Diabetic Ketoacidosis: Difference between revisions

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==Overview==
==Overview==
[[Diabetic ketoacidosis]] is diagnosed in the presence of symptoms like lethargy, fruity breath, thirst, weight loss, abdominal pain, and Kussmaul breathing and laboratory findings of [[hyperglycemia]] ([[Plasma glucose]] > 250 mg/dL), [[Metabolic acidosis|anion gap metabolic acidosis]] (pH < 7.3) and [[Serum bicarbonate]] < 15 mEq/L) and [ketonemia]]/ [[ketonuria]]. The mainstay of treatment involves agressive hydration with normal saline, glucose correction with insulin, potassium repletion and correction of acidosis.
[[Diabetic ketoacidosis]] is diagnosed in the presence of symptoms like lethargy, fruity breath, thirst, weight loss, abdominal pain, and Kussmaul breathing and laboratory findings of [[hyperglycemia]] ([[Plasma glucose]] > 250 mg/dL), [[Metabolic acidosis|anion gap metabolic acidosis]] (pH < 7.3) and [[Serum bicarbonate]] < 15 mEq/L) and [[ketonemia]]/ [[ketonuria]]. The mainstay of treatment involves agressive hydration with normal saline, glucose correction with insulin, potassium repletion and correction of acidosis.


==Causes==
==Causes==

Revision as of 01:39, 29 July 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ifrah Fatima, M.B.B.S[2]

Overview

Diabetic ketoacidosis is diagnosed in the presence of symptoms like lethargy, fruity breath, thirst, weight loss, abdominal pain, and Kussmaul breathing and laboratory findings of hyperglycemia (Plasma glucose > 250 mg/dL), anion gap metabolic acidosis (pH < 7.3) and Serum bicarbonate < 15 mEq/L) and ketonemia/ ketonuria. The mainstay of treatment involves agressive hydration with normal saline, glucose correction with insulin, potassium repletion and correction of acidosis.

Causes

The following are the causes of diabetic ketoacidosis (DKA):

Common Causes

Less common causes

Nonadherence to insulin treatment plans:[17][18]

Physiological stressors:

Diagnosis

VARIABLE DIABETIC KETOACIDOSIS
MILD (Plasma Glucose > 250mg/dL or 13.88 mmol/L) MODERATE (Plasma Glucose > 250mg/dL or 13.88 mmol/L) SEVERE (Plasma Glucose > 250mg/dL or 13.88 mmol/L)
Arterial pH 7.25 to 7.30 7.00 to < 7.24 < 7.00
Serum bicarbonate 15 to 18 mEq/L 10 to < 15 mEq/L < 10 mEq/L
Urine ketone (Nitroprusside reaction method) Positive Positive Positive
Serum ketone (Nitroprusside reaction method) Positive Positive Positive
Effective serum osmolality Variable Variable Variable
Anion gap > 10 mEq/L (10 mmol/L) > 12 mEq/L (12 mmol/L) > 12 mEq/L (12 mmol/L)
Mental status Alert Alert/drowsy Stupor/coma

Treatment

Shown below is an algorithm summarizing the treatment of Diabetic ketoacidosis according the American Association of Clinical Endocrinologists (AACE) guidelines [31] and American Diabetes Association guidelines. [29]

Step-wise approach to management of diabetic ketoacidosis

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
DKA treatment protocol according to ADA guidelines
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Fluids
 
 
 
 
 
 
 
 
Bicarbonate
 
 
 
 
 
 
Insulin
 
 
 
 
 
 
 
 
Potassium
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Hydration status
 
 
 
 
 
 
pH greater than equal to 6.9
 
pH less than 6.9
 
 
0.1 u/kg/B.WT. as IV bolus
 
 
0.14 u/kg/B.WT/hr as continous IV infusion
 
K < 3.3 mEq/L
 
K = 3.3 - 5.2 mEq/L
 
 
K > 5.2 mEq/L
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Severe hypovolemia
 
Mild dehydration
 
Cardiogenic shock
 
 
 
 
 
 
 
 
 
 
 
0.1 u/kg/B.WT. as IV continous infusion
 
 
 
 
 
 
 
Hold insulin and give 20-30mEq/L of potassium until K+ > 3.3mEq/L
 
Give 20-30mEq/L in each liter of IV fluids to maintain serum K 4-5mEq/L
 
 
Do not give potassium but check serum potassium every 2 hours
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
0.9% Nacl (1L/hr) as IV infusion
 
Check corrected serum sodium
 
Hemodynamic monitoring and add pressors accordingly
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
If serum glucose does not fall by 10 % within one hour of therapy then give 0.14 U/Kg as IV bolus and continue previous regimen
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
High serum Na (>145 mEq/L)
 
Normal serum Na (135-145 mEq/L)
 
Low serum Na (< 135 mEq/L)
 
 
 
 
 
 
 
 
 
