Hypoglycemia
Background
- Brain depends on glucose as primary source of energy, but is unable to synthesize or store glucose
Common Anti-hyperglycemic Drugs and Pharmacology
Drug | Pharmacology | ||
---|---|---|---|
Onset | Peak | Duration | |
Rapid-acting insulin
|
15-30min | 1-2h | 3-5h |
Short-acting insulin
|
30-60min | 2-4h | 6-10h |
Intermediate-acting insulin
|
1-3h | 4-12h | 18-24h |
Long-acting insulin
|
2-4h | None | 24h |
Sulfonylurea
|
– | 2-6h | 12-24h |
See also GLP-1 agonists
Clinical Features[1]
Neuroglycopenic
- Altered mental status, lethargy, confusion
- Focal neurologic deficits
- Unresponsiveness
Autonomic
- Anxiety, nervousness, irritability
- Nausea and vomiting
- Palpitations
- Tremor
- Changes in pupil size
- Tachycardia or bradycardia
- Salivation
Differential Diagnosis
- Adrenal insufficiency
- Head trauma
- Hepatic failure
- Insulinoma
- Medication-induced
- Self-induced insulin overdose
- Seizure
- Sepsis
- Stroke
- Sympathomimetic toxicity
- Toxic ingestion
Diagnosis
Workup
- 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:
Evaluation[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
Management
- If altered mental status
- Dextrose 50% 50mL bolus (equals "one amp")
- Contains 25mg glucose
- Dextrose 50% 50mL bolus (equals "one amp")
- 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
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
- ↑ Jalili M. Type 2 Diabetes Mellitus In: Tintinalli's Emergency Medicine. 7th ed. McGraw Hill. 2011:1431-1432
- ↑ Jalili M. Type 2 Diabetes Mellitus In: Tintinalli's Emergency Medicine. 7th ed. McGraw Hill. 2011:1431-1432
- ↑ 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
- ↑ 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.
- ↑ Rowden AK, Fasano CJ. Emergency management of oral hypoglycemic drug toxicity. Emerg Med Clin N Am 2007; 25:347-356
- ↑ 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
- ↑ Tran D et al. Oral Hypoglycemic Agent Toxicity Treatment & Management. Jul 14, 2015. http://emedicine.medscape.com/article/1010629-treatment#showall.
- ↑ 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
- ↑ Self, W. H., & McNaughton, C. D. (2013). Hypoglycemia. In Emergency Medicine (2nd ed., pp. 1379-1390). Elsevier.