Tuberculous Meningitis Fitting the Shoes of Incomplete Kawasaki Disease
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SCIENTIFIC LETTER
Tuberculous Meningitis Fitting the Shoes of Incomplete Kawasaki Disease Kaviarasan Lingesan 1 & Malini Maya 1 & Jaikumar Govindaswamy Ramamoorthy 1 & Pediredla Karunakar 1 & Dhandapany Gunasekaran 1 & Nanmaaran Periyannan Thangavel 1 & Routhu Santhosh Kumar 1 & Venkataraman Ranjith Kumar 1 Received: 17 April 2020 / Accepted: 5 May 2020 # Dr. K C Chaudhuri Foundation 2020
To the Editor: A 10-mo-old female infant presented with fever for 7 d. On examination, she was febrile, without obvious foci. Her anthropometry was normal except stunting. General and systemic examinations were non-contributory. Urine microscopy, Chest radiograph, and abdominal ultrasonogram were normal. Empirical intravenous antibiotics were administered for pyrexia of unknown origin. Blood and urine cultures were sterile. Persistent fever >7 d, normocytic anemia (9.2 g/dl), leucocytosis (15.2×109/L), thrombocytosis (472×109/L), and elevated erythrocyte sedimentation rate (100 mm/h) fulfilled the criteria for incomplete Kawasaki disease (KD). Echocardiogram was normal. For a clinical diagnosis of incomplete KD, intravenous immunoglobulin (2 g/kg) with anti-inflammatory dose of aspirin were administered. On day 4 of hospital stay, she developed left hemiparesis with left upper motor neuron facial palsy. Contrast-enhanced Computed tomography of brain showed basal exudates, meningeal enhancement with right gangliocapsular infarct and communicating hydrocephalus. The cerebrospinal fluid (CSF) analysis revealed 30 lymphocytes/mm3, low glucose (31 mg/dl) and elevated protein (58 mg/dl). Diagnosis of stage II Tuberculous meningitis (TBM) was made; child was initiated on antitubercular treatment with oral prednisolone, despite negative CSF and gastric aspirate for acid fast bacilli and GeneXpert. TBM is the most debilitating childhood TB with significant neuromorbidity in up to 50% cases [1]. TB vasculopathy contributes to 8% of strokes in Indian children with basal ganglia infarcts being commonest [2]. Cerebral vasculitis secondary to
KD can also cause gangliocapsular infarct [3]. Clinical features, blood and CSF investigations in children with TBM may simulate KD as seen in our case. However, basal exudates and ventricular dilatation are tell-tale findings of TBM in neuroimaging. Diagnosis of incomplete KD is challenging in the absence of more specific findings like BCG-itis (BCG vaccine site erythema) or coronary artery abnormalities [4]. The mere presence of laboratory abnormalities in a febrile child may not be sufficient to diagnose KD in a country with rampant malnutrition. Newer serum biomarkers like pro-brain natriuretic peptide are more specific (96%) in diagnosing KD than the current clinical criteria [5]. We emphasize the need for lumbar puncture and CSF analysis in such cases to rule out TBM before considering the Kawasaki disease. To conclude, TB meningitis may mimic incomplete KD with cerebral vasculitis. In an endemic area for TB, diagnosis of incomplete KD with the available non-specific clinical criteria should be ma
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