Acalculous Cholecystitis as an Atypical Presentation of Viral Pericarditis: A Case Report

Introduction

Pericarditis involves inflammation of the pericardial sac and is the most common disease of the pericardium seen in clinical practice [1]. Acute pericarditis in the Western hemisphere affects 27.7 per 100 000 people per year [1]. It commonly affects young and middle-aged individuals [2]. It is usually a benign and self-limiting disease, but in some cases complications such as cardiac tamponade, recurrent pericarditis, and permanent constrictive pericarditis occur [3]. The aetiology of pericarditis can include infectious or non-infectious causes. Viral infections are the most common, making up around 85% of all pericarditis cases [1]. Viral and idiopathic pericarditis are terms often used interchangeably, based on the assumption that the idiopathic cause has a presumed, but not proven, viral origin [3]. Other non-infectious causes include autoimmune, neoplastic, metabolic, and drug-related [3]. Diagnosis requires at least 2 of the following: pleuritic chest pain, pericardial friction rub, ECG changes, or presence of pericardial effusions [1].

Acalculous cholecystitis is acute inflammation of the gallbladder without the presence of gallstones [4]. It is a rare cause of cholecystitis, making up around 10% of all cholecystitis cases [5]. Typically, acalculous cholecystitis cases are seen in patients that are critically ill, intubated, or in a coma [6]. Clinically, these patients present with right upper-quadrant pain, fever, leukocytosis, and abnormal liver function tests [7]. However, it is difficult to diagnose and a combination of clinical symptoms with supportive imaging findings is usually required [4]. Ultrasound findings include a thickened gallbladder wall, no gallstones, and pericholecystic fluid [4]. Nonetheless, it is crucial to diagnose acalculous cholecystitis early, as it is associated with high mortality [8]. Definitive treatment with cholecystectomy is suggested if it can be performed [8].

In the literature, there are only a handful of cases in which acalculous cholecystitis and pericarditis presented simultaneously [9–14]. Concurrent presentation of these conditions is uncommon. In all described cases, a bacterial, rheumatological, or malignant etiology was found to be driving the presentation. Here, we present a unique case where a viral illness resulted in both pericarditis and acalculous cholecystitis. Unusually, the initial presentation of pericarditis was with clinical symptoms and imaging findings consistent with acute acalculous cholecystitis.

Case Report

INVESTIGATIONS:

Blood tests showed a normocytic normochromic anemia with hemoglobin 112 g/L (normal 130–170), mean corpuscular volume 93 fL (normal 80–99), mean corpuscular hemoglobin concentration 332 fL (normal 315–365), normal white cell count of 9.0×10⁹/L, (normal 4–12), and an elevated C-reactive protein 96.6 mg/L (normal <5). A mixed-picture mild derangement in liver function was found, with bilirubin 28 (normal <21), ala-nine transaminase 78 units/L (normal 5–40), aspartate transferase 54 units/L (normal 5–35), gamma-glutamyl transferase 84 units/L (normal 5–50), and alkaline phosphatase 108 units/L (30–110). Troponin was normal, at 3 ng/L (normal <20). Blood cultures revealed no growth, and urine culture was clear.

A chest X-ray showed the lungs and pleural spaces were clear, with no focal collapse or consolidation. A repeat abdomen ultrasound was performed, which demonstrated borderline gallbladder wall thickening, distended gallbladder, a small amount of pericholecystic fluid, and no gallstones (Figure 1). A CT chest, abdomen, and pelvis scan was performed, which revealed an incidental finding of a pericardial effusion and bilateral pleural collections, with no features of lymphoma. The known pericardial cyst was reduced in size. Subsequently, a transthoracic echocardiogram was performed, which demonstrated a moderately large circumferential pericardial effusion without definite evidence of tamponade (Figure 2). The pericardial effusion appeared to be organized with fibrinous strands in-situ, and the pericardium was also noted to be thickened. Left ventricular size and systolic function were normal, and there was a possible finding of impaired apical right ventricular function.

Due to ongoing fevers, more bloods tests were conducted. D-dimer was elevated at 3999 ng/mL (normal <500), and a subsequent ventilation perfusion scan was negative for pulmonary embolus. Infectious diseases screening for cytomegalovirus, coronavirus, Epstein-Barr virus, hepatis A/B/C, human immunodeficiency virus, and QuantiFERON mycobacterium tuberculosis was negative. Polymerase chain reaction tests for respiratory viruses, including influenza A/B, respiratory syncytial virus, rhinovirus/enterovirus, parainfluenza, adenovirus, human metapneumovirus, and Bordetella parapertussis were also negative. Rheumatological tests assessing for antinuclear antibody, antineutrophil cytoplasmic antibodies, rheumatoid factor, complement 3/4, and angiotensin-converting enzyme levels were all negative.

