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Transient Hilar Lymphadenopathy Due to Bacterial Endocarditis
Transient Hllar Lymphadenopathy Due to Bacterial Endocarditis· Stuart E. Mirois, M.D.; Kevin] Doyle, M.D.; and John N. Diaconu, M.D.
Transient hilar and mediastinal lymphadenopathy accompanying right-sided bacterial endocarditis without concurrent roentgenographically-demonstrable pulmonary parenchymal abnormalities has not, to our knowledge, been previously reported. The roentgenographic Bnding of hilar or mediastinal lymphadenopathy should not be considered incompatible with the diagnosis of bacterial endocarditis in the appropriate clinical setting. Possible mechanisms for the development of lymphadenopathy secondary to bacterial endocarditis are discussed.
H
ilar and mediastinal lymphadenopathy associated with some pulmonary infections has been well documented. Among these are tuberculosis, fungal infections, Mycoplasma pneumonia, viral pneumonias, including rubeola and varicella-zostet; and bacterial pneumonias such as tularemia, anthrax, and Hemophilus infections. 1 Hilar and mediastinal lymphadenopathy has also been shown to occur with pyogenic lung abscesses including those developing from septic thrombophlebitis or right-sided endocarditis. 2.3 lhmsient hilar and mediastinal lymphadenopathy accompanying right-sided bacterial endocarditis without concurrent roentgenographically demonstrable pulmonary parenchymal abnormalities has not to our knowledge been previously described. CASE REPORT
A 23-year-old black woman presented to the emergency room of the University of Maryland Hospital with a two-week history of diffuse myalgias, anorexia, fever, and night sweats, in addition to vomiting and diarrhea which had developed over the preceding four days. She also complained ofintermittent right-sided pleuritic chest pain associated with mild shortness of breath, without cough or signmcant sputum production. She offered a history of daily drug abuse of intravenous heroin and contacts with individuals possibly infected with tuberculosis and hepatitis. She visited another hospital four days earlier and ampicillin was prescribed, but the patient took only two doses on the first day. The patient did not appear acutely ill, but her vital signs revealed a pulse rate ofllO; blood pressure, 90160 mm Hg; respirations, 20; and an oral temperature of 39.3°C (102.8°F). The lungs were clear to auscultation and percussion. A grade 2/6 systolic ejection murmur was heard along the left: sternal border, without radiation or respiratory variation. The tip of the spleen was palpable, but the abdominal examination was otherwise unremarkable. Several small «1 cm) mobile, tender nodes were identified in the posterior cervical and inguinal regions bilaterally and in the right axilla. The remainder of the physical exam was normal. Laboratory studies revealed a hematocrit value of38 percent and a white blood cell count of 10.9 K with a normal differential. Serum *From the University of Maryland Hospital, and the Department of Diagnostic Radiology, De~ent ofMedicine, Veterans Administration Medical Center, Baltimore Reprint requests: Dr. Mirois, Department oj'Diagnostic Radiology, University of Maryland Hospital, Baltimore 21201
potassium level was 3.4 mEq/L. Urinalysis demonstrated 2 + protein with 0-4 white cells per high power field. Sputum Gram stain showed mixed flora with multiple white blood cells and epithelial cells. A frontal and lateral chest roentgenogram demonstrated enlargement of the right hilum and a density in the region of the aorta and pulmonary artery compatible with lymphadenopathy. No infiltrates or other abnormal densities were noted in the lungs. A pleural effusion was not demonstrated (Fig 1). With the history of recent intravenous drug abuse and several weeks of fever and cardiac murmur, therapy was initiated for probable bacterial endocarditis with penicillin, nafcillin, and gentamicin. The presence of hilar nodes was enigmatic, and other diagnoses such as infectious mononucleosis, tuberculosis and sarcoid were considered. Blood cultures on admission subsequently revealed a growth of Staphylococcus