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Pulmonary Sarcoidosis Presenting as Bronchogenic Carcinoma
the orifice of the right coronary a r t e ~ y . ~ ? l l W e believe that intermittent coronary artery. spasm as the cause of angina pectoris in the absence of atherosclerotic coronary artery disease is a definite entity. Holter monitoring a n d coronary angiography during t h e attacks of pain may b e fruitful in establishing the diagnosis.
1 Prinzmetal MD, Kennamer R, Merliss R, et al: Angina pectoris 1: A variant form of angina pectoris. Preliminary report. Am J Med 27: 375, 1959 2 Prinzmetal M, Ekmekci A, Kennamer R, et al: Variant form of angina pectoris. Previously undelineated syndrome. JAMA 174:1974, 1960 3 Silvermann ME, Flamm MD: Variant angina pectoris: Anatomic and prognostic implications. Ann Intern Med 75:339, 1971 4 Cheng TO, Bashour T, Kelser GA Jr, et al: Variant angina of Prinzmetal with normal coronary arteriogriuns: A variant of the variant. Circulation 37:476, 1973 5 Oliva PD, Potts DE, Pluss RG: Coronary arterial spasm in Prinzmetal angina. N Engl J Med 288:745, 1973 6 White PD: Coronary artery spasm. N Engl J Med 288: 1355, 1973 7 Andersson R, Holmberg S, Svedmyr N, et al: Adrenergic a and j3 receptors in coronary vessels in man. An in oitro study. Acta Med Scand 191:241, 1972 8 Malindzak GA Jr, VanDyke AH, Green HD, et al: a and j3 adrenergic receptors in coronary vascular bed. Arch Int Pliarmacodyn Ther 197: 112, 1972 9 Demany MA, Tambe A, Zimmerman HA: Coronary arterial spasm. Chest 53:714, 1968 10 O'Reilly RJ, Spellberg RD, King TW: Recognition of proximal right coronary artery spasm during coronary arteriography. Radiology 95: 305, 1970 11 Bouchek RJ, Takeshita R, Brady AH: Intimal hypertrophy in coronary arteries and considerations of the papillary muscle arteries (man). Anat Rec 153:243,1965
Pulmonary Sarcoidosis Presenting as Bronchogenic carcinoma* Jerome C . A m t t , Jr., M.D.OOand Hurst B. Hatch, Jr., M.D., F.C.C.P.
Massive pulmonary fibrosis simulating bronchogenic carcinoma on chest roentgenograms, planigrams and bronchograms is a d i i c t l y unusual manifestatioo of sarcoidosis. Bronchial stenosis can result from any of three types of bronchial involvement: compression of the major bronchi by enlarged perihilar nodes, sarcoid lesions in the bronchial wall, and diffuse bronchial constriction 'From the Department of Internal Medicine, Sedion on Pulmonary Disease, Alton Ochsner Medical Foundation and Ochsner Clinic, New Orleans. "Presently at Elkins, West Virginia. Re rint requests: Dr. Amett, 1514 J d e r s o n Highway, New 0 r L a n s 70121
CHEST, 67: 6, JUNE, 1975
associated with massive fibrosis. The symptoms produced by sarcoidosis can be quite similar to those commonly associated with bnmchogenic carcinoma, and when combiied with suspicions findings on chest roentgenograms, planigrams, and bronchograms, can lead to a strong clinical suspicion of carcinoma. Since the two diseases can co-exist in the same patient, diagnostic thoracotomy is usually required even with a prior diagnmis of sarcoidosis.
T
he pulmonary fibrosis seen in patienis with advanced sarcoidosis can roentgenographically simulate pulmonary tuberculosis, idiopathic pulmonary fibrosis, congestive heart failure, pulmonary involvement with scleroderma, rheumatoid lung, pneumoconiosis, or lymphangitic carcinoma.' T h e presence of a mass lesion simulating bronchogenic carcinoma is distinctly unusual. W e report a case where massive fibrosis suggested bronchogenic carcinoma on chest roentgenogram, a t bronchoscopy, and on bronchograms.
