Long-standing isolated traumatic tricuspid insufficiency in an elderly patient is reported. The hernodynamics and benign course of this lesion are compared ...
Pleural Effusion: Unusual Presentation of Prostatic Cancer Volker Scheidemandel, Brian Salisbury and Charles F. Tate, Jr. Chest 1972;61;686-689 DOI 10.1378/chest.61.7.686 The online version of this article, along with updated information and services can be found online on the World Wide Web at: http://chestjournal.chestpubs.org/content/61/7/686
Chest is the official journal of the American College of Chest Physicians. It has been published monthly since 1935. Copyright1972by the American College of Chest Physicians, 3300 Dundee Road, Northbrook, IL 60062. All rights reserved. No part of this article or PDF may be reproduced or distributed without the prior written permission of the copyright holder. (http://chestjournal.chestpubs.org/site/misc/reprints.xhtml) ISSN:0012-3692
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SCHEIDEMANDEL, SALISBURY AND TATE
FIGURE1A (left). Normal chest roentgenogram. B (right). Chest roentgenogram demonstrating the large increase in heart size. without evidence of cardiac tamponade; pericardial tap returned 50 ml of fluid.= Evidence of pericardial effusion in idiopathic lupus erythematosus is more common. Of 142 cases of idiopathic lupus reviewed by Hejtmancik and co- worker^,^ 12 percent had a pericardial rub. Two patients had massive pericardial effusion and cardiac tamponade. One patient developed constrictive pericarditis. Of 30 cases autopsied by Kong and colleaguess with idiopathic lupus, 12 had evidence of pericardial effusion, and four of the 12 had cardiac tamponade. Estes and Christians observed 150 patients with idiopathic lupus in a prospective study. Twenty-nine patients developed pericarditis, of which two progressed to cardiac tamponade. -
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Pleural Effusion: UnusualPresentation of Prostatic cancer* Volker Scheidemandel, M.D.," Brian Salisburg, M.D.,t and F. ,Jr.. - , M.D.- F.C.C.P.f 7
Pleural effusion complicating pleural metastases from prostatic carcinoma occurred in a patient and is a feature of this disease not previously reported. The possible pathogenesis of malignant pleural effusion in general and the patient presented specifically are discussed.
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1 Ladd AT: Procainamide-induced lupus erythematosus New Eng J Med 267: 1357,1962 2 Dubois EL: Procainamide induction of a systemic lupus erythematosus-likesyndrome. Medicine 48:217, 1969 3 Kaplan JM, Wachtel HL, Czamecki SW, et al: Lupus-like illness precipitated by procainamide. JAMA 192:444, 1965 4 Paine R: Procainamide and lupus erythematosus. JAMA 194:23, 1965 5 Fakhro AM, Ritchie RF, Lown B: Lupus-like syndrome induced by procainamide. Arner J Cardiol20:367,1967 6 Sanford HS, Michaelson AK, Halpem MM: Procainamide induced lupus erythematosus syndrome. Dis Chest 50: 172, 1967 7 Hejtrnancik MR, Wright JC, Quint R, et al: Cardiovascular manifestations of systemic lupus erythematosus. Arner Heart J 69: 119, 1964 8 Kong TQ, Kellum RE, Haserick JR: Clinical diagnosis of cardiac involvement in systemic lupus erythematosus. Circulation 26:7, 1962 9 Estes D, Christian CL: The natural history of systemic lupus erythematosus by prospective analysis. Medicine 50:85, 1971
rostatic cancer is the second most common cause of death from cancer in men, second to cancer of the bronchus and lung, and exceeding that of any portion of the digestive tract.' Although in autopsies of patients dead of cancer of the prostate, the incidence of metastases to the lung has varied from 25 percent to 38 p e r ~ e n t , the ~ . ~finding of pulmonary metastases on chest roentgenograms of patients with prostatic carcinoma is relatively uncommon, ranging from 5 percent to 7 per~ e n t . This ~ - ~ discrepancy can possibly be explained by the small size of the lung metastases which can often be detected only by microscopic e~amination,~ and the observation by several authors?.3.5.7 that nodular pleural metastases do not lead to secondary pleural effusion as a rule. Review of the literature indicates that pleural effusion ' ~ r o m the Department of Medicine, Pulmonary Disease Division, University of Miami School of Medicine, Jackson Memorial Hospital, Miami, Florida. "Fellow, Pulmonary Disease Division, Department of Medicine. +Intern. Department of Medicine. $Associate Professor of Medicine, University of Miami School of Medicine; Chief, Pulmonary Disease Section. Jackson Memorial Hospital.
