Diabetes Over View

Nonketotic Hyperglycemic - Hyperosmolar Coma

A syndrome characterized by hyperglycemia, extreme dehydration, and hyperosmolar plasma leading to impaired consciousness, sometimes accompanied by seizures.

Nonketotic hyperglycemic-hyperosmolar coma (NKHHC) usually develops after a period of symptomatic hyperglycemia in which fluid intake is inadequate to prevent extreme dehydration from the hyperglycemia-induced osmotic diuresis. It is a complication of type II DM and has a mortality rate of over 50%. The precipitating factor may be a coexisting acute infection or some other circumstance (e.g., elderly patient living alone).

Symptoms, Signs, and Diagnosis

NKHHC can also be induced by peritoneal dialysis or hemodialysis, by tube feeding, and by large IV glucose loads. In some patients, an infection, particularly pneumonia or gram-negative sepsis, is an initiating event; but NKHHC can also occur when patients with undiagnosed or neglected type II DM receive drugs that impair glucose tolerance (e.g., glucocorticoids) or increase fluid loss (e.g., diuretics).

The consistent and diagnostic features of NKHHC are CNS alterations, extreme hyperglycemia, dehydration and hyperosmolarity, mild metabolic acidosis without marked hyperketonemia, and prerenal azotemia (or preexisting chronic renal failure). The state of consciousness at presentation varies from mental cloudiness to coma. In contrast to DKA, focal or generalized seizures may occur. Transient hemiplegia may occur. The plasma glucose is usually in the range of 1000 mg/dL (55.5 mmol/L) (much higher than in most cases of DKA). The calculated serum osmolality on admission is about 385 mOsm/kg, whereas the normal level is about 290 mOsm/kg. Initial plasma bicarbonate levels are slightly depressed (17 to 22 mmol/L), and the plasma generally is not strongly positive for ketones. Serum Na and K levels are usually normal, but BUN and serum creatinine levels are markedly increased.

The average fluid deficit is 10 L, and acute circulatory collapse is a common terminal event in NKHHC. Widespread in situ thrombosis is a frequent finding on autopsy, and in some cases bleeding ascribed to disseminated intravascular coagulation or gangrenous-appearing digits has been observed.

Treatment

Treatment is started by infusing 2 to 3 L of 0.9% sodium chloride solution over 1 to 2 h. The immediate aim of treatment is to rapidly expand the contracted intravascular volume to stabilize BP and to improve circulation and urine flow.

If this stabilizes BP and circulation and restores good urine flow, then the IV infusion can be changed to 0.45% sodium chloride solution to provide additional water. The rate of the 0.45% sodium chloride solution infusion must be adjusted in accordance with frequent assessments of BP, cardiovascular status, and the balance between fluid input and output. K replacement is usually started by adding 20 mmol/L potassium as a phosphate salt to the initial liter of the IV-infused 0.45% sodium chloride solution, provided urine flow is adequate and the resulting initial rate of K infusion does not exceed 20 to 40 mmol/h.

Patients with NKHHC are often very sensitive to insulin, and large doses can precipitously decrease plasma glucose. Insulin treatment should not be aggressive and may be unnecessary because adequate hydration will usually decrease plasma glucose levels. A too-quick reduction in osmolality can lead to cerebral edema. However, many obese type II DM patients with NKHHC require larger insulin doses to reduce their marked hyperglycemia. If insulin is administered, 5% glucose should be added to the IV fluids when the plasma glucose reaches approximately 250 mg/dL (13.88 mmol/L) to avoid hypoglycemia. After recovery from the acute episode, patients are usually switched to adjusted doses of subcutaneous regular insulin at 4- to 6-h intervals. Many patients who are treated effectively for NKHHC with insulin initially may maintain their glucose control with diet or with oral hypoglycemics.