Pericarditis in renal disease

SPECIAL ARTICLE

Pericarditis in Renal Disease

Sudarshan Kumar and Michael Lesch

P ERICARDITIS in renal disease was first described by Richard Bright at autopsy in

1836.’ He also noticed involvement of the other serous membranes of the body and tabulated “six instances of old adhesions, eight of recent inflammation and twenty three of serious accumulation.” Additional early reports came from Barach in 1925’ and Richter in 1936.’ Barach aspirated 200 ml of fluid from the pericardium of one of his patients and noted its hemorrhagic appearance. All his patients died within an aver- age interval of 16 days after the appearance of a pericardial rub. Richter, while discussing a group of 41 patients with renal failure and pericarditis, stated that “the diagnostic rub is one of the very few single signs in medicine which enables the physician to prognosticate the death of his patient within a few days or weeks.” His statement and the earlier experience of Barach amply confirm the dismal outlook of these patients at that time. The introduction of dialysis for the management of renal disease now permits longer survival of many of these patients, with the eventual prospect of potential cure with renal transplantation. These important therapeutic advances necessitate a revision of the traditional concepts of pericarditis in renal disease as outlined by Barach and Richter. Its early recog- nition, an appreciation of pathogenesis, and proper management have become matters of great practical importance. The purpose of this article is to review current thinking as to the etiology, diagnosis, and management of pericardial disease in patients with renal disease.

PREVALENCE

The reported incidence of pericarditis in renal disease varies considerably in the literature. Bright’ described it in 8% of his 100 autopsied patients at Guys Hospital in London. Richter and O’Hare4 found it in 44% of patients at the Peter Bent Brigham Hospital. In a later study from the same institution, Wacker and Merrill’ described an incidence of 18% in patients with acute renal failure and 51% in patients with chronic renal disease. In a Scandinavian series reported by Skov et a1.6 in 1964, it was diagnosed

in 32% of cases, and in a more recent paper by Marini and HulL7 it was present in 35%.

In patients maintained on hemodialysis, new onset pericarditis was variably reported in 14% (Bailey et al. 19688), 16% (Comty et al. 1971’), 10% (Marini and Hull 1975’). and 8% (Connors et al. 1976”) of cases.

CLINICAL FEATURES

In patients with uremia, pericarditis has been observed to appear quite unexpectedly. Although pericarditis has been described as a complication of acute renal failure, most patients usually have had long-standing chronic renal insufficiency of varying etiology. There is no evidence to suggest

that renal disease of a particular etiology has an increased predilection to the development of pericarditis. Pericarditis occurs in patients who have never been dialyzed or who have been on dialysis for variable lengths of time. In some patients who are well controlled on dialysis, pericarditis develops late in the course of their illness, whereas in others, pericarditis may be noted for the first time at the time of the initial hemodialysis. In some instances, a metabolic stress, surgical intervention, or an infection8 have been suspected to precipitate pericarditis, whereas in most cases, no such predisposing factor is obvious. Although most frequent in severe uremia, there is no consistently good correlation between the level of blood urea or creatinine and the appearance of pericarditis. As with pericarditis of other etiologies, the clinical picture of uremic pericarditis is determined by the nature, rapidity and extent of pathologic changes in the pericardium. Thus, the presenting feature may be a pericardial rub, i.e.,fihrinous pericarditis, or the presence of variable quantities of pericardial fluid, i.e., effusive pericardi-

From the Section of Cardiology, Department of Medicine. Northwestern University School of Medicine, Chicago, Ill.

Reprint requests should be addressed to Sudarshan Kumar. M.D., Veterans Administration, Lakeside Hospital, 333 East Huron Street, Chicago. Ill. 60611.

ic) 1980 by Grune & Stratton. Inc. 00334620~80/220S4005$02.00/0

f%WSS in cardiOvascu/ar Diseases, Vol. XXII, No. 5 (March/April), 1980 357

358 KUMAR AND LESCH

tis; the latter, when associated with the signs of circulatory impairment, comprise the symptom complex of pericardial efusion with tamponade. In addition, several recent case reports have drawn attention to the evolution of subacute or chronic constriction resulting in the syndrome of constrictive pericarditis. However, it should be appreciated that in practice, the clinical picture may not be easily categorized. For example, it is not uncommon to encounter a patient who has a pericardial friction rub, evidence of pericardial effusion, and in addition, some element of constriction.

Chest Pain

Chest pain has been a striking feature in most of the reported series. Its severity varies from mild chest discomfort to severe pain requiring narcotics for relief. It is often aggravated by breathing, swallowing, and recumbent posture, and is relieved by sitting up and leaning forward (the sign of Mohammedan prayer-signe de la priere mahometane). The relief of discomfort obtained by the assumption of this posture has been considered quite characteristic of pericarditis. The location of pain varies widely and may be felt anywhere in the precordium, or even in the lower neck or across the shoulders.

