Case Of Pericardial Effusion Research Articles

Collapse of three cardiac chambers due to a pericardial effusion

We report a case of pericardial effusion with collapse of three cardiac chambers including the left atrium, a very specific sign of tamponade always urging for quick pericardiocentesis.

Application of ultrasonography to postmortem examination: Diagnosis of pericardial tamponade

In postmortem examination, it is difficult to diagnose pericardial tamponade in a dead body from the findings of conventional external examination alone. However, ultrasonography is a common diagnostic tool for pericardial tamponade in clinical practice. We studied the postmortem diagnosis of pericardial tamponade at external examination level by applying an ultrasonographic device. The ultrasonographic findings were compared with the conventional autopsy findings. Among 455 cases of forensic autopsy in Hamburg and Tokyo conducted within 5 days after death, we successfully diagnosed 11 cases of pericardial tamponade by ultrasound imaging prior to autopsy, and failed to diagnose pericardial tamponade in only two cases. In addition, 79 cases of external examination conducted at the Tokyo Medicinal Examiner's Office were also examined with ultrasonography, and we diagnosed three cases of pericardial tamponade and five cases of pericardial effusion. The differences in ultrasonographic findings between tamponade and effusion were relatively clear. Although autopsy provides definitive evidence for the cause of death, sometimes autopsy cannot be performed due to some social factors. In such cases, conventional external examination alone cannot establish a cause of death by pericardial tamponade, and application of diagnostic imaging technique will be helpful. While CT and/or MRI may provide more detailed information than ultrasound imaging, these techniques require special equipment, room and specialist, and most of all involves high cost, which is perhaps the most important consideration in the present atmosphere of medical cost containment. On the other hand, the ultrasonographic devices we use are compact, and can be used directly at the scene of death. Postmortem application of ultrasonography may be a valuable adjunct in the work of medical examiners and forensic pathologists.

Incidental Massive Pericardial Effusion Diagnosed by Myocardial Perfusion Imaging

A report on an unusual case of pericardial effusion and tamponade that was found incidentally on myocardial perfusion imaging. This was later confirmed by echocardiography and subsequently treated with pericardiocentesis. Two-dimensional echocardiography is still the "gold standard" for diagnosing pericardial effusion. Nuclear cardiac imaging will probably never have a primary role in the diagnosis of pericardial effusion. However, it may be helpful when the diagnosis of pericardial effusion has not been considered and when this condition is suggested by nuclear imaging findings. The echocardiogram underestimated the amount of pericardial effusion compared to myocardial perfusion imaging in this case, and in contrast to previous published reports. Further, prospective studies need to focus on the sensitivity and specificity of sestamibi nuclear scans in the qualitative and quantitative assessment of pericardial effusions.

Pericardial effusion leading to acute renal failure: Two case reports and discussion of pathophysiology

We describe two patients who developed acute renal failure secondary to severe pericardial effusion. In one patient, the pericardial effusion was due to coxsackievirus infection, and in the other patient, it was due to lung cancer. One patient was in cardiac tamponade, and the other was not yet in tamponade, as per echocardiographic criteria. Kidney function was relatively normal in both patients before the pericarditis episodes. In both patients, pericardiocentesis caused immediate massive diuresis with quick recovery of renal function back to baseline. In the first patient, blood urea nitrogen and serum creatinine decreased from 82 mg/dL and 7.6 mg/dL to 71 mg/dL and 4.6 mg/dL in the next 48 hours, then to 23 mg/dL and 1.3 mg/dL 5 days after the pericardiocentesis. In the second patient, blood urea nitrogen and serum creatinine decreased from 109 mg/dL and 2.9 mg/dL to 40 mg/dL and 0.9 mg/dL in the next 48 hours and 17 mg/dL and 0.7 mg/dL 3 days after release of tamponade. Pericardial effusion can affect renal hemodynamics in many different ways, including increased atrial natriuretic peptide secretion, increased renal efferent nerve activity, and increased secretion of renin and vasopressin. Although pericardial effusion is a complication of uremia, acute renal failure per se can occur in nonuremic cases of pericardial effusion. Two cases of acute renal failure resulting from pericardial effusion were reported in the literature in the past. Pericardial effusion should be included in the broad list of prerenal causes of acute renal failure. © 2002 by the National Kidney Foundation, Inc.

