Nonketotic hyperosmolar coma


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

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 Hyperglycemic Hyperosmolar State (HHS), as some patients may have some ketonuria and it does not necessarily cause coma.

Contents

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 (excessive urination, 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.

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 flaccidity, depressed reflexes, tremors or fasciculations.
  • Ultimately, if untreated, will lead to death.

Management

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]

Electrolyte replacement

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

Insulin

Insulin is given to reduce blood glucose concentration; however, as it also causes the movement of potassium into cells, serum potassium levels must be sufficiently high or dangerous hypokalemia may result. Once potassium levels have been verified to be greater than 3.3 mEq/l, then an insulin infusion of 0.1 units/kg is begun.[5]

References

  1. ^ Cirasino L, Thiella G, Invernizzi R, Silvani A, Ragaini S (1992). "Hyperosmolar hyperglycemic nonketotic coma in Waldenström's macroglobulinemia associated with type II diabetes and complicated by pulmonary tuberculosis". Recenti progressi in medicina 83 (4): 194–6. PMID 1626111. 
  2. ^ Stoner, GD (May 2005). "Hyperosmolar hyperglycemic state". American Family Physician 71 (9): 1723–1730. PMID 15887451. http://www.aafp.org/afp/20050501/1723.html. 
  3. ^ Tintinalli, Judith (2004). Emergency Medicine: A Comprehensive Study Guide, Sixth edition. McGraw-Hill Professional. p. 1309. ISBN 0071388753. 
  4. ^ Tintinalli, Judith (2004). Emergency Medicine: A Comprehensive Study Guide, Sixth edition. McGraw-Hill Professional. p. 1320. ISBN 0071388753. 
  5. ^ Tintinalli, Judith (2004). Emergency Medicine: A Comprehensive Study Guide, Sixth edition. McGraw-Hill Professional. p. 1310. ISBN 0071388753. 

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