Fever

In some studies, fever with or without leukocytosis has been a common symptom,7-9.““2 although this is not uniformly reported. For example fever was present in 96% of patients with leukocytosis in one series.’ Thus, the presence of unexplained pyrexia in a patient with uremia on or off dialysis should lead to a careful search for the presence of pericarditis.

Pericardial Rub

The presence of a pericardial friction rub is pathognomonic of pericarditis. It is found at one time or another in over 90% of cases. Sometimes repeated auscultation is required to detect its presence. As is well known, it is a superficial, harsh, scratchy sound, which has been likened to the rubbing of chamois leather. It can and is frequently heard over any part of the precordium. To disregard its presence because of “atypical location” is a common mistake, and similarly, to characterize it as “to and fro” is

imprecise. Pericardial rubs have a typical triphasic quality corresponding to atria1 systole. ventricular systole, and ventricular diastole. As it is often fleeting in nature, all three compo- nents may not be heard at one auscultation. The presence of this auscultatory finding indicates pericardial inflammation, but contrary to popular impression, a rub does not always disappear with the accumulation of pericardial effusion. Although it usually disappears with successful dialysis, however, occasionally it may persist in spite of adequate control of uremia, and in two of the patients described by Beaudry et al.,13 it was said to have persisted for several months after the initiation of hemodialysis, disappearing only after successful renal transplant.

Other Symptoms

A variety of other nonspecific symptoms are frequently present. These include general mal- aise, weakness, and lassitude. Breathlessness from pericardial effusion is a frequent com- plaint. The presence of hypotension is an important finding. Most patients with uremia are normotensive or have systemic hypertension. An unexplained episode of hypotension in these patients on, off, or during dialysis should alert the physician to the possibility of pericarditis and particularly pericardial tamponade. The onset of hypotension during hemodialysis was an initial manifestation of pericarditis in I4 patients of the series reported by Comty et a1.9 In these patients, elevated venous pressure and hepatomegaly were also present. Pleural effusion, commonly left-sided, occasionally bilateral, and rarely right-sided, may be present.

Special Signs

Various special clinical signs are described in the literature pertaining to the diagnosis of pericardial disease. With the availability of modern noninvasive techniques, the practical value of these signs has somewhat diminished.

Electrocardiogram. Classical ST segment elevation without reciprocal depression was present in 11 of the 40 cases of Skov et a1.6 In the experience of most other workers, this change has been infrequent; the most common electro- cardiographic feature being nonspecific repolar- ization abnormalities. In the presence of electro- lyte derangement, multiple drug therapy and

PERICARDITIS IN RENAL DISEASE 359

possible concomitant coronary ischemia, the diagnostic value of these abnormalities is limited. A sequential decrease in the voltage of QRS complexes in serial electrocardiograms in patients with rapidly accumulating fluid is inter- esting but seldom seen in practice. The presence of electrical alternans, for some obscure reason, is uncommon in uremic patients, but when present, is pathognomonic of cardiac tamponade.14 Supraventricular arrhythmia, vertical axis of QRS complexes in the frontal plane, and bifid P waves may be noted, particularly in the constrictive cases.

Radiology. It should be remembered that there really is no single feature diagnostic of pericardial effusion on x-ray. More often than not, too much confidence expressed in such a diagnosis is only a source of later embarrassment. According to Jefferson and Rees,15 between 250 and 500 ml of fluid must accumu- late before any change in heart size or shape can be detected on x-ray. They have suggested the following radiologic signs to be helpful in the diagnosis of pericardial effusion: (1) rapid change in heart size and shape with normal lungs, (2) absence of pulmonary venous hypertension and superior vena caval distension with a large heart, (3) loss of normal cardiac cantors with only slight or moderate cardiac enlargement, and (4) dominant enlargement of the heart laterally and anteriorly but not posteriorly.

In constrictive pericarditis, contrary to popular belief, the heart is frequently large and not small. The cardiac shape may be abnormal, depending on the site of constriction, and the right atria1 border is typically flat. Calcification of the pericardium, when present, is best seen in the lateral view.”

Echocardiography. Echocardiography is one of the most rewarding techniques currently available for the diagnosis of pericardial effusion; the only limitation being a small number of patients in whom, because of technical reasons, an adequate “window” cannot be obtained. It has been claimed that as little as 16 ml of fluid can be detected by echocardiography.” Pericar- dial fluid is recognized by the presence of an echo-free space between the epicardium and the pericardium posteriorly, or both anteriorly and posteriorly, or in some cases only on the anterior

surface of the heart. This feature is associated with greatly decreased or absent normal pericardial motion. In massive effusions, particularly those with tamponade, a wide exercusion of the heart is observed anteriorly and posteriorly-the so-called “swinging heart.” Alternation of the QRS complexes in the electrocardiogram, i.e., electrical alternans, is frequently observed to correspond with this excursion and has been invoked as a mechanism for its production.‘R In contrast to effusion, echocardiographic criteria for the diagnosis of constriction are less completely defined. Echocardiographic changes attributed to constriction include (1) Bat motion of the posterior left ventricular epicardium and pericardium during mild and late diastole; (2) abnormal septal motion; (3) a rapid diastolic slope (EF slope) of mitral valve; and (4) prema- ture opening of the pulmonic valve. None of these signs is specific, and all are found in many other conditions.”