Campylobacter fetus pericarditis in a patient with β-thalassemia: case report and review of the literature

A case of pericardial effusion due to Campylobacter fetus in a patient with thalassemia is presented. The patient failed to respond to ceftriaxone and clarithromycin despite in vitro susceptibility, but improved after pericardiectomy and ampicillin. Pericarditis due to C. fetus has rarely been reported. A high index of suspicion is essential to recognise this organism, because of its special microbiological characteristics.

Microfilaria of Wuchereria bancrofti identified in pericardial fluid.

A case of pericardial effusion in which cytologic examination revealed numerous sheathed microfilariae of Wuchereria bancrofti is described. The patient had no symptoms suggestive of filarial infection in the past. Following antifilarial therapy, the effusion resolved and the patient became asymptomatic. The possible etiologic role of the microfilariae in the genesis of the effusion is discussed.

Tuberculous pericarditis in children

This retrospective study reports experience in 44 children with pericardial tuberculosis seen during a 6-year period, 1986 to 1991. Thirty-seven children presented with pericardial effusion (PE), 4 with constrictive pericarditis and 3 with effusive constrictive disease. Features of cardiac tamponade were present in 90%, and in 91% radiologic cardiomegaly was found. A two-dimensional echocardiogram is diagnostic for PE. Culture and biopsy yields for Mycobacterium tuberculosis were low (18%). The Mantoux test was positive (> 10 mm) in 75%. In 14 patients doubt about etiology necessitated treatment for possible pyogenic infection with anterior pericardiotomy as opposed to diagnostic pericardiocentesis with catheter drainage. Twelve cases with PE were treated with steroids and the other 25 received only anti-tuberculous medication. Five cases of PE developed constrictive pericarditis during treatment of whom none received steroids. No statistically significant differences were demonstrated between the two groups. Only 5 of the 12 cases with constrictive pericarditis required pericardiectomy. There were no deaths and recovery has been complete in 43 cases. This study shows that tuberculous pericardial disease is common in areas with a high prevalence of tuberculosis. Prognosis is excellent for a condition in which morbidity and mortality have previously been high.

An unusual presentation of cardiac tamponade

A case of pericardial effusion with tamponade that presented as an acute abdomen is described.

Pericardial effusion as a clinical sign of legionnaires' disease

Legionnella often causes systemic manifestations. The clinical spectrum now includes cardiac legionnellosis. The first case of pericardial effusion was reported in September, 1981. To date, few additional cases have been reported. We hereby report a case of asymptomatic pericardial effusion with simultaneous pulmonary involvement. Pericardial involvement, if sought, would probably be more frequent than supposed in legionnaires' disease.

Pericardial fluid distribution: CT analysis.

Ultrasound and computed tomographic (CT) descriptions of pericardial effusion commonly indicate that fluid accumulates posteriorly within the pericardial sac before filling other areas. However, in a retrospective study of 68 cases of pericardial effusion identified on chest CT, most of the effusions were noted to be located solely or predominantly anterior to the right ventricle. Anatomic features of the pericardium and its fibrous attachments, and the physical principle of buoyancy account for this observation.

Simultaneous Electrical and Mechanical Alternans in Pericardial Effusion

A case of pericardial effusion and tamponade with echocardiographic documentation of both electrical and mechanical alternans is described. Alternation of the magnitude of the aortic valve opening reflected the mechanical alternation of the left ventricle. Analysis of the left atrial echoes may provide a possible explanation of the underlying mechanism. The cyclic variations in the magnitude of aortic opening in the weak beats, which are probably respiratory, may represent an echocardiographic counterpart of pulsus paradoxus. Echocardiograms of the aortic root and left atrium in pericardial effusion may help determine the true incidence of simultaneous electrical and mechanical alternans and may have potential value in the diagnosis of cardiac tamponade.

Angiocardiography in Constrictive Pericarditis

The conventional x-ray film examinations and the angiocardiographic features of 13 cases of constrictive pericarditis are analyzed and compared with those in five cases of pericardial effusion and four cases of congestive cardiomyopathy. The conventional x-ray film examination can contribute to the diagnosis of constrictive pericarditis if the following combination of features is present: absent to moderate cardiomegaly with poorly pulsating straightened heart borders, together with left atrial enlargement and signs of pulmonary venous hypertension. The angiocardiographic features described in the literature for the diagnosis of constrictive pericarditis are confirmed, namely: reflux of contrast material into the dilated inferior vena cava; straightening of the opacified right atrial lateral border; increased thickness of the right atrial extraluminal shadow; straightening of the opacified right ventricular cavity's septal border; and increased pulmonary circulation time. It is stressed that the following signs, not widely appreciated, should prove helpful for the diagnosis of constrictive pericarditis: (a) not only straightening but concavity of the right atrial lateral border persisting throughout the cardiac cycle; (b) not only straightening but concavity of the septal border of a small right ventricular cavity; (c) a small left ventricular cavity displaying forceful contractions; and (d) a concavity of the parietal border of the left ventricular cavity. It is noted that in our patients, left atrial enlargement and pulmonary venous hypertension were the rule rather than the exception. In our opinion, the above mentioned features may be particularly helpful in the differentation of constrictive pericarditis from pericardial effusion in which the cardiac cavities are of normal size, shape and display normal contractility; or from constrictive cardiomyopathy in which there is dilatation of these cavities with diminished contractions.

