Purulent Pericarditis in End-Stage Renal Disease: A Rare Case of Citrobacter freundii Infection

Background: Purulent pericarditis is a rare but life-threatening condition, particularly challenging when it occurs in immunocompromised individuals. Case report: We present the case of a 68-year-old man with end-stage renal disease who developed purulent pericarditis secondary to Citrobacter freundii infection. Despite initial challenges in diagnosis and management, the patient showed a favorable response to antibiotic therapy. Conclusions: This case highlights the importance of prompt recognition and treatment of purulent pericarditis, especially in patients with underlying immunosuppression and comorbidities.


Introduction
Acute pericarditis is the most prevalent inflammatory heart disease, being more common than acute myocarditis and acute endocarditis [1] and being responsible for 5% of non-ischemic chest pain in emergency departments [2].Although generally manifesting with a benign and self-limited course, there are cases where short-term complications arise, with the most serious and potentially fatal being cardiac tamponade due to rapid expansion of the pericardial effusion compromising cardiac chamber filling and impairing adequate cardiac output [1,3].
In developed countries, 80-90% of acute pericarditis cases are idiopathic, most likely of viral etiology [2].The remaining cases are divided among pericarditis associated with connective tissue diseases, post-myocardial infarction pericarditis, and neoplastic pericarditis [2].Purulent pericarditis, once much more prevalent before the advent of antibiotic therapy, has become increasingly rare [4].Among purulent pericarditis cases, the most frequently isolated bacteria are Gram-positive cocci, specifically Staphylococcus spp.and Streptococcus spp.[4].Although rare, purulent pericarditis is a severe form of pericarditis characterized by the presence of pus in the pericardial sac.It usually results from bacterial infections and can rapidly progress to life-threatening conditions if not promptly treated.
We present a case of a 68-year-old man with known chronic pericardial effusion experiencing exacerbation of symptoms and developing obstructive shock due to cardiac tamponade.

Case Presentation
A 68-year-old man with end-stage renal disease (ESRD) had multiple emergency department (ED) visits for chest pain for the past two months.Acute coronary syndrome was always excluded, and the pain was interpreted as secondary to musculoskeletal pathology.The patient's medical history is significant for hypertension and autosomal dominant polycystic kidney disease (ADPKD), and he has a relevant family history, with his father also affected by the last condition.The patient's usual medications included antihypertensives (Nifedipine and losartam), phosphate binders (sevelamer), erythropoiesis-stimulating agents (darbopoietin), and vitamin D supplementation (calcitriol).
The patient returned to the ED due to a new episode of precordial chest pain with pleuritic characteristics.Additionally, he reported an isolated fever episode accompanied by anorexia and generalized myalgias.During evaluation in the emergency department, he experienced a syncopal episode.On physical examination, the patient was hypotensive, with a blood pressure of 69/53 mmHg, a heart rate of 112/min, a temperature of 37.2ºC, and a respiratory rate of 15/min.The patient also had muffled cardiac sounds and lower limb edema, and, upon evaluation by cardiology with point-of-care ultrasound (POCUS), a largevolume pericardial effusion was noted.
Analytically, there was an elevation of liver enzymes consistent with ischemic hepatitis (aspartate aminotransferase of 9716 U/L [laboratory reference values 12-40 U/L]; alanine aminotransferase of 4620 U/L [laboratory reference values 7-40 U/L]) and a slight elevation of myocardial necrosis markers (Troponin I of 0.057 ng/mL [laboratory reference values <0.045 ng/mL]).Additionally, there was an elevation of inflammatory parameters, namely reactive C protein, of 137.70 mg/L.The detailed laboratory findings are presented in Table 1.

