- Email: [email protected]
Recurrent High-Altitude Illness Associated with Right Pulmonary Artery Occlusion from Granulomatous Mediastinitis
Recurrent High-Altitude Illness Associated with Right Pulmonary Artery Occlusion from Granulomatous MedlastlnHis* Kenneth G. 10rrlngton, M.D., F.C.C.P.t
While travelling across the intermountain West at an altitude of approximately 2,300 m, a 35-year-old man developed symptoms o£ HAPE. Delay in diagnosis and treatment was nearly lethal. Subsequent evaluation demoostrated unilateral pulmonary artery occlusion, presumably resulting from antecedent granulomatous mediastinitis. This case report supports the concept of evaluating anyone developing HAPE at relatively low altitude for an underlying predisposition. (Chest 1989; 96:1422-23) HAPE =high-altitude pulmonary edema; HAl= high-altitude
illDess
recent years the issue of HAl in mountain climbers has I nreceived increased attention in the medical literature;•·•
however, among sojourners at moderate altitudes (1,500 to 2,500 m), the nonspecific early symptoms of altitude illness are often unrecognized by the affected individuals and undiagnosed by medical personnel. Congenital absence of a pulmonary artery has been reported to predispose to HAPE .w In the following case history, I describe the association of recurrent HAl with acquired unilateral pulmonary artery stenosis induced by fibrosing mediastinitis. CASE REPORT
While travelling across central Wyoming (elevation approximately 2,300 m), a 35-yeaM>Id man began to complain of headache and mild breathlessness. On the following day, he drove 300 miles to Yellowstone National Park (elevation, 2,000 to 2,500 m), and complained of worsening headache, progressive dyspnea, and sweats. No fever or productive cough was noted. A physician's assistant evaluated and treated his headache with intramuscular meperidine and promethazine. After 24 hours of bed rest, Midrin was prescribed for worsening headache, and "migraine" was diagnosed. The increasing dyspnea was ignored. On the fourth day of his illness, the patient concluded that the altitude was affecting him and requested his wife drive him to the Oregon coast. Along the way, dyspnea and orthopnea became extreme, and hemopytsis began. He presented to a hospital emergency room (elevation, 1,500 m), where arterial blood gas levels on nasal oxygen at 5 Umin showed Pa01 of 40 mm Hg and PaC01 of35 mm Hg. After evaluation and initiation of treatment with intravenous heparin, intravenous erythromycin, and 100 percent oxygen via a nonrebreathing mask, the patient was transferred by ambulance to Boise, Idaho (altitude, 850m). *From St. Lukes Regional Medical Center, Boise, Idaho. tCurrently: Pulmonary Disease Service, Walter Reed Army Medical Center, Washington, DC. . The view, opinions, and/or findings contained in this paper are those of the author and should not be construed as official Department of the Army position, policy or decision unless so stated by other official documentation. Reprint 111queats: Dr. 10rrlngton, 1\dmooory Disease Service, Wlrd 77, Wllter Reed Army Medical Center; Washington, DC 20307-5001
1422
The patient denied prior symptoms of chronic pulmonary disease. For years. he had smoked two cigars per day without inhaling. He was a lifelong resident of Arkansas. On two previous trips to the western United States (Leadville, CO, at altitude of 3,100 m and Flagstaff, AZ, at altitude 2,500 m), the patient had developed similar but less severe headache and dyspnea and had improved upon returning to lower altitude. He had not consulted a physician on either occasion. The patient had had several episodes of childhood pneumonia and at the age of eight years had required hospitalization and right thoracocentesis. As a teenager, he had developed a traumatic right pneumothorax during a football game and had been treated overnight with tube thoracostomy. The patient denied a history of tuberculosis or pulmonary emboli. His employment as a machinist and mechanic had resulted in exposure to limited quantities of solvent fumes and dusts, without known ill effects. He took no medications regularly. On arriving in Boise, Idaho, only mild respiratory distress was present. Oral temperature was 37.6"C (99. 