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PubMed · 2680468

Hyperosmolar hyperglycemic nonketotic coma.

D W Pope·D Dansky
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Abstract

HHNC is a syndrome of abnormally high serum glucose and osmolality coupled with depressed consciousness and an absence of ketoacidosis. It represents as many as 20 per cent of all cases of severe hyperglycemia and constitutes a life-threatening medical emergency; however, the absence of acidosis and the insidious presentation of the disorder frequently mislead clinicians into dangerously inadequate therapeutic interventions. Aggressive therapy with intravenous fluids and potassium and the judicious use of insulin, in conjunction with careful monitoring of central venous pressure and urine output, form the mainstays of treatment. There is a strong association of HHNC with other underlying serious diseases, the detection and treatment of which are imperative to the adequate resolution of the syndrome.

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D W Pope, D Dansky. 1989. Hyperosmolar hyperglycemic nonketotic coma.. https://pubmed.ncbi.nlm.nih.gov/2680468/

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PubMed1992

Treatment of diabetic ketoacidosis and non-ketotic hyperosmolar diabetic coma.

Although mortality of diabetic ketoacidosis (KA) has decreased during the past 20 yr to 1-2%, hyperosmolar non-ketotic coma (HNC) is still lethal in 20-30% of cases due to severe underlying conditions or to complications. The most frequent causes of death are infections and thromboembolic disorders. The strategies of initial treatment of KA and HNC are similar; in KA, insulin, fluid and electrolyte replacement have first priority. In HNC, rehydration and electrolyte administration are of primary importance. It is now generally recognized that insulin therapy is best performed using low doses (4-8 units/h); after institution of insulin treatment and rehydration there are rapid changes of fluid and electrolytes from the extra- into the intravascular space. In this situation it is a major therapeutic challenge to avoid complications due to hypokalaemia, hypophosphataemia, hypomagnesaemia and hypovolaemia. These complications should be avoided by adequate replacement, and particularly by regular clinical and laboratory monitoring. When blood glucose concentrations decrease below 14 mmols/l, blood glucose concentrations should initially be maintained at this level because rapid lowering below this level may increase the risk of brain oedema. Too-vigorous fluid replacement with crystalline solutions also increases the risk that brain oedema or complications like the adult respiratory distress syndrome will develop. If hypovolaemia persists in spite of adequate crystalloid solutions, colloid-containing fluids such as albumin should be administered. It is not established whether replacements of phosphate and magnesium have clinical benefits. Nevertheless, it is probably justified to administer phosphate and magnesium when their serum concentrations are below the normal range, particularly if the clinical situation is critical. Mortality from diabetic coma in industrialized countries may only be decreased by prophylaxis, i.e. by education of all diabetic patients and physicians to detect metabolic decompensation early.

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