CHEST, VOL. 61, NO. 7, JUNE 1972
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PLEURAL EFFUSION
3. Bone marrow aspirate showing cluster of metastatic FIGURE tumor cells.
FIGURE1. Chest roentgenogram showing pleural effusion on the left, (right pleural thickening is unchanged from three years previously ). as a complication of prostatic carcinoma has not been reported and must be uncommon. This report describes a patient who presented with unilateral malignant pleural effusion most likely caused by widespread metastases of cancer of the prostate.
CASEREPORT A 70-year-old Negro man was admitted to Jackson Memorial Hospital for the evaluation of pleural effusion. He had a
FIGURE2. Section of Cope needle pleural biopsy showing conglomerate of malignant cells.
history of vague left lateral chest pain, moderate dry nonproductive cough, and lumbar pain of three weeks' duration. For two months he had been anorectic and lost 20 lbs in weight. He denied dyspnea, edema, dysuria and fever. Three years before, on his first admission for pneumococcal pneumonia of the right lower lobe, tube drainage had to be performed for postpneumonic empyema. The empyema was sterile and acidfast and fungus cultures gave negative results, as did the cytology studies. The patient was discharged with x-ray evidence of significant right residual pleural thickening. Moderate hypertension and slight left ventricular enlargement were found on chest roentgenogram at that time and blood pressure was controlled ever since on daily 500 mg of thiazide, and ranged around 150/90 mm Hg. On physical examination, he was an alert thin man with a pulse rate 66 per minute and regular, blood pressure 140/70 mm Hg, respiratory rate 16 per minute, and temperature of 97.4O F. There was flatness to percussion, absent tactile fremitus and decreased to absent breath sounds at the left base posteriorly and laterally, with an area of Skodaeic resonance above the area of flatness. Breath sounds were slightly diminished at the right base laterally. Lower lumbar vertebrae were tender to percussion and the left lobe of the prostate was hard and enlarged. Roentgenogram of the chest (Fig 1) showed significant left pleural effusion; left
FIGURE4. Roentgenogram of the pelvis showing diffuse osteoblastic lesions.
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SCHEIDEMANDEL, SALISBURY AND TATE ventricular enlargement and right pleural thickening were unchanged from the 1968 film. Electrocardiogram showed voltage of left ventricular hypertrophy. Hemoglobin was 9.2 G percent, hematocrit 28 percent, reticulocyte count 0.4 percent; the white blood cell count was 4,850, with 41 percent neutrophils, 23 percent band forms, 27 percent lymphocytes, 7 percent monocytes and 2 percent eosinophils. Platelet count was 156,000. Serum electrolytes, serum calcium, serum phosphorus, uric acid and total bilirubin were normal. The alkaline phosphatase was 400 IU (normal is up to 75 in this laboratory) with a normal leucine aminopeptidase. The acid phosphatase was 36.0 GU (normal range 0.1 to 2.2 GU). Urinalysis showed a specific gravity of 1.023 with no sugar, ketones, protein or red blood cells. There were 3 to 6 white blood cells per high power field and culture result was negative. Multiple sputum specimens were negative for acid-fast bacilli; cytology and fungi showed normal respiratory flora on culture. Intermediate strength PPD was negative. Thoracentesis of left pleural effusion revealed 300 rnl of serous fluid with a protein of 3.0 G percent; there were 1.650 red blood cells with 24 white blood cells with 44 Dercent neutrophils, 48 percent lymphocytes and 8 percent large mononuclear cells. Blood sugar was 139 mg percent; amylase and LDH were normal. Results of Gram stain, bacterial cultures and acid-fast bacilli stains were negative. Cell block of pleural fluid showed malignant cells with several mitotic figures. Pleural biopsy was done with a Cope needle and showed conglomerates of cells of irregular size with hyperchromatic, large nuclei and prominent nucleoli ( Fig 2 ). Bone marrow aspirate from left iliac crest showed clusters of bizarre-looking cells with multinucleoli compatible with metastatic tumor cells (Fig 3 ) . Chest fiLn obtained eight days after thoracentesis showed no reaccumulation of fluid. Because of the patient's increasing lumbar pains, an x-ray of the pelvis was done which showed diffuse osteoblastic lesions (Fig 4 ) . The patient repeatedly refused orchiectomy and prostatic biopsy. Diethylstilbestrol was started at 1 mg per os daily and resulted in almost complete disappearance of bone pain. He was discharged on the 11th hospital day and was doing well in the outpatient clinic when he was seen six weeks after discharge.
