio]ogical mechanism of this previously unreported complication are discussed. [Balk M, Goldman JM: Alveolar hemorrhage as a manifestation of pulmonary barotrauma after scuba diving. Ann Emerg Med August 1990;19:930-934.]
INTRODUCTION More than 2 million Americans participate in scuba diving, for commercial and recreational purposes. The medical complications associated with this activity include decompression sickness ("bends"), pulmonary barotrauma (pneumothorax, pneumomediastinum, and subcutaneous emphysema), and arterial gas embolism. Hemoptysis has been noted in a few divers in association with pulmonary barotrauma or air embolism.l There is little in the literature about hemoptysis in scuba divers, and we could find no reference to pulmonary hemorrhage as the sole manifestation of pulmonary barotrauma in the diving, environmental, or medical literature since 1940. 2-6 We present the following case to alert emergency physicians to the risk of alveolar hemorrhage as a complication of scuba diving.
Michael Balk, MD Jay M Goldman, MD Philadelphia, Pennsylvania From the Emergency Department, Hospital of the University of Pennsylvania, Philadelphia. Received for publication April 5, 1989. Revision received September 28, 1989. Accepted for publication December 1, 1989. Address for reprints: Jay M Goldman, MD, Division of Emergency Medicine, Thomas Jefferson University Hospital, 11th and Walnut Street, Philadelphia, Pennsylvania 19107.
CASE REPORT A previously healthy 46-year-old man was transferred to our hospital with hemoptysis, severe hypoxemia, and bilateral alveolar infiltrates. He was well until four hours before admission when he suffered a scuba diving accident at a depth of 85 ft seawater (fsw) and an ambient water temperature of 10 C. His bottom time was 25 minutes when his regulator malfunctioned. During ascent, which lasted approximately 30 seconds, he attempted to exhale continuously. His mask and regulator remained in place during his ascent, and he denied aspiration of seawater. On surfacing, he coughed up approximately 15 mL of bright red blood, became short of breath, and noted pleuritic substernal chest pressure. He denied vertigo, otalgia, sinus pain, joint pain, skin rash, epistaxis, paresthesias, or other neuromuscular complaints. The patient was a commercial diver with more than 20 years of experience and training in the US Navy. His last dive, one week previously, was to a depth of 150 fsw and was without complication. He had no history of cardiopulmonary disease or systemic illness and did not smoke cigarettes. He was taken to a local hospital where he was found to be cyanotic and in moderate respiratory distress. His examination was reported to be otherwise normal. Hemoglobin was 17 g/dL; arterial blood gases while the patient was receiving 6 L of supplemental oxygen were pH 7.34; Pco2, 40 m m Hg; and Po2, 42 m m Hg. His ECG was normal. His chest radiograph (Figure 1) with inspiratory and expiratory views revealed bilateral alveolar infiltrates without cardiomegaly, cephalization of vessels, pneumothorax, or pneumomediastinum. He was transferred to our hospital for further Care.
On arrival, the patient was in moderate respiratory distress with a blood pressure of 130/70 m m Hg; pulse, 100; and respirations, 24. He was afebrile. He had diffusely diminished breath sounds, rhonchi that cleared with coughing, and rare expiratory wheezes. The remainder of his physical ex-
19:8 August 1990
Annals of Emergency Medicine
930/125
ALVEOLAR HEMORRHAGE Balk & Goldman
FIGURE 1. Chest radiograph taken one hour after surfacing. Note fluffy bilateral alveolar infiltrates. FIGURE 2. Chest radiograph on arrival at our hospital, four hours after accident. Infiltrates have progressed.
