Older patients with type 2 diabetes are most likely to present with nonketotic hyperglycemia (NKH). Precipitating factors include infection, surgery, dialysis, tube feedings, and stress.
Neurologic signs are common, and include:31,32
Focal seizures may present variably from patient to patient. Stereotypic tonic changes in body posture and speech arrest, associated with supplementary motor area seizures, have been well described.33 The syndrome of transient focal reflex epilepsy and neurologic deficits in elderly patients is highly suggestive of NKH.34
Relatively late symptoms are reduced consciousness and cessation of seizures as hyperglycemia and hyperosmolality worsen.35
Epilepsia partialis continua (EPC) can be an early symptom and persist in association with the presence of hyponatremia.35 The pathogenesis of EPC is thought to require metabolic disturbances including hyperglycemia, mild hyperosmolality, hyponatremia, lack of ketoacidosis, and an area of pre-existing focal cerebral damage.35
In addition to plasma glucose concentrations that typically exceed 1,000 mg/dL, NKH is characterized by hyperosmolality and dehydration from hyperglycemia-induced osmotic diuresis.30 Unlike diabetic ketoacidosis, there is no ketoacid accumulation.
Laboratory findings confirm the hyperglycemia and hyperosmolality and may also demonstrate a mild metabolic acidosis, as well as hypokalemia, hyponatremia, and elevations of blood urea nitrogen and creatinine.
The mortality rate is more than 50%, typically from circulatory collapse, and therefore NKH represents a medical emergency. Treatment consists of insulin, correction of electrolyte abnormalities, and reversal of the hyperosmolality with rehydration. (The average fluid deficit is 10 liters.)
Focal seizures are often resistant to antiepileptic drugs but do respond to insulin and restoration of circulatory volume.36,37
Adapted from: Schachter SC and Lopez MR. Metabolic disorders. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;195–208. With permission from Elsevier (www.elsevier.com).
Reviewed and revised April 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.
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