A 53-year-old white farmer from Texas was referred to the Ochsner Medical Center in December, 1973 for evaluation of a mass lesion in his left upper lobe demonstrated on chest roentgenogram. He had smoked approximately six cigars daily for the ten years between 1946 and 1956. In 1956 a "spot" had been discovered in the lower left lung field on chest roentgenogram, which was no longer present on repeat study one year later. A routine chest roentgenogram in 1969 had revealed a diffuse interstitial infiltrate predominantly in the upper half of both lung fields. He remained asymptomatic, and a repeat study in 1971 revealed no change in the infiltrate. Evaluation at another hospital had included a left scalene node biopsy which had revealed a noncaseating granulomatous adenitis. Upon.admission, the patient reported malaise with a persistent nonproductive cough for the preceding six months, but he denied dyspnea, wheezing, chest pain, hemoptysis, fever, or weight loss. Auscultation of the lungs revealed a prolonged expiratory phase without rales or wheezes. There was no adenopathy or finger clubbing. Skin tests for tuberculosis, histoplasmosis, and mumps were negative. The chest roentgenogram revealed diffuse interstitial changes with a marked prominence of the left upper lobe hilus, suggesting a mass lesion, with radiation of fibrotic strands toward the periphery (Fig 1 ) . Tomograms revealed stenosis of the apicoposterior segment bronchus of the left upper lobe. Pulmonary function studies revealed a pure restrictive impairment, with the vital capacity 76 percent of predicted, the FEVl 83 percent of predicted, and the maximum breathing capacity 111percent of predicted. The resting alveolar-arterial oxygen gradient was elevated to 28 mm Hg, and the resting arterial oxygen pressure was normal (77 mm H g ) , with no change on exercise. Fiberoptic bronchoscopy revealed stenosis of the apicoposterior and anterior segmental bronchi of the left upper lobe, with normal-appearing mucosa. Brush biopsies of the segmental bronchi were negative for malignancy, and multiple washings were negative for fungi and acid-fast bacilli. A bronchogram showed a persistent filling defect of the anterior segment bronchus, with definite narrowing of the apicoposterior segment bronchus ( Fig 2 ) .
PULMONARY SARCOlDOSlS PRESENTING AS CARCINOMA 723
F I G ~ 1. R EPA ~ roentgenogram of chest demonstrating d8use interstitial changes with a mass lesion at the upper left hilum with stranding toward the periphery. Because of the suspicion of malignancy, exploratory thoracotomy was performed. Multiple hard, whitish plaques were present throughout the parenchyma of the left lung. A large, hard, fixed hilar mass was present near the left upper lobe bronchus, which had caused collapse of a portion of the anterior segment of the left upper lobe. The mass was very finn and fixed to the pulmonary artery. Multiple biopsies of areas of the mass and of distal parenchymal lesions were all compatible with sarcoidosis. Because of this finding, and because of the risk involved in attempted removal of the mass, resectional surgery was not performed. Microscopic examination of the biopsies revealed extensive granulomatous inflammation of undetermined etiology, consistent with sarcoidosis. Special stains for acid-fast bacilli and fungal organisms were
FIGURE2. Left bronchogram demonstrating occlusion of the anterior segment bronchus with narrowing of the apicoposterior segment bronchus.
730 ARNETT, HATCH
3. EPA chest roentgenogram 7 months after operation FIGURE demonstrating little change from preoperative roentgenogram. negative, as were cultures for bacteria, fungi, and Mycobactetium tuberculosis. The patient was discharged on a regimen of 40 mg of prednisone daily, which was tapered gradually to 10 mg daily, and he remained asymptomatic. A repeat chest roentgen* gram after seven months of low dose prednisone revealed little change ( Fig 3) Repeat bronchograms revealed an apparent decrease in the stenosis of the apicoposterior segment bronchus, with persistent occlusion of the anterior segment bronchus (Fig 4). Repeat pulmonary function studies at this time were unchanged from the preoperative ones.
.