amination was normal. His hemoglobin was 16.7 g/dL with WBCs of 20,300 cells/mm 3. Electrolytes, p l a t e l e t count, coagulation panel, and c r e a t i n i n e kinase were normal. Arterial blood gases while the patient was breathing 70% oxygen by a nonrebreather face-mask were pH 7.37; Pco~, 41 m m Hg; and Po2, 92 m m Hg. His chest radiograph (Figure 2) revealed progression of the bilateral patchy alveolar infiltrates without cardiomegaly or pleural effusion; his ECG was normal. The p a t i e n t ' s chest pressure resolved two hours later. Evaluation by an otorhinolaryngologist revealed no bleeding sites or other abnormalities. A nuclear cardiology scan (MUGA) revealed a normal ejection fraction of 50% with normal wall motion. Two days after admission, when he had i m p r o v e d c l i n i c a l l y and r a d i o graphically (Figure 3), sputum cytology showed hemosiderin-laden macrophages. Pulmonary function tests performed w h e n the patient had a Po~ of 65 m m Hg and a hemoglobin of 15.4 g/dL revealed a diffusing capacity (DLco) of 101% of the predicted value. P u l m o n a r y f u n c t i o n tests were otherwise normal. The patient continued to improve; at discharge four days after admission, his chest radiograph was norm a l (Figure 4). On f o l l o w - u p six weeks later, his Po 2 on room air was 101 m m Hg.
DISCUSSION Our patient presented with dyspnea, hemoptysis, severe hypoxemia, and diffuse alveolar infiltrates after experiencing a rapid free ascent. The differential diagnosis initially included pulmonary hemorrhage, aspiration, cardiogenic or noncardiogenic pulmonary edema, hypersensitivity pneumonitis from an unidentified allergen, toxin exposure, and pulmonary embolism. The patient denied aspiration, and the DLco would be r e d u c e d in p u l m o n a r y e d e m a or pneumonia. There was no evidence of toxin or allergen exposure, and the 126/931
patient had no atopic history. In the setting of an acute central nervous system event such as a cerebral arterial gas embolus, neurogenic pulmonary edema with capillary leak could have produced this syndrome. Annals of Emergency Medicine
However, the patient had a normal neurologic examination and no evidence of arterial gas emboli. T h r o m b o e m b o l i c p u l m o n a r y embolism could account for the sudden onset of pleuritic pain, dyspnea, he19:8 August 1990
FIGURE 3. Chest radiograph two
days later, showing considerable resolution of infiltrates.
moptysis, and hypoxia. However, this degree of hypoxia would be expected to be associated with a massive clot burden and hemodynamic instability (which were not seen in our patient). Furthermore, it would be most unusual for a massive pulm o n a r y embolus to resolve completely in the absence of thrombolysis or anticoagulation. In addition, the patient was an active, healthy man with no risk factors for pulmonary embolism. Pulmonary venous congestion can also slow pulmonary blood flow and produce pulmonary infarction. In a diver, this syndrome is k n o w n as "chokes" and is attributed to precipitation of occlusive gas bubbles in the pulmonary venous circulation after an i n a d e q u a t e l y d e c o m p r e s s e d dive.5, 6 Our patient's dive profile, however, did not require any decompression according to US Navy diving tables,7 and he had no other symptoms referrable to decompression sickness. The initial chest radiographs showed diffuse alveolar infiltrates (Figures 1 and 2}. This radiographic appearance was c o m p a t i b l e w i t h both intra-alveolar hemorrhage and p u l m o n a r y edema, s The normal ECG, MUGA scan, and absence of coronary artery disease argued against cardiogenic pulmonary 19:8 August 1990
edema. Further, chest radiograph findings of pulmonary edema clear rapidly, usually within 24 hours. 9 With pulmonary hemorrhage, however, the resolution is s o m e w h a t slower, t°, 1~ as it was in our patient. In addition, the presence of hemosiderin-laden alveolar macrophages in sputum (whether collected by expectoration or bronchoalveolar lavage) is a sensitive indicator of pulmonary hemorrhage. ~2,13 It takes 24 to 48 hours for alveolar macrophages to i n c o r p o r a t e the digested RBC products and produce hemosiderinstaining cells that can be identified on cytologic examination. Our patient's sputum samples collected two and four days after the alveolar hemorrhage revealed these typical hemosiderin-laden macrophages. The measurement of DLco is an accepted adjunct in the diagnosis of p u l m o n a r y hemorrhage.llA4, Is In this setting, the presence of RBCs and free hemoglobin in the alveolar space increases the number of available binding sites for carbon monoxide and thus increases DLc:o. In contrast, the DLco is decreased below the predicted value when other alveolar space-filling processes (eg, pulmonary edema, pneumonia) produce hypoxia and pulmonary infiltrates. 16 Our patient's D~co was 101% Of the predicted value at a time when he Annals of Emergency Medicine
