Ketamine
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Diabetes insipidus: case report A 15-year-old boy developed diabetes insipidus following administration of ketamine for analgesia [outcome not stated]. The boy presented for posterior spinal fusion as part of a two-stage repair of thoracolumbar scoliosis. He had undergone an uneventful thoracotomy and anterior release during previous week. He had a history of cerebral palsy, epilepsy and gastrooesophageal reflux disease, and his medications included sodium valproate, levetiracetam and esomeprazole. Prior to the surgery, a brain MRI showed normal cranio-cervical junction, but intraventricular distension with porencephaly. Routine blood tests showed sodium 129 mmol/L and Hb 111 g/L. Total IV anaesthesia was induced and maintained with propofol. Remifentanil was administered as an aid for intubation, followed by infusion. Following thoracotomy, adjuvant analgesic infusions were started following turning him to the prone position: IV infusion of ketamine 2–10 µg/kg/min along with lidocaine. Tranexamic acid was also administered. Cefuroxime and gentamicin were administered as antibiotic prophylaxis. Cervical traction was applied in anticipation of high thoracic vertebrae fusion. Somatosensory evoked potential and motor evoked potential monitoring was started. However, consistent high-quality signals were not obtained. An electroencephalogram indicated an appropriate depth of anaesthesia. Anaesthetic depth was decreased to improve signal. Ringer’s lactate [Hartmann’s solution] 10 mL/kg was administered along with norepinephrine [noradrenaline] 0.01 µg/kg/min to maintain a mean arterial BP. Ketamine infusion was increased to 10 µg/kg/min. However, no improvement was noted. Due to the advanced nature of the scoliosis, it was decided to proceed with surgery without neurophysiological monitoring. Initially during the surgery, the urine output was 4 mL/kg/h. However, by 210 minutes into the surgery, the urine output increased to 11 mL/kg/h. After further 45 minutes, it increased to 18 mL/kg/h. The appearance of the urine was dilute. Arterial blood gas analysis showed increased sodium (from 132 to 141 then 144 mmol/L). Despite good arterial pressure and oxygen saturations, the concern for diabetes due to impaired intracranial perfusion increased. Consequently, cervical traction was removed. After removing the cervical traction, the urine output transiently decreased before increasing again, with rise in sodium. Diabetes insipidus secondary to ketamine was suspected. The boy received additional Ringer’s lactate 10 mL/kg boluses (total 55 mL/kg) to maintain euvolaemia and vasopressin was started. By the time of completion of surgery, his urine output decreased to 1 mL/kg/h and sodium of 142 mmol/L. Following the surgery, he was transferred to the paediatric ICU, where sedation and mechanical ventilation were continued. Blood biochemistry results of perioperative blood sample showed: urinary sodium < 10 mmol/L, urine osmolality 86 mOsm/kg, plasma osmolality 294 mOsm/kg and plasma sodium 141 mmol/L. On the next day, vasopress
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