FIGURE4. Repeat left bronchogram after 7 months therapy with prednisone demonstrating apparent decrease in stenosis of the apicoposterior segment bronchus with persistent occlusion of the anterior segment bronchus.
CHEST, 67: 6, JUNE, 1975
Although the roentgenographic changes due to pulmonary sarcoidosis may resolve completely in a large percentage of cases, probably 20 percent will ultimately develop widespread fibrosis with eventual distortion of the lung a r c h i t e ~ t u r e This . ~ distortion is caused by a gradual upward migration of parenchymal lesions over a period of years, which results in dense fibrosis with upward retraction of the hila.' Coarse, irregular strands commonly extend from the hila toward the periphery. The presence of a mass lesion simulating bronchogenic carcinoma is an unusual finding, and was not mentioned in a series of 1,254 patients with proven sarcoidosis, 94 percent of whom had abnormal chest roentgenog r a m ~ On . ~ reviewing the literature we could find only four cases similar to Hahn's6 patient was found to have multiple hard, dense nodules which resulted in a "frozen hilus." Multiple biopsies of the lung, hilar mass, and pleural implants were suggestive of sarcoidosis. Resectional surgery was deemed inadvisable, and the patient remained well for 11 years after operation without further specific therapy. Sarcoidosis commonly causes symptoms which are also usually associated with bronchogenic carcinoma, including fatigue, malaise, weight loss, cough, dyspnea, chest pain, and occasionally hemoptysis.3 When these are combined with suspicious chest roentgenogram, planigrams, bronchoscopic findings, and bronchograms, the clinical suspicion of carcinoma is even stronger. Since bronchogenic carcinoma has been reported to co-exist with sarcoidosis,s-" even if the diagnosis of sarcoidosis has been M y established previously, diagnostic thoracotomy will be required to rule out co-existent carcinoma. The finding of bronchial stenoses in o w patient contributed further to the suspicion of carcinoma. Three different types of bronchial involvement have been described in sarcoidosis.1?,13 The first is caused by enlarged hilar nodes which compress the major bronchi and which may result in collapse or eventual bronchiectasis. This is quite rare, in spite of frequent massive enlargement of the mediastinal nodes. The second type is the occurrence of sarcoid lesions in the bronchial wall. This type is not unusual and diagnosis can frequently be made by means of bronchoscopic biopsy.l2-l5 The third type is the diffuse bronchial constriction which occurs in the later stages of fibrosis and results in narrowing of the major bronchi. Longcope and Freiman4 suggest that this is not infrequent. ACKNOWLEDGMENT: The authors express their appreciation to the Department of Medical Communications of the Alton Ochsner Medical Foundation for assistance in preparation of the manuscript.
1 Siltzbach LE: Sarcoidosis: Clinical features and management. Med Clin N Am 51:483-502, 1967
2 Fraser RG, Pare JAF': Diagnosis of Diseases of the Chest (vol2). Philadelphia, Saunders, 1970, pp 1090-1091 3 Mayock RL, Bertrand P, Morrison CB, et al: Manifesta-
CHEST, 67: 6, JUNE, 1975
