A 29–year–old African American male with no prior medical history was admitted to the hospital with substernal chest pain and cough with minimal expectoration for the past 3 months. He reported a 25 lb unintentional weight loss and subjective fever without chills or night sweats for a week. He denied any prior blood transfusion, smoking, alcohol or IV drug use. On exam he was afebrile, tachycardic at a rate of 111. Oxygen saturation was 93% on room air. He was delirious yet able to follow commands. He had bilateral axillary lymphadenopathy, bibasilar rales, no neck rigidity or focal neurological signs. His initial blood work was normal. Arterial blood gas analysis showed hypoxemia with respiratory alkalosis. Chest x–ray revealed consolidation in the right upper lobe. High resolution CT chest confirmed multifocal infiltrates and cavitary lesion in the right upper lobe. Bronchoscopy was negative for AFB, viral, bacterial and fungal stains. CT head with contrast showed two ring enhancing lesions compressing fourth ventricle and cerebellum along with hydrocephalus. The lesions were 1.7 cm and 1.9 cm in size respectively. Two days after admission he became obtunded and developed right occulomotor palsy. Neurosurgery was consulted and ventriculostomy was placed. Empiric TB treatment along with steroids were started based on the clinical presentation and CSF analysis showing lymphocytic predominance. Subsequently, workup was positive for HIV with CD4 count of 172 cells/cmm. His toxoplasma, histoplasma, EBV serologies and flow cytometry were all negative. Brain biopsy was pursued for definitive diagnosis and pathology showed caseous necrosis with multinucleated langerhans giant cells and acid fast bacilli consistent with tuberculosis. Subsequently, his clinical condition improved and antiretroviral therapy was initiated. His AFB cultures from bronchoalveolar lavage came back positive after 6 weeks. Patient was discharged with anti–TB regimen, HAART therapy and bactrim for PCP prophylaxis.
There are many potential etiologies for CNS mass lesions in patients with HIV: bacterial, mycobacterial, fungal, parasitic, neoplastic including lymphoma. Stereotactic brain biopsy is the gold standard for the diagnosis of focal CNS lesions in AIDS when the diagnosis cannot be made by clinical acumen and laboratory data. Our patient had serological evaluations which were negative and hence biopsy was pursued for definitive diagnosis.
This case reinforces the need to pursue aggressive evaluation in patients with CNS mass lesions associated with HIV. Often, the differential is so broad that empiric treatment alone is not recommended. The mortality in tuberculomas is 5–60% and can be avoided by timely approach. Our case proves that early diagnosis by tissue biopsy helped in guiding us towards providing a more accurate treatment plan, avoiding any delay in care.