Cerebral edema generally develops in the first 4–12 h of therapy; however, it can occur prior to therapy initiation and 24 h or more into therapy.[35,55–58] It is a clinical bedside diagnosis based on diagnostic, major and minor criteria (Box 4).[3,52] One diagnostic, two major or one or more minor criteria have a sensitivity of 92% and false-positive rate of only 4%.
For high-risk CE patients, mannitol or hypertonic saline needs to be at hand, at the bedside and ready to be used, with a precalculated dose (0.5–1 g/kg mannitol, 5–10 ml/kg 3% 'hypertonic' saline) for the setting of neurological deterioration in overt CE. Doses are administered over more than 30 min may be repeated if there is no response. The intravenous fluid rate must be reduced by 30%.
There are many other potential complications of DKA and its management, as summarized in Table 1. These include electrolyte disturbances, vascular insults, infection, pancreatitis and rhabdomyolysis.
Expert Rev Endocrinol Metab. 2012;7(4):433-443. © 2012 Expert Reviews Ltd.