EFFUSIVE PERICARDITIS

Effusive pericarditis may be present with or without tamponade. In effusion without tamponade, the symptoms are few, and its presence may go unnoticed. Some patients, usually those with large effusions, may complain of heaviness in the chest or dyspnea. Enlargement of heart shadow is present in the chest x-ray, and the diagnosis can be confirmed easily be echocardiography.

Cardiac Tamponade

This vexing and life-threatening complication of uremic pericarditis was first reported by Goodner and Brown” in two fatal cases in 1956, and in 1960, Keleman and Kloff” reported its occurrence in a patient during hemodialysis. Since these initial reports, several additional cases have been published.7,9.‘01’3.‘4.20.21-23 It is estimated that in a series of regularly dialyzed patients with uremic pericarditis, cardiac tamponade arose in 3 l%, and in 942 unselected regular dialysis patients, tamponade occurred in 5%~~~ Its incidence in patients who have never been dialyzed is not known but is probably quite low. All patients usually have severe renal impairment, and the onset of cardiac tamponade may cause further deterioration of renal function by virtue of low cardiac output, thus creating a dangerous vicious circle. For example. in the

360 KUMAR AND LESCH

series reported by Skov et aL6 the worst creatinine clearance (O-4 ml/min) and highest blood urea (410 mg/lOO ml) were found in patients who had tamponade. It should be appreciated though that all severely uremic patients do not develop tamponade and that the evidence for nitrogen retention may be minimal, i.e., highest blood urea nitrogen (BUN) values may be recorded prior to the development of this complication.32’33 The pericardial fluid is almost always hemorrhagic, and in an occasional case, the pericardium may be filled with blood clots.

There has been an increasing awareness of the possible interrelationship between the institution of dialysis and development of tamponade. However, the relationship is extremely complex, and no satisfactory explanation has emerged that fully explains all observations. In the experience of Beaudry et al., spanning a period from 1956 to 1964, 15 to 27 patients developed tamponade. However, only in one case did tamponade develop before the initiation of dialysis. In the remaining 26, it occurred at variable intervals after dialysis had been instituted; usually within the first month and often within 1-2 days after dialysis. As total body heparinization was routinely used at that time in their patients, these authors raised the possibility that total body heparinization may encourage additional intrapericardial bleeding and thus precipitate tamponade. In the experience of Skov et al.,’ the type of heparinization did not seem to be an important factor, as the incidence of tamponade was only 12.5% when they used total body heparinization for hemodialysis. It should also be remembered that anticoagulants were not used in several other patients with tamponade reported in the literature, and disconcertingly, tamponade had developed in some of the patients who had been treated with peritoneal dialysis.26327 In an occasional instance, cardiac tamponade may follow pericardiocentesis. Intra- pericardial bleeding resulting from trauma to myocardial structures is the probable mechanism in the majority of cases. In those where this possibility could be excluded with reasonable certainty, the mechanism is obscure and is perhaps related to sudden shifts in intravascular volume during aspiration.

Hemodynamic changes caused by tamponade

have been recorded both in the experimental animal and in man by various workers. This topic has been extensively reviewed in the literature,3s-60 and the reader is referred to these sources. In the setting of uremia, the diagnosis of cardiac tamponade is often difficult because circulatory congestion may be due either to coex- isting heart failure or fluid overload. Patients may be completely asymptomatic or may complain of progressive dyspnea or chest discomfort. A high index of suspicion is essential to quickly arrive at the correct diagnosis. The explanation for elevated venous pressure and distant heart sounds should be diligently sought and pulsus paradoxus looked for. It should be remembered that a third heart sound is not present in tamponade. In severe tamponade. pallor, sweating, impaired cereberation, and collapse may be the presenting symptoms. In an occasional patient, rapid deterioration of renal function may be the only manifestation of tamponade. Patients on dialysis are not protected from tamponade. Not infrequently, tamponade may develop for the first time during dialysis or soon after the initiation of dialysis. Presence of a pericardial rub on auscultation or evidence of effusion on echocardiography before beginning dialysis should alert the physician to the possible development of this complication during dialysis. A sudden fall in blood pressure during dialysis is a common finding in tamponade. It is worth remembering that since many uremic patients are hypertensive, the observed blood pressure may be normal at the time of tamponade. It should be appreciated that inspiratory distension of neck veins (Kussmaul’s sign) and early diastolic collapse of neck veins (Fred- erick’s sign) are not typical of tamponade and are frequently absent. At cardiac catheterization, there is elevation of the mean pressure in both atria and of the diastolic pressure in both ventricles. The systemic arterial pressure. in contrast, is usually low with a decrease in pulse pressure. In the right and left atria1 pressures there is a characteristic diminution or absence of the y descent. The cardiac output is always low. The aspiration of even relatively small quantities of fluid from the pericardium may result in a dramatic fall in atria1 and ventricular diastolic pressures and a rise in cardiac output.