tions of sarcoidosis: Analysis of 145 patients with a review of 9 series selected from the literature. Am J Med 35 :67-89, 1963 4 Longcope W, Freirnan DC:A study of sarcoidosis based on combined investigation of 160 cases including 30 autopsies from Johns Hopkins Hospital and Massachusetts General Hospital. Medicine 31: 1-132, 1952 5 Siltzbach LE, Som ML: Sarcoidosis with bronchial involvement. Mt Sinai J Med (NY) 19:473-480, 1953 6 Hahn R: Unusual forms of sarcoidosis. South Med J 64: 541645,1971 7 Westcott JL, Noehren TH: Bronchial stenosis in chronic sarcoidosis. Chest 63:893-897,1973 8 Sakula A: Bronchial carcinoma and sarcoidosis. Br J Cancer 17:206-212,1963 9 Jefferson M, Smith WT, Taylor AB, et al: A report of 2 cases of sarcoidosis with brochial carcinoma. Thorax 9:291-298, 1954 10 Ellman P, Hanson A: The co-existence of bronchial carcinoma and sarcoidosis. Br J Tuberc 52:218-221, 1958 11 Sarkar TK: Anaplastic carcinoma of the lung and sarcoidosis. Br J Clin Pract 24:297-299, 1970 12 Honey M, Jepson E: Multiple bronchostenoses due to sarcoidosis. Report of 2 cases. Br J Med 2: 1330-1334, 1957 13 Kalbian W: Bronchial involvement in pulmonary sarcoidosis. Thorax 12:18-23,1957 14 Friedman OH, Blaugrund SM, Siltzbach LE: Biopsy of the bronchial wall as an aid in diagnosis of sarcoidosis. JAMA 183:646-850, 1963 15 Siltzbach LE, Cahn LR: Random biopsy of bronchial and palatal mucosa in the diagnosis of sarcoidosis. Acta Med Scand Suppl425:230-236, 1964
A Technique for Unknotting an lntracardiac Flow-Directed Balloon catheter* Harry G. Mond, M.D.;" Dwight W. Clark, M.D., F.C.C.P.;? Stuart 1. Nesbitt, B.A.;$ and Robert C. Schlont, M.D.11
Described is an unusual complication occurring during right-sided cardiac catheterization using a 7F flow-directed balloon catheter. During an attempt to direct the catheter from the main pulmonary artery into the pulmonary wedge position, the tip became entangled in a loop of catheter and knotted. Initially, all attempts to unkad or remove the catheter faikd. A movable-core guide wire was passed through the major lumen of the catheter, resulting in the immediate unkn~ttingof the catheter, thus allowing its withdrawal. 'From the Cardiolo Division, Department of Medicine, Emory University ~%oolof Medicine and Grady Memorial Hospital, Atlanta, Ga. "Fellow in Medicine ( Cardiology). +Assistant Professor of Medicine ( Cardiology). $Technician, Cardiovascular Laboratory. I I Director, Division of Cardiology. Su ported in part by NHLI Training grant nos. HE5653 an8 HE-05731. Reptint requests: Dr. Schlont, 69 Butler Street, SE, Atlanta
30303
UNKNOTTIN6 INTRACARDIAC FLOW-DIRECTED BALLOON CATHETER 731
1 Prinzmetal MD, Kennamer R, Merliss R, et al: Angina pectoris 1: A variant form of angina pectoris. Preliminary report. Am J Med 27: 375, 1959 2 Prinzmetal M, Ekmekci A, Kennamer R, et al: Variant form of angina pectoris. Previously undelineated syndrome. JAMA 174:1974, 1960 3 Silvermann ME, Flamm MD: Variant angina pectoris: Anatomic and prognostic implications. Ann Intern Med 75:339, 1971 4 Cheng TO, Bashour T, Kelser GA Jr, et al: Variant angina of Prinzmetal with normal coronary arteriogriuns: A variant of the variant. Circulation 37:476, 1973 5 Oliva PD, Potts DE, Pluss RG: Coronary arterial spasm in Prinzmetal angina. N Engl J Med 288:745, 1973 6 White PD: Coronary artery spasm. N Engl J Med 288: 1355, 1973 7 Andersson R, Holmberg S, Svedmyr N, et al: Adrenergic a and j3 receptors in coronary vessels in man. An in oitro study. Acta Med Scand 191:241, 1972 8 Malindzak GA Jr, VanDyke AH, Green HD, et al: a and j3 adrenergic receptors in coronary vascular bed. Arch Int Pliarmacodyn Ther 197: 112, 1972 9 Demany MA, Tambe A, Zimmerman HA: Coronary arterial spasm. Chest 53:714, 1968 10 O'Reilly RJ, Spellberg RD, King TW: Recognition of proximal right coronary artery spasm during coronary arteriography. Radiology 95: 305, 1970 11 Bouchek RJ, Takeshita R, Brady AH: Intimal hypertrophy in coronary arteries and considerations of the papillary muscle arteries (man). Anat Rec 153:243,1965
Pulmonary Sarcoidosis Presenting as Bronchogenic carcinoma* Jerome C . A m t t , Jr., M.D.OOand Hurst B. Hatch, Jr., M.D., F.C.C.P.
