Hyperosmolar hyperglycemic state natural history, complications and prognosis
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Husnain Shaukat, M.D [2]
Overview
The symptoms of hyperosmolar hyperglycemic state (HHS) develop slowly over a period of days to weeks as compared to diabetic ketoacidosis (DKA) which presents within hours of inciting event. The symptoms range from fatigue, weakness, leg cramps, polyuria, dehydration and eventually seizures and coma. If left untreated, patients may develop multiorgan failure and eventually death. Common complications are renal failure, thrombotic events, and cardiovascular complications. The complications due to treatment can be cerebral edema, pulmonary edema, hypoglycemia, and electrolyte imbalance. The mortality rate ranges from a low of less than 5000 per 100,000 individuals to a high of 20,000 per 100,000 individuals which is ten times higher than diabetic ketoacidosis. The prognosis of the hyperosmolar hyperglycemic state (HHS) depends on the hemodynamic status, comorbidities, and age at the time of presentation.
Natural History, Complications, and Prognosis
Natural History
If left untreated, the evolution of hyperosmolar hyperglycemic state (HHS) can be insidious. The following features are associated with the natural course of the disease:[1][2][3][4][5]
- The symptoms of hyperosmolar hyperglycemic state (HHS) usually develop over several days to weeks as compared to diabetic ketoacidosis which presents within hours of inciting event.
- Early in the course of a disease, HHS usually presents with symptoms of hyperglycemia such as polyuria, polydipsia, leg cramps, weakness, nausea, and dehydration.
- As HHS progresses, it leads to increase in serum osmolality which can present with neurological manifestations such as altered sensorium, focal signs, confused state or even coma. Neurological symptoms rarely present with an osmolality of less than 320 mOsm/kg.
- The severity of dehydration in HHS is due to insidious onset and longer duration of metabolic decompensation and also due to the reduced fluid intake.
- The increase in plasma osmolality leads to water shifts out of the cells and causes intracellular dehydration and with insulin deficiency, it further exacerbates potassium movement out of the cell.
- The dehydration leads to decrease glomerular filtration rate (GFR) and renal clearance of glucose, which further exacerbates hyperglycemia and ultimately renal failure.
- Hypotension or shock during HHS is nearly always the result of dehydration and hypovolemia.
- Heart failure, myocardial infarction, and arrhythmias are seen commonly in an untreated hyperosmolar hyperglycemic state.
- If left untreated, HHS may progress to multi-organ failure, seizures, coma and eventually death.
Complications
People with hyperosmolar hyperglycemic state (HHS) need close and frequent monitoring for complications. Surprisingly, the most common complications of HHS are related to the treatment:[6][7][8][9][10]
Complications of hyperosmolar hyperglycemic state (HHS) include:
Complications due to the treatment of hyperosmolar hyperglycemic state (HHS) include:
- Cerebral edema due to aggressive hydration
- Pulmonary edema
- Hypoglycemia
- Hypokalemia
Prognosis
The mortality of hyperosmolar hyperglycemic state ranges from 5% to 20%, which is ten times higher than diabetic ketoacidosis. The signs of poor prognosis in hyperosmolar hyperglycemic state (HHS) at the time of diagnosis include:[11][12][13][14]
- Advanced age
- Severe dehydration
- Hypothermia
- Coma
- Hemodynamic instability
- Comorbidities such as chronic kidney disease or heart failure
References
- ↑ Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN (2009). "Hyperglycemic crises in adult patients with diabetes". Diabetes Care. 32 (7): 1335–43. doi:10.2337/dc09-9032. PMC 2699725. PMID 19564476.
- ↑ "Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar Syndrome | Diabetes Spectrum".
- ↑ "Hyperosmolar Hyperglycemic State - American Family Physician".
- ↑ Atchley DW, Loeb RF, Richards DW, Benedict EM, Driscoll ME (1933). "ON DIABETIC ACIDOSIS: A Detailed Study of Electrolyte Balances Following the Withdrawal and Reestablishment of Insulin Therapy". J. Clin. Invest. 12 (2): 297–326. doi:10.1172/JCI100504. PMC 435909. PMID 16694129.
- ↑ "care.diabetesjournals.org" (PDF).
- ↑ Muir AB, Quisling RG, Yang MC, Rosenbloom AL (2004). "Cerebral edema in childhood diabetic ketoacidosis: natural history, radiographic findings, and early identification". Diabetes Care. 27 (7): 1541–6. PMID 15220225.
- ↑ "Diabetic ketoacidosis". Diabetic ketoacidosis. Mayo Foundation for Medical Education and Research. 2006. Retrieved 2007-06-15. Text " By Mayo Clinic Staff " ignored (help)
- ↑ "Diabetic Coma > Diabetic ketoacidosis". Diabetic ketoacidosis. Armenian Medical Network. 2006. Retrieved 2007-06-15. Text " Umesh Masharani, MB, BS, MRCP " ignored (help)
- ↑ "Diabetic ketoacidosis complications". Diabetic ketoacidosis. The Diabetes Monitor. 2007. Retrieved 2007-06-15.
- ↑ Kitabchi AE, Umpierrez GE, Fisher JN, Murphy MB, Stentz FB (2008). "Thirty years of personal experience in hyperglycemic crises: diabetic ketoacidosis and hyperglycemic hyperosmolar state". J Clin Endocrinol Metab. 93 (5): 1541–52. doi:10.1210/jc.2007-2577. PMC 2386681. PMID 18270259.
- ↑ Liu WY, Lin SG, Wang LR, Fang CC, Lin YQ, Braddock M, Zhu GQ, Zhang Z, Zheng MH, Shen FX (2016). "Platelet-to-Lymphocyte Ratio: A Novel Prognostic Factor for Prediction of 90-day Outcomes in Critically Ill Patients With Diabetic Ketoacidosis". Medicine (Baltimore). 95 (4): e2596. doi:10.1097/MD.0000000000002596. PMC 5291578. PMID 26825908.
- ↑ Gale EA, Tattersall RB (1978). "Hypothermia: a complication of diabetic ketoacidosis". Br Med J. 2 (6149): 1387–9. PMC 1608617. PMID 102402.
- ↑ Al-Matrafi J, Vethamuthu J, Feber J (2009). "Severe acute renal failure in a patient with diabetic ketoacidosis". Saudi J Kidney Dis Transpl. 20 (5): 831–4. PMID 19736483.
- ↑ Nyenwe EA, Kitabchi AE (2011). "Evidence-based management of hyperglycemic emergencies in diabetes mellitus". Diabetes Res Clin Pract. 94 (3): 340–51. doi:10.1016/j.diabres.2011.09.012. PMID 21978840.