 
 
 
When serum glucose drops to 200 mg/dl, reduce regular insulin to 0.02-0.05 U/Kg/hour, or give rapid-acting insulin at 0.1 U/kg SC every 2 hours, maintain serum glucose between 150 mg/dl to,200 mg/dl until resolution
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
0.45% NaCl (250-500 ml per hour depending on hydration status
 
 
 
 
0.9% NaCl (200-500 ml per hour) depending on hydration status
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
When serum glucose decreases to 200 mg/dl, switch to 5% dextrose with 0.45% NaCl at 150-250 ml/hour
 
 
 
 
 
 
 
 
 

Do's

  • Correct hypovolemia and dehydration aggressively.
  • In patients with potassium(K) < 3.3 mEq/L, fluids and potassium replacement must be done before initiating insulin therapy, to prevent further hypokalemia.
  • Monitor plasma glucose levels every hourly.
  • Monitor serum electrolytes and pH levels every 2-3 hourly.

Don'ts

  • Avoid rapid correction of plasma osmolality and serum sodium, to prevent fatal cerebral edema.
  • Maximum reduction in plasma osmolality should be 3 mOsmol/kg per hour.

References

  1. ↑ 1.0 1.1 Evans K (2019). "Diabetic ketoacidosis: update on management". Clin Med (Lond). 19 (5): 396–398. doi:10.7861/clinmed.2019-0284. PMC 6771342 Check |pmc= value (help). PMID 31530688.
  2. ↑ Razavi Z (2010). "Frequency of ketoacidosis in newly diagnosed type 1 diabetic children". Oman Med J. 25 (2): 114–7. doi:10.5001/omj.2010.31. PMC 3215499. PMID 22125712.
  3. ↑ 3.0 3.1 Casqueiro J, Casqueiro J, Alves C (2012). "Infections in patients with diabetes mellitus: A review of pathogenesis". Indian J Endocrinol Metab. 16 Suppl 1: S27–36. doi:10.4103/2230-8210.94253. PMC 3354930. PMID 22701840.
  4. ↑ Ramaswamy K, Kozma CM, Nasrallah H (2007). "Risk of diabetic ketoacidosis after exposure to risperidone or olanzapine". Drug Saf. 30 (7): 589–99. PMID 17604410.
  5. ↑ Guenette MD, Hahn M, Cohn TA, Teo C, Remington GJ (2013). "Atypical antipsychotics and diabetic ketoacidosis: a review". Psychopharmacology (Berl.). 226 (1): 1–12. doi:10.1007/s00213-013-2982-3. PMID 23344556.
  6. ↑ Alavi IA, Sharma BK, Pillay VK (1971). "Steroid-induced diabetic ketoacidosis". Am. J. Med. Sci. 262 (1): 15–23. PMID 4327634.
  7. ↑ Alberti KG (1975). "Role of glucagon and other hormones in development of diabetic ketoacidosis". Lancet. 1 (7920): 1307–11. PMID 49515.
  8. ↑ Nakamura K, Kawasaki E, Imagawa A, Awata T, Ikegami H, Uchigata Y, Kobayashi T, Shimada A, Nakanishi K, Makino H, Maruyama T, Hanafusa T (2011). "Type 1 diabetes and interferon therapy: a nationwide survey in Japan". Diabetes Care. 34 (9): 2084–9. doi:10.2337/dc10-2274. PMC 3161293. PMID 21775762.
  9. ↑ Lu CP, Wu HP, Chuang LM, Lin BJ, Chuang CY, Tai TY (1995). "Pentamidine-induced hyperglycemia and ketosis in acquired immunodeficiency syndrome". Pancreas. 11 (3): 315–6. PMID 8577688.
  10. ↑ Lambertus MW, Murthy AR, Nagami P, Goetz MB (1988). "Diabetic ketoacidosis following pentamidine therapy in a patient with the acquired immunodeficiency syndrome". West. J. Med. 149 (5): 602–4. PMC 1026553. PMID 3150636.
  11. ↑ Borberg C, Gillmer MD, Beard RW, Oakley NW (1978). "Metabolic effects of beta-sympathomimetic drugs and dexamethasone in normal and diabetic pregnancy". Br J Obstet Gynaecol. 85 (3): 184–9. PMID 24459.
  12. ↑ Rodgers BD, Rodgers DE (1991). "Clinical variables associated with diabetic ketoacidosis during pregnancy". J Reprod Med. 36 (11): 797–800. PMID 1684993.
  13. ↑ Bouter KP, Diepersloot RJ, van Romunde LK, Uitslager R, Masurel N, Hoekstra JB, Erkelens DW (1991). "Effect of epidemic influenza on ketoacidosis, pneumonia and death in diabetes mellitus: a hospital register survey of 1976-1979 in The Netherlands". Diabetes Res. Clin. Pract. 12 (1): 61–8. PMID 1906798.