Massive pulmonary fibrosis simulating bronchogenic carcinoma on chest roentgenograms, planigrams and bronchograms is a d i i c t l y unusual manifestatioo of sarcoidosis. Bronchial stenosis can result from any of three types of bronchial involvement: compression of the major bronchi by enlarged perihilar nodes, sarcoid lesions in the bronchial wall, and diffuse bronchial constriction 'From the Department of Internal Medicine, Sedion on Pulmonary Disease, Alton Ochsner Medical Foundation and Ochsner Clinic, New Orleans. "Presently at Elkins, West Virginia. Re rint requests: Dr. Amett, 1514 J d e r s o n Highway, New 0 r L a n s 70121
CHEST, 67: 6, JUNE, 1975
associated with massive fibrosis. The symptoms produced by sarcoidosis can be quite similar to those commonly associated with bnmchogenic carcinoma, and when combiied with suspicions findings on chest roentgenograms, planigrams, and bronchograms, can lead to a strong clinical suspicion of carcinoma. Since the two diseases can co-exist in the same patient, diagnostic thoracotomy is usually required even with a prior diagnmis of sarcoidosis.
T
he pulmonary fibrosis seen in patienis with advanced sarcoidosis can roentgenographically simulate pulmonary tuberculosis, idiopathic pulmonary fibrosis, congestive heart failure, pulmonary involvement with scleroderma, rheumatoid lung, pneumoconiosis, or lymphangitic carcinoma.' T h e presence of a mass lesion simulating bronchogenic carcinoma is distinctly unusual. W e report a case where massive fibrosis suggested bronchogenic carcinoma on chest roentgenogram, a t bronchoscopy, and on bronchograms.
A 53-year-old white farmer from Texas was referred to the Ochsner Medical Center in December, 1973 for evaluation of a mass lesion in his left upper lobe demonstrated on chest roentgenogram. He had smoked approximately six cigars daily for the ten years between 1946 and 1956. In 1956 a "spot" had been discovered in the lower left lung field on chest roentgenogram, which was no longer present on repeat study one year later. A routine chest roentgenogram in 1969 had revealed a diffuse interstitial infiltrate predominantly in the upper half of both lung fields. He remained asymptomatic, and a repeat study in 1971 revealed no change in the infiltrate. Evaluation at another hospital had included a left scalene node biopsy which had revealed a noncaseating granulomatous adenitis. Upon.admission, the patient reported malaise with a persistent nonproductive cough for the preceding six months, but he denied dyspnea, wheezing, chest pain, hemoptysis, fever, or weight loss. Auscultation of the lungs revealed a prolonged expiratory phase without rales or wheezes. There was no adenopathy or finger clubbing. Skin tests for tuberculosis, histoplasmosis, and mumps were negative. The chest roentgenogram revealed diffuse interstitial changes with a marked prominence of the left upper lobe hilus, suggesting a mass lesion, with radiation of fibrotic strands toward the periphery (Fig 1 ) . Tomograms revealed stenosis of the apicoposterior segment bronchus of the left upper lobe. Pulmonary function studies revealed a pure restrictive impairment, with the vital capacity 76 percent of predicted, the FEVl 83 percent of predicted, and the maximum breathing capacity 111percent of predicted. The resting alveolar-arterial oxygen gradient was elevated to 28 mm Hg, and the resting arterial oxygen pressure was normal (77 mm H g ) , with no change on exercise. Fiberoptic bronchoscopy revealed stenosis of the apicoposterior and anterior segmental bronchi of the left upper lobe, with normal-appearing mucosa. Brush biopsies of the segmental bronchi were negative for malignancy, and multiple washings were negative for fungi and acid-fast bacilli. A bronchogram showed a persistent filling defect of the anterior segment bronchus, with definite narrowing of the apicoposterior segment bronchus ( Fig 2 ) .
