BRIEF CLINICAL
OBSERVATIONS
were characteristic of a carcinoid (Figure 2). Multifocal necrosis and hemorrhage were present. An occasional cell with mitotic figures was seen. Hyalinized connective tissue and osteoid tissue intersected the sheets of tumor cells. There was tumor cell invasion in the vascular channels and overlying osteoid tissue. Immunostaining was positive for serotonin and chromogranin but negative for vasoactive intestinal polypeptide/bombesin, enolase, and calcitonin. The patient had an uneventful postoperative course. Three years later, there was no visual field defect and a subsequent CT scan has not shown any recurrence of tumor. Patchell and Posner [l] reported that brain metastases occurred in 6% of their patients with carcinoid tumors, but they could find only a few other references in the literature. The CT scan appearance of carcinoid brain metastases could not be differentiated from that of other tumors. However, Deleu et al [2] described a hyperdense carcinoid metastasis to the brain with adjacent bone thickening suggestive of a meningioma. Histologically, no bone invasion was present. The CT scan in our case was very similar, although there was contrast enhancement. Although osseous invasion may have been partially responsible for the bone thickening, osteoid within and surrounding the tumor appeared to be responsible for most of the hyperdense areas seen on CT scan. Stroma1 bone formation has been described in carcinoid tumors [3]. Furthermore, an osteoblastic reaction can be seen with bone involvement [4]. In a patient with a carcinoid tumor and a hyperdense cerebral mass on CT scan, differentiation of a metastasis from the more common, unrelated meningioma would prove difficult. Carcinoid tumors may be slowgrowing and distant metastases can occur many years after the initial diagnosis. In our patient, the cerebral metastasis occurred 25 years after removal of the bronchial tumor. Such a long time interval could add confusion to the diagnosis. Finally, Smith et al [5] reported a carcinoid tumor that was found at postmortem examination to have metastasized to a meningioma. Therefore, even with a history of a carcinoid tumor, a patient with
316
March
1990
The American
Journal
a hyperdense intracranial tumor would require a biopsy as the only method to conclusively diagnose this type of tumor.
Loyola
DONALD L. GORDON, M.D. JOHN F. SHEA, M.D. KETTY BADRINATH, M.D. MICHAEL FINE, M.D. MEENA GUJRATI, M.D. University Medical Center Maywood, Illinois
1. Patchell PA. Posner JB: Neuroloe~c comokcations of carclnold. Neurology 1986; 36: 745-749. 2.Deleu D, DeGeeter F. Buisseret T, Goossens A, Caemaert J. Eblnger G: Dural metastasis from laryngeal malignant carcinold. Am J Med 1989; 86. 502% 505. 3. Kuhn C. Askln F: Lung and medlastinum, carclnoid. In: Klssane J, ed. Anderson’s pathology, 8th ed. St. LOUIS: CV Mosby. 1985; 927. 4. Powell JM: Metastatic carclnold of bone. Clin Orthop 1988; 230: 266-272. 5. SmithTW, Wang SY, Schoene WC. MalIgnant carclnoid tumor metastatlc to a meningloma. Cancer 1981; 47: 1872-1877. SubmItted September
11. 1989, and accepted In revised form October 24, 1989
COCAINE-ASSOCIATED RHABDOMYOLYSIS AND HEMOPNSIS MIMICKING PULMONARY EMBOLISM Pulmonary embolism is a potentially life-threatening event that should be considered in the differential diagnosis of any patient presenting with acute onset of either pleuritic pain, tachypnea, or bloody sputum. Since these findings are nonspecific, a large number of differential diagnoses should be considered [1,2]. We recently observed the case of a young adult who presented with chest pain, blood-streaked sputum, and rhabdomyolysis associated with “crack” cocaine use, closely mimicking an acute pulmonary embolism. This is an association heretofore not included in the differential diagnosis of pulmonary thromboembolic disease [1,2]. The patient was a 34-year-old man admitted with a 6-hour history of shortness of breath and rightsided pleuritic chest pain; he had noticed blood-streaked sputum during the last 24 hours and admittedtocrackcocaineuseevery2to3 days over the past year, including heavy cocaine smoking the day before his presentation. He denied any recent period of unconsciousness, seizures, trauma, syncopal episodes, palpitations, chills, or fe-
of Medicine
Volume
88
