aspiration to identify these pathogens suggests an obstructed bronchus with resistant bacteria sequestered distal to the site or the presence of loculated abscesses within the infiltrate. Recovery of peptococci from a sample obtained by transtracheal aspiration led to complacence about change in therapy since most peptococci are penicillin susceptible. However, the choice of penicillin in anaerobic pulmonary infections is not supported by data in experimental animals with lung abscess where penicillin treatment results in high failure rates." Although an excellent study has shown equal efficacy of penicillin and clindamycin in human anaerobic lung abscess and pneumonitis.s in spite of the presence of penicillin-resistant organisms in some patients, more recent experience with human infections would support the animal data cited above. For instance, the Philadelphia study of anaerobic lung abscess" showed that five of 21 penicillin-treated patients failed to defervesce, extended the pulmonary lesions, or developed empyema. Three additional patients had a relapse of infection (one while on therapy and two within a month of completion of treatment). Hence, there were eight failures in 21 patients (38 percent). There was no failure or relapse in 17 patients treated with clindamycin. Clindamycin has several unique properties which may account for its success in anaerobic infections. It is very active in vitro against most anaerobes. It achieves high concentrations in infected tissue, presumably as a result of antibiotic uptake by polymorphonuclear leukocytes and, unlike chloramphenicol, it is not inactivated at those infected sites. In an animal model for the chemoprophylaxis of experimental anaerobic lung abscess, only clindamycin and carbenicillin were effective, whereas procaine penicillin, chloramphenicol, doxycyline, and cefoxitin were ineffective (personal communication: H. Thadepalli). In situations where patients with anaerobic pulmonary infections do not respond to penicillin, or where sputum samples obtained by transtracheal aspiration have one or more penicillin-resistant anaerobes, clindamycin therapy may be more reliable. With the increasing frequency of isolation of such organisms, it is likely that more penicillin failures will be noted in anaerobic pleuropulmonary infections. Based on such considerations, the initial choice of penicillin in the treatment of anaerobic pulmonary infections requires a reappraisal. REFERENCES
1 Lorber B, Swenson RM. Bacteriology of aspiration pneumonia: a prospective study of community and hospital acquired cases. Ann Intern Med 1974; 81:329-31 ! Bartlett JG, Gorbach SL, Finegold SM. The bacteriology of aspiration pneumonia. Am J Med 1974; 56:202-07 3 Bartlett JG, Gorbach SL. Treatment of aspiration pneumonia and primary lung abscess: penicillin G vs clindamycin. JAMA 1975; 234:935-37 4 Salyers AA, Wong J, Wil1dns TO. Beta lactamase activity in strains of Bacteroides melaninogenicus and Bacteroides ortJ1Js. Antimicrob Agents Chemother 1977; 11:142-46 5 Levison ME, ALA Collaborative Group. Treabnent of anaerobic lung abscess: interscience conference on anti-
microbial agents and chemotherapy, abstract 356, November, 1981 6 Kannangara DW, Thadepallt H, Bach TV. Comparative efficacy of ave antibiotics in experimental anaerobic lung abscess. Am Soc Microbiology, abstract No. A20, May 12, 1980
Unsuspected ,Malignant Pericardial Effusion Causing Cardiac Tempenade" Rapid Diagnosis by Computed Tomography Frank E. Johnson, M.D.; Michael K. Woloerson, M.D.; Mural; Sundaram, M.D.; and Elisabeth Heiberg, M.D.
We report a patient in whom the diagnosis of cardiac tamponade due to cancer first suggested by computed tomography (Cf). Because rapid diagnosis and correct treatment of cardiac tamponade Improve results, we present helpful radiographic details which should Increase awareness of this entity.
ersonnel working in emergency departments encounter patients with acute cardiac tamponade due to trauma, uremia, hemorrhagic diatheses, and other causes. Similarly, patients who have undergone cardiac surgery may exhibit cardiac tamponade in the intensive care unit. Only rarely does a patient with this condition present without historic features suggestive of a predisposing condition. The differential diagnosis for acute hypotension is lengthy, and unsuspected malignant pericardiac effusion causing tamponade is sufficiently rare that it may not enter a working differential diagnosis in such cases. However, because it is eminently treatable, this entity should always be suspected in the hypotensive patient until positively ruled out. We have encountered instances recently which support the role of computed tomography (CT) in the diagnosis of malignant pericardial effusion. This article outlines radiographic and pathologic features in one such case. CASE REPORT
A 49-year-old caucasian man was admitted to St Louis University Medical Center with a four-week history of dyspnea, cough, and weight loss. One week before admission a right pulmonary infiltrate had been noted on chest radiograph. His admission temperature was 37.3°C; pulse rate, 9-2 per minute and regular; respiratory rate, 36 per minute and labored; blood pressure, 120nO rom Hg; cardiac tones were distant; and coarse rhonchi were heard over the right chest. Admission laboratory data included a white blood cell count of 7,800/mm 3 • A chest roentgenogram (Fig 1) revealed moderate cardiomegaly, a prominent right perihilar area, and a right pulmonary infiltrate. The work.ing clinical diagnosis was pneumonitis with a possible under·From the Deparbnents of Surgery and Radiology, St. Louis University Medical Center St. Louis. Reprint requests: Dr. Johnson, Department of SurB611/, 1325 South Grand Blod, St. Louis 63104 CHEST I 82 I 4 I OCTOBER, 1982
