HIV in Children
Metabolic Acidosis and Encephalopathy in an HIV Exposed Infant on Breast Feeding
Ira Shah, Jagdish Kathwate
Pediatric HIV Clinic, B.J.Wadia Hospital for Children, Mumbai

A 4 months old HIV exposed female infant presented to emergency department with multifocal convulsion, dystonic posturing and altered sensorium. She was born at 35-36 weeks of gestation, by emergency caesarean section due to cord prolapse. Mother was diagnosed to be HIV infected before pregnancy and was on ART consisting of AZT, lamivudine (3TC) and nevirapine (NVP) which she continued till date. Her CD4 count was 560 cell/cumm at the time of delivery. Baby also received single dose NPV after birth and then AZT prophylaxis for 6 weeks. Child was exclusively breastfeed. At presentation, the child had pallor, altered sensorium and dystonic posturing. Anterior fontanel was at level and reflexes were brisk though tone was normal and there was no focal neurological deficit. She had acidotic breathing with hepatomegaly. Other systemic examination was normal. Complete blood count was normal except hypochromic, microcytic anemia (hemoglobin was 9 gm/dl). Liver and renal functions were normal, but arterial blood gas analysis showed severe metabolic acidosis (pH-7.14, bicarbonate-4.2 mEq/L) with high anion gap of 30. Serum electrolytes were sodium -138mEq/L and potassium -4.3 mEq/L. Septic screen in form of CRP and blood culture were negative. Plasma sugar was 256 mg/dl and urine was negative for ketones. Child was treated with IV fluids and anticonvulsants. Her sensorium gradually improved. CT brain revealed bilateral basal ganglia hypodensities suggestive of metabolic encephalopathy (Figure 1). Serum lactate levels were sent after 24 hours of hospitalization and after correction of acidosis which was normal. [14 meq/L (normal: 12-22)]. Serum ammonia was 70 mmols/L (normal: 30-90mmols/L) and urinary organic acids screen was normal. EEG revealed generalized slowing.

What is the cause of the acute encephalopathy?
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