A boy aged 4 months 7 days from a middle-class family (monthly family-income of Tk 10,000-15,000 equivalent to US dollar 121-181) living in Dhaka district was brought to the Dhaka Hospital of icddr,b on 9 January 2011 and admitted to the Short Stay Unit on the same day. Immediately after admission, he was shifted to the hospital's ICU for his respiratory distress and irritability. He had a history of watery diarrhoea for 3 days, associated with vomiting for the same duration, fever and respiratory distress for the last 12 hours. His stool frequency was 12 times/day, vomiting 2 times/day, and fever was high and continued but not associated with chills and rigours, and respiratory distress was not associated with cough. The child had passed urine half-an-hour before admission in the ICU. He received 6 packets (3 litre) of inappropriately-prepared (concentrated) ORS at home but no drugs. History of his past illness was unremarkable. He did not have a history of contact with any persons known or suspected to have tuberculosis, and his family members were in good health. He was the second and the last issue of his non-consanguineous parents and was delivered normally at home at full term. His weight and height at birth could not be obtained. He was breastfed at birth, and it continued up to 2 months. Since then, he was given mixed-milk (formula milk and breastmilk). His developmental milestones were age-appropriate, and his vaccinations were up-to-date according to the local EPI (Expanded Programme on Immunization) schedule. Both the parents were literate (education of the father and the mother was up to college and high school level respectively); the father was a garments worker, and the mother was a housewife. They were living in a tinshed house, used to drink tubewell water but their sanitation was poor.
On admission, the infant was initially irritable and excessively thirsty but he became very lethargic soon after admission. His pulse rate was 146 per minute with normal volume, blood pressure was 85/60 mmHg, capillary refill time was <2 sec, rectal temperature was 39.5 °C, and respiration rate was 80 per minute. He weighed 6.4 kg and had a length of 60 cm; his anthropometric measurements showed a z-score of <-2 [>-3 of the median of WHO growth charts] for all of the three indices—weight-for-age, weight-for-length, and length-for-age. He had some dehydration but did not have pallor, cyanosis, jaundice, oedema, or clubbing.
There was no increased work of breathing (no marked use of accessory muscles of respiration, and he did not have nasal flaring, head-nodding, stridor, wheezing, grunting respiration, or lower chest-wall in-drawing). His trachea was centrally placed, and the respiration sounds were vesicular with no adventitious sounds (rales, rhonchi, or pleural rub). Other systemic examinations of the infant were not remarkable. His blood glucose, measured at bedside, was 7.30 mmol/L, and his arterial oxygen saturation (SPO2) was 96% in room-air (WHO defines SPO2 of <90% at sea-level as hypoxaemia).
Thus, the initial problems were: (a) acute watery diarrhoea with some dehydration, (b) hypernatraemia (on the basis of history and cardinal clinical signs), (c) pneumonia (according to WHO definition), and (d) lethargy (differentially thought to be due to hypernatraemia itself, and also sepsis).
The laboratory work included: blood for total and differential white blood cell (WBC) count; blood culture and sensitivity; serum electrolytes, including serum total calcium, total magnesium, serum creatinine; rectal swab culture for isolation and identification of enteric pathogens; urine for routine and microscopic examinations (RME); and urine for culture and sensitivity (as a part of routine investigations in a febrile infant); and a chest x-ray.
We started management of dehydration with ORS following WHO guideline (12
). Parenteral ceftriaxone and levofloxacin was also started to cover aetiologic agent in pneumonia and probable sepsis. Feeding was initiated according to standard protocolized management of diarrhoea.
His total WBC was 9,600/mm3, with 55.1% neutrophils, 0.0% bands, 33.5% lymphocytes, 11.2% monocytes, 0.1% eosinophil, and 0.1% basophil. Serum sodium was 201.0 mmol/L, chloride 165.3 mmol/L, potassium 3.6 mmol/L, TCO2 20.3 mmol/L, total calcium 1.94 mmol/L, total magnesium 1.31 mmol/L, and serum creatinine 66.6 micromol/L. The chest x-ray and urine RME revealed normal findings.
