Diagnostic delay in ankle and foot tuberculosis resulting in tuberculoma and tuberculous meningitis in a middle-aged female: A case report

Abstract

A middle-aged woman presents with chronic foot arthritis which progressed to a non-healing ulcer, which was unresponsive to conventional antibiotics and debridement. She then developed cerebral manifestations and was empirically treated with antitubercular medications which led to healing of the ulcer. Unfortunately, delays in initiating treatment resulted in development of other extrapulmonary tuberculosis complications such as cerebral tuberculoma with tuberculous meningitis. She was subsequently diagnosed with neurocysticercosis which continued to worsen during her hospital stay. She eventually succumbed to her illness due to the complications and a possible nosocomial infection. This case highlights the challenges with diagnosis of uncommon presentations of common diseases in an endemic area, leading to diagnostic delays and development of serious complications.

Keywords: Extrapulmonary tuberculosis; ankle and foot tuberculosis; tuberculoma; tuberculous meningitis.

Figure 1.

MRI of the right lower extremities showed thick fluid collection with heterogeneous signal intensities (complex collection) in subtalar joint and signal changes in most hind foot bones and some midfoot. There was narrowing of the tibiotalar joint space and destruction of the tibial subchondral bone (at the tibia talar dome), talus bone, and the fibular lateral malleolus. Tibial, fibular, talus, and mild calcaneus bone marrow edema surrounding the tibial lesions was seen with edematous infiltration of the per malleolar soft tissues with skin discontinuation suggesting an ulcer. There was diffuse marrow infiltration in the distal tibial (epiphysial-metaphyseal region), talus and distal epiphysis of fibula. MRI: magnetic resonance imaging.

Figure 2.

Yellowish cheese-like discharge seen after debridement of the ankle ulcer.

Figure 3.

MRI brain showing few punctate focal lesions involving the cerebral hemispheres, brainstem, and cerebellum. The lesions were isointense on T1 and had high signals on T2/FLAIR. There was a lesion in the right cerebellum showing low T2/FLAIR intensity center with peripheral hyperintensity and mild surrounding edema which showed ring enhancement after contrast administration (white arrow). There was no significant mass effect. MRI: magnetic resonance imaging.

Figure 4.

Non-contrast brain CT showing effacement of cerebral sulci and basal cisterns consistent with brain edema. There was leptomeningeal enhancement marked in the right occipital lobe and the cerebellum. CT: computed tomography.

Figure 5.

Brain MRI revealed dilatation of the ventricular system with widening of the temporal horns, due to communicating hydrocephalus. Post-contrast images demonstrated thick nodular leptomeningeal enhancement predominantly in the basal cisterns. MRI: magnetic resonance imaging.

Figure 6.

Brain MRI revealing left caudate hematoma, ventriculomegaly, prominent cerebrospinal fluid (CSF) at the fourth ventricle extending inferiorly to posterior of foramen magnum. There were multifocal intracranial hypodense lesions with associated multifocal calcifications—most likely neurocysticercosis. MRI: magnetic resonance imaging.

Figure 7.

CT-pulmonary angiography revealed pulmonary embolism with dilated right atrium and mild contrast backflow to inferior venacava (IVC), consistent with signs of pulmonary hypertension. CT: computed tomography.