Posterior reversible encephalopathy syndrome complicating diabetic ketoacidosis

Case report A previously healthy 12 year old boy presented to the emergency department with pain in abdomen and vomiting for 7 days. On examination, he had normal sensorium and maintained saturation in room air. He had tachypnoea, tachycardia and a normal blood pressure (BP). He was severely dehydrated but the neurological examination was normal. His blood gases showed severe metabolic acidosis (pH=6.95, bicarbonate 7, base deficit 21, pCO2 23). He was diagnosed to have severe DKA (blood glucose 372mg/dl, ketones ++ in urine). The child was managed with intravenous (IV) fluids and insulin infusion according to protocol. Monitoring continued with capillary blood glucose, arterial blood gas (ABG) and serum electrolytes. On day 2, severe hypokalaemia was noted (K=2.1 mmol/l), which was corrected as per standard protocol, but other electrolytes were within normal range. Over the next 48 hours, the child remained irritable and confused with episodes of tachyarrhythmia. His BP and urine output remained normal throughout. After 48 hours of treatment, the child improved and oral feeds and subcutaneous insulin were started. ___________________________________________ Peerless Hospital India, BK Roy Research Centre, India *Correspondence: monidipa.banerjee@gmail.com (Received on 22 August 2016: Accepted after revision on 23 September 2016) The authors declare that there are no conflicts of interest Personal funding was used for the project. Open Access Article published under the Creative


Introduction
Posterior reversible encephalopathy syndrome (PRES) was first described by Hinchey et al. in 1996 1 .The most common clinical features are headache, altered sensorium and seizures 2 .According to our knowledge there is only a single reported case of PRES associated with diabetes ketoacidosis (DKA) in a child 3 .

Case report
A previously healthy 12 year old boy presented to the emergency department with pain in abdomen and vomiting for 7 days.On examination, he had normal sensorium and maintained saturation in room air.He had tachypnoea, tachycardia and a normal blood pressure (BP).He was severely dehydrated but the neurological examination was normal.His blood gases showed severe metabolic acidosis (pH=6.95,bicarbonate 7, base deficit 21, pCO2 23).He was diagnosed to have severe DKA (blood glucose 372mg/dl, ketones ++ in urine).The child was managed with intravenous (IV) fluids and insulin infusion according to protocol.Monitoring continued with capillary blood glucose, arterial blood gas (ABG) and serum electrolytes.On day 2, severe hypokalaemia was noted (K=2.1 mmol/l), which was corrected as per standard protocol, but other electrolytes were within normal range.Over the next 48 hours, the child remained irritable and confused with episodes of tachyarrhythmia.His BP and urine output remained normal throughout.After 48 hours of treatment, the child improved and oral feeds and subcutaneous insulin were started.Computed tomography (CT) scan of the brain, done to rule out cerebral oedema, was normal.His vision improved with no headache and the child was discharged after 10 days on subcutaneous insulin.The same day the child was brought back to the emergency department in status epilepticus, with up-rolling of eyes, tongue biting, stiffening of body, altered sensorium and involuntary passage of urine.
In the emergency department, blood glucose was 295 mg/dl, ABG was normal, and there was a trace of ketones in the urine.His BP was recorded at 140/90 mm Hg.Convulsions subsided with antiepileptic drugs which were continued.Next day he had two further episodes of generalized tonic-clonic seizures.
He was put on maintenance valproate, with no further seizures.EEG was consistent with diffuse encephalopathy.But confusion and irritability persisted.CT scan of brain showed bilateral parieto-occipital oedema.Magnetic resonance imaging (MRI) with FLAIR was consistent with the diagnosis of PRES (Figure 1).Venous sinus thrombosis was excluded by MRI venography.

Discussion
In the only reported case of PRES associated with DKA in the literature, a 17 year old girl developed seizures, encephalopathy and cortical blindness due to PRES, after resolution of her DKA 3 .In this patient, hypertension was identified as the likely trigger for PRES 3 .Abrupt arterial hypertension is a known trigger for PRES 4 .In our patient, too, PRES occurred after resolution of the DKA and sudden onset of hypertension was the probable trigger for PRES.Typical MRI changes in the brain in PRES comprise bilateral hyperintensities predominantly in the parieto-occipital region 4 .This was present in our patient.The clinical outcome of PRES is excellent, recovery occurring within a few days although the resolution of the MRI abnormalities takes much longer 4 .Our patient showed clinical improvement within a week and the repeat MRI will be done in about 6 months.PRES is an unusual but nevertheless treatable complication of DKA.Any child with DKA with late deterioration, with seizures and altered sensorium merits exclusion of PRES, preferably by MRI brain.

___________________________________________ 1
Peerless Hospital India, 2 BK Roy Research Centre, India *Correspondence: monidipa.banerjee@gmail.com(Received on 22 August 2016: Accepted after revision on 23 September 2016) The authors declare that there are no conflicts of interest Personal funding was used for the project.Open Access Article published under the Creative Commons Attribution CC-BY License On day 4, the child started complaining of blurring of vision.Pupillary response to light, funduscopic examination and eye movements were all normal.