An 8-year-old girl with T1DM was admitted to the hospital with fever, lethargy, anorexia, and vomiting.  She was diagnosed three years ago and had been on insulin therapy (four daily injections) since. According to the history obtained from her family, she had experienced nausea, vomiting, fever, lethargy, and headache for the last 24 hours. There was no history of previous neurological disease.  On physical examination, her temperature was 38.1 C, pulse rate was 112 beats/min, and respiratory rate was 30/min. She had Kussmaul respiration and was mildly dehydrated. Her history revealed no BCG vaccination. On neurological examination, lethargy and irritability were observed. There were no signs of meningeal irritation.
Laboratory Findings
On initial laboratory examination, the patient's hemoglobin level was 15.5 g/dL. C-reactive protein (CRP) level was 5 mg/dL. Leukocyte count was 36 100/muL and differential count showed a shift to the left with toxic granulations in neutrophils. Blood glucose level was 444 mg/dL. Metabolic acidosis was present with a pH of 7.19. The other biochemical values were as follows: blood urea nitrogen level: 16 mg/dL, serum creatinine: 0.86 mg/dL, sodium: 124 mmol/L, potassium: 3.6 mmol/L, chloride: 102 mmol/L, serum osmolarity: 312 mOsm/kg. Hemoglobin  A1c was 8.1%. The patient's urine was strongly positive for sugar and ketones.
Management and Course
DKA treatment was started with intravenous fluids and insulin infusion. In view of the presence of fever, elevated CRP and elevated white blood cell count with neutrophilia, antibiotics were also started. Plasma glucose was monitored regularly. During the course of treatment, bradycardia developed and the lethargic state progressed to stupor.  Cranial computed tomography (CT) scan displayed cerebral edema. Lumbar puncture was not performed because of cerebral edema. Antiedema therapy was started with mannitol and dexamethasone. After 24 hours of treatment with intravenous insulin, blood glucose level decreased to 186 mg/dL. On the second day of treatment, diabetes insipidus occurred, and thus, desmopressin was added to the therapy.  With treatment, the metabolic parameters became normal, but the neurological status was not improved. Magnetic resonance imaging (MRI) was performed in order to detect any central nervous system (CNS) infection and revealed structures which were consistent with tuberculoma, such as is seen in tuberculous meningitis (Figure 1). After the resolution of the cerebral edema on repeat MRI, a lumbar puncture was performed. In the cerebrospinal fluid (CSF) examination, glucose level was 129 mg/dL, protein: 44 mg/dL, and leukocyte count was 3 ([i][/i]2 lymphocytes, 1 polymorphonuclear leukocyte). CSF staining demonstrated acid-fast bacilli, implying a diagnosis of tuberculosis (Figure 2). The patient was started on antituberculosis treatment (rifampicin, isoniazid, pyrazinamide, ethambutol).