7"F). Blood pressure was 142198 mm Hg, pulse rate was 82 beats per minute, and respiratory rate was 24 min. Auscultation of the lungs revealed bilateral inspiratory crackles, predominantly located in the left lung. Breath sounds were significantly decreased throughout the right hemithorax. The patient was obese, but the findings from his examination were otherwise normal. At admission, the WBC count was 11,700/cumm. Arterial blood gas analysis with a 40 percent Venturi mask showed a Pa01 of67.5 mm Hg, PaC01 of 46.5 mm Hg, and pH, 7.41. The presenting chest roentgenogram (Fig I) showed conftuent, central alveolar infiltrates throughout the left lung plus chronic right hilar and mediastinal calcifications. Interstitial markings were increased in the right lung, predominantly at the base. Xenon-133 lung scan showed normal ventilation bilaterally. Following injection of 4 mCi of technetium 99m macroaggregated albumin, complete absence of right lung perfusion and normal left lung perfusion were noted (Fig 2); HAPE was diagnosed, and antibiotic and anticoagulant therapy was withdrawn. Supplemental oxygen administration was continued, and diuresis was begun. To rule out massive pulmonary embolism, pulmonary arteriagrams were performed on the second day of hospitalization. Measurements of pressure (in millimeters of mercury) showed the following values: right atrium, 1210; right ventricle, 4015; right pulmonary artery, 36116; and left pulmonary artery, 45123. A selective pulmonary arteriogram demonstrated a mass of enlarged,
FIGURE 1. Posteroanterior chest roentgenogram shows conftuent, central alveolar infiltrates throughout left lung. Densely calcified mass of lymph nodes is located in right hilum and mediastinum. Interstitial markings are increased in right lung, especially at base. Recunent Hlgh-allllude IIIMM (Ksnneth G. Torrington)
calci6ed right hilar and right paratracheal nodes in the area where the right pulmonary artery was occluded. The occlusions sharp weD-defined border without evidence tOr tapering suggested extrinsic compression, rather than intravascular clot (Fig 3). The left pulmonary arteriogram was normal, as was the levophase examination. An ECG, two-dimensional echocardiography, and bilateral Doppler examination of the lower extremity venous systems were subsequently normal. FoDow-up chest roentgenograms demonstrated rapid improvement of the left pulmonary infiltrate within 12 hours and complete clearing within 72 hours. By then, the patient had become asymptomatic. He was advised to obtain local (sealevel) evaluation tOr possible pulmonary hypertension and to avoid future travel at altitudes over 1,500 m unless using supplemental oxygen.
DISCUSSION
FIGURE 2. Posterior view of technetium 99m macroaggregated albumin perfusion scan demonstrates complete absence of right lung perfusion and normal left lung perfusion.
FIGURE 3. Selective right pulmonary arteriogram demonstrates complete occlusion. Occlusion's border is sharp and weD defined. Occlusion is located adjacent to mass of enlarged, calci6ed right hilar and right paratracheal nodes.
Granulomatous mediastinitis, a condition usually associated with antecedent tuberculosis or histoplasmosis, is a pathologic process capable of affecting any structure traversing the mediastinum. 8 Although the tracheobronchial tree, esophagus, and superior vena cava are most commonly involved, pulmonary arterial or venous obstructions (or both) have been reported. 7•8 The densely calcified right hilar and mediastinal mass adjacent to an obstructed right pulmonary artery in a lifelong resident of Arkansas provides compelling evidence in favor of this diagnosis. The chronicity of the process can be inferred from finding roentgenographic stability onthis patient's chest x-ray films from 1968, as well as from the extent of calcification present. When the lung scan demonstrates unilateral absence of perfusion, possible etiologies include congenital abnormality (often associated with congenital heart disease), massive pulmonary embolism, and neoplasm. Rarely, fibrosing mediastinitis or unilateral hyperlucent lung syndrome (SwyerJames-Macleod) may produce this finding.• Interestingly, patients with proximal interruption of a pulmonary artery are usually asymptomatic unless they develop pulmonary hypertension, as happens in 19 percent.• Since the report by Hackett et al• in 1980, physicians have been aware of the susceptibility to HAl caused by unilateral pulmonary artery occlusion. Such cases support the presumed pathophysiology of RAPE, in which edema is thought to result from overperfusion of the microvasculature initiated by uneven arteriolar vasoconstriction and pulmonary hypertension. 1 Additionally, this patient may have a blunted hypoxic ventilatory response (manifested by a PaC02 of 46.5 mm Hg on his second blood gas determination) characteristically seen in persons susceptible to RAPE . Because he refused further arteriotomies, this possibility cannot be proven. All previously reported cases of unilateral pulmonary artery occlusion have been associated with congenital absence of the pulmonary artery.:l-3 My patients combination of presumed childhood granulomatous infection, development of fibrosing mediastinitis with right pulmonary artery obstruction, and susceptibility to recurrent episodes of HAl appears to be unique. Nevertheless, I believe that similar patients must exist among the millions of Americans with prior infection by tuberculosis or histoplasmosis. Because of the mobility of the US population, medical providers in mountainous regions of the country must become sensitized to ''high"-altitude illness occurring at moderate elevations. CHEST 196 I 6 I DECEMBER, 1989
