Case report: Acute Kidney Injury, Liver impairment, Severe Anemia in a child with Malaria and Hyperparasitaemia

P.falciparum Malaria is the most dangerous type of Malaria, it is often associated with high level of parasitemia in the blood. If untreated it is known to cause fatal complications. P.falciparum as suggested by many epidemiological studies happens to be the most prevalent of them all in Africa. Red blood cells that are infected with the parasite undergo hemolysis and sludging leading to microinfarctions in capillaries of the brain, liver, adrenal gland, intestinal tract, kidneys, lungs, and other organs.


Case report
A 12-year-old boy from Bondo, a town in Western Kenya with no previous co-morbidities was brought into the emergency department with prostration. He had a 2-day history of episodic high-grade fever associated with chills and rigors, yellowness of eyes which began since the morning of admission and multiple episodes of vomiting. This was associated with right upper quadrant abdominal pain, the patient was born in Western Kenya a highly endemic Malaria zone, there was no recent history of travel. Past history was notable for a single episode of Malaria 7 years previous to this admission which was managed with oral Artesunate-Lumefantrine combination along with Paracetamol for the fever in an outpatient setting. Physical examination revealed pallor, deep scleral jaundice, dry mucous membranes, and capillary refi ll >2 seconds. Vital signs were as follows-BP ( auscultation. The patient was resuscitated with intravenous fl uids and shifted to the ICU. Table 1 shows the laboratory parameters on admission Microscopic examination of blood smear revealed P. falciparum parasitemia of 35%, urine dipstick revealed presence of urine bilirubin , leukocytes, hemoglobin (confi rmed with urine microscopy) and proteins. Arterial blood gas revealed state compensated Metabolic Acidosis which was measured at intervals to determine correction of Acidosis and Metabolic derangement. Blood culture was done as a percentage of patients have been shown to present with concurrent gramnegative Septicemia or Meningitis. Ultrasound of the abdomen revealed minimal ascites, edematous gall bladder wall and sludge in the gall bladder. CT scan of the head showed brain edema necessitating I.V. Mannitol therapy.
The patient was diagnosed with Severe Malaria and was managed with I.V. Artesunate, I.V. Meropenem (considering renal dosage adjustment) was initiated for an initial broadspectrum prophylaxis, and I.V. fl uids Dextrose in Normal Saline. Meropenem was added as a prophylaxis to prevent gram negative Septicemia commonly seen in Severe Malaria and due to elevated procalcitonin and CRP levels. At 12 hours of admission, oliguria was noted with generalized edema. Fluid input by this time was 2000ml against an output of 150ml.
Renal consult was obtained, and a diagnosis of AKI stage 3 was made. A femoral dialysis catheter was inserted, and dialysis subsequently started. 24 hours after initiation of treatment the patient developed cola colored urine and worsening hemoglobin   • Metabolic acidosis.
The rarity of this case is in several aspects, fi rstly blackwater fever in itself is a rare occurrence in the modernday era [1], with most cases being reported in sub-Saharan Africa [2], secondly a majority of the documented cases occur following administration of Quinine salts [3,4]. Although there are documented cases of blackwater fever occurring with Artemisinin combinations like Mefl oquine-Artesunate combination and Artemether-Lumefantrine combination [4,5], there is only very few reported cases of blackwater fever following Artesunate monotherapy [6]. Thirdly AKI and jaundice although reported in adults are rare in children with Malaria [7,8].
Blackwater fever has been documented in 2 main groups of people it occurs in either non-immune immigrants or indigenous population in endemic areas [9], the latter being

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