A two year old boy was admitted to the children emergency unit of the Ladoke Akintola University of Technology Teaching Hospital, Osogbo on account of intermittent fever noticed about a week prior to presentation. Convulsions were observed five days prior to presentation. The patient had convulsed five times before presentation and the first noticed convulsion was generalized and lasted 15 mins. The patient had not regained consciousness till presentation. He has also had similar convulsions lasting for less than a minute on four consecutive days. The patient had not accepted any feed since the day he lost consciousness. The amount of urine produced had markedly reduced on the day the child presented. Vomiting of recently ingested feeds which later became bloody was observed a day prior to presentation.
Both parents of the child are 27 years old and tailors. They live in a village and have access to potable water. They have two other children that are well.
On examination the child was unconscious, mildly pale and afebrile with a temperature of 36.3ºC. He was well hydrated and had a capillary refill time less than 2 seconds. The patient weighed 12 kg. There was no cyanosis or icterus.
The central nervous system
examination revealed an unconscious child with a Glasgow coma score of 6. The occipito-frontal conference was 49.1 cm. Kernigs and brudzinski signs were negative. Hypertonia and hyperreflexia
were elicited in the upper limbs, while the tone and reflexes were normal in the lower limbs.
The cardiovascular system examination revealed normal volume and regular pulses at a rate of 116 beats per minute. The blood pressure was 94/60 mm/Hg and only the first and second heart sounds were heard. Examination of the respiratory system and the abdomen were essentially normal.
A tentative assessment of cerebral malaria was made and the full blood count examination on admission revealed a packed cell volume of 29 percent, total white blood count of 6,500 mm3
with neutrophils, lymphocyte and eosinophil
differential counts of 73, 26 and 1 percent respectively. A platelet count of 371,000 mm3
was recorded. The cerebrospinal fluid microscopy and chemistry were essentially normal. Trophozoites of Plasmodium falciparum
were detected in the blood film however. The random blood sugar and the pulse oximetry at admission were normal. The possibility of septicaemia complicating severe anemia was entertained because of the dominance of neutrophils
in the white cells.
The tentative diagnosis of cerebral malaria was still left in view. The patient was therefore started on 1 g of intravenous ceftriaxzone daily and intravenous artesuntae to manage the cerebral malaria. The convulsions were treated with daily administration of 60 mg of phenorbabitone and intramuscular paraldehyde when necessary. Although a nasogastric tube was passed for feeding, the child was not fed because the tube kept draining blood and so a diagnosis of upper gastrointestinal tract bleeding was made. Intravenous fluid
was administered at maintenance rate for calorie and adequate hydration.
The condition of the child became worse after 24 hours of admission with the development of facial puffiness and deepening coma evidenced by a Glasgow coma score of 3. Fluid input and output were 1010 and 160 mls respectively. Thus the output was 0.56 ml/kg/hr. Round worms were noticed to be migrating out of the anus. A picture of the round worms exiting the anus is found in Figure 1. A diagnosis of Ascariasis and acute kidney injury
was therefore made. The electrolytes, urea and creatinine were requested. The prothombrin time, partial thromboplastin
, urinalysis and random blood sugar were also requested. The results of the urinalysis was essentially normal, while the results of the other tests are displayed in Table 1.
The bleeding from the upper gastrointestinal tract persisted for 48 hours and there was no real improvement in the sensorium, mucosa
and pallor was still mild in the patient. There was no marked difference in the amount of urine produced. Therefore the electrolytes, urea and creatinine were re-requested. The results of the electrolytes, urea and creatinine are also displayed in Table 1.
On completion of the course of intravenous artesuate, the blood film examination by microscopy still revealed the presence Plasmodium falciparum
in the peripheral blood and the patient was commenced on intravenous quinine at 10 mg/kg body weight 8 hourly. At 72 hours of admission the patient went into cardio-respiratory arrest, which was managed by ambu-bagging and cardiac massage. While on the first course of quinine infusion the patient developed hypoglycaemia
with a random blood sugar of 1.6 mmol/l which rose to 2.1 mmol/l while on the second course of quinine infusion. Both episodes of hypoglycaemia were corrected with infusion of 4 mls/kg of 10% dextrose water. The strength of the quinine containing dextrose was also increased from 10% to 12%. Three other cardiopulmonary arrests were recorded and they were managed with cardiac massage and ambu-bagging. Consequently the child was transferred to the intensive care unit and placed on a ventilator and intensive care. However clinical condition of the child did not significantly improve and the patient died after 12 hours of care at the intensive care unit. The parents refused to consent to our autopsy