1423
REFERENCES
1 Schoene RB. Pulmonary edema at high altitude: review, pathophysiology, and update. Clin Chest Med 1985; 6:941-507 2 Hackett PH, Roach RC. Medical therapy of altitude illness. Ann Emerg Med 1987; 16:980-86. 3 Hackett PH, Creagh CE, Grover RF, Honigman B, Houston CS, Reeves JT, et al. High-altitude pulmonary edema in persons without the right pulmonary artery. N Engl J Med 1980; 302:107~ 73 4 Rios B, Driscoll DJ, McNamara DG. High-altitude pulmonary edema with absent right pulmonary artery. Pediatrics 1985; 75: 314-17 5 Levine SJ, White DA, Fels AOS. An abnormal chest radiograph in a patient with recurring high altitude pulmonary edema. Chest 1988; 94:627-28 6 Dines DE, Payne WS, Bernatz PE, Pairolero PC. Mediastinal granuloma and 6brosing mediastinitis. Chest 1979; 75:320-24 7 Berry DF, Buccigrossi BS, Peabody J, Peterson KL, Moser KM. Pulmonary vascular occlusion and 6brosing mediastinitis. Chest 1986; 89:296-301 8 Arnett EA, Baros JM, Macher AM, Marsh HB, Savage DD, Fulmer JD, et al. Fibrosing mediastinitis causing pulmonary arterial hypertension without pulmonary venous hypertension. AM J Med 1977; 63:634-43 9 Kinard RE, Orrison WW, Williams, JE. Absent right pulmonary artery ftow in a young man. Invest Radiol1985; 20:785-89
to the onset of symptoms. The patient had no history of lung disease or infections but had a smoking history of 40 pack years before stopping three years prior to admission. Other medications included Zantac, verapamil, furosemide (Lasix), prednisone, azathioprine (Imuran) and cyclosporine. He was afebrile and the physical examination was remarkable for a prominent right thyroid nodule and expiratory wheezes and rhonchi bilaterally. There was no peripheral edema. The chest x-ray 6lm findings were normal as were his blood studies except for a white blood cell count of 12.4 with a mild left shift (ll bands). The sputum was clear without polymorphonuclear leukocytes. The patient was begun on therapy with sulfamethoxazole (Bactrim), double strength twice a day, for possible upper respiratory infection and the yohimbine was stopped. Respiratory treatments with aerosolized atropine and albuterol were started. Initial pulmonary function studies showed moderate obstruction with a good response to bronchodilators with the FVC of 2.86 L (60 percent of predicted), increasing to 4. 13 L-a 44 percent improvement. The patient continued with his respiratory treatments and was started on oral theophylline on day 2. He began to feel better almost immediately with a decrease in mucus production and wheezing which cleared entirely by hospital day 5 . There was continued improvement and he was discharged on day 9 on a regimen including use ofa long-acting theophylline and an albuterol inhaler. Pulmonary function studies prior to discharge showed improvement with an FVC of 3.94 L (83 percent of predicted). All bronchodilators were successfully stopped three weeks after discharge. DISCUSSION
Yohimbine-Induced Bronchospasm* Eric lAndll, M.D., F.C.C .P.; and Eric Shoni, M.D.
Yohimbine is an alpba-2 blocking agent which also increases cholinergic activity. This medication is used to treat male impoleoce. We report a case of yohimbine-induced bronchospasm. (CM.t 1989; 96:1424)
I ~forced vital capacity; FDA= Food .oo Drus Adminis-1
Y autonomic effect is to decrease sympathetic activity and
ohimbine is an alpha-2 blocking agent. Its peripheral
to increase parasympathetic activity. • The increase in cholinergic activity and the decrease in adrenergic activity both can cause an increase in mucus secretion and bronchocoostriction.• Fbllowing is the report ofa patient with yohimbineinduced bronchospasm. CASE REPORT
A ~year-old man who was two years post-heart transplant for idiopathic cardiomyopathy presented to the emergency room with a ten-day history of cough productive of large amounts of clear to white sputum, headaches and progressive shortness of breath. The coughing was complicated by gagging and occasional vomiting of large amounts of sputum. The patient denied any fever, chills, diaphoresis, sore throat or chest pain. He had been started on yohimbine, 5.4 mg orally three times a day, for impotence just prior *From the Pulmonary Section and the Department of Medicine of Hartford Hospital, Hartford, Reprint requem: Dr. Shoni, 85 Seymour Stnlet, Hartford 06106
cr.