CONSTRICTIVE PERICARDITIS

The first case of uremic constrictive pericarditis, “Pericardite uremique a evolution constrictive subaigue,” was reported by a group of French workers in 1964.6’ This patient was a young man, 30 yr of age, with uremia who had been treated with repeated hemodialysis. A pericardectomy was attempted to relieve constriction, but the patient died of ventricular fibrilla- tion during surgery. At autopsy, the parietal pericardium was diffusely thickened and the pericardial cavity was transformed into small spaces by adhesions. Since this report, additional patients have been described by various authors, and up to the present review, 25 cases of uremic constriction could be collected from the literature.6’-78

The presence of adhesions at autopsy in patients dying of renal failure is probably quite common, but the presence of true clinical constriction during life is relatively rare. Thus, in a series of 482 patients maintained on chronic dialysis program at one institution, pericarditis was detected in 217-an incidence of 45%-but only 2 had developed constriction7’ In another large series, Comty et a1.9 found uremic pericarditis in 25 of 125 patients, with constriction present in 3 cases. Pericardial adhesions, however, were present in 8 cases at autopsy in their series and presumably 11 cases of “healed” pericarditis, observed at autopsy by Beaudry et a1.13 in their patients, were also probably examples of varying degrees of adhesive pericarditis. Whether adhesive pericarditis would have even- tually evolved into constrictive pericarditis is impossible to speculate.

In all the reported cases, the onset of clinical pericarditis was heralded by the appearance of a pericardial rub, and patients had been treated by various modalities for the control of uremia. Thus, Spaulding’s62 patient had received peritoneal dialysis only for 3 days earlier in the course of her disease, whereas case 2 of Reyman66 died during the first cycle of peritoneal dialysis; and in the patient described by Weiss et a1.76 renal failure was acute and the duration of hemodialysis 4 wk when death ensued. As with effusive- constrictive disease of other etiologies, such as malignancy, the symptom complex is frequently a combination of constriction and tamponade,

and in subacute cases, the course of the disease is relatively rapid, lasting for l-12 mo. Patients often present with what appears to be the clinical picture of “congestive heart failure” with the complaints of dyspnea, fatigue, and chest discomfort. Lethargy and general weakness are frequent, and mental confusion may be present. Increased central venous pressure, peripheral edema, hepatomegaly, and ascites are seen in more severe cases. Tachycardia, reduced blood pressure, narrow pulse pressure, and occasionally pulsus paradoxus may be present. Heart sounds are usually normal, a third heart sound (pericardial knock) is infrequent but may become prominently audible after pericardiocentesis. Similarly, the presence of electrical alternans on electrocardiogram indicates a predomi- nant element of tamponade rather than constriction. X-ray of the chest invariably shows enlargement of the cardiac shadow, and the presence of fluid can be reliably substantiated by means of echocardiography or by contrast right atria1 angiography. Instillation of small quantities of air in the pericardium (although a somewhat antiquated procedure) may show a thick loculated pericardial sac at the time of aspiration.

Cardiac catheterization data on these patients are scanty. In one of the two patients described by Pillay et a1.,78 the pressure pattern was described as “restrictive” but no values were given. In another case reported by Reyman,64 there was elevation of both right and left ventricular diastolic pressures with the suggestion of a plateau configuration. The pulmonary capillary wedge pressure was elevated, and the wedge and right atria1 pressure differed by 7 mm Hg. The right atria1 pressure was also elevated, but the phasic tracings did not show an abnormal pattern.

On pericardiocentesis, variable quantities of fluid are usually aspirated. The fluid has been always bloody, and in none of the cases reported has there been any evidence of bacterial, fungal, or viral infection. In the absence of surgical resection, the course has been uniformly fatal. Two survivors have been reported following pericardiectomy.‘*

Patients with effusive constrictive disease are constantly in a precarious state of circulatory

362 KUMAR AND LESCH

balance. Hypovolemia and depletion in blood volume from any cause are particularly poorly tolerated and should be avoided. Hypervolemia on the other hand can aggravate peripheral edema, ascites, and precipitate pulmonary edema. Mental confusion, drowsiness, dizziness, and in extreme cases even syncope during or soon after dialysis may be manifestations of hypovolemia and poor perfusion. Judicious handling of fluid balance is therefore very important. Persistent hypotension during dialysis has been a striking feature in some case reports.