was markedly hypoxic and had diffuse alveolar infiltrates; this lends further support to the diagnosis of pulmonary hemorrhage. We could locate only one report of p u l m o n a r y hemorrhage in a diver, which probably resulted from "thoracic squeeze" during an unconscious descent.17 This rare syndrome occurs when air in the lungs is compressed below the residual volume during a breath-hold descent. At a depth of 80 to 100 fsw, the ambient pressure squeezes the lung to the diver's residual volume, and alveoli are compressed to their smallest noncollapsible volume. On further descent, the pressure in the thoracic vasculature exceeds intra-alveolar pressure, and there is a tendency for distension ot alveolar capillaries and movement oi fluid into the alveoli. If the pressure differential is sufficient, the alveolar capillaries rupture and bleed into the interstitium and the alveolar space. This m e c h a n i s m of p u l m o n a r y hemorrhage, occurring only on descent, is the physiological opposite of the mechanism responsible for pulmonary barotrauma. Because our patient surfaced immediately on noticing malfunction of his regulator, he could not have developed "thoracic squeeze." Unless a diver exhales throughout ascent, the lungs will be exposed to an expanding volume of gas (Boyle's law). As ascent continues, alveoli increase in volume to the limit of distensibility and eventually rupture. This allows air to escape into the interstitium, pleural cavity, or pulmonary circulation is and results in pulmonary barotrauma. Manifestations of p u l m o n a r y b a r o t r a u m a include subcutaneous emphysema, pneumothor0x, pneumomediastinum, and arterial gas embolism. Diving accidents resulting in pulm o n a r y b a r o t r a u m a are rare. In a study of 50,000 ascents made in 100 fsw during submarine escape training, o n l y 25 a c c i d e n t s were reported. 19 The majority of these were cerebral gas embolism; there were four cases of mediastinal emphysema and one pneumothorax. Elliot et al 2° recently reported more than 200,000 trainee ascents during the past 20 932/127
ALVEOLAR HEMORRHAGE Balk & Goldman
FIGURE 4. Normal chest radiograph on discharge, four days after accident. years in which there were only 88 cases of p u l m o n a r y b a r o t r a u m a . Again, most patients had central nervous system findings, usually manifested by confusion, poor coordination, or loss of consciousness. There were ten cases of subcutaneous emphysema and several cases of pneumomediastinum and pneumothorax. Leitch and Gieen 1 reviewed civilian and naval diving accidents reported to the British Institute of Naval Medicine from 1965 t h r o u g h 1985. One hundred forty cases of pulmonary barotrauma were identified during this 20-year period with hemoptysis noted in 27 patients. No mention of major hemoptysis or pulmonary hemorrhage was made. However, this retrospective case review did not indicate the number of patients who had chest radiographs or give details about the subgroup with hemoptysis. It is probably the overdistension and stretching of lungs and not the elevated intrapuhnonary pressure per se that causes the pathology seen in p u l m o n a r y b a r o t r a u m a . This has been shown in a group of elegant yet simple experiments with rabbits, dogs, and fresh human cadavers. ~1-~3 A n i m a l s with o c c l u d e d tracheas were decompressed from significant depths and suffered air embolism and puhnonary interstitial emphysema as their lungs became distended with entrapped air. However, the air emboli and emphysema were prevented by the application of thoracoabdominal binders. These prevented overdistension of the lung despite a significant rise in transtracheal pressure with decompression. Similarly, the transtracheal pressure required to produce p u l m o n a r y barotrauma in fresh c a d a v e r s was s i g n i f i c a n t l y higher when both the chest and abdomen were bound, z2 If, during ascent, the diver's exhalation flow rate is insufficient to prcvent alveolar overdistention, pulmonary hemorrhage may result from rupture of alveolar walls. This has been demonstrated in rabbits decompressed very rapidly from 1 to 0.053 atm. a3 Alveolar hemorrhage occurred in 89% of animals. The change in ambient pressure produced in this 128/933
experiment was much greater than the change in ambient pressure imposed on our patient, but the mechanism of injury was similar.