1424
Yohimbine has recently been used experimentally for the treatment of male erectile impotence although it currently has no FDA sanctioned uses. 3 This treatment is based on the theory that in male sexual performance, erection is linked to both cholinergic activity and alpha-2 adrenergic blockade, which increase inflow and decrease outflow of blood to the penis, thereby causing an erection. Yohimbine was prescribed to treat this patient's impotence. The increased peripheral cholinergic tone caused by the yohimbine could result in contraction of the bronchial smooth muscle and stimulation of the bronchial mucous glands. • Thus, the use of yohimbine could cause bronchospasm and increased mucus production as occurred in our patient. We believe this patient's symptoms were caused primarily by the yohimbine rather than a respiratory infection. This conclusion is supported by the pharmacologic capacity of the drug, the temporal relationship of the symptoms to starting the drug, the unusually large quantity of clear secretions and no prior history of bronchospastic disease. Multiple medications can induce bronchospasm, 5 and yohimbine should be added to this eve~growing list. REFERENCES
1 Yocon R. Brand of yohimbine. In: Physicians diagnostic reference, 28th ed. Oradell, NJ: Medical Economics Company, 1988: 1521 2 Nettor F. The CIBA collection of medical illustrations: Vol 7. Summit City, NJ: Ciba-Geigy Corporation, 1980 3 Boyd JR, ed. Facts and comparisons drug information. St. Louis: JB Uppincott Company, 1988: 731 4 MayerS. Neurohumeral transmission and the autonomic nervous system In: Goodman, R. Goodman and Gilman"s The pharmacological basis of therapeutics. New York: MacMillan Publishing Co, 1980: 56-90 5 Mathison DA, Stevenson DD, Simon RA. Precipitating factors in asthma: aspirin, sul.6tes and other drugs and chemicals. Chest 1985; 87 (suppi):50S-54S YoNmbine-induced Bronchospasm (Landis, Shote)
While travelling across the intermountain West at an altitude of approximately 2,300 m, a 35-year-old man developed symptoms o£ HAPE. Delay in diagnosis and treatment was nearly lethal. Subsequent evaluation demoostrated unilateral pulmonary artery occlusion, presumably resulting from antecedent granulomatous mediastinitis. This case report supports the concept of evaluating anyone developing HAPE at relatively low altitude for an underlying predisposition. (Chest 1989; 96:1422-23) HAPE =high-altitude pulmonary edema; HAl= high-altitude
illDess
recent years the issue of HAl in mountain climbers has I nreceived increased attention in the medical literature;•·•
however, among sojourners at moderate altitudes (1,500 to 2,500 m), the nonspecific early symptoms of altitude illness are often unrecognized by the affected individuals and undiagnosed by medical personnel. Congenital absence of a pulmonary artery has been reported to predispose to HAPE .w In the following case history, I describe the association of recurrent HAl with acquired unilateral pulmonary artery stenosis induced by fibrosing mediastinitis. CASE REPORT
While travelling across central Wyoming (elevation approximately 2,300 m), a 35-yeaM>Id man began to complain of headache and mild breathlessness. On the following day, he drove 300 miles to Yellowstone National Park (elevation, 2,000 to 2,500 m), and complained of worsening headache, progressive dyspnea, and sweats. No fever or productive cough was noted. A physician's assistant evaluated and treated his headache with intramuscular meperidine and promethazine. After 24 hours of bed rest, Midrin was prescribed for worsening headache, and "migraine" was diagnosed. The increasing dyspnea was ignored. On the fourth day of his illness, the patient concluded that the altitude was affecting him and requested his wife drive him to the Oregon coast. Along the way, dyspnea and orthopnea became extreme, and hemopytsis began. He presented to a hospital emergency room (elevation, 1,500 m), where arterial blood gas levels on nasal oxygen at 5 Umin showed Pa01 of 40 mm Hg and PaC01 of35 mm Hg. After evaluation and initiation of treatment with intravenous heparin, intravenous erythromycin, and 100 percent oxygen via a nonrebreathing mask, the patient was transferred by ambulance to Boise, Idaho (altitude, 850m). *From St. Lukes Regional Medical Center, Boise, Idaho. tCurrently: Pulmonary Disease Service, Walter Reed Army Medical Center, Washington, DC. . The view, opinions, and/or findings contained in this paper are those of the author and should not be construed as official Department of the Army position, policy or decision unless so stated by other official documentation. Reprint 111queats: Dr. 10rrlngton, 1\dmooory Disease Service, Wlrd 77, Wllter Reed Army Medical Center; Washington, DC 20307-5001