After receiving the electrolyte report (around 4 hours after initiation of hydration), we re-evaluated the dehydration status and found no signs of dehydration. Then we decided to manage the correction of hypernatraemic dehydration, using ORS only. The volume required was calculated following a formula [10÷(molecular concentration of sodium in a given solution–measured serum sodium)/(0.6×weight in kg+1)=litre/24 hours] (2
) aiming not to reduce the serum sodium by >10 mmol/L/24 hours. We also maintained hydration by replacing the ongoing loss of each purging. ORS was administered through a nasogastric tube. In spite of having his dehydration under control, the patient was still experiencing fast breathing, indicating pneumonia even in absence of radiological evidence (13
Correction of hypernatraemia was started with a calculated rate of ORS of 15 mL per hour through nasogastric tube, and the correction of hypocalcaemia was tried with 10% calcium gluconate injection (0.5 mL/kg), and oral supplementation with calcium carbonate tablet was continued during hospitalization. Ten hours after initiating the treatment of hypernatraemia (14 hours after admission), the patient developed a generalized tonic clonic seizure. The seizure was difficult to control and required a total of three doses (0.1 mg/kg/dose) of injection lorazepam (10 minutes apart), followed by a loading dose of injection phenobarbitone (20 mg/kg) and injection phenytoin (20 mg/kg). Simultaneously, a maintainance dose of phenobarbitone (5 mg/kg/day in two divided doses) and phenytoin (2.5 mg/kg/dose 12 hourly) were continued to prevent further convulsions. After cessation of the convulsion, we re-examined the child and did not find any signs of meningism except extreme lethargy. We differentially thought that convulsion was either due to hypernatraemia itself or due to cerebral oedema from a probable rapid fall in sodium. The serum sodium level after 24 hours was 185 mmol/L, and the fall was >0.5 mmol/L/hr. We examined the fundi and did not find any evidence of cerebral haemorrhage or cerebral oedema. However, there was another episode of generalized tonic clonic convulsion which was not controlled by an additional dose of injection lorazepam (0.1 mg/kg/dose), and an empirical dose of 20% mannitol injection [0.5 g (2.5 mL)/kg/dose] was given due to the likelihood of cerebral oedema; the convulsion was controlled after infusion of mannitol. We gave another dose [0.5 g (2.5 mL)/kg/dose] of mannitol 6 hours after the initial dose. We re-examined the fundi and still did not find any evidence of cerebral oedema and, therefore, stopped mannitol. Then approximately every 24 hours, the serum sodium was checked (which was 174 mmol/L, 157 mmol/L, 152 mmol/L, and 145 mmol/L), and the volume of ORS needed for the correction of hypernatraemic dehydration was re-calculated each day. On average, the fall was <0.5 mmol/L/hr for the next 4 days during the correction. In the mean time, by day 3, diarrhoea was controlled, and clinical signs of pneumonia disappeared but the patient was still lethargic. The lethargy might have been due to the use of two anticonvulsants and as there were no further episodes of convulsion, the anticonvulsants were weaned after a convulsion-free period of 48 hours; all the anticonvulsants were gradually weaned successfully by day 7. On day 7, the patient was active and alert, took food orally and was gradually becoming afebrile. There were no CNS abnormalities. In the mean time, no organism was isolated from blood, rectal swab or urine culture, and we stopped antibiotics and planned to discharge the patient.
Before discharge (on day 12 of his hospitalization), a computed tomography scan of brain was performed, which revealed mild ischaemic changes in both the temporal lobes (). After review by a paediatric neurologist from a local tertiary-care centre, a Magnetic Resonance Image (MRI) scan was performed, which revealed ischaemic changes in left temporal lobe (), and this was consistent with the CT scan findings. The patient has been under regular follow-up at our hospital and at the last follow-up on 15 November 2011, the patient was found to be playful, and his developmental curve was up-to-date. However, there was a history of occasional episodes of absence seizure persisting for a few seconds over the last two months.
CT scan: Bilateral low-attenuation areas are seen in both temporal poles, overlying cortex is spared
MRI scan: T2 hyper-intense area is seen in the left temporal pole