Nonketotic hyperosmolar coma
Classification and external resources
ICD-9	250.2
DiseasesDB	29213
eMedicine	emerg/264
MeSH	D006944

Diabetes mellitus Related articles
Types of diabetes
Prediabetes:    • Impaired fasting glycaemia    • Impaired glucose tolerance Diabetes mellitus type 1 Diabetes mellitus type 2 Gestational diabetes
Blood tests
Blood sugar Glycosylated hemoglobin Glucose tolerance test Fructosamine
Diabetes management
Diabetic diet Anti-diabetic drugs Insulin therapy Glossary of diabetes
Complications
Cardiovascular disease Diabetic comas:    • Diabetic hypoglycemia    • Diabetic ketoacidosis    • Nonketotic hyperosmolar Diabetic myonecrosis Diabetic nephropathy Diabetic neuropathy Diabetic retinopathy Diabetes and pregnancy

Nonketotic hyperosmolar coma (nonketotic hyperglycaemia) is a type of diabetic coma associated with a high mortality seen in diabetes mellitus type 2. The preferred term used by the American Diabetes Association is hyperosmolar nonketotic state (HNS). Other commonly used names are hyperosmolar hyperglycemic nonketotic coma (HHNKC)^[1] or hyperosmotic non-ketotic coma (HONKC). It is also called Hyperglycaemic Hyperosmolar State (HHS), as some patients may have some ketonuria and it does not necessarily cause coma.

Contents 1 Pathophysiology 2 Clinical presentation 3 Management 3.1 Intravenous fluids 3.2 Electrolyte replacement 3.3 Insulin 4 References

[edit] Pathophysiology

Nonketotic coma is usually precipitated by an infection,^[2] myocardial infarction, stroke or another acute illness. A relative insulin deficiency leads to a serum glucose that is usually higher than 33 mmol/l (600 mg/dl), and a resulting serum osmolarity that is greater than 350 mOsm. This leads to polyuria (an osmotic diuresis), which, in turn, leads to volume depletion and hemoconcentration that causes a further increase in blood glucose level. Ketosis is absent because the presence of some insulin inhibits lipolysis, unlike diabetic ketoacidosis.

[edit] Clinical presentation

The increasing hemoconcentration and volume depletion may result in:

• Hyperviscosity and increased risk of thrombosis.
• Disordered mental functioning.
• Neurologic signs including focal signs such as sensory or motor impairments or focal seizures or motor abnormalities, including flacidity, depressed reflexes, tremors or fasciculations.
• Ultimately, if untreated, will lead to death.
• Vomiting.

[edit] Management

[edit] Intravenous fluids

Treatment of HHS begins with reestablishing tissue perfusion using intravenous fluids. People with HHS can be dehydrated by 8 to 12 l. Attempts to correct this usually take place over 24 hrs with initial rates of normal saline often in the range of 1 l/hr for the first few hours.^[3]

[edit] Electrolyte replacement

Severe potassium deficits often occur in HHS. They usually range around 350 mEq in a 70 kg person. This is generally be replaced at a rate 10 mEq per hour as long as there is urinary output.^[4]

[edit] Insulin

Once potassium levels have been verified to be greater than 3.3 mEq/l or greater an insulin infusion of 0.1 units/kg is begun.^[5]

[edit] References

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