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Challenges in identifying and managing cerebral oedema at first presentation of type 1 diabetes
Author(s) -
Uday Suma,
Krone Ruth
Publication year - 2017
Publication title -
practical diabetes
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.205
H-Index - 24
eISSN - 2047-2900
pISSN - 2047-2897
DOI - 10.1002/pdi.2084
Subject(s) - medicine , diabetic ketoacidosis , anesthesia , capillary refill , glasgow coma scale , metabolic acidosis , acidosis , tachypnea , bolus (digestion) , tachycardia , surgery , insulin , blood pressure
PRACTICAL DIABETES VOL. 34 NO. 2 COPYRIGHT © 2017 JOHN WILEY & SONS 65 An 11-year-old girl with known asthma presented to the emergency department with a 24-hour history of dyspnoea and chest pain. Examination revealed tachycardia, tachypnoea with normal oxygen saturation in air, intermittent drowsiness, poor perfusion peripherally and clinical dehydration with a central capillary refill time of 3 seconds. Initial investigations (electrocardiogram and chest X-ray) ruled out arrhythmia and/or pneumothorax. Subsequ ently, a venous blood gas at 2 hours (Table 1) revealed marked metabolic acidosis and hyperglycaemia and severe diabetic ketoacidosis (DKA) was confirmed in the presence of ketonuria. As per DKA guidance1 fluid resuscitation was given, followed by correction for 8% dehydration over 48 hours alongside maintenance fluids, followed by insulin after an hour. The patient continued to have severe acidosis and tachycardia, Glasgow Coma Scale dropped to 8 (E2M4V2) and cerebral oedema (CE) secondary to DKA was suspected, and thus hypertonic saline (5ml/kg of 3%) was administered. As the patient remained cardiovascularly unstable, a further fluid bolus was administered followed by intubation and ventilation; CT-head was in keeping with CE. A third fluid bolus was administered for circulatory shock and inotropes commenced. Maintenance fluids were halved and correction time for dehydration extended to 72 hours. Intravenous calcium was administered for myocardial protection and antibiotics for presumed sepsis. Sodium bicarbonate was considered. The parents were given a grave prognosis, but the patient eventually stabilised. Subsequent treatment was tailored to allow for controlled rise of PaCO2, fall in blood glucose and correction of metabolic acidosis (Table 1). A full clinical recovery with no acute neurological deficits was observed. Retrospectively, a history of weight loss despite an increased appetite over a month was established but osmotic symptoms (polyuria, polydipsia) and lethargy were Challenges in identifying and managing cerebral oedema at first presentation of type 1 diabetes