Abstract
The records of 200 patients, nutritionally supported by synthetic means, were reviewed for evidence of clinical hyperosmolar hyperglycemic nonketotic dehydration (HHND). There was a 3% incidence of morbidity, with a single mortality. Laboratory values demonstrated a positive correlation between persistent glucosuria and HHND. The pathophysiology of HHND demonstrated a relative insulin lack with sufficient insulin to prevent lipolysis, but insufficient to prevent hyperglycemia, glucosuria and osmotic diuresis. The mechanism and management of the pseudodiabetes of stress is reviewed. It is concluded that HHND is an avoidable iatrogenic morbidity. Prevention of osmotic diuresis secondary to glucosuria and, therefore, prevention of HHND is achieved by providing exogenous insulin sufficient to prevent glucosuria.
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