Hyperglycemic crises resident survival guide: Difference between revisions
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==Overview== | ==Overview== | ||
[[Diabetic ketoacidosis]] (DKA) and [[hyperosmolar hyperglycemic state]] (HHS) are life threatening complications of untreated or inadequately treated [[diabetes mellitus]]. [[DKA]] is characterized by [[hyperglycemia]], [[acidosis]] and [[ketosis]]; whereas HHS is characterized by [[hyperglycemia]], [[hyperosmolarity]] and [[dehydration]] without [[ketosis]].<ref name="pmid19564476">{{cite journal| author=Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN| title=Hyperglycemic crises in adult patients with diabetes. | journal=Diabetes Care | year= 2009 | volume= 32 | issue= 7 | pages= 1335-43 | pmid=19564476 | doi=10.2337/dc09-9032 | pmc=PMC2699725 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19564476 }} </ref> | [[Diabetic ketoacidosis]] (DKA) and [[hyperosmolar hyperglycemic state]] (HHS) are life threatening complications of untreated or inadequately treated [[diabetes mellitus]]. [[DKA]] is characterized by [[hyperglycemia]], [[acidosis]] and [[ketosis]]; whereas HHS is characterized by [[hyperglycemia]], [[hyperosmolarity]], and [[dehydration]] without [[ketosis]].<ref name="pmid19564476">{{cite journal| author=Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN| title=Hyperglycemic crises in adult patients with diabetes. | journal=Diabetes Care | year= 2009 | volume= 32 | issue= 7 | pages= 1335-43 | pmid=19564476 | doi=10.2337/dc09-9032 | pmc=PMC2699725 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19564476 }} </ref> | ||
==Causes== | ==Causes== | ||
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==Management== | ==Management== | ||
The diagnostic approach and management management of [[DKA]] and [[HHS]] are | The diagnostic approach and management management of [[DKA]] and [[HHS]] are based on the 2009 Diabetic Care recommendations.<ref name="pmid19564476">{{cite journal| author=Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN| title=Hyperglycemic crises in adult patients with diabetes. | journal=Diabetes Care | year= 2009 | volume= 32 | issue= 7 | pages= 1335-43 | pmid=19564476 | doi=10.2337/dc09-9032 | pmc=PMC2699725 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19564476 }} </ref> | ||
===General Approach=== | ===General Approach=== | ||
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❑ [[Polyuria]]<br> | ❑ [[Polyuria]]<br> | ||
❑ [[Polydipsia]]<br> | ❑ [[Polydipsia]]<br> | ||
❑ Weight loss<br> | ❑ [[Weight loss]]<br> | ||
❑ Vomiting<br> | ❑ [[Vomiting]]<br> | ||
❑ [[Dehydration]]<br> | ❑ [[Dehydration]]<br> | ||
❑ Weakness<br> | ❑ Weakness<br> |
Revision as of 00:32, 22 October 2014
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Vidit Bhargava, M.B.B.S [2], Rim Halaby, M.D. [3]
Overview
Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are life threatening complications of untreated or inadequately treated diabetes mellitus. DKA is characterized by hyperglycemia, acidosis and ketosis; whereas HHS is characterized by hyperglycemia, hyperosmolarity, and dehydration without 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. Diabetic ketoacidosis and hyperosmolar hyperglycemic state are life-threatening conditions and must be treated as such irrespective of the causes.
Common Causes
- Alcohol
- Cholecystitis
- Cerbrovascular accident
- Dehydration
- Drug intoxication
- Failure of pump therapy[2][3]
- Inadequate treatment of DM
- Insulin deficiency
- Medications (corticosteroid, pentamidine,[4] thiazide diuretics, clozapine[5])
- MI
- Pancreatitis
- Pneumonia[6]
- Pregnancy[7]
- Surgery[8]
- UTI
Management
The diagnostic approach and management management of DKA and HHS are based on the 2009 Diabetic Care recommendations.[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 DKA: ❑ Blood glucose <200 mg/dl, AND Determine the resolution of HHS: | ||||||||||||||||||||||||||||||||||||||||||||||||||
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 200 mg/dL in DKA (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+>3.3 mEq/L ❑ 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 200 mg/dL for DKA (300 mg/dL for 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 and 200 mg/dL until resolution of DKA (200-300 mg/dL for HHS) | |||||||||||||||||
❑ Check glucose every 3-4 hours until stable | |||||||||||||||||
❑ Confirm resolution of DKA 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 DKA | |||||||||||||||||||||||
Management: Bicarbonate
❑ Assess pH | |||||||||||||||
pH≥6.9 | pH<6.9 | ||||||||||||||
❑ No HCO3- | ❑ 100 mmol HCO3- in 400 mL H20 and 20 mEq KCl infusion for 2 hours | ||||||||||||||
❑ Repeat every 2 hours until pH≥7 ❑ Monitor serum K+ every 2 hours | |||||||||||||||
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.
- 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 SC insulin is administered because it needs time to kick in.
- Do not give insulin if K+ levels are below 3.5 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.
- Do not supplement phosphate excessively, clinical trials have not shown any benefits. Supplement phosphate only if there is an actual deficit.
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.
- ↑ Rosenbloom, AL. (2010). "The management of diabetic ketoacidosis in children". Diabetes Ther. 1 (2): 103–20. doi:10.1007/s13300-010-0008-2. PMID 22127748. Unknown parameter
|month=
ignored (help) - ↑ Baird, JS. (2009). "Relapse of diabetic ketoacidosis secondary to insulin pump malfunction diagnosed by capillary blood 3-hydroxybutyrate: a case report". Cases J. 2: 8012. doi:10.4076/1757-1626-2-8012. PMID 19918445.
- ↑ 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. PMID 3150636. Unknown parameter
|month=
ignored (help) - ↑ Ai, D.; Roper, TA.; Riley, JA. (1998). "Diabetic ketoacidosis and clozapine". Postgrad Med J. 74 (874): 493–4. PMID 9926128. Unknown parameter
|month=
ignored (help) - ↑ Umpierrez, GE.; Kitabchi, AE. (2003). "Diabetic ketoacidosis: risk factors and management strategies". Treat Endocrinol. 2 (2): 95–108. PMID 15871546.
- ↑ Parker, JA.; Conway, DL. (2007). "Diabetic ketoacidosis in pregnancy". Obstet Gynecol Clin North Am. 34 (3): 533–43, xii. doi:10.1016/j.ogc.2007.08.001. PMID 17921013. Unknown parameter
|month=
ignored (help) - ↑ MacGillivray, MH.; Bruck, E.; Voorhess, ML. (1981). "Acute diabetic ketoacidosis in children: role of the stress hormones". Pediatr Res. 15 (2): 99–106. doi:10.1203/00006450-198102000-00002. PMID 6789292. Unknown parameter
|month=
ignored (help)