ver. He had a history of recurrent episodes of deep venous thrombosis and venous stasis ulcers of the lower extremities since age 25, as well as three episodes of pulmonary embolism, the last one in 1983, when he underwent plication of the inferior vena cava. His temperature was 37.4’C, pulse 72 beats/minute, respirations 34/minute, and blood pressure 1201 85 mm Hg. He was utilizing his accessory muscles of respiration and was diaphoretic. He had decreased diaphragmatic excursion and decreased breath sounds bilaterally. There were multiple hyperpigmented circular scars on both lower legs. His arterial oxygen tension was 74 mm Hg on room air, with an oxygen saturation of 91.8%. The electrocardiogram was unchanged from previous tracings, and there were no further changes; chest radiography demonstrated a linear subsegmental atelectasis of the left base, and a rounded, prominent vessel on the right hilum. A working diagnosis of pulmonary embolism was established. A ventilation/perfusion lung scan was interpreted as “low probability” for pulmonary embolism, and a pulmonary angiogram revealed no evidence of pulmonary embolism. Urine and blood samples showed high levels of cocaine. Total creatine-phosphokinase (CPK) peaked at 661 U/L on the second hospital day. Results of testing for CPK-MB isoenzyme, however, were negative three times over a 24-hour period, and levels of lactate dehydrogenase cardiac isoenzymes did not rise above normal limits, ruling out myocardial infarction. Urine myoglobin was positive at 179 ng/mL, confirming the diagnosis of rhabdomyolysis. The patient steadily improved with decreased respiratory distress, relief of chest pain, and a decrease in total CPK to near-normal values. He was discharged asymptomatic 3 days after initial presentation. Rhabdomyolysis [3-61 and myocardial ischemic events [7,8] have been reported in association with cocaine abuse. By blocking re-uptake of catecholamines, cocaine produces pronounced stimulation of a-adrenergic receptors, leading to muscle damage induced by prolonged ischemia secondary to vasoconstriction [4,7]. Recently, Rubin and Neugarten [6] reported six pa-
BRIEF CLINICAL
tients with cocaine-associated rhabdomyolysis presenting with chest pain simulating a myocardial infarction. We suspect our patient’s chest pain was secondary to rhabdomyolysis associated with his use of “crack” cocaine. He also presented with blood-streaked sputum, a finding that has been reported after smoking “freebase” cocaine [9,10]. Intense cocaine-induced vasoconstriction has also been suggested as the mechanism for pulmonary hemorrhage [9]. We postulate that our patient’s hemoptysis was also associated with his use of “crack” cocaine, contributing to a clinical picture that closely simulated pulmonary embolism. With the rapid escalation in consumption of “crack” cocaine in recent years, physicians should be alerted to this clinical presentation not previously described. Rhabdo-
myolysis and pulmonary hemorrhage associated with smoking “crack” cocaine should be considered in the differential diagnosis of patients presenting with a clinical picture suggestive of pulmonary embolism. We strongly suggest that in the appropriate clinical setting, while the possible diagnoses of pulmonary embolism and acute myocardial ischemic event are pursued, a toxicology screen and an active search for evidence of rhabdomyolysis should be simultaneously initiated. FEDERICO R. JUSTINIANI, M.D. CARMEN CABEZA, B.S. BRUCE A. MILLER, M.D. Mount Sinai Medical Center Miami Beach, Florida and University of Miami School of Medicine Miami, Florida
March
1990
The American
OBSERVATIONS
1. Senior R: Pulmonary embolism. In: Wyngaarden JB, Smith LH Jr, eds. Cecil textbook of medicine. Phrladelphia: WB Saunders, 1988; 442-450. 2. Hull RD, Raskob GE, Carter CJ. et al: Pulmonary embolism in outpatients wrth pleuritrc chest pain. Arch Intern Med 1988; 148: 838-844 3. Krohn KD, Slowman-Kovacs S, Leapman SB: Cocaine and rhabdomyolysrs (letter). Ann Intern Med 1988; 108: 639-640. 4. Herzlich BC, Arsura EL, Pagala M, Grob D: Rhabdomyolysrs related to cocaine abuse. Ann Intern Med 1988; 109: 335-336. 5. Roth D. Alarcon FJ. Fernandez JA. ef al: Acute rhabdomyolysis associated with cocarne intoxrcation. N Engl J Med 1988; 319: 673-677. 6. Rubtn RB, Neugarten J: Cocarne-induced rhabdomyolysis masquerading as myocardial ischemra. Am J Med 1989; 86: 551-553. 7. Cregler LL, Mark H: Medical complrcations of cocaine abuse. N Engl J Med 1986; 315: 1495-1500. 8. Smith HWB Ill, Liberman HA. Brodv SL. eta/:Acute myocardial infarction temporally related to cocaine use. Ann Intern Med 1987; 107: 13-18. 9. Murray RJ. Albin RJ. Mergner W, Criner GJ: Drffuse alveolar hemorrhage temporally related to cocaine smokrng. Chest 1988; 93: 427-429. 10. Godwin JE, Harley RA. Miller KS, Hefner JE: Cocaine, pulmonary hemorrhage and hemoptysis (letter). Ann Intern Med 1989; 110: 843. Submitted August 23, 1989, and accepted October 2, 1989
Journal
of Medicine
Volume