PULMONARY SARCOlDOSlS PRESENTING AS CARCINOMA 723
F I G ~ 1. R EPA ~ roentgenogram of chest demonstrating d8use interstitial changes with a mass lesion at the upper left hilum with stranding toward the periphery. Because of the suspicion of malignancy, exploratory thoracotomy was performed. Multiple hard, whitish plaques were present throughout the parenchyma of the left lung. A large, hard, fixed hilar mass was present near the left upper lobe bronchus, which had caused collapse of a portion of the anterior segment of the left upper lobe. The mass was very finn and fixed to the pulmonary artery. Multiple biopsies of areas of the mass and of distal parenchymal lesions were all compatible with sarcoidosis. Because of this finding, and because of the risk involved in attempted removal of the mass, resectional surgery was not performed. Microscopic examination of the biopsies revealed extensive granulomatous inflammation of undetermined etiology, consistent with sarcoidosis. Special stains for acid-fast bacilli and fungal organisms were
FIGURE2. Left bronchogram demonstrating occlusion of the anterior segment bronchus with narrowing of the apicoposterior segment bronchus.
730 ARNETT, HATCH
3. EPA chest roentgenogram 7 months after operation FIGURE demonstrating little change from preoperative roentgenogram. negative, as were cultures for bacteria, fungi, and Mycobactetium tuberculosis. The patient was discharged on a regimen of 40 mg of prednisone daily, which was tapered gradually to 10 mg daily, and he remained asymptomatic. A repeat chest roentgen* gram after seven months of low dose prednisone revealed little change ( Fig 3) Repeat bronchograms revealed an apparent decrease in the stenosis of the apicoposterior segment bronchus, with persistent occlusion of the anterior segment bronchus (Fig 4). Repeat pulmonary function studies at this time were unchanged from the preoperative ones.
.
FIGURE4. Repeat left bronchogram after 7 months therapy with prednisone demonstrating apparent decrease in stenosis of the apicoposterior segment bronchus with persistent occlusion of the anterior segment bronchus.
CHEST, 67: 6, JUNE, 1975
Although the roentgenographic changes due to pulmonary sarcoidosis may resolve completely in a large percentage of cases, probably 20 percent will ultimately develop widespread fibrosis with eventual distortion of the lung a r c h i t e ~ t u r e This . ~ distortion is caused by a gradual upward migration of parenchymal lesions over a period of years, which results in dense fibrosis with upward retraction of the hila.' Coarse, irregular strands commonly extend from the hila toward the periphery. The presence of a mass lesion simulating bronchogenic carcinoma is an unusual finding, and was not mentioned in a series of 1,254 patients with proven sarcoidosis, 94 percent of whom had abnormal chest roentgenog r a m ~ On . ~ reviewing the literature we could find only four cases similar to Hahn's6 patient was found to have multiple hard, dense nodules which resulted in a "frozen hilus." Multiple biopsies of the lung, hilar mass, and pleural implants were suggestive of sarcoidosis. Resectional surgery was deemed inadvisable, and the patient remained well for 11 years after operation without further specific therapy. Sarcoidosis commonly causes symptoms which are also usually associated with bronchogenic carcinoma, including fatigue, malaise, weight loss, cough, dyspnea, chest pain, and occasionally hemoptysis.3 When these are combined with suspicious chest roentgenogram, planigrams, bronchoscopic findings, and bronchograms, the clinical suspicion of carcinoma is even stronger. Since bronchogenic carcinoma has been reported to co-exist with sarcoidosis,s-" even if the diagnosis of sarcoidosis has been M y established previously, diagnostic thoracotomy will be required to rule out co-existent carcinoma. The finding of bronchial stenoses in o w patient contributed further to the suspicion of carcinoma. Three different types of bronchial involvement have been described in sarcoidosis.1?,13 The first is caused by enlarged hilar nodes which compress the major bronchi and which may result in collapse or eventual bronchiectasis. This is quite rare, in spite of frequent massive enlargement of the mediastinal nodes. The second type is the occurrence of sarcoid lesions in the bronchial wall. This type is not unusual and diagnosis can frequently be made by means of bronchoscopic biopsy.l2-l5 The third type is the diffuse bronchial constriction which occurs in the later stages of fibrosis and results in narrowing of the major bronchi. Longcope and Freiman4 suggest that this is not infrequent. ACKNOWLEDGMENT: The authors express their appreciation to the Department of Medical Communications of the Alton Ochsner Medical Foundation for assistance in preparation of the manuscript.
