Miliary Tuberculosis Presenting With GI Bleed From Hepatic Artery Pseudoaneurysm Rupture in an HIV Infected Patient

Abstract

INTRODUCTION: Miliary tuberculosis (TB) is more common among HIV infected patients. However, hepatic artery pseudoaneurysms are extremely rare. This is the first reported case of a hepatic artery tuberculous pseudoaneurysm in an HIV-infected patient. CASE PRESENTATION: A 35 year old homosexual male from Mexico, HIV-positive, with CD4 count of 74 cells/mcl presented with a one year history of weight loss, and 6 months of daily fevers, shaking chills, abdominal pain and distention. One week prior to presentation he developed non-productive cough and dyspnea. On admission, he was ill appearing, with rigors, fever and tachycardia. A chest radiograph showed bilateral reticulonodular infiltrates and an air fluid level projecting over the T-12 vertebral body. Computed tomography (CT) revealed innumerable pulmonary nodules, a 5.3 x 3.7 cm fluid collection in the porta hepatis region with pneumoblia and diffuse retroperitoneal lymphadenopathy. Miliary TB was suspected and empiric therapy was started on hospital day 3. TB skin test resulted in 0 mm of induration and three sputum samples were negative for acid fast bacilli (AFB). CT-guided aortocaval lymph node biopsy revealed granulomas and numerous AFB. Nucleic acid amplification test revealed TB and the culture grew Mycobaterium tuberculosis 16 days after biopsy. Interferon Gamma Release Assay for TB obtained on day 6 was positive. The patient improved until hospital day 12, when he suddenly experienced severe epigastric pain followed by hematemesis, fever and shock. CT demonstrated a new bilobed pseudoaneurysm originating from the hepatic artery traversing the previously noted porta hepatis fluid collection, associated with hemobilia. Two stents were placed across the neck of the pseudoaneurysm extending along the right hepatic artery followed by coil embolization. The patient improved with antituberculous therapy and started antiretroviral treatment 45 days later. DISCUSSION: TB involvement of the hepatic artery may have resulted from ingested mycobacteria traversing the intestinal wall and lymphoid tissue and causing caseous necrotic lymphadenopathy adhering to the porta hepatis region. Effective treatment requires vascular repair and antituberculous therapy. In patients with shock, endovascular placement of stents and microcoil embolization may lead to superior outcomes compared with open surgical intervention. Antituberculous therapy should be started as soon as tuberculosis is suspected and continued for 6 to 9 months. CONCLUSIONS: Vascular lesions due to TB should be considered in patients presenting with pain and suspected TB infection. Early diagnosis and institution of surgical and medical treatment is essential.