88
317
OBSERVATIONS
were characteristic of a carcinoid (Figure 2). Multifocal necrosis and hemorrhage were present. An occasional cell with mitotic figures was seen. Hyalinized connective tissue and osteoid tissue intersected the sheets of tumor cells. There was tumor cell invasion in the vascular channels and overlying osteoid tissue. Immunostaining was positive for serotonin and chromogranin but negative for vasoactive intestinal polypeptide/bombesin, enolase, and calcitonin. The patient had an uneventful postoperative course. Three years later, there was no visual field defect and a subsequent CT scan has not shown any recurrence of tumor. Patchell and Posner [l] reported that brain metastases occurred in 6% of their patients with carcinoid tumors, but they could find only a few other references in the literature. The CT scan appearance of carcinoid brain metastases could not be differentiated from that of other tumors. However, Deleu et al [2] described a hyperdense carcinoid metastasis to the brain with adjacent bone thickening suggestive of a meningioma. Histologically, no bone invasion was present. The CT scan in our case was very similar, although there was contrast enhancement. Although osseous invasion may have been partially responsible for the bone thickening, osteoid within and surrounding the tumor appeared to be responsible for most of the hyperdense areas seen on CT scan. Stroma1 bone formation has been described in carcinoid tumors [3]. Furthermore, an osteoblastic reaction can be seen with bone involvement [4]. In a patient with a carcinoid tumor and a hyperdense cerebral mass on CT scan, differentiation of a metastasis from the more common, unrelated meningioma would prove difficult. Carcinoid tumors may be slowgrowing and distant metastases can occur many years after the initial diagnosis. In our patient, the cerebral metastasis occurred 25 years after removal of the bronchial tumor. Such a long time interval could add confusion to the diagnosis. Finally, Smith et al [5] reported a carcinoid tumor that was found at postmortem examination to have metastasized to a meningioma. Therefore, even with a history of a carcinoid tumor, a patient with
316
March
1990
The American
Journal
a hyperdense intracranial tumor would require a biopsy as the only method to conclusively diagnose this type of tumor.
Loyola
DONALD L. GORDON, M.D. JOHN F. SHEA, M.D. KETTY BADRINATH, M.D. MICHAEL FINE, M.D. MEENA GUJRATI, M.D. University Medical Center Maywood, Illinois
1. Patchell PA. Posner JB: Neuroloe~c comokcations of carclnold. Neurology 1986; 36: 745-749. 2.Deleu D, DeGeeter F. Buisseret T, Goossens A, Caemaert J. Eblnger G: Dural metastasis from laryngeal malignant carcinold. Am J Med 1989; 86. 502% 505. 3. Kuhn C. Askln F: Lung and medlastinum, carclnoid. In: Klssane J, ed. Anderson’s pathology, 8th ed. St. LOUIS: CV Mosby. 1985; 927. 4. Powell JM: Metastatic carclnold of bone. Clin Orthop 1988; 230: 266-272. 5. SmithTW, Wang SY, Schoene WC. MalIgnant carclnoid tumor metastatlc to a meningloma. Cancer 1981; 47: 1872-1877. SubmItted September
11. 1989, and accepted In revised form October 24, 1989
COCAINE-ASSOCIATED RHABDOMYOLYSIS AND HEMOPNSIS MIMICKING PULMONARY EMBOLISM Pulmonary embolism is a potentially life-threatening event that should be considered in the differential diagnosis of any patient presenting with acute onset of either pleuritic pain, tachypnea, or bloody sputum. Since these findings are nonspecific, a large number of differential diagnoses should be considered [1,2]. We recently observed the case of a young adult who presented with chest pain, blood-streaked sputum, and rhabdomyolysis associated with “crack” cocaine use, closely mimicking an acute pulmonary embolism. This is an association heretofore not included in the differential diagnosis of pulmonary thromboembolic disease [1,2]. The patient was a 34-year-old man admitted with a 6-hour history of shortness of breath and rightsided pleuritic chest pain; he had noticed blood-streaked sputum during the last 24 hours and admittedtocrackcocaineuseevery2to3 days over the past year, including heavy cocaine smoking the day before his presentation. He denied any recent period of unconsciousness, seizures, trauma, syncopal episodes, palpitations, chills, or fe-
of Medicine
Volume
88