1422
The patient denied prior symptoms of chronic pulmonary disease. For years. he had smoked two cigars per day without inhaling. He was a lifelong resident of Arkansas. On two previous trips to the western United States (Leadville, CO, at altitude of 3,100 m and Flagstaff, AZ, at altitude 2,500 m), the patient had developed similar but less severe headache and dyspnea and had improved upon returning to lower altitude. He had not consulted a physician on either occasion. The patient had had several episodes of childhood pneumonia and at the age of eight years had required hospitalization and right thoracocentesis. As a teenager, he had developed a traumatic right pneumothorax during a football game and had been treated overnight with tube thoracostomy. The patient denied a history of tuberculosis or pulmonary emboli. His employment as a machinist and mechanic had resulted in exposure to limited quantities of solvent fumes and dusts, without known ill effects. He took no medications regularly. On arriving in Boise, Idaho, only mild respiratory distress was present. Oral temperature was 37.6"C (99. 7"F). Blood pressure was 142198 mm Hg, pulse rate was 82 beats per minute, and respiratory rate was 24 min. Auscultation of the lungs revealed bilateral inspiratory crackles, predominantly located in the left lung. Breath sounds were significantly decreased throughout the right hemithorax. The patient was obese, but the findings from his examination were otherwise normal. At admission, the WBC count was 11,700/cumm. Arterial blood gas analysis with a 40 percent Venturi mask showed a Pa01 of67.5 mm Hg, PaC01 of 46.5 mm Hg, and pH, 7.41. The presenting chest roentgenogram (Fig I) showed conftuent, central alveolar infiltrates throughout the left lung plus chronic right hilar and mediastinal calcifications. Interstitial markings were increased in the right lung, predominantly at the base. Xenon-133 lung scan showed normal ventilation bilaterally. Following injection of 4 mCi of technetium 99m macroaggregated albumin, complete absence of right lung perfusion and normal left lung perfusion were noted (Fig 2); HAPE was diagnosed, and antibiotic and anticoagulant therapy was withdrawn. Supplemental oxygen administration was continued, and diuresis was begun. To rule out massive pulmonary embolism, pulmonary arteriagrams were performed on the second day of hospitalization. Measurements of pressure (in millimeters of mercury) showed the following values: right atrium, 1210; right ventricle, 4015; right pulmonary artery, 36116; and left pulmonary artery, 45123. A selective pulmonary arteriogram demonstrated a mass of enlarged,
FIGURE 1. Posteroanterior chest roentgenogram shows conftuent, central alveolar infiltrates throughout left lung. Densely calcified mass of lymph nodes is located in right hilum and mediastinum. Interstitial markings are increased in right lung, especially at base. Recunent Hlgh-allllude IIIMM (Ksnneth G. Torrington)
calci6ed right hilar and right paratracheal nodes in the area where the right pulmonary artery was occluded. The occlusions sharp weD-defined border without evidence tOr tapering suggested extrinsic compression, rather than intravascular clot (Fig 3). The left pulmonary arteriogram was normal, as was the levophase examination. An ECG, two-dimensional echocardiography, and bilateral Doppler examination of the lower extremity venous systems were subsequently normal. FoDow-up chest roentgenograms demonstrated rapid improvement of the left pulmonary infiltrate within 12 hours and complete clearing within 72 hours. By then, the patient had become asymptomatic. He was advised to obtain local (sealevel) evaluation tOr possible pulmonary hypertension and to avoid future travel at altitudes over 1,500 m unless using supplemental oxygen.
DISCUSSION
FIGURE 2. Posterior view of technetium 99m macroaggregated albumin perfusion scan demonstrates complete absence of right lung perfusion and normal left lung perfusion.