aureus, sensitive to penicillin, in all six samples. Splinter hemorrhages on multiple digits later appeared. EchocaJ'ldiographyobtained three days after admission revealed a 0.5 cm vegetation on the septal leaflet ofthe tricuspid valve compatible with bacterial endocarditis. Because ofpersistent pleuritic chest pain and the detection of an intermittent pleural friction rub repeat chest roentgenograms were obtained. Enlargement of the right hilum representing lymphadenopathy and aortopulmonary lymphadenopathy were demonstrated without evidence of infiltrates or effusions. Antibiotic therapy was changed to penicillin G, 3.3 million units intravenously every four hours. Another roentgenographic examination of the chest obtained five days later was surprising, due to the disappearance ofthe previously noted adenopathy (Fig 2). The patient at this time was improving clinically. The subsequent hospital course was complicated by a no~ mochromic, normocytic anemia and transient renal insufficiency believed to be related to immune complex induced nephritis or interstitial nephritis caused by antibiotics. The patient was discharged after six weeks of intravenous antibiotics and has remained well. DISCUSSION
Infectious endocarditis, usually bacterial, is a well-known complication of intravenous drug abuse. The development of transient, roentogenographically detectable hilar adenopathy as a consequence of endocarditis has not, to the authors' knowledge, been reported. 4-9 The hilar adenopathy observed in this patient could have theoretically occurred due to lymphatic stimulation from one of several possible causes including chronic intravenous drug uS"le, a direct effect of the infected tricuspid valve, pulmonary "parenchymal disease, not detectable roentgenographically, or remotely as a generalized response to persistent staphylococcal sepsis. Joseph and Gealhoed10 reviewed the surgical complications in 250 long-term intravenous drug abusers. They noted that 34 of these patients had asymptomatic "addict" hilar adenopathy with absent pulmonary parenchymal disease. About two-thirds of these patients also had some evidence of generalized adenopathy with firm nontender nodes mainly in the axillary, epitrochlear, and posterior cervical regions. Histologic examination of hilar nodes obtained to exclude sarcoidosis, tuberculosis, and lymphoma revealed a nonspecific lymphocytic hyperplasia similar to that obtained from peripheral nodes. They postulated that long-term lymphatic over-stimulation by injected particulate foreign matter accounted for hilar lymphadenopathy. In the English medical literature, there are no other reports of lymphadenopathy associated with intravenous heroin abuse. While our patient did manifest a peripheral adenopathy similar to that described by Joseph and Gealhoed, the rapid resolution CHEST I 89 I 3 I MARCH, 1988
481
FICURE 1. Posteroanterior and lateral chest roentgenograms obtained on admission demonstrate enlargement of the right hilum and increased soft tissue in the aortopulmonary window compatible with hilar and mediastinal adenopathy (arrowheath). The lung fields are normal.
of the hilar adenopathy during antibiotic therapy suggests a direct relationship to the patients endocarditis. The anatomy of the lymphatic drainage of the mammalian heart was recently reviewed by Miller. 10 In the usual pattern, a small right and a large left epicardial collecting lymphatic fOllows the course of the right and left coronary vein respectively. These lymphatics unite and enter a pretracheallymph
node, consistently located between the arch of the aorta and the pulmonary artery. From there, one or two lymphatics ascend to the cardiac lymph node, located between the superior vena cava and the right brachiocephalic artery. The cardiac lymph node drains by several lymph vessels into the right lymphatic duct system. The distribution oflymph node enlargement seen in our patient does not conform to the
FICURE 2. Repeat posteroanterior and lateral chest roentgenograms nine days after initiation oftreatment for bacterial endocarditis reveal resolution of previous abnormalities. Again, the lung parenchymal appears normal.