Despite initiating treatment for pericarditis, his fevers continued; there were concerns for sepsis, and a pericardial window was planned. A transoesophageal echocardiogram was performed, showing an adherent inflammatory mass between the pericardium and myocardium, which was fused at the apex of the left ventricle. Therefore, due to limited access, only a diagnostic pericardial and pleural biopsy was taken. Pericardial tissue biopsy showed non-specific changes, with no growth and negative cytology. A left pleural biopsy showed non-specific inflammatory/reactive changes and no growths.

TREATMENT:

On admission, the patient was treated with IV Augmentin as empiric treatment for intra-abdominal infection for his cholecystitis. Due to suboptimal response to antibiotics and imaging findings suggestive of an underlying viral pericarditis, he was started on colchicine 500 µg BD and ibuprofen 400 mg TDS, and antibiotics were stopped. Ibuprofen was stopped after 1 week and colchicine was continued for 3 months. He was discharged home on day 12 of admission after extensive investigations.

OUTCOME AND FOLLOW-UP:

The patient was seen in an outpatient clinic 3 weeks after discharge. He had made a complete recovery, with resolution of his symptoms. A repeat outpatient echocardiogram showed no pericardial fluid and preserved cardiac function. A repeat chest CT was performed and demonstrated no pleural or pericardial effusion, and complete resolution of the right pericardial cyst. He continued to prophylactically take colchicine for 3 months in total to minimize the risk of recurrence.

Discussion

There are 7 documented cases where pericarditis and acalculous cholecystitis present simultaneously [9–15]. Four of these cases involved rheumatological conditions, including systemic lupus erythematosus and Churg-Strauss Syndrome [10,11,14,15]. The patients were all women aged 21–38 years, who presented with a variety of symptoms, including fever, pleuritic chest pain, abdominal pain, and shortness of breath. All but 1 patient had no significant medical or prior history of autoimmune conditions. Two patients underwent more extensive investigation, with one receiving a laparoscopic cholecystectomy and the other required intubation and a pericardial window [10,11]. All patients responded to steroid treatment, with resolution of symptoms.

In 2 other cases, infections were implicated. A young woman developed a parasitic infection caused by Ascaris lumbricoides after consuming fresh vegetables prior to onset of abdominal pain [13]. Another case involved a young man who was diagnosed with leptospirosis after travelling to areas where there were recent cases of similar infections [12]. Lastly, a case of pulmonary carcinoma was confirmed through pericardial biopsy in a patient experiencing both conditions [9].

Our patient was a previously healthy, middle-aged man who presented with ultrasound findings of gallbladder distention and pericholecystic fluid. These radiological findings suggest a diagnosis of acalculous cholecystitis [4]. Furthermore, comprehensive investigation was done with our patient given his ongoing fevers and weeks of systemic symptoms prior to admission. All investigations for rheumatological, malignant, and bacterial causes were all negative. This is in contrast with cases previously described. Recurrent pericarditis is also unlikely in this context, as cases typically reoccur within 18 months [16]. Furthermore, our patient had a history of a pericardial cyst. These are uncommon, occurring in only 1/100 000 of the population, with most being asymptomatic [17]. It is unclear whether the cyst contributed to this presentation, but it was noted that the cyst resolved on interval serial imaging. There are case reports of spontaneous resolution of pericardial cysts without intervention [17]. Given our patient’s history of a viral illness, good response to colchicine, and a pericarditis episode 10 years before, it is likely that an isolated acute virus led to both the pericarditis and acalculous cholecystitis.

This case demonstrates the need to maintain a high index of suspicion in patients who present with acalculous cholecystitis and pericarditis. The literature indicates viral infections such as Epstein-Barr, coronavirus, hepatitis A/B, dengue, cytomegalovirus, and some upper respiratory viruses can result in acalculous cholecystitis in healthy individuals [18–21]. The exact pathogenesis is unclear, but a recent case report proposed cytokine release syndrome as the underlying mechanism [18]. This was in a patient who recovered from coronavirus infection, with many other similar documented cases [7,18]. Viruses implicated in acalculous cholecystitis such as Epstein-Barr virus are also associated with viral pericarditis [22]. It is possible that a dysregulated inflammatory response mediated through cytokine release resulted in systemic inflammation of both the gallbladder and pericardium, potentially explaining the co-existence of these conditions.

Conclusions

Simultaneous presentation of acalculous cholecystitis and pericarditis is uncommon, and it is essential to investigate other potential underlying conditions. Our case highlights an atypical presentation of acute viral pericarditis with acalculous cholecystitis. Recognizing this is crucial, as management for these conditions differs significantly – acalculous cholecystitis often requires more invasive interventions, while pericarditis is typically managed with non-steroidal medications. Notably, our case report is one of the few in which both these conditions appeared without a clear underlying rheumatological, malignant, or bacterial cause.