FIGURE 3. Selective right pulmonary arteriogram demonstrates complete occlusion. Occlusion's border is sharp and weD defined. Occlusion is located adjacent to mass of enlarged, calci6ed right hilar and right paratracheal nodes.
Granulomatous mediastinitis, a condition usually associated with antecedent tuberculosis or histoplasmosis, is a pathologic process capable of affecting any structure traversing the mediastinum. 8 Although the tracheobronchial tree, esophagus, and superior vena cava are most commonly involved, pulmonary arterial or venous obstructions (or both) have been reported. 7•8 The densely calcified right hilar and mediastinal mass adjacent to an obstructed right pulmonary artery in a lifelong resident of Arkansas provides compelling evidence in favor of this diagnosis. The chronicity of the process can be inferred from finding roentgenographic stability onthis patient's chest x-ray films from 1968, as well as from the extent of calcification present. When the lung scan demonstrates unilateral absence of perfusion, possible etiologies include congenital abnormality (often associated with congenital heart disease), massive pulmonary embolism, and neoplasm. Rarely, fibrosing mediastinitis or unilateral hyperlucent lung syndrome (SwyerJames-Macleod) may produce this finding.• Interestingly, patients with proximal interruption of a pulmonary artery are usually asymptomatic unless they develop pulmonary hypertension, as happens in 19 percent.• Since the report by Hackett et al• in 1980, physicians have been aware of the susceptibility to HAl caused by unilateral pulmonary artery occlusion. Such cases support the presumed pathophysiology of RAPE, in which edema is thought to result from overperfusion of the microvasculature initiated by uneven arteriolar vasoconstriction and pulmonary hypertension. 1 Additionally, this patient may have a blunted hypoxic ventilatory response (manifested by a PaC02 of 46.5 mm Hg on his second blood gas determination) characteristically seen in persons susceptible to RAPE . Because he refused further arteriotomies, this possibility cannot be proven. All previously reported cases of unilateral pulmonary artery occlusion have been associated with congenital absence of the pulmonary artery.:l-3 My patients combination of presumed childhood granulomatous infection, development of fibrosing mediastinitis with right pulmonary artery obstruction, and susceptibility to recurrent episodes of HAl appears to be unique. Nevertheless, I believe that similar patients must exist among the millions of Americans with prior infection by tuberculosis or histoplasmosis. Because of the mobility of the US population, medical providers in mountainous regions of the country must become sensitized to ''high"-altitude illness occurring at moderate elevations. CHEST 196 I 6 I DECEMBER, 1989
1423
REFERENCES
1 Schoene RB. Pulmonary edema at high altitude: review, pathophysiology, and update. Clin Chest Med 1985; 6:941-507 2 Hackett PH, Roach RC. Medical therapy of altitude illness. Ann Emerg Med 1987; 16:980-86. 3 Hackett PH, Creagh CE, Grover RF, Honigman B, Houston CS, Reeves JT, et al. High-altitude pulmonary edema in persons without the right pulmonary artery. N Engl J Med 1980; 302:107~ 73 4 Rios B, Driscoll DJ, McNamara DG. High-altitude pulmonary edema with absent right pulmonary artery. Pediatrics 1985; 75: 314-17 5 Levine SJ, White DA, Fels AOS. An abnormal chest radiograph in a patient with recurring high altitude pulmonary edema. Chest 1988; 94:627-28 6 Dines DE, Payne WS, Bernatz PE, Pairolero PC. Mediastinal granuloma and 6brosing mediastinitis. Chest 1979; 75:320-24 7 Berry DF, Buccigrossi BS, Peabody J, Peterson KL, Moser KM. Pulmonary vascular occlusion and 6brosing mediastinitis. Chest 1986; 89:296-301 8 Arnett EA, Baros JM, Macher AM, Marsh HB, Savage DD, Fulmer JD, et al. Fibrosing mediastinitis causing pulmonary arterial hypertension without pulmonary venous hypertension. AM J Med 1977; 63:634-43 9 Kinard RE, Orrison WW, Williams, JE. Absent right pulmonary artery ftow in a young man. Invest Radiol1985; 20:785-89
to the onset of symptoms. The patient had no history of lung disease or infections but had a smoking history of 40 pack years before stopping three years prior to admission. Other medications included Zantac, verapamil, furosemide (Lasix), prednisone, azathioprine (Imuran) and cyclosporine. He was afebrile and the physical examination was remarkable for a prominent right thyroid nodule and expiratory wheezes and rhonchi bilaterally. There was no peripheral edema. The chest x-ray 6lm findings were normal as were his blood studies except for a white blood cell count of 12.4 with a mild left shift (ll bands). The sputum was clear without polymorphonuclear leukocytes. The patient was begun on therapy with sulfamethoxazole (Bactrim), double strength twice a day, for possible upper respiratory infection and the yohimbine was stopped. Respiratory treatments with aerosolized atropine and albuterol were started. Initial pulmonary function studies showed moderate obstruction with a good response to bronchodilators with the FVC of 2.86 L (60 percent of predicted), increasing to 4. 13 L-a 44 percent improvement. The patient continued with his respiratory treatments and was started on oral theophylline on day 2. He began to feel better almost immediately with a decrease in mucus production and wheezing which cleared entirely by hospital day 5 . There was continued improvement and he was discharged on day 9 on a regimen including use ofa long-acting theophylline and an albuterol inhaler. Pulmonary function studies prior to discharge showed improvement with an FVC of 3.94 L (83 percent of predicted). All bronchodilators were successfully stopped three weeks after discharge. DISCUSSION
Yohimbine-Induced Bronchospasm* Eric lAndll, M.D., F.C.C .P.; and Eric Shoni, M.D.