1tanslent Hiler Lymphadenopathy (MlrvIs, Doyle, DlaconIs)
pattern one would expect to see if the nodes receiving lymph directly from the heart were enlarged. Recently, Gumbs and McCauley! described four patients with septic pulmonary emboli in whom hilar and mediastinal adenopathy appeared and regressed on antibiotic therapy. Three of their patients were intravenous drug abusers with S aureus tricuspid endocarditis. However, in all of their patients, there was clear roentgenographic evidence on plain film chest studies of cavitating peripheral lesions typical of septic pulmonary emboli. 2 Although the reticuloendothelial system ofthe pulmonary vascular bed may playa role in the clearance oforganisms in the setting of persistent bacteremia, there has been no previous association noted between right-sided staphylococcal endocarditis and the presence of hilar adenopathy. Although this mechanism cannot be excluded as the cause of hilar node enlargement in our patient, it is believed that a more likely etiology is metastatic pulmonic inoculation that could not be detected roentgenographically. This patient was unique in that chest x-ray films failed to reveal any evidence of concurrent pulmonary parenchymal lesions or pleural effusions. She experienced pleuritic chest pain, mild dyspnea, and had an intermittent pleural friction rub, suggesting that she had septic pulmonary emboli which responded to treatment prior to manifesting infiltration or cavitation on roentgenograms. Buar adenopathy in a patient with fevet; nausea, and other constitutional symptoms raises the possibility of a variety of diagnoses including infectious mononucleosis, tuberculosis, sarcoidosis, and lymphoma among others. In patients with a history ofintravenous drug abuse, hilar adenopathy could be secondary to particulate injections, but right-sided bacterial endocarditis without roentgenographically evident concurrent pulmonary parenchymal disease should also be considered. Although the initial impression was that the patient suffered from some entity in addition to endocarditis, fortunately the correct therapy was initiated to treat the most urgent probability. The roentgenographic finding of hilar adenopathy should not be considered incompatible with the diagnosis of bacterial endocarditis in the appropriate clinical setting.
Chronic Pulmonary Emboll* Sparing of Affected Regions of Lung from Noncardlogenlc Pulmonary Edema Janis Jackson, M.D.;t Norman Thompson, M.D.;; and York E. Miller, M.D.'
In chronic pulmonary emboli, lung perfusion may be main-
tained by either recanalization of occluded pulmonary artery segments or collateral bronchial circulation. We present a case of noncardiogenic pulmonary edema superimposed on chronic pulmonary emboli, in which the occluded segments of lung were spared from pulmonary edema, but not from neutrophil in6Itration. This case demonstrates that chronic emboli may lead to roentgenographic sparing in noncardiogenic pulmonary edema, similar to that previously reported in acute pulmonary emboli superimposed on noncardiogenic edema.
S
everal studies have suggested that acute pulmonary emboli prevent development of pulmonary edema in occluded lung segments. 1-3 The mechanism appears to involve a local decrease in hydrostatic perfusion pressure secondary to acute occlusion of the pulmonary vascular supply. Since patients with chronic pulmonary emboli may develop collateral circulation from the bronchial arteries or recanalize the occluded segments of pulmonary artery, it is unclear whether chronic pulmonary emboli may similarly prevent pulmonary edema in lung segments. We report a case of chronic pulmonary emboli with superimposed pulmonary edema. Pulmonary edema did not occur in lung segments with chronically occluded pulmonary arterial vascular supplies. Therefore, chronic pulmonary emboli can be as effective as acute pulmonary emboli in preventing pulmonary edema in affected regions of the lung. The development of characteristic roentgenographic findings in a patient with pre-existing pulmonary hypertension should lead the clinician to suspect this situation and may provide a clue to the etiology of the pulmonary hypertension.
