Hyperglycemic crises resident survival guide
For more information about DKA, click here.
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2], Husnain Shaukat, M.D [3]
Hyperglycemic crises Resident Survival Guide Microchapters |
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Overview |
Classification |
Causes |
FIRE |
Diagnosis |
Treatment |
Do's |
Don'ts |
Overview
Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are life threatening complications of untreated or inadequately treated diabetes mellitus. HHS is characterized by hyperglycemia, hyperosmolarity and dehydration; whereas DKA is characterized by hyperglycemia, acidosis, and ketosis.[1]
Causes
Life Threatening Causes
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. Hyperosmolar hyperglycemic state is a life-threatening condition and must be treated as such irrespective of the causes.
Common Causes
Common causes of hyperosmolar hyperglycemic state (HHS) include:
- Infections:
- Drugs:[7][8]
- Myocardial infarction[16]
- Pancreatitis[17]
- Shock/hypovolemia[18]
- Trauma[19]
- Undiagnosed diabetes mellitus[20]
- Noncompliance to insulin treatment:[21][22]
- Body image issues
- Financial problems
- Lack of insulin[5]
- Psychological factors
- Self-neglect
- Accidental
- Neglect by caregivers
Management
The diagnostic approach and management management of HHS and DKA are based on the ADA guidelines published in 2009.[1]
General Approach
Characterize the symptoms:
❑ Polyuria Examine the patient: ❑ Poor skin turgor Identify precipitating factors: ❑ Infections ❑ Insulin deficiency ❑ Myocardial infarction ❑ New onset DM type 1 ❑ Pregnancy ❑ Stress | |||||
Order tests: ❑ Serum glucose ❑ EKG ❑ CXR ❑ Urine, sputum, blood cultures (not routine) | |||||
Start the management of the following SIMULTANEOUSLY: (Urgent) (Check the algorithms below for more details) ❑ IV fluids | |||||
Check the following every two hours until the patient is stable: ❑ Glucose ❑ Electrolytes ❑ BUN ❑ Venous pH ❑ Creatinine | |||||
Determine the resolution of HHS: ❑ Blood glucose <200 mg/dl, AND Determine the resolution of HHS: | |||||
- The diagnosis of diabetic ketoacidosis is made in the presence of:
- Hyperglycemia- Plasma glucose > 250 mg/dL
- Anion gap metabolic acidosis- pH < 7.3; Serum bicarbonate < 15 mEq/L
- Ketonemia/ Ketonuria
- Shown below is a table summarizing the diagnosis of Diabetic ketoacidosis according the the American Diabetes Association (ADA) guidelines. [23] [24]
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 |
Management: IV Fluids
Initial IV fluid ❑ 0.9% NaCl (15-20ml/kg/hour), OR ❑ 1-1.5L during the first hour | |||||||||||||||||||||||||||||
❑ Evaluate the hydration status | |||||||||||||||||||||||||||||
Severe hypovolemia | Mild hypovolemia | Cardiogenic shock ❑ Hemodynamic monitoring/pressors | |||||||||||||||||||||||||||
❑ Assess the corrected [Na+] | |||||||||||||||||||||||||||||
❑ Administer 0.9% NaCl (1.0L/hour) | High or normal [Na+] ❑ Administer 0.45% NaCl (250-500 ml/hour) depending on the hydration status | Low [Na+] ❑ Administer 0.9% NaCl (250-500 ml/hour) depending on the hydration status | |||||||||||||||||||||||||||
Hemodynamic monitoring: | |||||||||||||||||||||||||||||
When serum glucose reaches 200mg/dL in DKA and 300mg/dl in HHS ❑ Change to 5% dextrose with 0.45% NaCl (150-250 mL/hour) | |||||||||||||||||||||||||||||
Management: Insulin
Check K+ before administering insulin | |||||||||||||||||
K+<3.3 mEq/L ❑ Hold insulin and give K+ 20-30 mEq/h until K+>3.3 mEq/L | K+>5.5 mEq/L ❑ Do not give K ❑ Proceed with insulin | ||||||||||||||||
Administer initial IV dose of insulin ❑ Continuous IV infusion of 0.14 U/Kg/h, OR ❑ IV bolus of 0.1 U/Kg, then continuous IV infusion of 0.1 U/Kg/h | |||||||||||||||||
❑ Check if serum glucose falls by 10% in the first hour | |||||||||||||||||
Yes | No | ||||||||||||||||
❑ Administer IV bolus of 0.14 U/Kg, then continue previous treatment | |||||||||||||||||
When serum glucose reaches 250mg/dl in DKA and 300mg/dl in HHS: ❑ Reduce IV regular insulin infusion to 0.02-0.05 U/kg/h, OR ❑ Administer SC rapid acting insulin at 0.1 U/kg every 2 hours ❑ Keep serum glucose between 150-200 mg/dL until resolution (200-300 mg/dL for HHS) | |||||||||||||||||