Yohimbine is an alpba-2 blocking agent which also increases cholinergic activity. This medication is used to treat male impoleoce. We report a case of yohimbine-induced bronchospasm. (CM.t 1989; 96:1424)
I ~forced vital capacity; FDA= Food .oo Drus Adminis-1
Y autonomic effect is to decrease sympathetic activity and
ohimbine is an alpha-2 blocking agent. Its peripheral
to increase parasympathetic activity. • The increase in cholinergic activity and the decrease in adrenergic activity both can cause an increase in mucus secretion and bronchocoostriction.• Fbllowing is the report ofa patient with yohimbineinduced bronchospasm. CASE REPORT
A ~year-old man who was two years post-heart transplant for idiopathic cardiomyopathy presented to the emergency room with a ten-day history of cough productive of large amounts of clear to white sputum, headaches and progressive shortness of breath. The coughing was complicated by gagging and occasional vomiting of large amounts of sputum. The patient denied any fever, chills, diaphoresis, sore throat or chest pain. He had been started on yohimbine, 5.4 mg orally three times a day, for impotence just prior *From the Pulmonary Section and the Department of Medicine of Hartford Hospital, Hartford, Reprint requem: Dr. Shoni, 85 Seymour Stnlet, Hartford 06106
cr.
1424
Yohimbine has recently been used experimentally for the treatment of male erectile impotence although it currently has no FDA sanctioned uses. 3 This treatment is based on the theory that in male sexual performance, erection is linked to both cholinergic activity and alpha-2 adrenergic blockade, which increase inflow and decrease outflow of blood to the penis, thereby causing an erection. Yohimbine was prescribed to treat this patient's impotence. The increased peripheral cholinergic tone caused by the yohimbine could result in contraction of the bronchial smooth muscle and stimulation of the bronchial mucous glands. • Thus, the use of yohimbine could cause bronchospasm and increased mucus production as occurred in our patient. We believe this patient's symptoms were caused primarily by the yohimbine rather than a respiratory infection. This conclusion is supported by the pharmacologic capacity of the drug, the temporal relationship of the symptoms to starting the drug, the unusually large quantity of clear secretions and no prior history of bronchospastic disease. Multiple medications can induce bronchospasm, 5 and yohimbine should be added to this eve~growing list. REFERENCES
1 Yocon R. Brand of yohimbine. In: Physicians diagnostic reference, 28th ed. Oradell, NJ: Medical Economics Company, 1988: 1521 2 Nettor F. The CIBA collection of medical illustrations: Vol 7. Summit City, NJ: Ciba-Geigy Corporation, 1980 3 Boyd JR, ed. Facts and comparisons drug information. St. Louis: JB Uppincott Company, 1988: 731 4 MayerS. Neurohumeral transmission and the autonomic nervous system In: Goodman, R. Goodman and Gilman"s The pharmacological basis of therapeutics. New York: MacMillan Publishing Co, 1980: 56-90 5 Mathison DA, Stevenson DD, Simon RA. Precipitating factors in asthma: aspirin, sul.6tes and other drugs and chemicals. Chest 1985; 87 (suppi):50S-54S YoNmbine-induced Bronchospasm (Landis, Shote)