With the longer survival of patients on dialysis, it is possible that more cases of constriction will emerge. There is no evidence to suggest so far that either aspiration of pericardial effusion or intrapericardial instillation of steroid prevents the development of constriction. The introduction of air into the pericardium at the time of pericardiocentesis, although sometimes effective in the experience of some workers in relieving pain, probably also does not prevent adhesions and constriction. In the absence of a positive evidence of bacterial, viral, or fungal infection, no satisfactory explanation of the mechanism of chronicity is available. As the pericardial fluid is always bloody, it has been suggested that repeated bleeding into the pericardial sac may predispose to the formation of adhesion and fibrosis and eventual development of constriction. This hypothesis remains unproven.

ETIOLOGY

Pericarditis complicating uremia has been described in patients with acute renal failure and in patients with chronic renal failure, in patients on various modes of dialysis and in patients who have never been dialyzed. In the series of patients described by Comty et aL9 the majority of patients were females, but in the 3 other large series where sex distribution was given, there were 9 females and 24 males (Bailey et al.,*); 2 1 females and 19 males (Skov et aL6); 10 females and 17 males (Beaudry et al.‘-‘). Adding all these patients from 4 series, the overall sex incidence was 54 females and 7 1 males.

Some authors are of the opinion that there are two broad categories of patients with pericarditis. In one, pericarditis develops in the end-stage of renal disease. These patients have either never

been dialyzed or have been inadequately dialyzed before with poor control of uremia, and on initiation of dialysis, resolution of pericarditis is usually readily achieved. In the second group are patients who have developed symptoms while undergoing regular dialysis. In these patients, the course of the disease may be protracted, the outcome less predictable, and intensification of dialysis may or may not alleviate the symptoms of pericarditis. This broad catagerization is clearly an attempt to seek some order in what otherwise is a very confused situation; no doubt there are occasional examples that transgress these boundaries.

No satisfactory explanation is available to explain the etiology of uremic pericarditis. The following hypotheses have been put forward.

(I) Biochemical Theory

It is well known that pericarditis usually occurs in patients with renal disease with severe biochemical disturbances; it was therefore expected that a chemical inflammation of the pericardium due to retained catabolic nitro- genous products in the body would attract the attention of medical investigators. Furthermore, the fact that pericarditis may reverse with the commencement of or intensification of dialysis and the frequent concomitant involvement of other serous membranes of the body would lend further weight to this hypothesis. Bright, while considering it to be a part of “the general involvement of serous membranes of the body,” presumably had this possibility in mind. But several other lines of evidence do not firmly establish this as the only causative factor. It is for example common knowledge that the severity of the retention of known products of catabolism have a poor correlation with the development of pericarditis: a specific nondialyzable uremic toxin with this unique effect has not yet been isolated, and given a similar degree of BUN and creatinine retention, one patient may develop pericarditis and the other may not. Also, pericarditis may develop de novo in patients otherwise seemingly well controlled on established dialysis. Marini and HulI’ found no statistical difference in blood urea nitrogen and creatinine levels in their patients with or without pericarditis. Simi- larly, in the experience of Fox et al.,79 BUN, serum creatinine, and creatinine clearance levels


did not significantly differ in patients who developed pericarditis from the rest of their dialysis population.

Clarkson” reported significantly higher levels of blood uric acid in a group of patients with pericarditis and speculated that supersaturated levels of uric acid with crystal precipitation in the pericardium could incite inflammation of the pericardium, much like the development of arthritis in gout. However, examination of pericardial fluid has not shown the presence of phagocytosed uric acid crystals, and polarization microscopy has not yielded postitive findings8’

Hypercalcemia from nephrogenic bone disease was present in 5 of 25 patients of Comty et al.’ In the experience of others, however, there has been no correlation between uremic pericarditis and renal osteodystrophy. Moreover, the presence of high concentrations of calcium in the pericardium has never been reported.

(2) Infection

In the setting of the metabolic derangement of renal disease, the general debility associated with uremia, and the frequent administration of corticosteroids and other immunosuppressive drugs, an enhanced predilection to infection could be postulated. Furthermore, personnel working in dialysis units and the dialysis equip- ment are both potential sources of infection. Despite this predilection for infection, an infec- tious origin has not been proven in the vast majority of patients with uremic pericarditis. Moreover, the typical pericardial fluid is bloody and not purulent. Routine fungal, bacteriologic, and viral cultures are negative,‘0.“.28 and antimicrobial agents have no effect on the course of the disease. It should be pointed out that loculated blood in the pericardial sac, until absorbed or removed, is per se capable of causing fever without the presence of an infection.