REFERENCES
CASE REPORT
1 Pare ~ Fraser RG. Synopsis of diseases of the chest. Philadelphia: WB Saunders Co, 1983:254-350 2 Gumbs R~ McCauley DI. Hilar and mediastinal adenopathy in septic embolic abscess. Radiology 1982; 142:313-15 3 Roh16ng BM, White EA, Webb WR, Goodman pc. Hilar and mediastinal adenopathy caused by bacterial abscess of the lung. Radiology 1978; 128:289-93 4 Stern WZ. Roentgenographic aspects of narcotic addiction. JAMA 1976; 236:963-65 5 Jaffe RB, Koschmann EB. Intravenous drug abuse: pulmonary, cardiac, and vascular complications. AJR 1970; 109:107-20 6 Cherubin CEo Infectious disease problems of narcotic addicts. Arch Intern Med 1971; 128:309-13 7 Jaffe RB, Koschmann EB. Septic pulmonary emboli. Radiology 1970; 96:527-32 8 Stein WZ, Spear P~ Jacobson HG. The roentgen findings in acute heroin intoxication. AJR 1968; 103:522-32 9 Ellis K, Jaffe C, Malm JR, Bowman FO. Infective endocarditis roentgenographic considerations. Radiol Clio N Am 1973; 11: 415-41 10 Miller AJ. Lymphatics ofthe heart. New York: Raven Press, 1982
A 61-year-old white man was admitted to the hospital for evaluation of new onset seizures. Past medical history was significant for a long history of deep venous thrombosis complicated by recurrent pulmonary emboli, pulmonary hypertension, and cor pulmonale. An umbrella had been inserted into the inferior vena cave many years prior to admission and the patient was receiving long-term coumarin therapy. Significantly, the patient had a two-week history ofpost-tussive syncope, and on admission, was noted to have several generalized tonic clonic seizures that were also immediately preceded by coughing. Neurologic examination was unremarkable, and remaining physical examination was significant only for signs consistent with pulmonary hypertension and cor pulmonale. Admission laboratory values included a normal glucose value, normal elec*From the Veterans Administration Hospital, UDiversity ofColorado Health Sciences Center, Denver. tFellow, Division of Pulmonary Science, Department of Medicine. ;Resident, Department of Pathology. 'Assistant Professor, Division of Pulmonary Sciences, Department of Medicine. Reprint requests: Dr. Miller, VA Medical Center, 1055 Clermont Street, Denver 80220 CHEST I 89 131 MARCH, 1986
483
Transient hilar and mediastinal lymphadenopathy accompanying right-sided bacterial endocarditis without concurrent roentgenographically-demonstrable pulmonary parenchymal abnormalities has not, to our knowledge, been previously reported. The roentgenographic Bnding of hilar or mediastinal lymphadenopathy should not be considered incompatible with the diagnosis of bacterial endocarditis in the appropriate clinical setting. Possible mechanisms for the development of lymphadenopathy secondary to bacterial endocarditis are discussed.
H
ilar and mediastinal lymphadenopathy associated with some pulmonary infections has been well documented. Among these are tuberculosis, fungal infections, Mycoplasma pneumonia, viral pneumonias, including rubeola and varicella-zostet; and bacterial pneumonias such as tularemia, anthrax, and Hemophilus infections. 1 Hilar and mediastinal lymphadenopathy has also been shown to occur with pyogenic lung abscesses including those developing from septic thrombophlebitis or right-sided endocarditis. 2.3 lhmsient hilar and mediastinal lymphadenopathy accompanying right-sided bacterial endocarditis without concurrent roentgenographically demonstrable pulmonary parenchymal abnormalities has not to our knowledge been previously described. CASE REPORT
A 23-year-old black woman presented to the emergency room of the University of Maryland Hospital with a two-week history of diffuse myalgias, anorexia, fever, and night sweats, in addition to vomiting and diarrhea which had developed over the preceding four days. She also complained ofintermittent right-sided pleuritic chest pain associated with mild shortness of breath, without cough or signmcant sputum production. She offered a history of daily drug abuse of intravenous heroin and contacts with individuals possibly infected with tuberculosis and hepatitis. She visited another hospital four days earlier and ampicillin was prescribed, but the patient took only two doses on the first day. The patient did not appear acutely ill, but her vital signs revealed a pulse rate ofllO; blood pressure, 90160 mm Hg; respirations, 20; and an oral temperature of 39.3°C (102.8°F). The lungs were clear to auscultation and percussion. A grade 2/6 systolic ejection murmur was heard along the left: sternal border, without radiation or respiratory variation. The tip of the spleen was palpable, but the abdominal examination was otherwise unremarkable. Several small «1 cm) mobile, tender nodes were identified in the posterior cervical and inguinal regions bilaterally and in the right axilla. The remainder of the physical exam was normal. Laboratory studies revealed a hematocrit value of38 percent and a white blood cell count of 10.9 K with a normal differential. Serum *From the University of Maryland Hospital, and the Department of Diagnostic Radiology, De~ent ofMedicine, Veterans Administration Medical Center, Baltimore Reprint requests: Dr. Mirois, Department oj'Diagnostic Radiology, University of Maryland Hospital, Baltimore 21201
