Hyperosmolar hyperglycemic state

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Hyperosmolar hyperglycemic state
Synonyms Hyperosmolar hyperglycemic nonketotic coma (HHNC), hyperosmolar non-ketotic coma (HONK), nonketotic hyperosmolar coma, hyperosmolar hyperglycemic nonketotic syndrome (HHNS)[1]
Video describing diabetes and its complications, including HHS.
Symptoms Signs of dehydration, altered level of consciousness[2]
Complications Disseminated intravascular coagulopathy, mesenteric artery occlusion, rhabdomyolysis[2]
Usual onset Days to weeks[3]
Duration Few days[3]
Risk factors Infections, stroke, trauma, certain medications, heart attacks[4]
Diagnostic method Blood tests[2]
Similar conditions Diabetic ketoacidosis[2]
Treatment Intravenous fluids, insulin, low molecular weight heparin, antibiotics[3]
Prognosis ~15% risk of death[4]
Frequency Relatively common[2]

Hyperosmolar hyperglycemic state (HHS) is a complication of diabetes mellitus in which high blood sugar results in high osmolarity without significant ketoacidosis.[4] Symptoms include signs of dehydration, weakness, legs cramps, trouble seeing, and an altered level of consciousness.[2] Onset is typically over days to weeks.[3] Complications may include seizures, disseminated intravascular coagulopathy, mesenteric artery occlusion, or rhabdomyolysis.[2]

The main risk factor is a history of diabetes mellitus type 2.[4] Occasionally it may occur in those without a prior history of diabetes or those with diabetes mellitus type 1.[3][4] Triggers include infections, stroke, trauma, certain medications, and heart attacks.[4] Diagnosis is based on blood tests finding a blood sugar greater than 30 mmol/L (600 mg/dL), osmolarity greater than 320 mOsm/kg, and a pH above 7.3.[2][3]

Initial treatment generally consists of intravenous fluids to manage dehydration, intravenous insulin in those with significant ketones, low molecular weight heparin to decrease the risk of blood clotting, and antibiotics among those in whom there is concerns of infection.[3] The goal is a slow decline in blood sugar levels.[3] Potassium replacement is often required as the metabolic problems are corrected.[3] Efforts to prevent diabetic foot ulcers are also important.[3] It typically takes a few days for the person to return to baseline.[3]

While the exact frequently of the condition is unknown, it is relatively common.[4][2] Older people are most commonly affected.[4] The risk of death among those affected is about 15%.[4] It was first described in the 1880s.[4]

Signs and symptoms[edit]

Symptoms include an altered level of consciousness. Additionally it may also lead to:

  • Neurologic signs including focal signs such as sensory or motor impairments or focal seizures or motor abnormalities, including flaccidity, depressed reflexes, tremors or fasciculations.
  • Hyperviscosity and increased risk of blood clot formation

Cause[edit]

The main risk factor is a history of diabetes mellitus type 2.[4] Occasionally it may occur in those without a prior history of diabetes or those with diabetes mellitus type 1.[3][4] Triggers include infections, stroke, trauma, certain medications, and heart attacks.[4]

Pathophysiology[edit]

Nonketotic coma is usually precipitated by an infection,[5] 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 320 mOsm. This leads to excessive urination (more specifically 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 hormone-sensitive lipase mediated fat tissue breakdown.

Diagnosis[edit]

Criteria[edit]

According to the consensus statement published by the American Diabetes Association, diagnostic features of HHS may include the following:[6][7]

  • Plasma glucose level >30 mmol/L (>600 mg/dL)
  • Serum osmolality >320 mOsm/kg
  • Profound dehydration, up to an average of 9L (and therefore substantial thirst (polydipsia))
  • Serum pH >7.30
  • Bicarbonate >15 mEq/L
  • Small ketonuria (~+ on dipstick) and absent-to-low ketonemia (<3 mmol/L)
  • Some alteration in consciousness

Imaging[edit]

Cranial imaging is not used for diagnosis of this condition. However, if MRI is performed, it may show cortical restricted diffusion with unusual characteristics of reversible T2 hypointensity in the subcortical white matter.[8]

Differential diagnosis[edit]

The major differential diagnosis is diabetic ketoacidosis (DKA). In contrast to DKA, serum glucose levels in HHS are extremely high, usually greater than 40-50 mmol/L, but an anion-gap metabolic acidosis is absent or mild. Delirium is also more common in HHS than DKA. Although traditionally DKA has been associated with Type I Diabetes, whereas HHS has been associated with Type II, HHS can be seen in people of both types. HHS also tends to have an elderly preponderance.

Management[edit]

Intravenous fluids[edit]

Treatment of HHS begins with reestablishing tissue perfusion using intravenous fluids. People with HHS can be dehydrated by 8 to 12  liters. Attempts to correct this usually take place over 24 hours with initial rates of normal saline often in the range of 1 L/h for the first few hours or until the condition stabilizes.[9]

Electrolyte replacement[edit]

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.[10]

Insulin[edit]

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 dangerously low blood potassium levels 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/hr is started.[11]

References[edit]

  1. ^ "Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNS)". American Diabetes Association. Retrieved 6 July 2012. 
  2. ^ a b c d e f g h i Stoner, GD (1 May 2005). "Hyperosmolar hyperglycemic state.". American family physician. 71 (9): 1723–30. PMID 15887451. 
  3. ^ a b c d e f g h i j k l Frank, LA; Solomon, A (2 September 2016). "Hyperglycaemic hyperosmolar state.". British journal of hospital medicine (London, England : 2005). 77 (9): C130–3. PMID 27640667. doi:10.12968/hmed.2016.77.9.C130. 
  4. ^ a b c d e f g h i j k l m Pasquel, FJ; Umpierrez, GE (November 2014). "Hyperosmolar hyperglycemic state: a historic review of the clinical presentation, diagnosis, and treatment.". Diabetes care. 37 (11): 3124–31. PMID 25342831. doi:10.2337/dc14-0984. 
  5. ^ Stoner, GD (May 2005). "Hyperosmolar hyperglycemic state". American Family Physician. 71 (9): 1723–30. PMID 15887451. 
  6. ^ Lewis P. Rowland; Timothy A. Pedley (2010). Merritt's Neurology. Lippincott Williams & Wilkins. pp. 369–370. ISBN 978-0-7817-9186-1. 
  7. ^ Magee MF, Bhatt BA (2001). "Management of decompensated diabetes. Diabetic ketoacidosis and hyperglycemic hyperosmolar syndrome.". Crit Care Clin. 17 (1): 75–106. PMID 11219236. 
  8. ^ Neuroradiology 2007 Apr;49(4):299-305.
  9. ^ Tintinalli, Judith E.; Kelen, Gabor D.; Stapczynski, J. Stephan; American College of Emergency Physicians (2004). Emergency Medicine: A Comprehensive Study Guide (6th ed.). McGraw-Hill Prof Med/Tech. p. 1309. ISBN 978-0-07-138875-7. 
  10. ^ Tintinalli, Kelen & Stapczynski 2004, p. 1320
  11. ^ Tintinalli, Kelen & Stapczynski 2004, p. 1310

External links[edit]

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