KE, a 23-year-old male prisoner, was referred to Mulago Hospital for specialized treatment after failure to improve during 3 days of management at the Murchison Bay Prison Referral Hospital where he was admitted with a history of new onset of left upper limb weakness. He had a past history of pulmonary tuberculosis and was on the continuation phase of anti-TB treatment. His present history included two weeks of a mild headache, convulsions, confusion, and limb weakness that was most pronounced in the left upper limb. On admission, he had healed scars suggestive of past generalized maculo-papular rash and oral candidiasis. He was afebrile, had no nausea or vomiting, and had an unremarkable cardiorespiratory physical exam. His Glasgow Coma Scale (GCS) was 15/15, Karnofsky score was 70%, neck was supple, Kerning's sign was negative, and papilledema was absent. His motor exam was significant for left upper limb monoplagia (power of 0/5), generalized brisk reflexes, right flexor plantar response, unresponsive left plantar response, and a normal sensory exam. Clinical studies were negative for serum Cryptococcal antigen (sCrAg), and a rapid HIV test was positive. A lumbar puncture (LP) was not performed due to focal neurological signs. The presumptive diagnosis was cerebral toxoplasmosis with a differential diagnosis of bacterial meningitis and tuberculous meningitis (TBM) secondary to history of tuberculosis with uncertain compliance to treatment. He was started on empiric treatment for toxoplasmosis (1440 mg Septrin po q8h), bacterial meningitis (2g IV ceftriaxone QD), continued oral anti-TB treatment (Isoniazid and Ethambutol), and phenytoin (300 mg po QD). The patient's condition progressively declined and on the 5th day after admission, he rapidly deteriorated clinically with a GCS of 7/15, slowing respiration, and right upper limb held in decorticate position. At that time, the ward team performed an LP. Cerebrospinal fluid (CSF) analysis revealed 10 cells/cm3, protein 200 mg/dL, Gram and Ziehl-Neelsen (ZN) stains were negative as was the bacterial culture. A CT scan was done on the same day and showed an extensive ill-defined, non-enhancing hypodense lesion involving most of the right parietal lobe with global sulcial effacement, right lateral ventricle compression with 0.9 cm mid-line shift to the left, all suggesting an inflammatory cerebral lesion with massive brain edema with imminent danger of infratentorial coning (figure 1). Based on the LP and CT results, diagnoses included toxoplasmosis, TBM, and cerebral brain abscess. Management was modified to include a corticosteroid (8mg IV dexamethasone q8h), a diuretic (40mg IV furosemide q12h), and the insertion of a nasogastric tube. Despite continued treatment for the presumed differential diagnoses, the patient continued to deteriorate and died on the 15th day after admission.
The case demonstrates several challenges unique to a resource-limited setting. At the Mulago hospital, patients are cared for by relatives, who feed the patient and provide basic nursing care, including bathing, changing, and turning the patient. For the prisoner, social support was poor as he received limited care from prison staff. For example, upon deterioration, the patient could no longer accept solid food. The prison changed the food to porridge, but its supply was not regular. Also, the basis for the original diagnosis of pulmonary TB was not certain and the patient's compliance was unknown.
In conclusion, the patient presented with progressively worsening signs of focal neurological deficits. He was managed for toxoplasmosis, TBM, and a bacterial cerebral abscess. The neurological clinical and diagnostic findings were suggestive of a progressive cerebral lesion that was unresponsive to treatment and complicated by limited social support, leading to death on the 15th day after admission.