  14. ↑ Nakamura K, Inokuchi R, Doi K, Fukuda T, Tokunaga K, Nakajima S, Noiri E, Yahagi N (2014). "Septic ketoacidosis". Intern. Med. 53 (10): 1071–3. PMID 24827487.
  15. ↑ Osuchowski MF, Craciun FL, Schuller E, Sima C, Gyurko R, Remick DG (2010). "Untreated type 1 diabetes increases sepsis-induced mortality without inducing a prelethal cytokine response". Shock. 34 (4): 369–76. doi:10.1097/SHK.0b013e3181dc40a8. PMC 2941557. PMID 20610941.
  16. ↑ Czaja CA, Rutledge BN, Cleary PA, Chan K, Stapleton AE, Stamm WE (2009). "Urinary tract infections in women with type 1 diabetes mellitus: survey of female participants in the epidemiology of diabetes interventions and complications study cohort". J. Urol. 181 (3): 1129–34, discussion 1134–5. doi:10.1016/j.juro.2008.11.021. PMC 2699609. PMID 19152925.
  17. ↑ Borus JS, Laffel L (2010). "Adherence challenges in the management of type 1 diabetes in adolescents: prevention and intervention". Curr. Opin. Pediatr. 22 (4): 405–11. doi:10.1097/MOP.0b013e32833a46a7. PMC 3159529. PMID 20489639.
  18. ↑ Gosmanov AR, Gosmanova EO, Dillard-Cannon E (2014). "Management of adult diabetic ketoacidosis". Diabetes Metab Syndr Obes. 7: 255–64. doi:10.2147/DMSO.S50516. PMC 4085289. PMID 25061324.
  19. ↑ Katz JR, Edwards R, Khan M, Conway GS (1996). "Acromegaly presenting with diabetic ketoacidosis". Postgrad Med J. 72 (853): 682–3. PMC 2398638. PMID 8944212.
  20. ↑ Burzynski J (2005). "DKA and thrombosis". CMAJ. 173 (2): 132, author reply 132–3. doi:10.1503/cmaj.1050103. PMC 1174837. PMID 16027420.
  21. ↑ Jovanovic A, Stolic RV, Rasic DV, Markovic-Jovanovic SR, Peric VM (2014). "Stroke and diabetic ketoacidosis--some diagnostic and therapeutic considerations". Vasc Health Risk Manag. 10: 201–4. doi:10.2147/VHRM.S59593. PMC 3986295. PMID 24748799.
  22. ↑ Pivonello R, De Leo M, Vitale P, Cozzolino A, Simeoli C, De Martino MC, Lombardi G, Colao A (2010). "Pathophysiology of diabetes mellitus in Cushing's syndrome". Neuroendocrinology. 92 Suppl 1: 77–81. doi:10.1159/000314319. PMID 20829623.
  23. ↑ Pasternak DP (1974). "Hemochromatosis presenting as diabetic ketoacidosis with extreme hyperglycemia". West. J. Med. 120 (3): 244–6. PMC 1129403. PMID 4205898.
  24. ↑ Trachtenbarg DE (2005). "Diabetic ketoacidosis". Am Fam Physician. 71 (9): 1705–14. PMID 15887449.
  25. ↑ Nair S, Yadav D, Pitchumoni CS (2000). "Association of diabetic ketoacidosis and acute pancreatitis: observations in 100 consecutive episodes of DKA". Am. J. Gastroenterol. 95 (10): 2795–800. doi:10.1111/j.1572-0241.2000.03188.x. PMID 11051350.
  26. ↑ Kamalakannan D, Baskar V, Barton DM, Abdu TA (2003). "Diabetic ketoacidosis in pregnancy". Postgrad Med J. 79 (934): 454–7. PMC 1742779. PMID 12954957.
  27. ↑ Umpierrez GE, Kitabchi AE (2003). "Diabetic ketoacidosis: risk factors and management strategies". Treat Endocrinol. 2 (2): 95–108. PMID 15871546.
  28. ↑ Dhatariya KK (2007). "Diabetic ketoacidosis". BMJ. 334 (7607): 1284–5. doi:10.1136/bmj.39237.661111.80. PMC 1895683. PMID 17585123.
  29. ↑ 29.0 29.1 Schmoldt A, Benthe HF, Haberland G (1975). "Digitoxin metabolism by rat liver microsomes". Biochem Pharmacol. 24 (17): 1639–41. PMID doi.org/10.2337/dc09-9032 Check |pmid= value (help).
  30. ↑ Kitabchi AE, Umpierrez GE, Murphy MB, Barrett EJ, Kreisberg RA, Malone JI; et al. (2001). "Management of hyperglycemic crises in patients with diabetes". Diabetes Care. 24 (1): 131–53. doi:10.2337/diacare.24.1.131. PMID 11194218.
  31. ↑ "www.aace.com" (PDF).


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