Diyabetik ketoasidozda tanı ve tedavi yaklaşımı

Year 2019, Volume: 2 Issue: 3, 92 - 98, 01.07.2019

Tuna Turan , İrfan Karahan , Aşkın Güngüneş

https://doi.org/10.32322/jhsm.452023

Abstract

Diyabetik
ketoasidoz,   hızlı tanı ve tedavi
gerektiren tip 1 ve tip 2 diyabetes mellitusun ciddi komplikasyonlarından
biridir.  Genellikle tip 1 diyabet ile
birlikteliği vardır. Bunun yanında tip 2 diyabet hastalarında katabolik strese
yol açan ciddi enfeksiyon, travma, kardiyovasküler veya diğer acil durumlarda diyabetik
ketoasidoz tablosu görülebilir. Hiperglisemi osmotik diüreze yol açar. Osmotik diürez
elektrolitten çok sıvı kaybı ile karakterizedir.  İntravasküler hacim azalır. Bu durum
ilerledikçe böbrek perfüzyonu azalır, idrarla glukoz atılımı azaltılır,
hiperosmolarite giderek artar. Hiperozmolarite >330 mOsm/kg’ı aşarsa merkezi
sinir sistemi depresyonu ve koma durumu ortaya çıkabilir. Tanının erken konulup
tedaviye hemen başlanması mortalitede ciddi oranda azalmalara yol açmaktadır.
Tedavide en önemli sıvı replasmanı, sonra insülin tedavisi ve ardından
ketoasidoza yol açan nedene yönelik tedavidir. Diyabet sıklığı giderek artmakta
olduğu için, her hekimin pratikte karşılaşabileceği ve mortal seyredebilecek bu
komplikasyona dikkat çekmek istedik.

Keywords

Diyabet, ketoasidoz, komplikasyon

Diagnostic and therapeutic approach to diabetic ketoacidosis

Abstract

Diabetic
ketoacidosis is one of the serious complications of type 1 and type 2 diabetes
mellitus which require prompt diagnosis and treatment. It is usually associated
with type 1 diabetes. In addition, diabetic ketoacidosis can occur in severe
infection, trauma, cardiovascular or other emergencies that lead to catabolic
stress in type 2 diabetic patients. Hyperglycaemia leads to osmotic diuresis.
The osmotic diuresis is characterized by very fluid loss from the electrolyte.
The intravascular volume is reduced. As this condition progresses, kidney perfusion
decreases, urinary glucose excretion decreases, hyperosmolarity progressively
increases. If hyperosmolarity exceeds 330 mOsm / kg, central nervous system
depression and coma may occur. The early introduction of the diagnosis and the
onset of treatment immediately lead to a serious decrease in mortality.
Treatment is the most important fluid replacement, followed by insulin therapy
followed by treatment for ketoacidosis. As the frequency of diabetes is
increasing, we would like to draw attention to this complication that every
physician may encounter in practice and in mortality.

Keywords

Diabetes, ketoasidosis, complication

References

• 1. Umpierrez G, Korytowski M. Diabetic emergencies ketoacidosis, hyperglycaemic hyperosmolar state and hypoglycaemia. Nature Reviews Endocrinol 2016; 12: 222–32.
• 2. Masharani U. Diabetes mellitus ve hipoglisemi. Papadakis MA, McPhee SJ, Rabow MW (eds). Lange Güncel Tıbbi Tanı ve Tedavi, 54. Baskı. 2016: 1222-6.
• 3. Centers for Disease Control and Prevention. Diabetes data&trends. [online], http://www.cdc.gov/nchs/fastats/inpatient-surgery.htm (2015).
• 4. Chiasson JL, Aris-Jilwan N, Belanger R, et al. Diagnosis and treatment of diabetic ketoacidosis and hyperosmolar state. CMAJ 2003; 168: 859-66.
• 5. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes Care 2009; 32: 1335.
• 6. Smith RJ. Diabetes Mellitus, Hipoglisemi. Benjamim IJ, Griggs RJ, Wing EJ, Fitz JG (eds). Andreoli and Carpenter's Cecil Essential of Medicine, 9. Baskı (Türkçe). 2016: 668.
• 7. TEMD Diabetes Mellitus ve Komplikasyonlarının Tanı, Tedavi ve İzlem Kılavuzu 2018. Diyabette Akut Komplikasyonlar 2018; 119: 126- 128.
• 8. ADA Clinical Practice Recommendations. Diabetes Care 2004; 27 (Suppl 1): 94-102.
• 9. Champe PC, Harvey RA, Ferrier DR (eds). Trikarboksilik asit döngüsü - Yağ asidi ve triaçilgliserol metabolizması. Lippincott’s Illustrated Reviews Serisinden: Biyokimya, 3. Baskı. 2007: 112: 195-6.
• 10. Masharani U, German MS. Pankreatik hormonlar ve diyabetes mellitus. Gardner DG, Shoback D (eds). Lange Greenspan's Temel ve Klinik Endokrinoloji, 9. Baskı. 2013: 629-32.
• 11. Kitabchi AE, Umpierrez GE, Murphy MB, et al. Management of hyperglycemic crises in patients with diabetes mellitus (Technical Review). Diabetes Care 2001; 24: 131.
• 12. Newcomer JW. Second-generation (atypical) antipsychotics and metabolic effects: a comprehensive literature review. CNS Drugs 2005; 19 Suppl 1: 1.
• 13. Warner EA, Greene GS, Buchsbaum MS, Cooper DS, Robinson BE. Diabetic ketoacidosis associated with cocaine use. Arch Intern Med. 1998; 158: 1799.
• 14. Polonsky WH, Anderson BJ, Lohrer PA, Aponte JE, Jacobson AM, Cole CF. Insulin omission in women with IDDM. Diabetes Care 1994; 17: 1178.
• 15. Umpierrez G, Amado XF. Abdominal pain in patients with hyperglycemic crises. J Crit Care. 2002; 17: 63.
• 16. Granner DK, Olgun A. Pankreas ve sindirim kanalı hormonları. Murray RK, Granner DK, Mayes PA, Rodwell WW (eds). Harper Biyokimya, 25. Baskı. 2004: 615.
• 17. Yadav D, Nair S, Norkus EP, Pitchumoni CS. Non specific hyperamylasemia and hyperlipasemia in diabetic ketoacidosis: incidence and correlation with biochemical abnormalities. Am J Gastroenterol 2000; 95: 3123.
• 18. Viallon A, Zeni F, Lafond P, et al. Does bicarbonate therapy improve the management of severe diabetic ketoacidosis? Crit Care Med 1999; 27: 2690.
• 19. DeFronzo RA, Matzuda M, Barret E. Diabetic ketoacidosis: a combined metabolic - nephrologic approach to therapy. Diabetes Rev 1994; 2: 209.
• 20. Wolfsdorf J, Glaser N, Sperling MA, American Diabetes Association. Diabetic ketoacidosis in infants, children, and adolescents: A consensus statement from the American Diabetes Association. Diabetes Care 2006; 29: 1150.
• 21. Kitabchi AE, Wall MB. Diabetic ketoacidosis. Med Clin North Am 1995; 79: 9-37.