The infrequency of the demonstration of lung metastases in patients with carcinoma of the prostate is indicated by Russo and Cavanaugh* who in an analysis of 105 patients with pulmonary metastases, found that in no case of their series was the primary site in the prostate. It is interesting to note that even though 11 percent to 13 percent of patients dead of cancer of the *~ pleural prostate show pleural m e t a ~ t a s e s , ~associated efFusion is not a recognized feature and is not mentioned in urology textbooksi and representative up-to-date reviews on diseases of the pleura.ll Pulmonary metastases are generally small in size and seem to appear very late in the clinical course of the patient's disease.2 The factors possibly influencing the appearance of effusions caused by secondary pleural carcinoma were recently . ~e studied the necropsy material analyzed by M e ~ e r H of 52 cases of metastatic carcinoma of the pleura and concluded that the development of pleural effusion was related closely to neoplastic infiltration of mediastinal nodes whereas the extent of pleural involvement by nodular metastases, as found in widespread prostatic
cancer, bore no such relationship. This finding is supported by several large series in which pleural nodular , ~ no , ~ mention is metastases were found at a ~ t o p s y , ~but made of concomitant pleural effusion. We believe that the finding in the patient presented, of a hard left prostatic lobe, osteoblastic changes as shown in the pelvic roentgenogram, maximally increased serum acid phosphatase, the presence of clusters of malignant appearing cells in a bone marrow aspirate along with significant anemia, are convincing evidence that widespread metastases from a primary prostatic lnalignancy had occurred. Moreover, severe and extensive metastases can be due to a minute primary focus in , ~ ~ can sometimes be documented the p r ~ s t a t e , ~which only by thorough examination of the gland at autopsy. The carcinoma cells seen in the pleural fluid cell block and confirmed by subsequent pleural biopsy were probably metastatic from the primary prostatic tumor. Bronchogenic carcinoma as a possible source of pleural metastases cannot be dismissed in this patient because of his history of cigarette smoking. However, as a cause of pleural effusion, it is nearly always associated with roentgenographically demonstrable pulmonary abnormalityl1 and for this reason is unlikely here. Prostatic carcinoma spreads by way of the perineural lymphatic sheaths through the capsule and over perivascular lymphatics to regional and lumbar periaortic nodes. From these nodes widespread dissemination most likely occurs through the blood and in a few cases in the series of Mintz and Smith5 there was microscopic evidence of tumor cells in the blood vessels. At autopsy, two-thirds of lung metastases from prostatic carcinoma are of the micronodular type with the remainder being lymphangitic, the combination of both Since there is eviforms occurring only occa~ionally.~ denceg that nodular pleural metastases as found in patients dead of carcinoma of the prostate show no appreciable incidence of secondary pleural effusion, it is interesting to speculate on its possible pathogenesis in the case presented. In the series of Elkin and h l ~ e l l e r , ~ spread of prostatic cancer to mediastinal and bronchopulmonary nodes occurred in 10 of 104 cases. Even though there was no lymph node involvement shown by chest x-ray examination in our patient, metastatic spread to hilar and mediastinal nodes has been observed at autopsy in spiteof there being no roentgenographic evidence of lymphadenopathy.ll It is therefore not unlikely that lymphatic obstruction caused by mediastinal involvement, though not obvious by chest x-ray film, had led to pleural effusion. It is interesting to note that pleural fluid did not reaccumulate following institution of estrogen therapy. This, with concomitant marked improvement of lumbar pain, suggests a diminution not only of the osseous but also of pulmonary metastases with resulting improvement in pulmonary lymphatic drainage.