❑ Check glucose, BUN, electrolytes, creatinine, venous pH every 3-4 hours until stable | |||||||||||||||||
❑ Confirm resolution and assess ability to eat | |||||||||||||||||
Inability to eat | Able to eat | ||||||||||||||||
❑ Continue IV insulin infusion and IV fluid replacement | Transfer from IV to SC insulin ❑ Initiate SC multidose insulin ❑ Continue IV insulin 1-2 hours after SC insulin is initiated | ||||||||||||||||
Patient previously on insulin? ❑ Recommence the insulin home dose | Insulin naive patient? ❑ Start at a multidose of 0.5-0.8 U/kg/day | ||||||||||||||||
Management: Potassium
❑ Assess K+ level ❑ Establish adequate renal function (urine output 50 ml/hour) | |||||||||||||||||||||||
K+<3.3 mEq/L | K+= 3.3-5.2 mEq/L | K+>5.2 mEq/L | |||||||||||||||||||||
❑ Hold insulin ❑ Administer 20-30 mEq/hour until K+>3.3 mEq/L | ❑ Administer 20-30 mEq/hour in each liter of IV fluid to keep serum K+ between 4 and 5 mEq/L | ❑ Do not give K+ | |||||||||||||||||||||
Keep K+= 4-5 mEq/L ❑ Check K+ every 2 hours until resolution of HHS | |||||||||||||||||||||||
Do's
- Check labs initially and every 2-4 hours.
- Immediately check urine for ketones with dipstick and send urine to the lab for analysis.
- Initiate IV insulin as soon as the patient arrives and satisfies the diagnostic criteria of DKA.
- Assess the trigger that precipitated DKA and treat the cause.
- In patients with potassium(K) < 3.3 mEq/L, fluids and potassium replacement must be done before initiating insulin therapy, to prevent further hypokalemia.
- Admit the patient to the floor; however, if the pH < 7.0 or the patient is unconscious then admit to ICU.
- Make sure to calculate the corrected sodium level when evaluating the sodium level. Sodium can be falsely low due to the elevated glucose level; in order to correct for this, add 1.6 mmol/L of Na+ for every 100 mg/dL of glucose > 100 mg/dL.
- Monitor for complications of DKA itself or of the therapy.
- In case the patient has cardiac or renal compromise, monitor serum osmolality and frequently assess the cardiac, renal and mental status.
Don'ts
- Do not stop IV insulin until DKA has resolved.
- Do not stop IV insulin, even if subcutaneous insulin is administered because it needs time to kick in.
- Do not give insulin if K+ levels are below 3.3 mEq/l because it may further exacerbate the hypokalemia.
- Do not use 0.9% NaCl if corrected Na+ levels > 145 mEq/l, use 0.45% instead.
- 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.
- Do not supplement phosphate excessively, clinical trials have not shown any benefits. Supplement phosphate only if there is an actual deficit.
- DO not use subcutaneous sliding scale insulin in management of hyperglycemia due to diabetes type 1.[25]
References
- ↑ 1.0 1.1 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 5.0 5.1 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Alavi IA, Sharma BK, Pillay VK (1971). "Steroid-induced diabetic ketoacidosis". Am. J. Med. Sci. 262 (1): 15–23. PMID 4327634.
- ↑ Alberti KG (1975). "Role of glucagon and other hormones in development of diabetic ketoacidosis". Lancet. 1 (7920): 1307–11. PMID 49515.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Rodgers BD, Rodgers DE (1991). "Clinical variables associated with diabetic ketoacidosis during pregnancy". J Reprod Med. 36 (11): 797–800. PMID 1684993.
- ↑ Trachtenbarg DE (2005). "Diabetic ketoacidosis". Am Fam Physician. 71 (9): 1705–14. PMID 15887449.
- ↑ 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.
- ↑ Umpierrez GE, Kitabchi AE (2003). "Diabetic ketoacidosis: risk factors and management strategies". Treat Endocrinol. 2 (2): 95–108. PMID 15871546.
- ↑ Dhatariya KK (2007). "Diabetic ketoacidosis". BMJ. 334 (7607): 1284–5. doi:10.1136/bmj.39237.661111.80. PMC 1895683. PMID 17585123.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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). - ↑ 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.
- ↑ Pasquel FJ, Lansang MC, Dhatariya K, Umpierrez GE (2021). "Management of diabetes and hyperglycaemia in the hospital". Lancet Diabetes Endocrinol. 9 (3): 174–188. doi:10.1016/S2213-8587(20)30381-8. PMID 33515493 Check
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value (help).