Uremic Pericarditis Research Articles

MRI of the abnormal pericardium.

To evaluate the use of MRI in the diagnosis of pericardial disease, 63 patients with pericardial abnormalities or clinically suspected pericardial disease were studied retrospectively. Twenty-three patients had pericardial effusion, 19 patients had pericardial thickening, and 11 patients were referred for evaluation of masses with possible pericardial involvement. The other 10 patients were referred for differentiation of constrictive pericarditis from restrictive cardiomyopathy and eventually were found to have pericardial hematoma or normal pericardium as assessed by MRI. The calculated size of pericardial effusion by MRI showed a good correlation with semiquantitative echocardiographic estimations. MRI could demonstrate fibrinous adhesions in patients with uremic pericarditis. It was also of great value in the differential diagnosis of constrictive pericarditis vs restrictive cardiomyopathy. Pericardial thickness of more than 4 mm was found in patients with constrictive pericarditis. Normal pericardial thickness was demonstrated by MRI in the three patients with restrictive cardiomyopathy. MRI diagnosed hemopericardium correctly as the cause of constrictive symptoms in two patients. Pericardial thickening in patients after cardiac surgery was commonly found by MRI and usually was not associated with clinical signs of constrictive pericarditis. MRI proved to be useful in the diagnosis of pericardial cysts and in the evaluation of paracardiac masses with possible pericardial involvement. MRI is an important technique in the evaluation of the pericardium. It can provide important additional information when diagnosis cannot be made adequately by other noninvasive imaging techniques.

Unusual Cardiac Complications of Wegener's Granulomatosis

Wegener's granulomatosis most commonly involves the sinuses, lungs and kidneys with necrotizing granulomatous vasculitis. In 12 percent of a large series of patients with Wegener's granulomatosis there was cardiac involvement, largely manifested by pericarditis and coronary arteritis. We present three patients with this disease who developed unusual cardiac complications. Patient 1 had renal failure requiring hemodialysis, pericardial tamponade requiring pericardiocentesis, and later developed constrictive pericarditis requiring pericardiectomy. Patient 2 developed pericarditis and high grade atrioventricular block, and patient 3 developed pericarditis and atrial tachycardia resistant to pharmacologic and transesophageal atrial pacing methods. All three patients greatly improved with cyclophosphamide therapy. The rhythm disturbances seen in patients 2 and 3 were attributed to coronary arteritis. The renal failure in patient 1 was due to Wegener's granulomatosis, but whether the constrictive pericarditis was due to uremic pericarditis or the pericarditis of Wegener's granulomatosis is uncertain. As patients with Wegener's granulomatosis live longer with cyclophosphamide therapy and because inpatient arrhythmia monitoring and recording has become more widespread, these uncommon manifestations of Wegener's granulomatosis may be seen more often.

Captopril and Pericarditis

To the Editor.— In the Jan 20 issue ofThe Journal, Dr Zatuchni 1 reports a case of pericarditis that he contends was caused by captopril therapy. There are several points that must be made. The author's case presentation is incomplete. Only in the last sentence does he state that "the serum urea nitrogen level continued to rise." How high was this level? I suspect that it was very high. The serum urea nitrogen level was very pertinent because it could justify a far better and much more common explanation for the patient's pericarditis, ie, uremic pericarditis, which the author discards so easily. The author states that the patient's heart failure was "refractory." A plausible explanation for this refractoriness could be the development of a larger pericardial effusion, again, probably caused by uremia. The patient's sedimentation rate of 126 mm/hr is remarkable and suggests a vasculitis or arteritis

Captopril and Pericarditis-Reply

In Reply.— The issues that Dr Garbitelli raises are important and relevant and were fully addressed in an original manuscript, which was reduced to a brief letter at the request of the editor. The serum urea nitrogen level was 103 mg/dL, and the creatinine level was 8.3 mg/dL. Uremic pericarditis was a definite possibility and could not be excluded with certainty but was considered unlikely for the reasons cited in the letter. Second, pericardial effusion was not responsible for refractory heart failure, for it was absent initially and, later, not large but small, as revealed by echocardiography. Third, the elevated ESR was thought to be part of a drug-induced immune dysregulatory phenomenon. Finally, to be sure, the evidence of a causal relationship is circumstantial but favored by findings and sequence of events.