potassium level was 3.4 mEq/L. Urinalysis demonstrated 2 + protein with 0-4 white cells per high power field. Sputum Gram stain showed mixed flora with multiple white blood cells and epithelial cells. A frontal and lateral chest roentgenogram demonstrated enlargement of the right hilum and a density in the region of the aorta and pulmonary artery compatible with lymphadenopathy. No infiltrates or other abnormal densities were noted in the lungs. A pleural effusion was not demonstrated (Fig 1). With the history of recent intravenous drug abuse and several weeks of fever and cardiac murmur, therapy was initiated for probable bacterial endocarditis with penicillin, nafcillin, and gentamicin. The presence of hilar nodes was enigmatic, and other diagnoses such as infectious mononucleosis, tuberculosis and sarcoid were considered. Blood cultures on admission subsequently revealed a growth of Staphylococcus aureus, sensitive to penicillin, in all six samples. Splinter hemorrhages on multiple digits later appeared. EchocaJ'ldiographyobtained three days after admission revealed a 0.5 cm vegetation on the septal leaflet ofthe tricuspid valve compatible with bacterial endocarditis. Because ofpersistent pleuritic chest pain and the detection of an intermittent pleural friction rub repeat chest roentgenograms were obtained. Enlargement of the right hilum representing lymphadenopathy and aortopulmonary lymphadenopathy were demonstrated without evidence of infiltrates or effusions. Antibiotic therapy was changed to penicillin G, 3.3 million units intravenously every four hours. Another roentgenographic examination of the chest obtained five days later was surprising, due to the disappearance ofthe previously noted adenopathy (Fig 2). The patient at this time was improving clinically. The subsequent hospital course was complicated by a no~ mochromic, normocytic anemia and transient renal insufficiency believed to be related to immune complex induced nephritis or interstitial nephritis caused by antibiotics. The patient was discharged after six weeks of intravenous antibiotics and has remained well. DISCUSSION
Infectious endocarditis, usually bacterial, is a well-known complication of intravenous drug abuse. The development of transient, roentogenographically detectable hilar adenopathy as a consequence of endocarditis has not, to the authors' knowledge, been reported. 4-9 The hilar adenopathy observed in this patient could have theoretically occurred due to lymphatic stimulation from one of several possible causes including chronic intravenous drug uS"le, a direct effect of the infected tricuspid valve, pulmonary "parenchymal disease, not detectable roentgenographically, or remotely as a generalized response to persistent staphylococcal sepsis. Joseph and Gealhoed10 reviewed the surgical complications in 250 long-term intravenous drug abusers. They noted that 34 of these patients had asymptomatic "addict" hilar adenopathy with absent pulmonary parenchymal disease. About two-thirds of these patients also had some evidence of generalized adenopathy with firm nontender nodes mainly in the axillary, epitrochlear, and posterior cervical regions. Histologic examination of hilar nodes obtained to exclude sarcoidosis, tuberculosis, and lymphoma revealed a nonspecific lymphocytic hyperplasia similar to that obtained from peripheral nodes. They postulated that long-term lymphatic over-stimulation by injected particulate foreign matter accounted for hilar lymphadenopathy. In the English medical literature, there are no other reports of lymphadenopathy associated with intravenous heroin abuse. While our patient did manifest a peripheral adenopathy similar to that described by Joseph and Gealhoed, the rapid resolution CHEST I 89 I 3 I MARCH, 1988
481
FICURE 1. Posteroanterior and lateral chest roentgenograms obtained on admission demonstrate enlargement of the right hilum and increased soft tissue in the aortopulmonary window compatible with hilar and mediastinal adenopathy (arrowheath). The lung fields are normal.
