Main Article Content

Fatimah Hussain Alzaher
Hashim Mohammed Alawi Aljarrash
Madhawi Ali Al-Mutairi
Aisha Ebrahim Al-Dossary
Khameal Hussain Mohammad Al-Zaher
Fatimah Hassan Al Sheef
Kareemah Abdullah Shokan
Aqeelh Abdulaziz Said Al Ibrahim
Akeelah Abdullah Hussain Al Khalaf
Faten Hassan Al Sheef Staff Nurse
Abdullah Mohammed Ahmed Alezzy
Fahad Ibrahim S Alotaibi
Ameerah Ibraheem Almredeef
Mona Mohammed Al Huzaia


Diabetic ketoacidosis (DKA), Pathophysiology, Management.


Type 1 diabetes mellitus is a medical condition characterized by the absence of proper insulin functioning in the body, leading to the unopposed effects of the glucagon hormone. Diabetic ketoacidosis (DKA) is recognized as a severe and acute life-threatening complication that can arise from type 1 diabetes mellitus. It is important to note that DKA might manifest as the initial presentation of this particular medical condition. Individuals who do not adhere to their insulin therapy regimen or fail to administer insulin as prescribed are at a significantly higher risk of developing DKA. The onset of this condition is often triggered by severe illnesses such as pneumonia or myocardial infarction, which can result in increased levels of hormones that oppose insulin, such as adrenaline and glucocorticoids. Consequently, DKA is closely linked with disturbances in Acid-Base balance and Electrolyte levels within the body, further complicating the individual's overall health status. In this review, we highlight the significance of DKA and its pathophysiology, specifically focusing on suggestions for managing and treating it based on the available evidence.

Abstract 40 | Pdf Downloads 14


1. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN: Hyperglycemic crises in adult patients with diabetes. Diabetes care. 2009, 32:1335.
2. Goguen J, Gilbert J, Committee CDACPGE: Hyperglycemic emergencies in adults. Canadian journal of diabetes. 2013, 37:S72-S76.
3. Clausen T, Everts ME: Regulation of the Na, K-pump in skeletal muscle. Kidney international. 1989, 35:1-13.
4. Van den Berghe G, Kitabchi AE, Fisher JN: Hyperglycemic crises: diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS). Acute Endocrinology: From Cause to Consequence. 2008:119-147.
5. Wachtel TJ, Tetu-Mouradjian LM, Goldman DL, Ellis SE, O’Sullivan PS: Hyperosmolarity and acidosis in diabetes mellitus: a three-year experience in Rhode Island. Journal of general internal medicine. 1991, 6:495-502.
6. Nyenwe EA, Loganathan RS, Blum S, et al.: Active use of cocaine: an independent risk factor for recurrent diabetic ketoacidosis in a city hospital. Endocrine Practice. 2007, 13:22-29.
7. Polonsky WH, Anderson BJ, Lohrer PA, Aponte JE, Jacobson AM, Cole CF: Insulin omission in women with IDDM. Diabetes care. 1994, 17:1178-1185.
8. John W: Second-Generation (Atypical) Antipsychotics and Metabolic Effects. CNS Drugs. 2005, 19.
9. Taylor SI, Blau JE, Rother KI: SGLT2 inhibitors may predispose to ketoacidosis. The Journal of Clinical Endocrinology & Metabolism. 2015, 100:2849-2852.
10. Lorber D: Nonketotic hypertonicity in diabetes mellitus. Medical Clinics of North America. 1995, 79:39-52.
11. Nyenwe EA, Razavi LN, Kitabchi AE, Khan AN, Wan JY: Acidosis: the prime determinant of depressed sensorium in diabetic ketoacidosis. Diabetes care. 2010, 33:1837-1839.
12. Malone ML, Gennis V, Goodwin JS: Characteristics of diabetic ketoacidosis in older versus younger adults. Journal of the American Geriatrics Society. 1992, 40:1100-1104.
13. Rugg-Gunn C, Deakin M, Hawcutt D: Update and harmonisation of guidance for the management of diabetic ketoacidosis in children and young people in the UK. BMJ Paediatrics Open. 2021, 5:e001079. 10.1136/bmjpo-2021-001079
14. Gowrishankar M, Kamel KS, Halperin ML: A brain protein–centered view of H+ buffering. Journal of the American Society of Nephrology. 2007, 18:2278-2280.
15. Hoorn EJ, Carlotti AP, Costa LA, et al.: Preventing a drop in effective plasma osmolality to minimize the likelihood of cerebral edema during treatment of children with diabetic ketoacidosis. The Journal of pediatrics. 2007, 150:467-473.
16. Halperin ML, Maccari C, Kamel KS, Carlotti AP, Bohn D: Strategies to diminish the danger of cerebral edema in a pediatric patient presenting with diabetic ketoacidosis. Volume 7. Wiley Online Library; 2006:191-195.
17. Napolova O, Urbach S, Davids MR, Halperin ML: Assessing the degree of extracellular fluid volume contraction in a patient with a severe degree of hyperglycaemia. Nephrology Dialysis Transplantation. 2003, 18:2674-2677.
18. Wolfsdorf J, Craig ME, Daneman D, et al.: Diabetic ketoacidosis in children and adolescents with diabetes. Pediatr Diabetes. 2009, 10:118-133.
19. Savage M, Dhatariya K, Kilvert A, et al.: Joint British Diabetes Societies guideline for the management of diabetic ketoacidosis. Diabetic medicine. 2011, 28.
20. Kamel KS, Lin S-H, Cheema-Dhadli S, Marliss EB, Halperin ML: Prolonged total fasting: a feast for the integrative physiologist. Kidney international. 1998, 53:531-539.
21. Glaser N, Barnett P, McCaslin I, et al.: Risk factors for cerebral edema in children with diabetic ketoacidosis. New England Journal of Medicine. 2001, 344:264-269.
22. Kamel KS, Halperin ML: Acid–base problems in diabetic ketoacidosis. New England Journal of Medicine. 2015, 372:546-554.
23. Zipf WB, Bacon GE, Spencer ML, Kelch RP, Hopwood NJ, Hawker CD: Hypocalcemia, hypomagnesemia, and transient hypoparathyroidism during therapy with potassium phosphate in diabetic ketoacidosis. Diabetes care. 1979, 2:265-268.