Treatment of Pericardial Effusion With Local Corticosteroid Injections-Reply

In Reply.— I am grateful to Dr Twardowski for calling to my attention his report of intrapericardial injections of corticosteroids as a treatment for uremic pericarditis, which no doubt led others later to try to perfect and popularize this method. However, he is not correct when he states that local steroids were always used in conjunction with In the references we cited for treatment of tamponade caused by rheumatoid pericarditis, the patients were treated with aspiration and instillation of deposteroids alone, without prolonged drainage. are also aware of a report of similar management to avoid prolonged drainage or pericardectomy in tamponade from other causes. 1 Those authors concluded, We feel that hemodynamically significant uremic pericardial effusions should be treated first by pericardiocentesis and intrapericardial instillation of triamcinolone hexacetomide. would reserve pericardiectomy for those cases in which loculations prevent adequate aspiration of the effusion or in which tamponade

Predicting Success of Intensive Dialysis in the Treatment of Uremic Pericarditis

No AccessJournal of Urology1 Jun 1984Predicting Success of Intensive Dialysis in the Treatment of Uremic Pericarditis N.L. De Pace, P.F. Nestico, A.B. Schwartz, G.S. Mintz, J.S. Schwartz, M.N. Kotler, and C. Schwartz N.L. De PaceN.L. De Pace More articles by this author , P.F. NesticoP.F. Nestico More articles by this author , A.B. SchwartzA.B. Schwartz More articles by this author , G.S. MintzG.S. Mintz More articles by this author , J.S. SchwartzJ.S. Schwartz More articles by this author , M.N. KotlerM.N. Kotler More articles by this author , and C. SchwartzC. Schwartz More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(17)50897-6AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "Predicting Success of Intensive Dialysis in the Treatment of Uremic Pericarditis." The Journal of Urology, 131(6), pp. 1252–1253 © 1984 by The American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 131Issue 6June 1984Page: 1252-1253 Advertisement Copyright & Permissions© 1984 by The American Urological Association Education and Research, Inc.MetricsAuthor Information N.L. De Pace More articles by this author P.F. Nestico More articles by this author A.B. Schwartz More articles by this author G.S. Mintz More articles by this author J.S. Schwartz More articles by this author M.N. Kotler More articles by this author C. Schwartz More articles by this author Expand All Advertisement PDF downloadLoading ...

Predicting success of intensive dialysis in the treatment of uremic pericarditis

To identify predictors of the success or failure of daily intensive dialysis in uremic pericarditis, a retrospective examination was made of initial clinical, laboratory, and echocardiographic data in 97 patients using univariate and multivariate statistical analysis. In this group, 67 patients showed response to intensive dialysis, and 30 patients did not (22 required surgery and eight died). By univariate analysis, nine factors correlated with intensive dialysis failure (p < 0.10): admission temperature over 102 °F, rales, admission blood pressure under 100 mm Hg, jugular venous distension, peritoneal dialysis treatment only because of severe hemodynamic instability, white blood cell count over 15,000/mm 3, white blood cell count left shift, large effusion by echocardiography, and both anterior and posterior effusion by echocardiography. Echocardiographic left ventricular size and function were not useful predictors of success or failure; there was no difference in response to hemodialysis in patients with pericarditis before dialysis (69 percent) versus patients with pericarditis during a maintenance program (67 percent). By discriminant analysis, a seven-variable function was constructed that divided the patients into three groups: (1) those likely to show response to intensive dialysis (48 patients, predictive value of 98 percent), (2) those with an intermediate (38 percent) chance of showing response to intensive dialysis (30 patients), and (3) those unlikely to show response to intensive dialysis (14 patients, predictive value of 100 percent). When the function was applied prospectively to 12 patients (eight with success and four with failure), all were classified correctly. Thus, discriminant analysis of patients with uremic pericarditis allows improved selection of patients with uremic pericarditis likely to have response to daily intensive dialysis and early consideration of alternative forms of treatment in patients unlikely to show response to intensive dialysis. However, the model should be validated in the particular institution where it is to be used before its application.

Surgical treatment of pericarditis in the dialysis patient

Eighteen patients with pericarditis complicating chronic renal failure who were unresponsive to medical therapy underwent surgical decompression of the pericardium for either pericardial tamponade [16] or constrictive pericarditis [2]. There was one perioperative death and minimal morbidity. Preoperative pericardiocentesis in nine patients afforded only temporary relief in most of the patients and caused a life-threatening pericardial tamponade in one patient. Creation of a pericardial window through a left anterior thoracotomy was the procedure of choice in patients without signs of constrictive pericarditis or posterior loculated effusions and had excellent long-term results. We recommend early surgical treatment of uremic pericarditis in all patients with hemodynamic instability, enlarging pericardial effusion, or effusion that is unresponsive to intensive medical therapy.

