ILLUSTRATIVE CASE

Neurologic Deterioration in a Child Undergoing Treatment for Tuberculosis Meningitis Gilad D. Birnbaum, BA,* Lucila Marquez, MD, MPH,*Þ Kevin M. Hwang, BA,* and Andrea T. Cruz, MD, MPH*Þþ

Abstract: Clinical deterioration while receiving antituberculosis (anti-TB) therapy can be due to a number of etiologies, including drug resistance, disease progression despite effective therapy, or alternative diagnoses. We present the case of a 22-month-old girl diagnosed with TB meningitis 4 months prior to presentation. At time of her initial diagnosis, computed tomography showed hydrocephalus and basilar meningitis with some evidence of ischemic damage. She required placement of a ventriculoperitoneal shunt and was discharged on multidrug anti-TB therapy and corticosteroids. At the time of her second emergency department presentation, she had developed new-onset seizures and hemiparesis. Her steroids had been tapered and discontinued. Differential diagnosis included shunt malfunction and/or shunt infection. Magnetic resonance imaging of the brain showed interval development of tuberculomas. Symptomatic and radiographic improvement was seen after initiation of corticosteroids for immune reconstitution inflammatory syndrome, which can be seen in immunocompetent children, with onset weeks to months after starting antituberculous therapy. Key Words: immune reconstitution inflammatory syndrome, tuberculomas, tuberculosis meningitis (Pediatr Emer Care 2014;30: 566Y567)

CASE A 22-month-old Latin American girl presented to the emergency department with difficulty walking, left-sided tremor and leaning to the left while ambulating, right eye ptosis, and 3 generalized tonic-clonic seizures. Symptoms began 10 days prior to admission. The child was diagnosed with tuberculosis (TB) meningitis 4 months prior; following the toddler’s diagnosis, her mother was diagnosed with cavitary pulmonary TB. The child’s imaging studies at that time demonstrated hydrocephalus, which required placement of a ventriculoperitoneal shunt, basilar meningitis, and a right basal ganglia infarct (Fig. 1A). Pan-susceptible Mycobacterium tuberculosis had been cultured from her cerebrospinal fluid and gastric aspirates. The child was HIV-seronegative. She was managed initially with corticosteroids and a 4-drug regimen (isoniazid, rifampin, pyrazinamide, and ethionamide) via directly observed therapy and subsequently transitioned to isoniazid and rifampin after 2 months. At the time of this emergency department visit, the family denied fever, weight change, or vomiting but reported constipation, rhinorrhea, and an occasional cough. Physical examination revealed an irritable child, weighing 11 kg (25th percentile), 79 cm in height (10th percentile), temperature of 98-F, pulse of 138 beats/min, respiratory rate of 36 breaths/min, and blood pressure of 110/50 mm Hg. The shunt was palpable over the

right scalp, and there was no associated erythema or tenderness. She had right-sided ptosis and a slight left-sided mouth droop. Left-sided dysmetria and coarse tremor also were noted. Her Glasgow Coma Scale score was 10. Her peripheral white blood cell count was 8500 cells/KL, with 54% neutrophils, 37% lymphocytes, and 8% monocytes. Serum chemistries were normal; sodium was 139 mEq/L. A shunt series showed an intact right-sided shunt. A noncontrast computed tomography scan of the brain demonstrated a large area of diffuse hypodensity involving the right frontal, parietal, and temporal lobes with ventricular and sulcal compression. Magnetic resonance imaging (MRI) of the brain with contrast (Fig. 1B) showed abnormal basilar enhancement and multiple new ring enhancing nodules along the surface of the brain, greatest within the basilar cisterns. There was right hemisphere edema with midline shift and ventricular and aqueduct compression. This child had interval development of tuberculomas while on effective anti-TB therapy. On admission, the patient was begun on intravenous dexamethasone 1.5 mg/kg per day divided every 6 hours and admitted to the pediatric intensive care unit. She did not require intubation for airway protection, and her anti-TB drug regimen was not changed. Three days into her admission, she demonstrated marked improvement of irritability. After 2 weeks, she was interactive and had significant improvement of the left-sided tremor and right eye ptosis. She also was able to ambulate without difficulty. She was discharged home on prednisolone 4 mg/kg per day divided twice daily, and she continued to improve. The steroids were tapered very slowly over the course of 3 months. Hearing and visual screening demonstrated no sensory losses. However, her risk of developmental delay as a consequence of her initial TB meningitis remains high.

DISCUSSION Tuberculomas are seen in a small fraction of children with TB meningitis at presentation,1 but improved imaging modalities such as MRI have made detection of tuberculomas more

From the *Department of Pediatrics, †Sections of Infectious Diseases and ‡Emergency Medicine, Baylor College of Medicine, Houston, TX. Disclosure: The authors declare no conflict of interest. Reprints: Andrea T. Cruz, MD, MPH, Department of Pediatrics, Baylor College of Medicine, 1102 Bates St, Suite 1850, Houston, TX 77030 (e

Neurologic deterioration in a child undergoing treatment for tuberculosis meningitis.

Clinical deterioration while receiving antituberculosis (anti-TB) therapy can be due to a number of etiologies, including drug resistance, disease pro...
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