Profile of pericarditis in peritoneal dialysis: about 5 cases

Abstract

Cardiovascular complications are common in peritoneal dialysis patients, but acute pericarditis is a rare occurrence. Early and appropriate diagnosis and management of acute pericarditis are crucial to prevent serious complications such as cardiac tamponade. Although anti-inflammatory treatments are often effective, particular attention needs to be paid to adverse effects, especially in patients with renal impairment. Further studies are needed to better understand the underlying mechanisms and optimize therapeutic strategies for this patient population. In this article, we present five clinical cases of acute pericarditis among 239 peritoneal dialysis patients.

Introduction

Acute pericarditis is an inflammation of the pericardial leaflets with or without associated effusion. Subdialysis is the leading cause of pericardial effusion in patients with chronic end-stage renal disease.[1]Other etiologies may also be present, notably tuberculosis. Studies carried out in Morocco have shown a high prevalence of acute pericarditis in chronic hemodialysis patients, ranging from 1% to 7%, compared with the general population. [2,3,4] Our aim is to describe the clinical and paraclinical features of acute pericarditis in 5 patients with this condition in 239 peritoneal dialysis (PD) patients who have been followed in our hospital.

OBSERVATIONS

Clinical Case 1

A 35-year-old female hypertensive patient on continuous ambulatory peritoneal dialysis (CAPD) since 2020, with 3 exchanges per day (two 2.27% glucose solutions during the day + icodextrin solution at night). The measured dialysis dose was a total Kt/V of 0.87 and a weekly creatinine clearance (WCC) of 28 L/week/1.73 m2, nPCR at 0.6 g/kg/D.

The patient presented to the emergency department with acute left lateral chest pain, worsening on inspiration and in a supine position. She also had a recent flu-like illness. Physical examination revealed an apyretic patient who was tachycardic at 100 bpm, with BP of 170/100 mmHg; eupneic, with SpO2 of 98% on room air; with pericardial rub on auscultation; and with no signs of overload. The electrocardiogram (ECG) showed no ST segment or PR interval abnormalities. Chest X-ray revealed cardiomegaly (Figure 1).

Figure 1.(A) Chest X-ray from 2021. (B) Admission chest radiograph showing cardiomegaly (cardiothoracic index 0.8).

Trans Thoracic Echocardiography (TTE) revealed a 14-mm circumferential pericardial effusion of moderate size, with no right chamber involvement and a left ventricular ejection fraction (LVEF) of 68% (Figure 2.). Biological tests revealed an inflammatory syndrome (CRP 58 mg/L) and negative troponin at 21 ng/dL.

Figure 2.Subcortical (A) and apical (B) echocardiographic sections, showing a 14-mm pericardial effusion.

The diagnosis of presumed viral acute pericarditis was made in view of pericardial effusion + biological inflammatory syndrome + recent influenza-like illness. We decided to intensify dialysis and optimize ultrafiltration. The evolution after 3 weeks was marked by worsening chest pain and dyspnea in a context of deteriorating general condition. The biological findings were hyponatremia of 128 mEq/L and CRP of 141 mg/L. TTE examination revealed minimal pericardial effusion with fibrin and suspicion of incipient constrictive pericarditis. We were unable to perform a pericardial puncture, given the minimal abundance of the pericardial effusion. In view of this clinical picture (deterioration in general condition + effusion with fibrin + worsening

of inflammatory markers + hyponatremia) and our epidemiological context, a tuberculosis workup was requested, which came back negative. The patient began trial treatment with anti-bacillary agents at appropriate doses: quadritherapy for 2 months, then dual therapy with rifampicin-isoniazid, for a total of 6 months, with a favorable clinical and biological evolution, and CRP negativation at 2 mg/L after 1 month.

Clinical case 2

A male patient aged 23, on automated peritoneal dialysis since 2021 (APD: total volume 10 L, 4 cycles of 2 h, injection volume 2 L, final stasis 1 L, concentrations 2.27%). The measured dialysis dose was a total Kt/V of 1.35 and a WCCr of 38 L/week/1.73 m2, nPCR at 0.85. One week prior to admission, the patient presented with non-radiating retrosternal chest pain with dyspnea. An ECG and chest X-ray were performed, which came back unremarkable. With worsening chest pain and dyspnea, the patient was admitted to the emergency department. Clinical examination revealed tachycardia at 115 bpm, BP 140/90 mmHg, apyrexia, decreased heart sounds, orthopnea, SpO2 of 95% on room air, no crepitus rales, and no signs of right heart failure. ECG showed diffuse microvoltage. Chest X-ray revealed cardiomegaly (ICT 0.7) with hilar overload (Figure 3.). TTE showed a large circumferential pericardial effusion at 23 mm without collapse, with fibrin deposits, dilated IVC, and 50% LVEF (Figure 4.). A biological inflammatory syndrome was present, with CRP of 160 mg/L without hyperleukocytosis, and negative troponin 28 ng/dL. The patient underwent emergency pericardiocentesis, yielding 500 mL of hematic, exudate fluid (protein 56 g/L). Cytobacteriological examination, BK testing, and GeneXpert in the puncture fluid were negative, with no cells suspected of malignancy on pathology.

Figure 3.Chest X-ray showing cardiomegaly (ICT 0.7) with hilar overload

Figure 4.Subcutaneous TTE section showing a large pericardial effusion with fibrin

At the end of these workups, the etiological diagnosis of presumed viral acute pericarditis was retained with an overload component after eliminating other probable etiologies. We decided not to give anti-inflammatory treatment and to optimize ultrafiltration. The evolution was marked by a clear clinical and biological improvement, with regression of pain and resumption of feeding and patient autonomy. A follow-up TTE revealed significant resolution of the pericardial effusion after 1 month.

Clinical case 3

A 41-year-old male patient on CAPD since 2023 with 3 exchanges per day (two 1.36% glucose solutions during the day + 2.27% glucose solution at night). The measured dialysis dose was a total Kt/V of 1.59 and a WCCr of 52 L/week/1.73 m2, nPCR at 0.71 g/kg/D. Two days prior to admission, he presented with retrosternal chest pain, dyspnea, and unquantified fever. The patient was admitted to the emergency department in a state of respiratory distress, tachycardia of 127 bpm, BP of 140/110 mmHg, and muffled heart sounds, with no signs of right heart failure. The ECG was unremarkable.

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