(3) Hemorrhagic Theory

Hemorrhage, spontaneous or provoked by heparin administration, is another possible etio- logic consideration. In favor of this hypothesis is the fact that the pericardial fluid is almost always bloody to the naked eye, and on microscopic examination, evidence of recent bleeding in the form of red blood cells or chronic bleeding characterized by hemosiderin particles may be

present. Both the naked eye and microscopic examination of the tissue obtained at pericardiectomy or autopsy frequently shows evidence of a highly vascular granulation tissue. A clini- cally increased bleeding tendency, as well as abnormalities of capillary and platelet function and coagulation are occasionally present in severely uremic patients. It is therefore reasonable to infer that bleeding within the pericardium is an important component in the initiation and/or progression of pericardial disease. Ali Regiaba et al.” believe that the effusion emanates from the rupture of many new small blood vessels that develop in inflamed pericardial layers that are subjected to the shearing force of cardiac motion. Attention has also been drawn by Beaudry et a1.13 to the possible contri- bution of total body heparinization in aggravat- ing pericarditis. Alfery et a1.,82 using tagged red cells, found no evidence of active blood loss in the pericardial sac during dialysis. However most of the patients studied by these workers were dialyzed with regional heparinization.

PATHOLOGY

The pathologic findings will obviously vary with the stage and nature of the disease. Thus, the pericardial reaction may be fibrinous, effusive, constrictive or a combination of all the three.x3m*4

in the fibrinous type, there may be nothing more than a layer of fibrinous material covering the visceral and parietal layer of pericardium giving rise to the so-called “bread and butter” appearance. The amount of fluid in these cases is usually minimal and straw colored.

In the effusive type, accumulation of pericardial effusion is the striking feature-the amount of fluid varying from several milliliters to a few liters in extreme cases. In patients who have been subjected to dialysis during life, the fluid is overwhelmingly hemorrhagic, and in extreme examples, the heart may be encased in thick layers of blood clots. This feature is uncommon in patients without dialysis wherein a straw- colored or serosanguinous effusion is more common. The pericardial surface appears raw and red. Microscopically, hemorrhage and fibrin dominate the picture. There may be evidence of attempted organization. Organization of the exudate leads to the formation of adehesions and

364 KUMAR AND LESCH

the pericardial cavity may be transformed into islands of fluid-filled spaces. With the further organization of fluid, the pericardium is mark- edly thickened, densely fibrotic, and may form a fibrous shell over the heart and demonstrate a so-called “onion peel” appearance. Microscopi- cally, connective tissue formation is more pronounced, and the clinical picture of constrictive pericarditis is seen. Pericardial effusion, hemorrhage into the pericardial sac, and col- lagenization of pericardial exudate have been considered as causes of cardiac tamponade in uremic patients.

MANAGEMENT

There is considerable controversy with regard to the management of patients with uremic pericarditis. Available modalities of treatment include:

Pericardiocentesis Dialysis Drugs

Corticosteroids Indomethacin

Surgical Pericardial window Resection of the pericardium

Pericardiocentesis

Aspiration of the pericardium has been a popular procedure in the past to establish the diagnosis of effusion, but with the recent advances in noninvasive techniques and the possible occasional occurrence of serious complications, physicians are increasingly becoming less enthusiastic to perform this procedure for this purpose. Current view is that pericardiocentesis has only a limited role to play in this regard in the routine management of patients with pericarditis. It is only required in those few cases for making the diagnosis of pericardial effusion where echocardiography has yielded unsatisfactory results because of technical reasons. A diagnostic tap is also indicated in patients where the presence of an infection is strongly suspected. Laboratory examination of the fluid in such cases would be helpful to isolate the causative organism and select proper antimicrobial thera- PY.

The other situation in which pericardiocentesis is consistently helpful is in the relief of acute circulatory embarrassment in severe tamponade.

This measure can be life-saving and the results are often impress. 1 e even in the most moribund patients. As a definitive mode of therapy, it is generally unsatisfactory because of frequent recurrences and occasional serious complications. Morin et al.,*’ on the basis of data collected from the literature, estimated that of 86 patients treated with pericardial aspiration, only 28 (32.5%) had complete resolution, 42 (48.9%) had a recurrence of sufficient degree to require operation, and 16 (18.6%) died suddenly during or just after pericardiocentesis. In none of their own 6 patients was pericardiocentesis definitive therapy, and 2 of the 6 died from cardiac arrest during or immediately following pericardiocentesis.

Complications

Various complications of pericardiocentesis have been reported in the literature and include: (1) trauma to cardiac structures: injury to the myocardium or its blood supply can lead to life-threatening bleeding; (2) cardiac arrhythmia: various cardiac arrhythmias, atria1 and ventricular, may be initiated; (3) damage to lung or creation of a pneumothorax; (4) damage to liver or other abdominal viscera; (5) increased accumulation of fluid with worsening of or development of fresh tamponade; (6) sudden death.