1 Siltzbach LE: Sarcoidosis: Clinical features and management. Med Clin N Am 51:483-502, 1967
2 Fraser RG, Pare JAF': Diagnosis of Diseases of the Chest (vol2). Philadelphia, Saunders, 1970, pp 1090-1091 3 Mayock RL, Bertrand P, Morrison CB, et al: Manifesta-
CHEST, 67: 6, JUNE, 1975
tions of sarcoidosis: Analysis of 145 patients with a review of 9 series selected from the literature. Am J Med 35 :67-89, 1963 4 Longcope W, Freirnan DC:A study of sarcoidosis based on combined investigation of 160 cases including 30 autopsies from Johns Hopkins Hospital and Massachusetts General Hospital. Medicine 31: 1-132, 1952 5 Siltzbach LE, Som ML: Sarcoidosis with bronchial involvement. Mt Sinai J Med (NY) 19:473-480, 1953 6 Hahn R: Unusual forms of sarcoidosis. South Med J 64: 541645,1971 7 Westcott JL, Noehren TH: Bronchial stenosis in chronic sarcoidosis. Chest 63:893-897,1973 8 Sakula A: Bronchial carcinoma and sarcoidosis. Br J Cancer 17:206-212,1963 9 Jefferson M, Smith WT, Taylor AB, et al: A report of 2 cases of sarcoidosis with brochial carcinoma. Thorax 9:291-298, 1954 10 Ellman P, Hanson A: The co-existence of bronchial carcinoma and sarcoidosis. Br J Tuberc 52:218-221, 1958 11 Sarkar TK: Anaplastic carcinoma of the lung and sarcoidosis. Br J Clin Pract 24:297-299, 1970 12 Honey M, Jepson E: Multiple bronchostenoses due to sarcoidosis. Report of 2 cases. Br J Med 2: 1330-1334, 1957 13 Kalbian W: Bronchial involvement in pulmonary sarcoidosis. Thorax 12:18-23,1957 14 Friedman OH, Blaugrund SM, Siltzbach LE: Biopsy of the bronchial wall as an aid in diagnosis of sarcoidosis. JAMA 183:646-850, 1963 15 Siltzbach LE, Cahn LR: Random biopsy of bronchial and palatal mucosa in the diagnosis of sarcoidosis. Acta Med Scand Suppl425:230-236, 1964
A Technique for Unknotting an lntracardiac Flow-Directed Balloon catheter* Harry G. Mond, M.D.;" Dwight W. Clark, M.D., F.C.C.P.;? Stuart 1. Nesbitt, B.A.;$ and Robert C. Schlont, M.D.11
Described is an unusual complication occurring during right-sided cardiac catheterization using a 7F flow-directed balloon catheter. During an attempt to direct the catheter from the main pulmonary artery into the pulmonary wedge position, the tip became entangled in a loop of catheter and knotted. Initially, all attempts to unkad or remove the catheter faikd. A movable-core guide wire was passed through the major lumen of the catheter, resulting in the immediate unkn~ttingof the catheter, thus allowing its withdrawal. 'From the Cardiolo Division, Department of Medicine, Emory University ~%oolof Medicine and Grady Memorial Hospital, Atlanta, Ga. "Fellow in Medicine ( Cardiology). +Assistant Professor of Medicine ( Cardiology). $Technician, Cardiovascular Laboratory. I I Director, Division of Cardiology. Su ported in part by NHLI Training grant nos. HE5653 an8 HE-05731. Reptint requests: Dr. Schlont, 69 Butler Street, SE, Atlanta
30303
UNKNOTTIN6 INTRACARDIAC FLOW-DIRECTED BALLOON CATHETER 731