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Hyperosmolar hyperglycemic state


Authors: Jaroslav Rybka;  Jerguš Mistrík
Authors‘ workplace: Diabetologické centrum Interní kliniky Krajské nemocnice T. Bati, a. s., Zlín, přednosta MUDr. Jiří Latta
Published in: Vnitř Lék 2015; 61(5): 451-457
Category: Reviews

Overview

The hyperglycemic hyperosmolar state (HHS) is a serious acute complication of diabetes decompensation, especially in type 2 diabetes (T2DM), and with critical prognosis. Primary characteristics of HHS include extreme hyperglycemia, severe dehydration (with prerenal hyperazotaemia), plasma hyperosmolarity, frequent disorders of consciousness, absent or minimum ketoacidosis (with higher values, only found in combined forms). Both DKA and HHS have a common pathogenetic mechanism, but both states are opposite extreme deviations, and the boundaries between them are not entirely clear. Significant hyperglycemia is at the forefront of HHS, while ketoacidosis dominates in DKA. Various etiopathogenic mechanisms of the onset and development of HHS are discussed, but a clear explanation of the absence of ketoacidosis in HHS is lacking. The most frequent cause of HHS is serious cardiovascular disease, acute stroke, particularly genitourinary and/or respiratory infections, conditions preventing the patient from adequate water intake during osmotic diuresis, the consequences of inappropriate medication therapy, social conditions, and last but not least, it is often the first manifestation especially in type 2 diabetes. The clinical picture is influenced mainly by dehydration, while circulatory changes can lead to heart or circulatory failure and renal insufficiency. HHS is the cause of frequent disturbances of consciousness, and a cerebrovascular event should always be considered. Given the seriousness of HHS prognosis, timely comprehensive and properly guided therapy is of major prognostic significance. HHS treatment (rehydration, insulin therapy, ion substitution) is governed by similar rules as the treatment of diabetic ketoacidosis, but it also varies in many respects. Particular attention should be paid mainly to the control of dehydration. The patient with HHS should always be admitted to the intensive care unit. The most serious complications include cardiovascular complications, acute renal failure, thrombotic events and infectious complications. Given the still high mortality of patients with HHS the research focuses not only on the uncertainties concerning etiopathogenesis, but particularly on establishing safe and effective therapeutic strategies.

Key words:
diabetic ketoacidosis (DKA) – HHS therapy – hyperglycemia – hyperosmolar hyperglycemic state (HHS) – pathogenetic mechanisms of HHS


Sources

1. Pasquel FJ, Umpierrez GE. Hyperosmolar Hyperglycemic State: A Historic Review of the Clinical Presentation, Diagnosis, and Treatment. Diabetes Care 2014; 37(11): 3124–3131.

2. Kitabchi AE, Umpierrez GE, Murphy MB et al. American Diabetes Association. Hyperglycemic crises in diabetes. Diabetes Care 2004; 27(Suppl.1): S94-S102.

3. Rybka J. Akutní příhody v diabetologii. In: Rybka J et al. Kritické stavy vnitřního lékařství ve všeobecné praxi. Avicenum: Praha 1992: 305–314. ISBN 80–201–0143–8.

4. Malkani S et al. Diabetic Coma. In: Irwin RS, Rippe JM. Intensive Care Medicine. 7th ed. Wolters Kluwer Health/Lippincott Williams & Wilkins: Philadelphia 2011: 1139–1151. ISBN 978–1608311835.

5. Šmahelová A, Škrha J (eds). Hyperglykemický hyperosmolární neketotický stav. In: Škrha J (ed). Diabetologie. Galén: Praha 2009: 162–166. ISBN 978–80–7262–607–6.

6. Wyckoff J, Abrahamson MJ. Diabetic ketoacidisis and hyperosmolar hyperglycemic state. In: Joslin EP, Ronald C (eds). Joslin´s diabetes mellitus. 14th ed. Lippincott Williams and Wilkins: Philadelphia 2005: 887–899. ISBN 10–0812115317. ISBN 13–9780812115314.