of the hilar adenopathy during antibiotic therapy suggests a direct relationship to the patients endocarditis. The anatomy of the lymphatic drainage of the mammalian heart was recently reviewed by Miller. 10 In the usual pattern, a small right and a large left epicardial collecting lymphatic fOllows the course of the right and left coronary vein respectively. These lymphatics unite and enter a pretracheallymph
node, consistently located between the arch of the aorta and the pulmonary artery. From there, one or two lymphatics ascend to the cardiac lymph node, located between the superior vena cava and the right brachiocephalic artery. The cardiac lymph node drains by several lymph vessels into the right lymphatic duct system. The distribution oflymph node enlargement seen in our patient does not conform to the
FICURE 2. Repeat posteroanterior and lateral chest roentgenograms nine days after initiation oftreatment for bacterial endocarditis reveal resolution of previous abnormalities. Again, the lung parenchymal appears normal.
1tanslent Hiler Lymphadenopathy (MlrvIs, Doyle, DlaconIs)
pattern one would expect to see if the nodes receiving lymph directly from the heart were enlarged. Recently, Gumbs and McCauley! described four patients with septic pulmonary emboli in whom hilar and mediastinal adenopathy appeared and regressed on antibiotic therapy. Three of their patients were intravenous drug abusers with S aureus tricuspid endocarditis. However, in all of their patients, there was clear roentgenographic evidence on plain film chest studies of cavitating peripheral lesions typical of septic pulmonary emboli. 2 Although the reticuloendothelial system ofthe pulmonary vascular bed may playa role in the clearance oforganisms in the setting of persistent bacteremia, there has been no previous association noted between right-sided staphylococcal endocarditis and the presence of hilar adenopathy. Although this mechanism cannot be excluded as the cause of hilar node enlargement in our patient, it is believed that a more likely etiology is metastatic pulmonic inoculation that could not be detected roentgenographically. This patient was unique in that chest x-ray films failed to reveal any evidence of concurrent pulmonary parenchymal lesions or pleural effusions. She experienced pleuritic chest pain, mild dyspnea, and had an intermittent pleural friction rub, suggesting that she had septic pulmonary emboli which responded to treatment prior to manifesting infiltration or cavitation on roentgenograms. Buar adenopathy in a patient with fevet; nausea, and other constitutional symptoms raises the possibility of a variety of diagnoses including infectious mononucleosis, tuberculosis, sarcoidosis, and lymphoma among others. In patients with a history ofintravenous drug abuse, hilar adenopathy could be secondary to particulate injections, but right-sided bacterial endocarditis without roentgenographically evident concurrent pulmonary parenchymal disease should also be considered. Although the initial impression was that the patient suffered from some entity in addition to endocarditis, fortunately the correct therapy was initiated to treat the most urgent probability. The roentgenographic finding of hilar adenopathy should not be considered incompatible with the diagnosis of bacterial endocarditis in the appropriate clinical setting.
Chronic Pulmonary Emboll* Sparing of Affected Regions of Lung from Noncardlogenlc Pulmonary Edema Janis Jackson, M.D.;t Norman Thompson, M.D.;; and York E. Miller, M.D.'