Study of the relationships between pericarditis and osteopathy in chronic haemodialysis

Statistically significant correlations were demonstrable between the incidence of bone abnormalities due to parathyroid hyperfunction and of pericarditis in 130 patients maintained on chronic haemodialysis. Parathyroid hormone is regarded on these grounds as one of the possible factors accounting for the production of non-infective uraemic pericarditis.

A controlled study of the effect of indomethacin in uremic pericarditis

AbstractA controlled study of the effect of indomethacin in uremic pericarditis. To determine the impact of indomethacin on the course of uremic pericarditis we performed a prospective, double blind study in which 24 patients with endstage chronic renal failure and pericarditis randomly received indomethacin, 25 mg four times daily, (11 patients) or a placebo (13 patients) for a 3-week period. All patients received peritoneal or hemodialysis treatment concurrently with the study drug. In contrast to the placebo, indomethacin produced an immediate and sustained reduction of fever in all but one patient. On the other hand, indomethacin had no effect on the duration of chest pain (mean days ±SE: placebo 1.4 ± 0.6, indomethacin 5.5 ± 3.3), duration of pericardial friction rub (placebo 10.3 ± 1.7, indomethacin 16.0 ± 3.8), or on the amount of pericardial effusion. Further, indomethacin did not diminish the need for invasive surgical procedures for relief of tamponade (three of 13 placebo patients, two of 11 indomethacin patients) or result in decreased mortality rate. Death (not due to pericarditis) occurred in two patients treated with indomethacin and one patient who received the placebo. In our patients pericarditis encompassed a wide spectrum ranging from a mild illness of several days duration to a painful and debilitating disease lasting weeks and requiring surgical intervention. Although the size of our population prohibits definitive conclusions, it would appear that, except for fever, the manifestations and natural history of this illness are unaffected by indomethacin.Une étude contrôlée de l'effet de l'indométhacine dans la péricardite urémique. Déterminer l'effet de l'indométhacine sur l'évolution de la péricardite urémique, nous avons effectué une étude prospective, en double insu, dans laquelle 24 malades avec une insuffisance rénale chronique terminale et une péricardite ont reçu au hasard 25 mg quatre fois par jour (11 malades) d'indométhacine ou de placebo (13 malades) pendant une période de 3 semaines. Tous les malades étaient en dialyse péritonéale ou en hémodialyse en même temps que l'étude du médicament. Par rapport au placebo, l'indométhacine a entraîné une réduction immédiate et prolongée de la fièvre chez tous les malades sauf un. Cependant, l'indométhacine n'a pas eu d'effet sur la durée de la douleur thoracique (nombre moyen de jours ±SE: placebo 1,4 ± 0,6, indométhacine 5,5 ± 3,3), la durée du frottement péricardique (placebo 10,3 ± 1,7, indométhacine 16,0 ± 3,8), ou sur l'importance de l'épanchement. En outre, l'indométhacine n'a pas diminué la nécessité de gestes chirurgicaux invasifs nécessaires pour améliorer la tamponnade (trois du 13 malades placebo, deux du 11 malades sous indométhacine), ni n'a diminué le taux de mortalité. La mort (non dûe à la péricardite) est survenue chez deux malades traités avec l'indométhacine et chez un malade qui avait reçu le placebo. Chez nos malades, la péricardite était caractérisée par un large spectre allant d'une maladie de gravité moyenne durant plusieurs jours à une maladie douloureuse et débilitante durant des semaines et nécessitant une intervention chirurgicale. Bien que la taille de notre population interdise des conclusions définitives, il semble apparaître qu'à l'exception de la fièvre, les manifestations et l'histoire naturelle de cette maladie ne sont pas affectées par l'indométhacine.

Early Drainage of Pericardial Effusion in Patients With Dialysis Pericarditis

Pericarditis in patients with renal failure remains a serious problem, with mortality as high as 20%.1The etiology is unknown and may be multifactorial. The conventional approach to treatment has been intensive (daily) dialysis, using minimal or regional heparinization for 10 to 14 days.2,3Steroids given for systemic effect and nonsteroidal anti-inflammatory agents have also been used, but controlled studies attesting to their benefit are lacking. With the advent of maintenance dialysis, two distinct forms of this disease have emerged. In patients with pericarditis who never received dialysis (uremic pericarditis), the response rate to intensive hemodialysis is almost 90%,2suggesting that uremia is a major causative factor. However, patients receiving maintenance hemodialysis who have pericarditis (dialysis pericarditis) have only a 10% to 40% response rate to intensified hemodialysis,1,2,4suggesting that accumulation of dialyzable uremic toxins may not be the sole cause of the pericarditis. In fact,