Hemodialysis

The usefulness of hemodialysis in the control of uremia is universally accepted, and there is general agreement among various workers that in patients who have not been on dialysis, this should be instituted, and in those who are already on dialysis, this should be intensified. Marini and Hull7 have recommended a 6-hr dialysis everyday for 6-7 days as the initial treatment of pericarditis. In a great majority of patients, vigorous dialysis will relieve symptoms and bring about resolution of pericarditis, whereas in a significant minority, this measure alone not only may prove inadequate but even dangerous with the further accumulation of fluid, sometimes leading to tamponade. Bailey et al.* reported resolution of pericarditis in 72% of their patients with intensive dialysis, whereas Morin et al.*’ reviewed major published series and found that dialysis was unsuccessful in preventing progressive pericardial effusion and tamponade in 60% of the reported cases. Thus, in

PERICARDITIS IN RENAL DISEASE

199 cases found by these authors, 80 (40%) resolved completely and 11 patients (5.5%) suffered sudden death. Unfortunately no reliable clinical or laboratory criteria have emerged to enable one to predict the likelihood of success with dialysis in a given patient. Close supervision of the patient during and following dialysis is therefore of great importance. Patients resistant to or deteriorating with hemodialysis present a difficult therapeutic problem, and various approaches in the management of these resistant cases have been suggested. Bailey et al.’ recommended continous pericardial drainage with an indwelling percutaneous catheter for prolonged periods. Cohen et a1.86 reported on 3 patients who developed pericardial effusion while on hemodialysis. Peritoneal dialysis brought improvement in all 3 patients. On the basis of this rather small experience, the authors recommended that “pericarditis and pericardial effusion occurring during hemodialysis should be treated by pericardiocentesis and subsequently by peritoneal dialysis for at least one week despite the tempta- tion to use a patent AV canula with a good and improving blood flow.” Other workers6,27 have reported the occurrence of tamponade in patients on chronic peritoneal dialysis programs with relief in some cases. In the others, relief was obtained only on further treatment with intensive hemodialysis.

Drugs

Corticosteroid Therapy

Both systemic and local steroids have been used in patients with uremic pericarditis. Comty et al.’ administered systemic steroids, i.e., prednisone 60 mg daily for a period of 1-12 wk to 8 patients. Pericarditis subsided in all patients, however, one patient died of purulent peritonitis from a perforated ulcer after 2 mo, and 2 other patients were discovered to have adhesive pericarditis at autopsy 2 mo after therapy when they died of an infection. Eliasson and Murphy” described a “dramatic” response in 3 patients with oral steroids-40 mg prednisone daily tapered over 28-32 days. One patient had no return of signs or symptoms of pericarditis for the last 20 mo on a dialysis program, the second died of a cerebral vascular accident, and the follow-up on the third patient was not given. On the basis of this experience, the authors stated that “patients who develop progressive symp-

toms and substantial pericardial effusion should be considered for steroid therapy if dialysis and rest are not followed by considerable improvement.” Lindsay et a1.6g reported on one patient with uremic pericarditis in whom considerable reduction in cardiac silhouette was observed after 60 mg of prednisone daily for 6 days, when it was discontinued because of a pronounced catabolic effect resulting in a marked increase in blood urea nitrogen. About 11 mo following the single additional intrapericardial administration of 60 mg of methylprednisone, the patient presented with clinical and hemodynamic features of constrictive pericarditis.

Local Steroids

Buselmeier et al.” described a group of 12 patients with uremic pericarditis treated with intrapericardial steroid therapy. The majority had fever, chest pain, dyspnea, and edema. These symptoms were aggravated by attempts at ultrafiltration during dialysis. All patients had been on adequate hemodialysis (3 times/week) for at least 1 mo prior to the development of effusion. Failure to respond to dialysis qualified these patients for admission to the study group. Eleven of the 12 patients had suffered from tamponade. Through an indwelling catheter placed in the pericardial sac, repeated aspiration and triamcinolone instillation was carried out for 24-72 hr. One of the 12 patients had an organiz- ing pericardial effusion with unsuccessful pericardiocentesis; in the 11 remaining patients, resolution of pericarditis was achieved. No complications were reported. Fuller et a1.88 treated 5 patients unresponsive to hemodialysis with a similar protocol. All 5 recovered, and no recurrence was observed 1-15 mo after treatment. These authors stated that “this method is an effective alternative to the surgical management of intractable uremic pericarditis and might be the treatment of choice in patients particularly susceptible to the risks of genera1 anesthesia and thoracotomy.”