ver. He had a history of recurrent episodes of deep venous thrombosis and venous stasis ulcers of the lower extremities since age 25, as well as three episodes of pulmonary embolism, the last one in 1983, when he underwent plication of the inferior vena cava. His temperature was 37.4’C, pulse 72 beats/minute, respirations 34/minute, and blood pressure 1201 85 mm Hg. He was utilizing his accessory muscles of respiration and was diaphoretic. He had decreased diaphragmatic excursion and decreased breath sounds bilaterally. There were multiple hyperpigmented circular scars on both lower legs. His arterial oxygen tension was 74 mm Hg on room air, with an oxygen saturation of 91.8%. The electrocardiogram was unchanged from previous tracings, and there were no further changes; chest radiography demonstrated a linear subsegmental atelectasis of the left base, and a rounded, prominent vessel on the right hilum. A working diagnosis of pulmonary embolism was established. A ventilation/perfusion lung scan was interpreted as “low probability” for pulmonary embolism, and a pulmonary angiogram revealed no evidence of pulmonary embolism. Urine and blood samples showed high levels of cocaine. Total creatine-phosphokinase (CPK) peaked at 661 U/L on the second hospital day. Results of testing for CPK-MB isoenzyme, however, were negative three times over a 24-hour period, and levels of lactate dehydrogenase cardiac isoenzymes did not rise above normal limits, ruling out myocardial infarction. Urine myoglobin was positive at 179 ng/mL, confirming the diagnosis of rhabdomyolysis. The patient steadily improved with decreased respiratory distress, relief of chest pain, and a decrease in total CPK to near-normal values. He was discharged asymptomatic 3 days after initial presentation. Rhabdomyolysis [3-61 and myocardial ischemic events [7,8] have been reported in association with cocaine abuse. By blocking re-uptake of catecholamines, cocaine produces pronounced stimulation of a-adrenergic receptors, leading to muscle damage induced by prolonged ischemia secondary to vasoconstriction [4,7]. Recently, Rubin and Neugarten [6] reported six pa-
BRIEF CLINICAL
tients with cocaine-associated rhabdomyolysis presenting with chest pain simulating a myocardial infarction. We suspect our patient’s chest pain was secondary to rhabdomyolysis associated with his use of “crack” cocaine. He also presented with blood-streaked sputum, a finding that has been reported after smoking “freebase” cocaine [9,10]. Intense cocaine-induced vasoconstriction has also been suggested as the mechanism for pulmonary hemorrhage [9]. We postulate that our patient’s hemoptysis was also associated with his use of “crack” cocaine, contributing to a clinical picture that closely simulated pulmonary embolism. With the rapid escalation in consumption of “crack” cocaine in recent years, physicians should be alerted to this clinical presentation not previously described. Rhabdo-
myolysis and pulmonary hemorrhage associated with smoking “crack” cocaine should be considered in the differential diagnosis of patients presenting with a clinical picture suggestive of pulmonary embolism. We strongly suggest that in the appropriate clinical setting, while the possible diagnoses of pulmonary embolism and acute myocardial ischemic event are pursued, a toxicology screen and an active search for evidence of rhabdomyolysis should be simultaneously initiated. FEDERICO R. JUSTINIANI, M.D. CARMEN CABEZA, B.S. BRUCE A. MILLER, M.D. Mount Sinai Medical Center Miami Beach, Florida and University of Miami School of Medicine Miami, Florida
March
1990
The American
OBSERVATIONS
1. Senior R: Pulmonary embolism. In: Wyngaarden JB, Smith LH Jr, eds. Cecil textbook of medicine. Phrladelphia: WB Saunders, 1988; 442-450. 2. Hull RD, Raskob GE, Carter CJ. et al: Pulmonary embolism in outpatients wrth pleuritrc chest pain. Arch Intern Med 1988; 148: 838-844 3. Krohn KD, Slowman-Kovacs S, Leapman SB: Cocaine and rhabdomyolysrs (letter). Ann Intern Med 1988; 108: 639-640. 4. Herzlich BC, Arsura EL, Pagala M, Grob D: Rhabdomyolysrs related to cocaine abuse. Ann Intern Med 1988; 109: 335-336. 5. Roth D. Alarcon FJ. Fernandez JA. ef al: Acute rhabdomyolysis associated with cocarne intoxrcation. N Engl J Med 1988; 319: 673-677. 6. Rubtn RB, Neugarten J: Cocarne-induced rhabdomyolysis masquerading as myocardial ischemra. Am J Med 1989; 86: 551-553. 7. Cregler LL, Mark H: Medical complrcations of cocaine abuse. N Engl J Med 1986; 315: 1495-1500. 8. Smith HWB Ill, Liberman HA. Brodv SL. eta/:Acute myocardial infarction temporally related to cocaine use. Ann Intern Med 1987; 107: 13-18. 9. Murray RJ. Albin RJ. Mergner W, Criner GJ: Drffuse alveolar hemorrhage temporally related to cocaine smokrng. Chest 1988; 93: 427-429. 10. Godwin JE, Harley RA. Miller KS, Hefner JE: Cocaine, pulmonary hemorrhage and hemoptysis (letter). Ann Intern Med 1989; 110: 843. Submitted August 23, 1989, and accepted October 2, 1989
Journal
of Medicine
Volume
88
317