Early drainage of pericardial effusion in patients with dialysis pericarditis

Pericarditis in patients with renal failure remains a serious problem, with mortality as high as 20%.¹The etiology is unknown and may be multifactorial. The conventional approach to treatment has been intensive (daily) dialysis, using minimal or regional heparinization for 10 to 14 days.^2,3Steroids given for systemic effect and nonsteroidal anti-inflammatory agents have also been used, but controlled studies attesting to their benefit are lacking. With the advent of maintenance dialysis, two distinct forms of this disease have emerged. In patients with pericarditis who never received dialysis (uremic pericarditis), the response rate to intensive hemodialysis is almost 90%,²suggesting that uremia is a major causative factor. However, patients receiving maintenance hemodialysis who have pericarditis (dialysis pericarditis) have only a 10% to 40% response rate to intensified hemodialysis,^1,2,4suggesting that accumulation of dialyzable uremic toxins may not be the sole cause of the pericarditis. In fact,

Cardiac arrhythmias in patients on maintenance hemodialysis.

17 patients on maintenance hemodialysis were monitored for cardiac arrhythmias using ambulatory electrocardiographic recording. Atrioventricular dissociation was found in a patient with an elevated serum digoxin concentration, intradialytic supraventricular tachycardia had been present in a second patient during acute uremic pericarditis prior to the study. Ventricular premature beats (VPB) were absent or of low grade (occasional/uniform) in 14 patients and did not increase on dialysis. 3 patients had potentially dangerous VPB of higher grades (multiform, salvos or R on T) which occurred on or after dialysis in 2. 2 of these 3 patients were overdigitalized, and 2 had severe cardiac disease (amyloid, old myocardial infarction). Several other risk factors (age, hypertension, cardiac hypertrophy, smoking, hyperlipidemia, electrolyte changes) did not seem to be of importance for VPB. In these patients on maintenance hemodialysis, potentially dangerous VPB were rare and occurred mainly during or after dialysis in patients with preexisting heart disease and/or digitalization.

The Subxiphoid Approach to Pericardial Disease

During the 36-month period from July, 1978, through July, 1981, 25 patients underwent a subxiphoid pericardial window procedure for diagnosis and therapy. Twelve patients were operated on for uremic pericarditis, 6 for malignancy, and 7 for etiological diagnosis of the pericarditis. All 12 patients with renal failure had enlarging effusions, despite aggressive dialysis. Eleven of the 12 are alive, free from recurrence, 3 to 36 months postoperatively. Six patients were operated on for suspected pericardial malignancy with hemodynamic compromise. Histological diagnosis was made from the pericardial tissue in all patients; only 1 patient lived more than 43 days following the procedure. In the group of 7 patients operated on for diagnosis, 4 were thought preoperatively to have tuberculous pericarditis. All 4 were treated with antituberculosis chemotherapy and are asymptomatic, without evidence of calcification, 12 to 31 months postoperatively. This diverse group of patients demonstrates that the subxiphoid pericardial window is an effective approach for relief of uremic effusions and may adequately treat effusive tuberculous pericarditis when combined with multidrug chemotherapy. Patients with suspected malignant pericardial disease and hemodynamic compromise need to be carefully studied before an operative procedure is considered as a means of diagnosis and therapy.

Positive Epicardial Fat Pad Sign Without Pericardial Effusion-Reply

In Reply.— Drs Engle and Upham, in their conclusion, state that a positive EFPS may be present not only with a pericardial effusion but also with pericardial thickening. We agree; however, the sign is more commonly seen with pericardial fluid than with thickening. We agree that the EFPS is positive in the patient described, and we can only speculate as to why the echocardiogram is negative for pericardial fluid. Considering the patient's clinical findings, it seems most likely that he had uremic pericarditis. The history of chronic renal failure and the presence of a friction rub in January 1981 when the EFPS was positive and also three months earlier support the diagnosis of uremic pericarditis. In uremic pericarditis there is fibrinous exudate that often results in adhesions between the visceral and parietal layers of the pericardium. This can cause fluid to be loculated and, if it is loculated anteriorly, a

Management of Acute Cardiac Tamponade by Subxiphoid Pericardiotomy

Eighteen patients with cardiac tamponade were treated by subxiphoid pericardiotomy performed with the patients under local anesthesia. This group included 9 cases of uremic pericarditis (50%), 5 cases of metastatic cancer (28%), 2 cases of trauma (11%), 1 case of tuberculosis (5.5%), and 1 case of unknown cause. Immediate relief from acute cardiac tamponade was obtained in all 18 cases with only minor and self-limiting postoperative complications, including transient supraventricular arrhythmias (five cases) and fever (five cases). There were no deaths related to either the operative procedure or reaccumulation of the pericardial effusion. The drainage period averaged 9.6 days (range, three to 28 days). Pericardial biopsy was performed in 15 of 18 cases. We conclude that subxiphoid pericardiotomy is a safe and effective method for the management of pericardial effusion of diverse causes. The ability to perform this technique safely using local anesthesia and the capacity to obtain a biopsy specimen under direct visualization make this technique superior to both needle pericardiocentesis and pericardiectomy in the acutely ill patient.