1. Cardiomegaly and right hilar prominence are apparent and there is a right pulmonary infiltrate.
lying bronchogenic carcinoma. Sputum cytology and culture results were unrevealing, and the patient's productive cough and dyspnea increased. Shortly after admission, cr of the chest was performed to investigate the possibility of a right hilar neoplasm. A mass was found, which involved the right hilum and the right peritracheal and subcarinal portions of the mediastinum. A sizeable pericardial effusion was apparent; its high attenuation coefficient (24 Hn ) was suggestive of bloody fluid or exudate (Fig 2) . Later that same day the patient experienced cardiac arrest. Resuscitation included pericardiocentesis which yielded a large amount of serosanguineous fluid. He improved dramatically, but cardiac arrest occurred again during the same hospitalization, and further attempts at resuscitation were fruitless. An autopsy was done, which revealed adenocarcinoma of the left kidney with metastases to the pericardium, mediastinal lymph nodes, right lung, left adrenal, and brain. DISCUSSION
The introduction of CT in the last decade made an immediate and dramatic impact upon the diagnosis of acute intracranial lesions. It is being used increasingly in the diagnosis of acute processes elsewhere in the body. Its impact upon diagnosis, staging, and treatment planning of malignant diseases is well established and growing. Preliminary experience with CT in the diagnosis of acute mediastinal disease such as dissecting thoracic aortic aneurysm has proved encouraging! and to some extent has supplanted more invasive procedures. Its utility in the diagnosis of pericardial effusion remains undefined, though our experience suggests a major role. In addition to the detection of pericardial fluid, associated solid masses can be appreciated by CT. The x-ray attenuation coefficient or Hounsfield number (Hn) provides further diagnostic information, with low values suggesting a serous effusion and higher numbers an exudative or hemorrhagic effusion. The use of intravenous contrast enhancement also allows evaluation of other mediastinal and pulmonary structures. Pericardial neoplasm should be suspected when there are local alterations in the cardiac silhouette on conventional chest radiography or when a patient with a known cancer develops cardiac abnormalities such as arrhythmia, heart failure, pericarditis, or pericardial 502
FiGURE 2. cr of thorax. A (upper). Section immediately below the carina. A mass involves the right hilum and adjacent mediastinum (curved arrouu}. Pericardial fluid is present at the level of the aortic root and pulmonary outflow tract (between maight arrows). B (lower). Section through low thorax 3 em below level of Figure 2A. Low attenuation area around the heart is due to a large pericardial effusion (between small a"ows). A thin layer of epicardial fat is demonstrated (large short arrow). There is a right pleural effusion (curved arrouis),
effusion . Malignant pericardial disease is suggested by several CT criteria, which we have reported in greater detail elsewhere." l)pericardial effusion with highC'I' density (in excess of 20 Hn) ; 2) localized or diffuse pericardial thickening; 3) masses arising from or contiguous with the pericardium; and 4) obliteration of normal tissue planes between a paracardiac mass and the heart or pericardium. The development of cardiac tamponade due to cancer is rare . The presence of pericardial effusion or hemorrhage, which is not uncommon in metastatic or primary pericardial neoplasms, usually does not result in tamponade. On the contrary, since the effusion is typically slow to form, the pericardium may tolerate very large amounts of effusion with the development of relatively few symptoms. Cytology is useful, though Lopez-Cardozo" reports false-positive and false-negative results in about 20 percent of patients. A recent Unsuspected Malignant Perlcard lal Effusion (Johnson lit al)
review of cardiac tamponade as the presenting sign of extracardiac malignancy' revealed only 29 cases, of which four were sarcomas and 25 were carcinomas. In this series, the most common primary type of extracardiac malignancy presenting with cardiac tamponade was lung cancer, though other varieties included pancreas, stomach, ovary, kidney, and lymphoma. Primary neoplasms of the heart and pericardium are quite rare, with a reported incidence rate of 0.001 to 0.28 percent of autopsy series." However, metastatic disease of the heart is surprisingly common with an incidence of about 10 percent of cancer-related deaths in autopsy series." Although cardiac symptoms during life are uncommon, clinical manifestations in such patients fan into recognizable patterns: 6 1) pericardial involvement, with findings such as effusion, tamponade, and constriction; 2) myocardial involvement, with findings such as rhythm disturbances, pump failure, cardiac rupture, and coronary artery occlusion; 3) endocardial involvement, with findings mimicking valvular stenosis and bacterial endocarditis; and 4) tumor thrombosis of cardiac chambers, with findings of chamber inflow and/or outflow obstruction. The lymphatic circulation of the heart and pericardium has been described in detail both in human and animal subjects." An extensive subendocardial plexus exists which empties through myocardial channels into a subepicardial plexus. Branches from this plexus then drain into larger trunks which generally parallel the coronary vasculature, ultimately exiting the heart into mediastinal nodal structures. Spread of tumor emboli through these lymphatics and direct invasion of the pericardium appear to be the major mechanisms for development of malignant pericardial disease. We emphasize the rapid and lethal progression of neoplastic cardiac tamponade which the current case exemplifies and which has been noted by others.' 1 However, Fraser et al" noted that the median survival time of those patients with neoplastic cardiac tamponade receiving pericardiectomy was 5~ months as compared to those who received either supportive care with pericardiocentesis (seven days) or radiation therapy or chemotherapy (five weeks). These considerations support an aggressive policy in dealing with this problem. Our experience with this case and others suggests that CT can be decisive in the establishment of this diagnosis and subsequent treatment planning.