In chronic pulmonary emboli, lung perfusion may be main-
tained by either recanalization of occluded pulmonary artery segments or collateral bronchial circulation. We present a case of noncardiogenic pulmonary edema superimposed on chronic pulmonary emboli, in which the occluded segments of lung were spared from pulmonary edema, but not from neutrophil in6Itration. This case demonstrates that chronic emboli may lead to roentgenographic sparing in noncardiogenic pulmonary edema, similar to that previously reported in acute pulmonary emboli superimposed on noncardiogenic edema.
S
everal studies have suggested that acute pulmonary emboli prevent development of pulmonary edema in occluded lung segments. 1-3 The mechanism appears to involve a local decrease in hydrostatic perfusion pressure secondary to acute occlusion of the pulmonary vascular supply. Since patients with chronic pulmonary emboli may develop collateral circulation from the bronchial arteries or recanalize the occluded segments of pulmonary artery, it is unclear whether chronic pulmonary emboli may similarly prevent pulmonary edema in lung segments. We report a case of chronic pulmonary emboli with superimposed pulmonary edema. Pulmonary edema did not occur in lung segments with chronically occluded pulmonary arterial vascular supplies. Therefore, chronic pulmonary emboli can be as effective as acute pulmonary emboli in preventing pulmonary edema in affected regions of the lung. The development of characteristic roentgenographic findings in a patient with pre-existing pulmonary hypertension should lead the clinician to suspect this situation and may provide a clue to the etiology of the pulmonary hypertension.
REFERENCES
CASE REPORT
1 Pare ~ Fraser RG. Synopsis of diseases of the chest. Philadelphia: WB Saunders Co, 1983:254-350 2 Gumbs R~ McCauley DI. Hilar and mediastinal adenopathy in septic embolic abscess. Radiology 1982; 142:313-15 3 Roh16ng BM, White EA, Webb WR, Goodman pc. Hilar and mediastinal adenopathy caused by bacterial abscess of the lung. Radiology 1978; 128:289-93 4 Stern WZ. Roentgenographic aspects of narcotic addiction. JAMA 1976; 236:963-65 5 Jaffe RB, Koschmann EB. Intravenous drug abuse: pulmonary, cardiac, and vascular complications. AJR 1970; 109:107-20 6 Cherubin CEo Infectious disease problems of narcotic addicts. Arch Intern Med 1971; 128:309-13 7 Jaffe RB, Koschmann EB. Septic pulmonary emboli. Radiology 1970; 96:527-32 8 Stein WZ, Spear P~ Jacobson HG. The roentgen findings in acute heroin intoxication. AJR 1968; 103:522-32 9 Ellis K, Jaffe C, Malm JR, Bowman FO. Infective endocarditis roentgenographic considerations. Radiol Clio N Am 1973; 11: 415-41 10 Miller AJ. Lymphatics ofthe heart. New York: Raven Press, 1982
A 61-year-old white man was admitted to the hospital for evaluation of new onset seizures. Past medical history was significant for a long history of deep venous thrombosis complicated by recurrent pulmonary emboli, pulmonary hypertension, and cor pulmonale. An umbrella had been inserted into the inferior vena cave many years prior to admission and the patient was receiving long-term coumarin therapy. Significantly, the patient had a two-week history ofpost-tussive syncope, and on admission, was noted to have several generalized tonic clonic seizures that were also immediately preceded by coughing. Neurologic examination was unremarkable, and remaining physical examination was significant only for signs consistent with pulmonary hypertension and cor pulmonale. Admission laboratory values included a normal glucose value, normal elec*From the Veterans Administration Hospital, UDiversity ofColorado Health Sciences Center, Denver. tFellow, Division of Pulmonary Science, Department of Medicine. ;Resident, Department of Pathology. 'Assistant Professor, Division of Pulmonary Sciences, Department of Medicine. Reprint requests: Dr. Miller, VA Medical Center, 1055 Clermont Street, Denver 80220 CHEST I 89 131 MARCH, 1986
483