SUMMARY The presence of hemoptysis, alveolar infiltrates, hemosiderin-laden macrophages, and DLco of 101% of predicted in the prescnce of hypoxemia made the diagnosis of pulmonary hemorrhage likely in our patient. The absence of prior cardiac disease or concurrent infection and the mechanism of injury supported this diagnosis, as did the rate of resolution of clinical symptoms and radiographic abnormalities. The most likely alternative explanation for our patient's symptoms, aspiration of water, was denied by the patient and would have resulted in an abnormally low DLco. The cause for the alveolar hemorrhage in the absence of any other signs of pulmonary barotrauma is unclear; it may have been Annals of Emergency Medicine
secondary to inadequate exhalation of the rapidly expanding gas within the diver's lungs during emergency ascent. Even with frec ascent from a sign i f i c a n t depth, p u l m o n a r y overpressure accidents are rare. Most of these accidents occur during inadvertent breath-holding by inexperienced divers; thus, the best prevention is proper training in the technique of ascent. Pulmonary barotrauma may also occur during normal ascent in patients with obstructive lung diseases. Arterial gas embolism and mediastihal emphysema are the most common manifestations of pulmonary barotrauma; p n e u m o t h o r a x , pneumopericardium, and p n e u m o p e r i toneum can also occur. Alveolar h e m o r r h a g e should be added to the list of rare complications of diving accidents associated with barotrauma. Pulmonary barotrauma can occur in shallow water 19:8 August 1990
such as in swimming pools, for it is near the surface that the air in the lungs expands at the greatest rate during ascent. 3 Thus, e m e r g e n c y physicians, regardless of practice location, may encounter patients with pulmonary barotrauma and should be familiar with its many manifestations. REFERENCES 1. Leiteh DR, Green RD: Pulmonary barotrauma in divers and the treatment of cerebral arterial gas embolism. Aviat Space Environ Med 1986;57:931-938. 2. Boettger ML: Scuba diving emergencies: Pulmonary overpressure accidents and decompression sickness. Ann Emerg Med 1983;12:563-567. 3. Arthur DC, Margulies KA: A short course in diving medicine. Ann Emerg Med 1987;16: 689-701. 4. Kizer KW: Management of dysbaric diving casualities. Emerg Med Clin North A m 1983; 1:659-670. 5. Calder IM: Dysbarism: A review. Forensic Sci Int 1986;30:237-266.
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14. Ewan PW, Jones HA, Rhodes CG, et ah Detection of intrapulmonary hemorrhage with carbon monoxide uptake. N Engl J Med 1976; 295:1391-1396 .
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15. Greening AP, Hughes JMB: Serial estima-
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tions of carbon monoxide diffusing capacity in intrapulmonary hemorrhage. Clin Sci 1981; 60:507-512. 16. Conrad SA: Gas diffusion, in Conrad SA, Kinasewitz GT~ George RB (eds): Pulmonary Function Testing, Principles and Practice. New York, Churchill Livingstone, 1984, p 185-201. 17. Strauss MB, Wright PW: Thoracic squeeze diving casualty. Clin Aviat Aerospace Med 1971;42:673-675. 18. Macklin CC: Transport of air along sheaths of pulmonic blood vessels from alveoli to mediastinum. Arch Intern Med 1939;64:913-926. 19. Miles S: Underwater Medicine, ed 3. London, Staples Press, 1969, p 340. 20. Elliot DH, Harrison JAB, Barnard EEP: Clinical and radiologic features of 88 cases of decompression barotrauma. Proceedings of the Sixth Symposium on Underwater Physiology. Bethesda, Maryland, 1978, p 527-535. 21. Schaefer KE, et ah Mechanisms in development of interstitial emphysema and air embolism on decompression from depth. J Appl Physiol 1958;13:15~29. 22. Miles S: Underwater Medicine, ed 3. London, Staples Press, 1969, p 83-85. 23. Fang HS, Hsu WT: The appearance of pulmonary hemorrhage following explosive decompression in rabbits. J Formos Med Assoc 1982; 81:843-847.
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