A 49-year-old man, smoker of 12 cigarettes a day and ex-drinker for 3 years. He came to the emergency department for presenting progressive dyspnoea in the previous days, accompanied by oedema, dizziness and syncope, without accompanying chest pain or orthopnoea. The relevant history included a case of infective endocarditis on a myxoid mitral valve, complicated by valve perforation and severe mitral insufficiency, initially treated with antibiotics and subsequently with replacement of the mitral valve with a mechanical prosthesis by sternotomy. He was discharged 10 days before the current admission on treatment with acenocoumarol, bisoprolol, furosemide and amiodarone. Examination revealed a fair general condition, arterial hypotension (TAS 90 mmHg), jugular ingurgitation and hepatomegaly of 3 fingerbreadths.
Laboratory tests showed a significant elevation of transaminases (AST: 5,550 U/L; ALT: 3,826 U/L) and LDH (10,375 U/L), with slightly elevated bilirubin levels (2 mg/dL). He also had anaemia (Hb: 9.2 g/dL), impaired renal function (Cr: 1.76 mg/dL; urea 88 mg/dL) and an I.N.R. of 9.86. Serologies for HAV, HBV, HCV, HIV, EBV, CMV and autoimmunity were negative. Ingestion of drugs and other hepatotoxic products was ruled out.
The electrocardiogram showed no alterations of interest and the ultrasound showed marked hepatomegaly with diffuse alteration of echogenicity related to steatosis, and the hepatic vascular study was normal.
Given the suspicion of a possible cardiac origin of the clinical picture, an echocardiogram was performed which confirmed the presence of massive pericardial effusion, predominantly in the free wall of the right ventricle, where it reached 60 mm thick, and in the left ventricle with 29 mm thick. The right ventricle as well as the initial portion of the pulmonary artery appeared completely collapsed, evidence of severe echocardiographic tamponade.

In view of these findings, the patient was transferred to the Coronary Unit where diagnostic and evacuative pericardiocentesis was performed using an anterior approach (3rd left parasternal intercostal space) with extraction of 600 cc of haemorrhagic fluid, leaving a slight effusion located at the apical level (encapsulated). Samples were sent for biochemistry, microbiology and cytology, confirming a haematic effusion with a haematocrit higher than the plasma haematocrit, with the microbiological study and cytology being normal. At the same time, corticosteroid treatment was started with a good clinical response. Laboratory tests showed normalisation of creatinine levels (0.72 mg/dL) and a progressive decrease in transaminase values (AST: 304 U/L; ALT: 227 U/L) and LDH (568 U/L). Prior to discharge, a control echocardiogram was performed which showed mild pericardial effusion of fibrinous appearance, loculated, asymmetrically distributed, predominantly located at the anterior level and apex of the right ventricle, with no evidence of haemodynamic compromise. Given the good clinical and analytical evolution, liver biopsy was not necessary and he was diagnosed with ischaemic hepatitis due to low cardiac output in relation to cardiac tamponade secondary to post-pericardiotomy syndrome with haemorrhagic transformation.