Lab values Reference values
Peripheral  The patient underwent an ECG in the emergency department, which revealed atrial fibrillation with a rapid ventricular response without signs suggestive of acute ischemia or electrical alternans.
Two weeks before, he was evaluated by cardiology, who identified a small-volume pericardial effusion and bilateral pleural effusion, both attributed to hypervolemia secondary to his ESRD.
Thoracoabdominopelvic CT scan (Figure 1) confirmed a pericardial effusion with a maximum thickness of 3.9 cm and small sub-centimetric hepatic cysts without other occupying lesions, as well as a small volume of ascites.Given this clinical picture, the patient was admitted to the intensive care unit (ICU) with the diagnosis of obstructive shock secondary to cardiac tamponade due to acute perimyocarditis of uncertain etiology complicated by ischaemic hepatitis.During the stay in the ICU, the patient remained hypotensive, requiring noradrenaline support for six days (maximum dose of 0.6 mcg/kg/min).Pericardiocentesis was performed, with the drain remaining in place throughout the patient's ICU stay.On the sixth day, due to an improvement in blood pressure, the patient was transferred to the internal medicine ward.Subsequently, the results of the pericardial fluid laboratory study were obtained, revealing 4288 cells/μL (72% neutrophils), and cytological examination showed abundant neutrophils consistent with purulent pericarditis.Microbiological culture of the pericardial fluid isolated Citrobacter freundii.The patient was initiated on piperacillin-tazobactam treatment, which was later adjusted based on his antimicrobial susceptibility profile to cotrimoxazole.
After initiation of antibiotic therapy as well as a combination of acetylsalicylic acid and colchicine, it was possible to remove the pericardial drain (total drainage of 4445 mL over nine days, removed three days after the transfer to the internal medicine ward).The removal of the pericardial drain was prompted by the progressively decreasing volume of pericardial fluid drainage, which suggested a favorable clinical evolution.Further investigation for infectious causes of pericarditis and immune-mediated pericarditis is summarized in Table 2.The laboratory findings revealed slight complement C3 consumption and serological testing indicated past exposure to hepatitis A, Epstein-Barr virus, and parvovirus B19 and were not compatible with the recent infection.In a follow-up evaluation, the patient remained asymptomatic for four weeks after continuing antibiotic therapy.A subsequent POCUS revealed only a thin layer of pericardial effusion, indicating a favorable resolution of the condition.

Discussion
This case reports purulent pericarditis due to a Citrobacter freundii infection of the pericardial fluid.This diagnosis, severe in itself, is compounded by the fact that it occurred in an immunocompromised patient [3,4] who was also hypervolemic due to ESRD, which predisposed the superinfection of the pericardial fluid.The accumulation of pus in the pericardial space increased intrapericardial pressure to such an extent that it restricted cardiac chamber filling, reducing cardiac output (cardiac tamponade), thereby explaining the syncope due to cerebral hypoperfusion and the development of secondary ischemic hepatitis.Blood pressure and liver enzyme levels improved as the pericardial effusion was drained, but it was observed that the pericardial effusion recurred daily, with over 4 liters of pericardial fluid drained over nine days.
The favorable response to antibiotic treatment, coupled with the isolation of Citrobacter freundii in the pericardial fluid, makes the diagnosis of purulent pericarditis highly probable.Regarding the etiological agent, it is known to be a gram-negative bacterium of the Enterobacteriaceae family, which is associated with infections in patients with known comorbidities and immunocompromised patients [5], as in this particular case.Furthermore, there is a reported case of cardiac tamponade associated with purulent pericarditis caused by this microorganism, which occurred in a pediatric 10-year-old individual [5].
This case further emphasizes the critical importance that the treatment of acute pericarditis always presupposes identifying the underlying cause for a more appropriate approach to this pathology.As demonstrated in this case, pericardiocentesis is a vital diagnostic tool for determining the etiology, as documented in the literature through different clinical case reports [6][7][8][9].

Conclusions
Purulent pericarditis remains a rare but serious complication, particularly in immunocompromised patients.
Early recognition and aggressive management, including appropriate antibiotic therapy and drainage of pericardial effusion, are crucial for favorable outcomes.This case underscores the need for a high index of suspicion, thorough diagnostic evaluation, and a multidisciplinary management approach in similar clinical scenarios.Furthermore, it highlights the critical importance of identifying the etiology of pericarditis to guide targeted treatment strategies and prevent recurrence and complications.Addressing underlying immunosuppression and comorbidities is essential for comprehensive management and improved patient outcomes.

FIGURE 1 :
FIGURE 1: A coronal section of the thoracoabdominopelvic CT scan demonstrated pericardial enhancement compatible with active inflammation as well as a markedly large pericardial effusion.