7. Bouček P. Hyperglykemie. In: Pelikánová T, Bartoš V (eds). Praktická diabetologie. 5th ed. Maxdorf: Praha 2011: 362–372. ISBN 978–80- 7345–244–5.

8. Šmahelová A. Akutní komplikace diabetu. Triton: Praha 2006. ISBN 80–7254–812–3.

9. Polko J. Diabetická ketoacidóza, hyperglykemický hyperosmolární syndrom a laktátová acidóza. In: Mokáň M, Martinka E, Galajda P (eds). Diabetes mellitus. P + M: Turany 2008: 481–495. ISBN 9788096971398.

10.

11. Kitabchi AE, Umpierrez GE, Murphy MB et al. Hyperglycemic crises in adult patients with diabetes: a consensus statement from the American Diabetes Assotiation. Diabetes Care 2006; 29(12): 2739–2748.

12. Geglia JL, Wyckoff J, Abrahamson MJ. Acute hyperglycemic crisis in the elderly. Med Clin North Am 2004; 88(4):1063–1084.

13. Fadini GP, de Kreutzenberg SV, Rigato M et al. Characteristics and outcomes of the hyperglycemic hyperosmolar non-ketotic syndrome in a cohort of 51 consecutive cases at single center. Diabetes Res Clin Pract 2011; 94(2): 172–179.

14. Hansen TK, Moller N. Acute Metabolic Complications of Diabetes: Diabetic Ketoacidosis and Hyperosmolar Hyperglykemia. In: Holt R, Cockram C (eds). Textbook of Diabetes. 4th ed. Wiley-Blackwell 2010: 546–552. ISBN 978–1405191814.

15. Vavřinec J. Diabetická ketoacidóza a hyperosmolární hyperglykemické stavy u dětí. In: Kvapil M (ed). Diabetologie 2014. Triton: Praha 2014: 41–75. ISBN 978–80–7387–755–2.

16. Canarie MF, Bogue CW, Banasiak KJ et al. Decompensated hyperglycemic hyperosmolarity without significant ketoacidosis in the adolescent and young adult population. J Pediatr Endocrinol Metab 2007; 20(10): 1115–1124.

17. Bagdure D, Rewers A, Campagna E et al. Epidemiology of hyperglycemic hyperosmolar syndrome in children hospitalized in USA. Pediatr Diabetes 2013; 14(1): 18–24.

18. Kitabchi AE, Umpierez GE, Murphy MB et al. Management of hyperglycemic crises in patients with diabetes. Diabetes Care 2001; 24(1): 131–153.

19. Rybka J. Diabetická ketoacidóza a hyperosmolární neacidotický dekompenzovaný diabetes. In: Rybka J (ed). Pokroky v diabetologii 1. Avicenum: Praha 1990: 220–245. ISBN 80–201–0040–7.

20. Gerich J, Penhos JC, Recant L. Effect of dehydration and hyperosmolarity on glucose, free fatty acid and ketone body metabolism in the rat. Diabetes 1973; 22(4): 264–271.

21. Rains JL, Jain SK. Oxidative stress, insulin signaling, and diabetes. Free Radic Biol Med 2011; 50(5): 567–575.

22. Stentz FB, Umpierrez GE, Cuervo R et al. Proinflammatory cytokines, markers of cardiovascular risks, oxidative stress, and lipid peroxidation in patients with hyperglycemic crises. Diabetes 2004; 53(8): 2079–2086.

23. Ekpebegh C, Longo-Mbenza B. Mortality in hyperglycemic crisis: a high association with infection and cerebrovascular disease. Minerva Endocrinol 2013; 38(2): 187–193.

24. Corwell B, Knight B, Olivieri L et al. Current Diagnosis and Treatment of Hyperglycemic Emergencies. Emerg Med Clin N Am 2014; 32(2): 437–452.

25. Savage MW, Dhatariya KK, Kilvert A et al. Joint British Diabetes Societies guideline for the management of diabetic ketoacidosis. Diabet Med 2011; 28(5): 508–515.

26. Gerich JE, Martin MM, Recant L. Clinical and metabolic characteristics of hyperosmolar nonketotic coma. Diabetes 1971; 20(4): 228–238.