Reflections on the role of carbon haemoadsorption in therapeutic medicine.

The selection of Norit RBX-1-activated carbon granules for blood detoxification by haemoadsorption is outlined. Synthetic polymer membranes have been coated on to this carbon by a specially developed process and perfusion devices prepared from these materials have been evaluated in animal models of acute poisoning and liver failure. Clinical application of carbon haemoadsorption has been explored in acute poisoning, liver failure and uraemia. The experience to date would suggest that carbon will have to be augmented by other adsorbent species before life support systems based principally on haemoadsorption become a reality especially in the treatment of uraemia and in liver failure. A secondary role as a temporary adjunct to dialysis has been established for carbon haemoperfusion in the treatment of uraemic pericarditis and is under further investigation in the treatment of pruritus, pigmentation and neuropathy.

Cimetidine clearance during intermittent and chronic peritoneal dialysis

A case report evaluating the clearance of cimetidine during intermittent peritoneal dialysis and chronic ambulatory peritoneal dialysis is presented. A 50-year-old white man with end-stage renal disease using chronic ambulatory peritoneal dialysis was hospitalized with uremic pericarditis. He was treated with indomethacin and aggressive intermittent peritoneal dialysis. Cimetidine 300 mg every 12 hours was prescribed for ulcer prophylaxis. After taking cimetidine for seven days, the clearance of cimetidine during intermittent peritoneal dialysis was evaluated by collecting blood and dialysate samples during a four-hour dialysis period. The patient was discharged using chronic ambulatory peritoneal dialysis. Cimetidine 300 mg every 12 hours was continued. One week after discharge, the clearance of cimetidine during a four-hour dwell period of chronic ambulatory peritoneal dialysis was measured. Cimetidine clearance was approximately 4 ml/min for both intermittent and chronic ambulatory peritoneal dialysis. Clinically unimportant quantities of cimetidine were removed by intermittent and chronic ambulatory peritoneal dialysis. The need for supplemental doses of cimetidine during peritoneal dialysis is not supported.

Metabolites of glucose in the blood of patients with renal failure.

The blood concentrations of pyruvate and of some of its metabolites and the red cell 2,3-diphosphoglycerate concentration were compared with the severity of uraemia in 103 patients with renal failure. In chronic renal failure 2,3-butylene glycol was distinctly elevated, and a positive linear correlation (2p Less Than 0.001) with the urea was found. The values were even higher in corresponding patients with uraemic pericarditis, but,--taking into account their relation to the urea--,they were not elevated in acute renal failure. Acetaldehyde, acetoin and acetate behaved in part likewise. Severe uraemia, which clinically was demonstrated by uraemic pericarditis, was characterized biochemically, without regard to the urea, by very elevated values of 2,3-butylene glycol and acetaldehyde and of the pyruvate: lactate ratio. In addition, the chronic patients who were not undergoing regular haemodialysis, did not show the expected rise of 2,3-diphospho-glycerate along with progressive anaemia. The data suggest that the uraemic state is characterized by the impairment of the oxidative glucose metabolism between pyruvate and the tricarbonic acid cycle more precisely than by the blood urea.

Pericarditis Pain in Uremic Patients-Reply

In Reply. —We appreciate Dr Spodick's comments regarding our observations on atherosclerosis as a possible cause of pain associated with uremic pericarditis. Appropriate testing for CPK and LDH did not indicate any elevation of the myocardial specific fraction. It should be noted, however, that the detection of such enzyme fractions does not necessarily rule out pericarditis as the underlying disease process. Profound subepicardial myocarditis has been increasingly recognized as a cause of elevated myocardial specific CPK and LDH fractions in subjects with pericarditis. In the usual case of isolated uremic pericarditis, this phenomenon generally is not observed. Dr Spodick's comments regarding relief by assumption of the upright position as equally characteristic of ischemic and pericardial pain are of great interest. Inspection of the leading textbooks of cardiovascular disease indicates that relief after sitting upright is characteristic of pericardial rather than ischemic pain. 1,2 Perhaps, some confusion concerning this point is related to