Case Presentation: A 30-year-old Spanish-speaking male, initially emigrated from Guatemala over 10 years ago now homeless in Central Park with active HCV and severe alcohol use disorder, presented with 2-months of persistent frontal headache, subjective fevers, chills, and weight loss. Initial exam unremarkable except for a fever of 100.6°F, mild hyponatremia (132 mmol/L) and elevated AST (126 U/L). Lumbar puncture showed lymphocytic pleocytosis, elevated protein, and low glucose (Table 1). CSF AFB stains were negative, and the Xpert MTB/RIfPCR testing volume was insufficient. MRI Head revealed a 2×2 cm rim-enhancing lesion in the right frontal lobe with leptomeningeal enhancement. CT of the chest, abdomen, and pelvis showed numerous bilateral pulmonary nodules and mesenteric/retroperitoneal/cardiophrenic lymphadenopathy. Course complicated by acute deterioration of clinical status, found to be febrile and obtunded requiring emergent right craniotomy for brain abscess resection. Intraoperative findings suggested TB, and tissue analysis was AFB stain and culture positive but rifampin-resistance negative. Subsequent MRI brain showed multiple small infarcts and left frontal sulci/insular leptomeningeal enhancement, likely due to TB meningitis. Treatment included high dose dexamethasone for TB meningitis 5 mg IV every 6 hours (20 mg /day total), rifampin 600 mg IV daily (initially 1200 mg IV daily), isoniazid 300 mg oral daily with B6 supplementation, pyrazinamide 1500 mg oral daily, and ethambutol 1200 mg oral daily.
Discussion: Miliary tuberculosis (MT) with tuberculous meningitis (TBM) is a severe consequence of Mycobacterium tuberculosis dissemination to the central nervous system (CNS) and carries high mortality rate. While nonspecific TBM symptoms often delay diagnosis, in our case, the patient’s history of immigration and alcohol use disorder raised suspicion for both MT and TBM, initiating prompt diagnosis and treatment.Hospitalists must recognize that TBM with MT my present atypically in immunocompromised hosts, necessitating a rapid integrative approach. Diagnosis requires the synthesis of clinical findings, neuroimaging, and CSF analysis. While MRI is highly sensitive for leptomeningeal enhancement and tuberculomas, the low sensitivity of CNS molecular testing must not exclude a diagnosis. CSF analysis typically shows lymphocytic pleocytosis, high protein, and low glucose, as was seen in our patient.Treatment follows established guidelines which recommend a 9–12-month regimen of first-line anti-tuberculosis drugs, including isoniazid, rifampin, pyrazinamide, and ethambutol. Adjunctive corticosteroid therapy plays a crucial role in mitigating CNS inflammation and improving neurological outcomes. Regular monitoring for the development of drug resistance and potential adverse effects from treatment is also essential for optimal patient care.
Conclusions: Given the high mortality risk and potential for neurological sequelae, early and aggressive treatment and regular monitoring for the development of drug resistance is crucial for hospital medicine.
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