Hypoglycemia: Difference between revisions
(Updated disposition guidelines.)
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** Generally symptomatic at <55mg/dL though threshold is variable depending on chronicity
** Generally symptomatic at <55mg/dL though threshold is variable depending on chronicity
* Resolution of symptoms after administration of glucose
* Resolution of symptoms after administration of glucose
*Determine etiology of hypoglycemia
 
==Evaluation==
Patients with known diabetes who are not systemically ill and can identify a clear precipitant, no extensive workup is required. In severely ill patients, consider:
* BMP
* LFT
* EtOH
* Infectious workup: CXR, UA, urine and blood cultures
* ECG, troponin
* Other studies: insulin, C-peptide, pro-insulin, glucagon, growth hormone, cortisol, B-OH, insulin antibodies


==Management==
==Management==
Line 57: Line 65:


==Disposition==
==Disposition==
*Admit for refractory hypoglycemia, sulfonylurea-induced hypoglycemia or long acting insulins
Admission or observation for oral anti-hyperglycemic agent or intermediate- to long-acting insulin. Consider discharge after 4h uneventful observation if:<ref>Self, W. H., & McNaughton, C. D. (2013). Hypoglycemia. In Emergency Medicine (2nd ed., pp. 1379-1390). Elsevier.</ref>
* Hypoglycemia fully and rapidly reversed without continuous infusion of dextrose
* Tolerated a full meal in ED
* Clear and innocuous cause identified with recurrence unlikely
* Adequate patient understanding, home support/monitoring, and ability to detect/prevent recurrence with close primary care follow-up


==See Also==
==See Also==

Revision as of 00:17, 7 June 2016

Background

  • Brain depends on glucose as primary source of energy, but is unable to synthesize or store glucose

Clinical Features[1]

  • Neuroglycopenic
    • Altered mental status, lethargy, confusion
    • Focal neurologic deficits
    • Unresponsiveness
  • Autonomic
    • Anxiety, nervousness, irritability
    • Nausea, vomiting
    • Palpitations
    • Tremor
    • Changes in pupil size
    • Tachycardia or bradycardia
    • Salivation

Differential Diagnosis

Diagnosis[2]

"Whipple's Triad"

  • Symptoms suggestive of hypoglycemia
    • See Clinical Features
  • Low glucose
    • Serum glucose <60mg/dL
    • Generally symptomatic at <55mg/dL though threshold is variable depending on chronicity
  • Resolution of symptoms after administration of glucose

Evaluation

Patients with known diabetes who are not systemically ill and can identify a clear precipitant, no extensive workup is required. In severely ill patients, consider:

  • BMP
  • LFT
  • EtOH
  • Infectious workup: CXR, UA, urine and blood cultures
  • ECG, troponin
  • Other studies: insulin, C-peptide, pro-insulin, glucagon, growth hormone, cortisol, B-OH, insulin antibodies

Management

  • If altered mental status
    • Dextrose 50% 50mL bolus (equals "one amp")
      • Contains 25mg glucose
  • If awake
    • Oral glucose
  • Glucagon[3]
    • Efficacy dependent on hepatic glycogen stores (less effective in chronic ETOH, cirrhosis, malnourished, neonate, in-born errors, glycogen storage disease, etc.)[4]
    • Onset of action slower than IV dextrose (7-10min)
    • 1mg SC or IM

Hypoglycemia from Sulfonylureas[5][6]

Activated charcoal[7]

  • Administer activated charcoal, preferably within 1 hr of ingestion
  • Multiple doses may be beneficial, especially for glipizide

Glucose Treatment

  • Initial therapy regardless of known cause
Adults
  • 50mL D50W bolus
  • Start a D10 1/2NS drip (100mL/hr)
Children
  • 1mL/kg of D50W OR
  • 2mL/kg D25W OR 5-10mL/kg D10W
  • Neonate: 5-10 mL/kg D10W

Octreotide[8]

  • Theoretical benefit to reduce risk of recurrent hypoglycemia
  • Hyperpolarization of the beta cell results in inhibition of Ca influx and prevents insulin release
  • 50-100 mcg subcutaneous in adults with repeat dosing Q6hrs
  • 2 mcg/kg (max 150mcg) subcutaneously Q6hrs should be used in children
  • Continuous infusion of 50-125 mcg/hr is an alternative in adults
  • Administer octreotide for 24 hours, then after discontinuing, monitor for hypoglycemia for another 24 hours

Special Considerations

  • Glucagon 5mg IM may be used as temporizing measure, e.g. while obtaining IV access
    • Dependent on glycogen stores which may be depleted in prolonged hypoglycemia
    • Also short duration of action
    • Caution in using glucagon drip
      • Glucagon also has an insulin-releasing effect
      • May subsequently cause initial paradoxical hypoglycemia

Hypoglycemia from Long Acting Insulin

  • Similar treatment as for Sulfonylureas except no role for Octreotide
  • Treatment should include oral intake as well as maintenance glucose containing drip either D5 or D10

Disposition

Admission or observation for oral anti-hyperglycemic agent or intermediate- to long-acting insulin. Consider discharge after 4h uneventful observation if:[9]

  • Hypoglycemia fully and rapidly reversed without continuous infusion of dextrose
  • Tolerated a full meal in ED
  • Clear and innocuous cause identified with recurrence unlikely
  • Adequate patient understanding, home support/monitoring, and ability to detect/prevent recurrence with close primary care follow-up

See Also

References

  1. ↑ Jalili M. Type 2 Diabetes Mellitus In: Tintinalli's Emergency Medicine. 7th ed. McGraw Hill. 2011:1431-1432
  2. ↑ Jalili M. Type 2 Diabetes Mellitus In: Tintinalli's Emergency Medicine. 7th ed. McGraw Hill. 2011:1431-1432
  3. ↑ Carstens S, Sprehn M. Prehospital treatment of severe hypoglycaemia: a comparison of intramuscular glucagon and intravenous glucose. Prehosp Disaster Med. 1998 Apr-Dec;13(2-4):44-50
  4. ↑ Cydulka RK, Maloney GE. Diabetes Mellitus and Disorders of Glucose Homeostasis, in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2013, (Ch) 126: p 1652-1667.
  5. ↑ Rowden AK, Fasano CJ. Emergency management of oral hypoglycemic drug toxicity. Emerg Med Clin N Am 2007; 25:347-356
  6. ↑ Howland MA. Antidotes in Depth: Octreotide. In: Flomenbaum NE, Goldfrank LR, Hoffman RS et al, eds: Goldfrank’s Toxicologic Emergencies. New York NY, 2006;770-773
  7. ↑ Tran D et al. Oral Hypoglycemic Agent Toxicity Treatment & Management. Jul 14, 2015. http://emedicine.medscape.com/article/1010629-treatment#showall.
  8. ↑ Fasano CJ et al. Comparison of Octreotide and standard therapy versus standard therapy alone for the treatment of sulfonylurea-induced hypoglycemia. Ann Emerg Med 2008; 51:400-406
  9. ↑ Self, W. H., & McNaughton, C. D. (2013). Hypoglycemia. In Emergency Medicine (2nd ed., pp. 1379-1390). Elsevier.
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