Tuberculosis Reactivation Following Plasmapheresis and Perioperative Intravenous Immunoglobulin for Heparin-Induced Thrombocytopenia and Mechanical Mitral Valve Replacement

Abstract Tuberculosis (TB) remains the leading infectious cause of death worldwide despite international efforts to eliminate it. Approximately 25% of the world population has a latent tuberculosis infection (LTBI), and 80% of new TB diagnoses in the US are due to reactivation. The reported incidence of TB in Micronesia is 53/100,000. While the tuberculin skin test (TST) provides high sensitivity and modest specificity for LTBI screening, newer screening methods like Interferon-gamma release assay are limited by modest sensitivity despite a higher level of specificity. Therefore, LTBI reactivation accounts for a significant number of active TB cases, highlighting the importance of screening, diagnosis, and treatment in high-risk patients/populations. We present a case of a 50-year-old Asian female from Micronesia, who had a prolonged hospitalization for severe mitral regurgitation with group 2 pulmonary hypertension and right ventricular failure, secondary to rheumatic heart disease, requiring mechanical mitral valve replacement. Her preoperative course was complicated by Serotonin release assay (SRA) negative heparin-induced thrombocytopenia (HIT) which was treated with plasmapheresis (PLEX) and perioperative intravenous immunoglobulin (IVIg). Post-operatively, the patient's clinical course was complicated with recurrent fevers and acute hypoxic respiratory failure requiring reintubations and tracheostomy. Despite empiric treatment for suspected ventilator-associated pneumonia (VAP), and confirmed mycoplasma pneumonia with doxycycline, her recurrent fevers persisted. One week after discharge, she was readmitted for tracheostomy site bleeding. A computed tomography (CT) scan of her chest for persistent fevers not responding to appropriate antibiotics revealed findings consistent with miliary TB. Subsequent sputum and CSF cultures/polymerase chain reaction confirmed diagnoses of pulmonary TB and TB meningitis. Abdominal imaging and colonoscopy demonstrated a psoas abscess and possible ileocecal TB. Anti-tubercular and steroid therapy initially provided positive outcomes. However, appropriate anticoagulation was hindered by reoccurring arterial GI bleeds in the setting of suspected ileocecal TB. Our patient's TB reactivation is likely multifactorial, with contributing factors including PLEX, IVIg, and surgically induced stress response. Prior research has demonstrated a 48% incidence rate of infection following treatment with PLEX, with approximately one-third (31%) developing septic shock. Her misleading symptoms and lack of CT imaging until after readmission likely contributed to the delayed diagnosis and prolonged hospital course. This case illustrates the importance, and potential benefit of, infectious disease screening in high-risk LTBI patients from TB endemic areas before undergoing immunosuppressive therapies or cardiopulmonary bypass. Early consideration, identification, and intervention of LTBI may help prevent devastating outcomes secondary to TB reactivation.