1 Vital Statistics of the United States (vol II), Part A, 1966, pp 1-59
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ISOLATED TRAUMATIC TRlCUSPlD REGURGITAT'ION 2 Elkin M, Mueller HP: Metastases from cancer of the prostate: autopsy and roentgenological findings. Cancer 7: 1246, 1954 3 Horstmann W: Pathologisch-Anatomische Untersuchungen iiber Geschwulstartige Erkrankungen der Prostata, insbesondere iiber das Karzinom. Zbchr Urol45:50, 1952 4 Bumpus HC Jr: Carcinoma of the prostate; a clinical study of one thousand cases. Surg Gynec Obstet 43:150, 1926 5 Mintz ER, Smith GG: Autopsy findings in 100 cases of prostatic cancer. New Eng J Med 211:479, 1934 6 Balogh F, Szendroi Z: Cancer of the Prostate. Budapest, Akadkmiai Kiad6,1968 7 Scott WW, Schirmer HKA: Carcinoma of the Prostate. In Urology (Vol 11) ed by Campbell MF and Hamson JH. Philadelphia, WB Saunders Company 1970, pp 1143-1189 8 Russo PE, Cavanaugh CJ: Diagnosis of pulmonary metastases; a study of 105 cases. Radiology 80:198, 1953 9 Meyer PC: Metastatic carcinoma of the pleura. Thorax 21:437, 1966 10 Tabbara W, Orgel L: Les metastases pulrnonaires des microcarcinomes prostatiques. Difficulties du diagnostic anatomo-clinique. Arch Anat Path 10:136, 1962 11 Fraser RG, Pare JAP: Diseases of the pleura. In Diagnosis of Diseases of the Chest (Vol 11). Philadelphia, WB Saunders Company, 1970, pp 1144-1164
Isolated Traumatic Tricuspid Regurgitation: Prolonged Survival without Operative intervention*
FIGURE1A. Electrocardiogram showing atrial fibrillation and incomplete right bundle branch block.
A 64-year-old white retired truck driver was first admitted to the hospital in July 1970 because of fever, dysuria and palpitation. In 1953, he fell out of a tree and sustained extensive injuries to the right side of his chest with multiple rib fractures, pneumomediastinum and hemopneumothorax. At the time of admission to another hospital, he was in shock and required several blood transfusions. He made a good recovery, and was discharged from the hospital after six weeks. The chest x-ray films from that admission are now unavailable. However, no mention was made of cardiomegaly in any of the x-ray reports. He was in good health until 1965 when he developed fatigue and dyspnea. He was seen by a physician and started on digitalis and diuretics. However, he took these on an intermittent basis and was not seen again until the time of his present illness. One week prior to this admission, he developed fever, chills and dysuria He was seen by a local physician who treated him with
N . S . Cahill, M.B.; B. M. Bell& M.D.; J . W . Linhart, M.D., F.C.C.P.; and R. G . Early, Ph.D.
Long-standing isolated traumatic tricuspid insufficiency in an elderly patient is reported. The hernodynamics and benign course of this lesion are compared briefly with the tricuspid insufficiency associated with rheumatic mitral and aortic vahrulitis. We conclude that this lesion, when isolated, may be well-tolerated and managed medically for a long period of time.
T
raumatic tricuspid insufficiency has been reported with increasing frequency in the past decade. To date, 14 cases have been described.'-" However, information concerning the clinical course of patients not undergoing surgery is sparse. The purpose of this report is to demonstrate the long survival and exercise tolerance of an elderly patient with long-standing traumatic tricuspid insufficiency who has been managed with only medical therapy for congestive heart failure. We emphasize how the natural history of this isolated lesion appears to differ from the tricuspid insufficiency that occurs in rheumatic heart disease, and other disorders of the pulmonary circulation. 'From the Section of Cardiovascular Disease, Department of Ph siology and Medicine, The University of Texas Medical s c & ~ at ~ lSan Antonio.
FIGURE 1B. Chest x-ray film showing cardiomegaly involving mainly the right atrium.
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Pleural Effusion: Unusual Presentation of Prostatic Cancer Volker Scheidemandel, Brian Salisbury and Charles F. Tate, Jr. Chest 1972;61; 686-689 DOI 10.1378/chest.61.7.686 This information is current as of July 16, 2011 Updated Information & Services Updated Information and services can be found at: http://chestjournal.chestpubs.org/content/61/7/686 Cited Bys This article has been cited by 1 HighWire-hosted articles: http://chestjournal.chestpubs.org/content/61/7/686#related-urls Permissions & Licensing Information about reproducing this article in parts (figures, tables) or in its entirety can be found online at: http://www.chestpubs.org/site/misc/reprints.xhtml Reprints Information about ordering reprints can be found online: http://www.chestpubs.org/site/misc/reprints.xhtml Citation Alerts Receive free e-mail alerts when new articles cite this article. To sign up, select the "Services" link to the right of the online article. Images in PowerPoint format Figures that appear in CHEST articles can be downloaded for teaching purposes in PowerPoint slide format. See any online figure for directions.
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