In a more recent publication, Buselmeier et a1.g4 have reported on 45 patients with pericarditis treated with intrapericardial instillation of triamcinolone and followed for a period of l-54 mo. Pericarditis resolved in all patients except one, who had a recurrence of her effusion 6 mo after therapy. One other patient was left with persistent pericardial pain despite resolution of

366 KUMAR AND LESCH

the pericardial effusion. An asymptomatic inter- nal mammary fistula was the only complication seen in a single case. It is obvious from the above reports that the role of local or systemic steroids is far from clear at present. It would appear that steroid therapy is beneficial in certain circum- stances in the suppression of pericarditis, but that it has its own definite hazards. The side effects of orally administered steroids could be serious, and the presence of adehesive pericarditis at autopsy observed in some patients raises questions of long-term effectiveness. Clearly, more data are needed to properly evaluate their use, particularly with regard to long-term prognosis of these patients. Whether or not steroids will prevent the development of constrictive pericarditis is at present an important, but unan- swered, question. It is sobering to note that pericarditis developed in three patients who were on large doses of steroids for renal transplant rejection crisis.”

Indomethacin

In patients with pericarditis, indomethacin administration has been reported to result in improvement with abatement of pain and fever and with the disappearance of rub and effusion.89 When effective, the improvement is usually dramatic and seen within 24-40 hr after the commencement of treatment. In unresponsive patients, increasing the dose or prolonging the duration of therapy is of little benefit. Various side effects have been reported that include anorexia, nausea, vomiting, headaches, and neutropenia.

Surgery

In the past few years and particularly following the observation by Hampers et aL9’ that dialysis patients tolerate surgery well, many reports of surgical treatment of uremic pericarditis have appeared in the literature.a-‘3.27- 29~3’~78X8239’~95 However, the precise criteria for patient selection, timing of the surgery, and the type of surgery still remain controversial. There is difference of opinion even to the site of incision for entry into the pericardium and to the extent of pericardial resection. Furthermore, the termi- nology of different procedures seems to carry different meaning to different surgeons. Basical- ly, there are two types of surgical procedures, i.e., pericardiotomy or pericardiectomy.

Pericardiotomy

Pericardiotomy implies opening of the pericardial sac to establish drainage. This has been further grouped according to the avenue of approach into anterior, inferior, and posterior pericardiotomy. Two of the most popular approaches have been the inferior or subxiphoid approach and the anterior approach through an anterolateral thoractomy. Satisfactory drainage can be established by both methods in most cases, and relief of effusion is impressive. Advan- tages of the subxiphoid approach are that the pleural space is not entered, and thus there is no compromise of respiratory function. In those instances where infection is a possibility, chances of pleural infection are also minimal. The disad- vantage of the subxiphoid approach is that one may not be able to break loculations quite as well to permit complete drainage of the pericardium. The anterolaterai approach permits relatively wider exploration of the pericardium and is the preferred method with large posterior loculated effusions.

Obliteration of the pericardiotomy, cardiac herniation and secondary infection are complications of this procedure, and there remains a small, albeit a real, possibility of the development of constrictive pericarditis in some patients in the future.

Pericardiectomy

Pericardiectomy implies resection of the pericardial sac. It is a more extensive procedure and requires general anesthesia. This is clearly the only effective mode of treatment in constrictive pericarditis. Initially, pericardiectomy was un- dertaken only as an extreme measure in patients with evidence of severe tamponade. Recently, the procedure has been used more liberally and has also included patients with recurrent or continous signs of tamponade and also patients with large lax pericardiai effusions. Further- more, there has been an increasing trend towards as complete resection as possible and most surgeons now try to remove pericardium from one phrenic nerve to the other. According to Wray et al.,95 a pericardial window should be reserved for the patient who is so debilitated that he would not tolerate general anesthesia. Their indications for pericardiectomy include: (1) full blown cardiac tamponade; (2) recurrent hypotension during dialysis without other evidence of

PERICARDITIS IN RENAL DISEASE

tamponade; (3) enlarging lax pericardial effusion while on dialysis. Published reports indicate that in the hands of a competent surgeon, the mortality is negligible and morbidity is minimal. However, before subjecting a patient to pericardiectomy, a careful assessment should be made to identify the role of myocarditis in the causa- tion of symptoms, for these are not hkely to respond to surgery.

CONCLUSION

Pericarditis is not an uncommon complication of uremia. The clinical picture varies from an accidentally discovered pericardial friction rub

367

on routine examination to the presence of vascular collapse due to cardiac tamponade and signs and symptoms of constriction in other cases.

The possible role of infection, intrapericardial bleeding, and the retention of metabolic products in the etiology of pericarditis are discussed.

Management techniques include pericardial aspiration, dialysis, drug treatment with corticosteroids and/or indomethacin, pericardiotomy and pericardiectomy. With early diagnosis and the judicious application of these modalities, most cases can be satisfactorily managed. The development of pericarditis need no longer be regarded as a preterminal or terminal event in the prognosis of patients with renal disease.

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Pericarditis in renal disease

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