Disseminated Tuberculosis and Takayasu Arteritis: A Fatal Case of Infectious Aortic Pseudoaneurysm
Fatal Aortic Pseudoaneurysm Unfolds in Young Patient With Suspected Takayasu Arteritis and Disseminated Tuberculosis
A 25-year-old agricultural worker from Nepal living in Portugal died following a massive gastrointestinal hemorrhage caused by an infectious aortic pseudoaneurysm, a fatal complication that developed while he was undergoing treatment for disseminated tuberculosis and pre-existing vascular disease, Cureus reported. The case highlights the severe diagnostic and therapeutic hurdles physicians face when managing destructive vascular infections in patients with chronic large-vessel vasculopathy.
- The patient had a history of renal artery stenosis diagnosed at age 17, which required bilateral renal artery stenting, raising strong clinical suspicion of underlying Takayasu arteritis.
- Microbiologic evaluation confirmed smear-positive pulmonary tuberculosis, prompting the initiation of standard first-line antituberculous therapy.
- Despite hospitalization at a tertiary center, the patient declined surgical intervention and vascular investigation, leading to fatal aortic rupture nine days later.
Patient Presents with Cough and Severe Vascular Occlusions
The patient presented to the emergency department with a subacute history of a progressively worsening cough, persistent fever, anorexia, asthenia, and mid-back pain that shifted to the right hypochondrium. Initial computed tomography angiography revealed diffuse reticulonodular pulmonary infiltrates featuring apical cavitary lesions, calcified mediastinal lymphadenopathy, and bilateral pleural effusions. Abdominal Doppler ultrasonography subsequently demonstrated critical stenosis of the celiac trunk, occlusion of the superior mesenteric artery, and bilateral renal artery occlusion. Transthoracic echocardiography revealed severe dilated cardiomyopathy with an estimated left ventricular ejection fraction of approximately 23 percent.
Cureus noted that the combination of early-onset renovascular hypertension, extensive multivessel arterial stenoses, and heavy aortic calcification heavily pointed toward underlying Takayasu arteritis. Meanwhile, a large periaortic collection measuring 80 by 35 millimeters, located inferior to the origin of the celiac trunk, displayed peripheral enhancement and disruption of adjacent intimal calcifications. These imaging features strongly suggested an infectious aortic pseudoaneurysm linked to active tuberculosis.
Autopsy Confirms Disseminated Necrotizing Granulomatous Disease
One month following his admission, the patient transferred to a tertiary center for vascular surgical assessment, where he ultimately refused further diagnostic workups and surgical intervention. During subsequent inpatient care, he remained febrile until experiencing sudden-onset abdominal pain, massive gastrointestinal hemorrhage, severe metabolic acidosis, and refractory shock. Cardiac arrest and death followed rapidly.
An autopsy confirmed disseminated necrotizing granulomatous disease affecting the lungs, kidneys, and aortic wall. Histopathological examination of lung tissue showed epithelioid granulomas with central necrosis and multinucleated giant cells. The aortic wall exhibited transmural arteritis featuring prominent neutrophilic infiltration, microabscess formation, and tissue necrosis. While histochemical stains performed on tissue samples yielded inconclusive results due to autolytic artifacts, the combination of microbiologically confirmed pulmonary tuberculosis and destructive aortic inflammation established the diagnosis of infectious aortitis.
Differentiating Overlapping Vascular Pathologies
The relationship between tuberculosis and Takayasu arteritis remains a subject of ongoing clinical debate in medical literature. A separate case report published in PMC examining a 10-year-old Tunisian child with childhood-onset Takayasu arteritis and concomitant pulmonary tuberculosis reinforces the recognized association between mycobacterial infection and chronic granulomatous large-vessel vasculitis. PMC-indexed literature highlights that abnormal immune responses to mycobacterial antigens and potential cross-reactivity involving heat shock proteins may contribute to vascular pathogenesis, though a direct causal link remains unproven.
In the fatal adult case reported by Cureus, clinicians confronted an intricate overlap where pre-existing large-vessel vasculopathy compromised the structural integrity of the aorta. Because infectious aortitis and inflammatory large-vessel vasculitis produce remarkably similar clinical and radiological findings, distinguishing between primary vasculopathy and secondary mycobacterial destruction remains exceptionally difficult. Management of tuberculous aortic pseudoaneurysms typically requires a dual strategy combining prolonged antituberculous drug regimens with definitive open surgical repair or endovascular intervention. The patient’s refusal of vascular intervention precluded surgical repair, leaving the destructive pseudoaneurysm untreated.
Autopsy results confirmed transmural aortitis with extensive tissue necrosis, but autolytic artifacts prevented the direct microbiological isolation of Mycobacterium tuberculosis within the aortic wall itself, leaving open the precise local mechanism of arterial destruction.
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