Unusual diastolic heart beat in pericardial effusion.

Unusual, hitherto undescribed form of, diastolic heart beat was reported in a case of tense pericardial effusion and in another case of seroconstrictive pericarditis. It consists of large and sharp early diastolic thrust, the peak of which conincides in time with the protodiastolic extrasound (pericardial knock). The mechanism and the diagnostic significance were discussed. Failure to recognize this diastolic heart beat in most cases of pericardial effusion or seroconstrictive (effusive-constrictive) pericarditis may be due to the absolute faintness of the precordial movement in these conditions. In addition, inspiratory widening of the split second heart sound due to the shortened electromechanical systole was described in a case of tense pericardial effusion without constriction

The role of angiocardiography in myxedema heart disease.

In 1918, Zondek (26) reported cardiac change in a number of patients with myxedema, emphasizing the increase in heart size as demonstrated by x-ray examination. In 1939, Scherf and Boyd (20) described 3 cases of pericardial effusion in myxedematous patients, offering this as a common cause of the enlarged cardiac silhouette. In recent years, there have been several reports of this association in the literature, usually in isolated cases (2, 3, 4, 6, 10, 12, 17, 21, 26). Most often, the diagnosis was established by pericardiocentesis (9); in other instances, by postmortem examination. Of interest is the report of Lerman et al. (14), who cited postmortem records showing 2 of 5 myxedematous patients to have pericardial effusions. In 1953, Marks and Roof (16) reviewed the literature on pericardial effusion in myxedema. In 13 of 44 cases of myxedema reported, there were associated pleural or peritoneal effusions, or both. The purpose of this paper is to show how angiocardiography may be decisive in documenting...

Importance of intracavitary pressure curves in chronic diffuse constrictive pericarditis

SummaryIn conclusion of the study of the intra-cardiac pressure curves in eight cases of constrictive pericarditis, one case of heart amyloidosis and one case of pericardial effusion, the authors conclude that the morphologic appearance of the intra-ventricular and intra-auricular pressure curves is not to be considered as specific.

Demonstration of L.E. cells in pericardial fluid; report of a case.

The value of the so-called lupus erythematosus (L. E.) inclusion phenomenon of bone marrow and blood as an aid in the diagnosis of acute disseminated lupus erythematosus has been amply demonstrated.1It is the purpose of this paper to report a case of pericardial effusion due to acute disseminated lupus erythematosus in which the diagnosis was first intimated by the finding of L. E. cells in the Wright-stained buffy coat smears of the patient's oxalated pericardial fluid. Subsequently, large numbers of L. E. cells were demonstrated in buffy coat preparations made from an oxalated marrow specimen from the same patient. Response to cortisone therapy was striking and led to rapid resorption of the pericardial effusion. REPORT OF A CASE A 38-year-old white woman was well until May, 1950, at which time pain developed in the right thigh, with subsequent pain and swelling in the right leg and foot. In

CORONARY ARTERY THROMBOSIS WITH PERICARDIAL EFFUSION

Within a short period of six months two cases of pericardial effusion following coronary artery occlusion have been observed. It is thought that this condition may be diagnosed clinically and that it is one which will be found more frequently. The reported incidence is indeed small. In a review of the etiology of 360 cases of pericarditis, Gerke 1 did not mention coronary artery occlusion. In Levine's monograph 2 on coronary thrombosis a pericardial effusion was encountered in only one patient in a series of 145. This effusion was not suspected during life, but 1,000 cc. of pericardial fluid was found at postmortem examination. White 3 in his book on heart disease did not cite coronary artery thrombosis as a cause of pericarditis with effusion. However, in 1932 Camp and White 4 reported their observations in 126 cases of pericardial effusion; and in two cases in which death occurred with