REFERENCES 1 Larde D, Belloir C, Vasile N, Frija J. Ferrane J. Computed tomography of aortic dissection. Radiol 1980; 136:147-51 2 Wolverson MK, Grider RD, Sundaram M, Heiberg E, Johnson F. Demonstration of unsuspected malignant disease of the pericardium by computed tomography. CT: J Computed Tomography 1980; 4:330-33 3 Lopez-Cardozo P. A critical evaluation of 3,000 cytologic analyses of pleural fluid, ascitic fluid and pericardiaI fluid. Acta Cytol 1966; 10:455-60 4: Fraser RS, Viloria JB, Wang N-S. Cardiac tamponade as a presentation of extracardiac malignancy. Cancer 1980; 45:1697-704
5 McAllister HA Jr. Primary tumors and cysts of the heart and pericardium. Curr Probl audiol 1979; 4:8-51 6 Hanfling SM. Metastatic cancer to the heart: Review of the literature and report of 127 cases. Circulation 1960; 22:474-83 7 Cusumano F, De Le1lis R, Piotti P. Mesothelioma of the pericardium: Report of a case. Tumori 1980; 66:269-72
Benign Mesenchymal Tumor of the Heart* Spontaneous Regression and Disappearance of Pulmonary Artery Stenosis Yu-Chen Lee, M.D.; Robert T. Singleton, M.D.; and Chi1c-Kwun Tang, M.D.t
We describe a patient who was found to have a large benign mesenchymal tumor of the right ventricular
wall and right pulmonary artery stenosis at the age of 20 months. FoDowing biopsy of the tumor, the patient's respiratory dktress improved graduaDy and cardiac catheterization at the age of ten yean showed normal Intracardiac pressures and disappearance of right pulmonary artery stenosis. He remained asymptomatic at age 20. Possible facton for the spontaneous regression of the tumor are discussed. partial or complete disappearance of a tumor in the absence of treatment is a rare but well known phenomenon.t'" However, to our knowledge, spontaneous regression of cardiac tumors has not been reported. The purpose of this article is to describe a patient who had a large benign mesenchymal tumor of the heart which has regressed; pulmonary artery stenosis disappeared following biopsy of the tumor. CASE REPoRT
A 20-month-old baby was admitted to the University of Maryland Hospital on December 14, 1959. The prenatal history was unremarkable and the delivery was uneventfu1. Since the age of 14 days, he had been admitted to a local hospital on numerous occasions due to dypsnea and wheezing. He was found to have marked cardiomegaly, and treatment with digitalis failed to improve the symptoms. Physical examination on admission revealed a well-developed, wellnourished boy without cyanosis or clubbing. Blood pressure was 100/60 mm Hg, and pulse rate was ISO/min with frequent premature beats. The chest was symmebic and coarse rhonchi were heard throughout. The heart was markedly enlarged; a grade 3/6 ejection systolic murmur was heard over the base and the second heart sound at the pulmonic area was widely split. The liver was palpable 2 em below the right costal margin. Hemoglobin was 10 g/dl, white blood cell count was 11,500/ml with 65 percent polymorphs, 22 percent lymphocytes, 12 percent monocytes, ·From the Division of Cardiology, Department of Medicine and Department of Pathology], University of Maryland Hospital, Baltimore. Reprint requests: Dr. Lee, Dimsion of Cardiology/Medfcine~ 22 Greene Street, Baltimore 21201 CHEST I 82 I 4 I OCTOBER, 1882