A 13-year-old boy was referred to our hospital with complaints of high-grade fever, non-bilious, non-bloody projectile vomiting, light headedness, generalized weakness, reduced appetite and passing black-coloured urine. Prior to his admission, the child was febrile (40  C) with blood pressure of 110/40 mmHg (considered to be low as per guidelines of the National Institute of Health), along with thrombocytopaenia (28 000 mm-3 blood; normal: 1.5-4.5 mm-3 blood), low haematological parameters of haemoglobin (12.3 g dl-1; normal: 10-15.5 g dl-1), haematocrit (35.8 %; normal: 35-44 %), mean corpuscular volume (66.1 fl; normal: 80-95 fl) and mean corpuscular haemoglobin (22.7 pg; normal: 32-36 pg). Blood urea (62 mg dl-1; normal: 5-18 mg dl-1) and random blood sugar (204 mg dl-1; normal: 70-140 mg dl-1) levels were significantly raised. Peripheral blood smear examination was positive for P. vivax. Other tests such as Dengue (Non-structural protein 1) NS1, scrub typhus card tests, Widal test and COVID 19 reverse transcriptase (RT)-PCR were negative. Despite thrombocytopaenia, the child had no bleeding manifestations and was administered a first dose of intravenous artesunate and intravenous fluids.
With the impending hypovolaemia, and persistent hypotension with an episode of loss of consciousness for 20 min, the child was referred to our hospital. He was afebrile, hypotensive (88/36 mmHg), with high pulse rate (110 bpm) and facial swelling. There was reduction in urine output of around 150 ml per day, but the oxygen saturation (SpO2) was well maintained. Liver was enlarged up to 2 cm below the right costal margin. Other systemic examinations were within normal limits. Upon laboratory investigations, his haemoglobin level was 11 g dl-1, with a low haematocrit (34.2 %), mean corpuscular volume (71 fl) and mean corpuscular haemoglobin (22.9 pg) values with platelet count of 36 000 mm-3 blood. Serum direct bilirubin and liver enzymes were elevated. Giemsa-stained peripheral blood smears revealed normal sized erythrocytes with microgametocytes containing malarial pigments (Fig. 1). Quantitative buffy coat (QBC) examination detected gametocytes of non-falciparum species. Blood sample was subjected to a multiplex nested PCR assay using published primers (Table 1), and an amplified product of 121 bp corresponding with P. vivax was detected by 1.5 % agarose gel electrophoresis using a molecular ladder of 100 bp (Thermo Scientific Gene Ruler 100 bp ladder) (Fig. 2). Buffer used for the agarose gel cast and running buffer in the gel electrophoresis tank was 10x Tris boric acid EDTA (TBE). The child was treated with injectable inotropes, intravenous fluids, oxygenation, the remaining two doses of artesunate and injectable antibiotics (ceftriaxone and vancomycin). Antibiotics were discontinued after malaria was reported. A repeat complete haemogram showed a fall of platelets to 19 000 mm-3 blood after 7 h of treatment, but the child became stable after 22 h with the same regimen and was discharged with advice to continue artemether-lumefantrine combination without any other drugs and/or antibiotics.