27. Arieff AI, Carroll HJ. Hyperosmolar nonketotic coma with hyperglycemia: abnormalities of lipid and carbohydrate metabolism. Metabolism 1971; 20(6): 529–538.

28. Kitabchi AE, Umpierrez GE, Miles JM et al. Hyperglycemic crises in adult patients with diabetes. Diabetes Care 2009; 32(7): 1335–1343.

29. Zeitler P, Haqq A, Rosenbloom A et al. Drugs and Therapeutics Committee of the Lawson Wilkins Pediatric Endocrine Society. Hyperglycemic hyperosmolar syndrome in children: pathophysiological considerations and suggested guidelines for treatment. J Pediatr 2011; 158(1): 9–14.

30. Alberti KG, Hockaday TD. Diabetic coma: a reappraisal after five years. Clin Endocrinol Metab 1977; 6(2): 421–455.

31. Poser CM. Hyperglycemic non-ketatic coma. Role of sodium in the pathogenesis of the neurologic manifestations. Dis Nerv Syst 1972; 33(11): 725–729.

32. Feng Y, Fleckman AM. Acute Hyperglycemic Syndromes: Diabetic Ketoacidosis and the Hyperosmolar State. In: Poretsky L (ed.) Principles of Diabetes Mellitus. 2nd ed. Springer 2010: 281–297. ISBN 978–0387098401.

33. Umpierrez GE, Murphy MB, Kitabchi AE. Diabetic ketoacidosis and hyperglycemic hyperosmolar syndrome. Diabetes Spectrum 2002: 15(1): 28–36.

34. Rybka J. Diabetická ketoacidóza a kóma hyperosmolární. In: Rybka J et al. Diabetes mellitus. Avicenum: Praha 1985: 269–291.

35. Genuth S. Diabetic ketoacidosis and hypercemic hypersmolar state in adults. In: Lebovitz HE et al (American Diabetes Association). Therapy for diabetes mellitus and related disorders. American Diabetes Association 2004: 87–99. ISBN 13: 978–1580403047. ISBN 10: 1580403042.

36. Kitabchi AE, Nyenwe EA. Hyperglycemic crises in diabetes mellitus: diabetic ketoacidosis and hyperglycemic hyperosmolar state. Endocrinol Metabol Clin North Am 2006; 35(4): 725–751.

37. Van Ness-Otunnu R, Hack JB. Hyperglycemic crisis. J Emerg Med 2013; 45(5): 797–805.

38. American Diabetes Association. Standards of medical care in diabetes – 2011. Diabetes Care 2011; 34(Suppl 1): S11-S61.

39. Gershengorn HB, Iwashyna TJ, Cooke CR et al. Variation in use of intensive care for adults with diabetic ketoacidosis. Crit Care Med 2012; 40(7): 2009–2015.

40. Keenan CR, Murin High S, White RH. High risk for venous thromboembolism in diabetics with hyperosmolar state: comparison with other acute medical illnesses. J Thromb Haemost 2007; 5(6): 1185–1190.

41. Langouche L, Vanhorebeek I, Vlasselaers D et al. Intensive insulin therapy protects the endothelium of critically ill patients. J Clin Invest 2005; 115(8): 2277–2286.

42. Arieff AI, Carroll HJ. Nonketotic hyperosmolar coma with hyperglycemia: clinical features, pathophysiology, renal function, acid-base balance, plasma-cerebrospinal fluid equilibria and the effects of therapy in 37 cases. Medicine (Baltimore) 1972; 51(2): 73–94.

43. Arieff AI. Cerebral edema complicating nonketotic hyperosmolar coma. Miner Electrolyte Metab 1986; 12(5–6): 383–389.

44. Arieff AI, Kleeman CR. Studies on mechanisms of cerebral edema in diabetic comas. Effects of hyperglycemia and rapid lowering of plasma glucose in normal rabbits. J Clin Invest 1973; 52(3): 571–583.

45. Svačina Š (ed). Metabolické účinky psychofarmak. Triton: Praha 2004. ISBN 80–7254–599-X.

Labels
Diabetology Endocrinology Internal medicine

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Internal Medicine

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