Blood Culture-negative Infective Endocarditis with Fatal Ischaemic Hepatitis in a Patient on Antitubercular Therapy: A Case Report

Infective Endocarditis (IE) in patients receiving Antitubercular Therapy (ATT) is easily missed, because rifampicin can sterilise blood cultures and blunt the febrile and inflammatory response, delaying recognition until multiorgan failure is already established. The present case report is of a 45-year-old male in the fourth month of HRZE (isoniazid, rifampicin, pyrazinamide, ethambutol) ATT for pulmonary tuberculosis who presented afebrile with a two-day history of dyspnoea and haemodynamic collapse. Emergency physician bedside Point-Of-Care Ultrasound (POCUS) showed a collapsible Inferior Vena Cava (IVC), an ejection fraction of 35%, a thickened calcified aortic valve with a mobile vegetation, severe aortic regurgitation, and moderate functional mitral regurgitation. Initial Arterial Blood Gas (ABG) showed pH 7.19 and lactate 15 mmol/L; over the next five hours the acidosis worsened (pH 7.12) although lactate was 12.8 mmol/L, despite initial supportive measures. Following IVC-guided fluid resuscitation, vasopressor optimisation, and Intermittent Haemodialysis (IHD) from day 3, lactate improved to a nadir of 5.1 mmol/L on day 3 before re-rising to 8.9 mmol/L by day 5, paralleling progressive multiorgan failure. Serum Glutamic-Oxaloacetic Transaminase (SGOT) was 7,279 IU/L (182 times the upper limit of normal) at presentation, indicating pre-arrival ischaemic hepatitis, and exceeded 20,000 IU/L by day 2. Two pre-antibiotic blood culture sets remained negative for growth at 96 hours (Day 4) of incubation, consistent with probable rifampicin-associated blood culture-negative endocarditis. The patient died on day 5 after a cardiac arrest unresponsive to resuscitation. This case demonstrates that IE on a tuberculosis-predisposed calcified valve can present afebrile with extreme hyperlactataemia and established ischaemic hepatitis, and that an early lactate-clearance response does not preclude terminal re-deterioration once hepatic and multiorgan failure are structurally established.