Hypoglycemia: Difference between revisions
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===Drugs=== | ===Drugs=== | ||
* Anti-hyperglycemic | *Anti-hyperglycemic | ||
** [[Insulin]] | **[[Insulin]] | ||
** Oral secretagogue | **Oral secretagogue | ||
* Other | *Other | ||
** [[EtOH]] | **[[EtOH]] | ||
** [[B-blocker]] | **[[B-blocker]] | ||
** ACE | **ACE | ||
** [[Acetaminophen Overdose|Acetaminophen (OD)]] | **[[Acetaminophen Overdose|Acetaminophen (OD)]] | ||
===Systemic Illness=== | ===Systemic Illness=== | ||
* Critical Illness | *Critical Illness | ||
** [[Sepsis]] | **[[Sepsis]] | ||
** [[MI]] | **[[MI]] | ||
* Organ Failure | *Organ Failure | ||
** Hepatic failure | **Hepatic failure | ||
** [[Renal failure]] | **[[Renal failure]] | ||
* Endocrinopathy | *Endocrinopathy | ||
** [[Adrenal insufficiency]] | **[[Adrenal insufficiency]] | ||
* [[Seizure]] | *[[Seizure]] | ||
===Malignancy=== | ===Malignancy=== | ||
* Insulinoma | *Insulinoma | ||
* Non-islet cell | *Non-islet cell | ||
* Insulin/receptor autoantibodies | *Insulin/receptor autoantibodies | ||
* High tumor burden | *High tumor burden | ||
===Other=== | ===Other=== | ||
* Artifactual | *Artifactual | ||
** Specimen collection | **Specimen collection | ||
** Consumption | **Consumption | ||
*** [[Leukemia]] | ***[[Leukemia]] | ||
*** Erythrocytosis | ***Erythrocytosis | ||
*** Hemolytic disease | ***Hemolytic disease | ||
* Post-surgical | *Post-surgical | ||
** [[Gastric bypass surgery|Gastric bypass]] | **[[Gastric bypass surgery|Gastric bypass]] | ||
** Gastrectomy | **Gastrectomy | ||
** Pyloroplasty | **Pyloroplasty | ||
* Starvation | *Starvation | ||
** [[Anorexia nervosa]] | **[[Anorexia nervosa]] | ||
===Precipitants of anti-hyperglycemic induced hypoglycemia=== | ===Precipitants of anti-hyperglycemic induced hypoglycemia=== | ||
* Decreased glucose | *Decreased glucose | ||
** Missed meal | **Missed meal | ||
** Consumption (exercise, illness) | **Consumption (exercise, illness) | ||
* Increased drug | *Increased drug | ||
** Error (patient, provider) | **Error (patient, provider) | ||
** Intentional overdose | **Intentional overdose | ||
** Increased availability | **Increased availability | ||
*** Hepatic failure | ***Hepatic failure | ||
*** Renal failure | ***Renal failure | ||
*** Drug interaction | ***Drug interaction | ||
==Diagnosis== | ==Diagnosis== | ||
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*Patients with known diabetes who are not systemically ill and can identify a clear precipitant, no extensive workup is required. | *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: | *In severely ill patients, consider: | ||
** BMP | **BMP | ||
** LFT | **LFT | ||
** EtOH | **EtOH | ||
** Infectious workup: [[CXR]], UA, urine and blood cultures | **Infectious workup: [[CXR]], UA, urine and blood cultures | ||
** [[ECG]], [[troponin]] | **[[ECG]], [[troponin]] | ||
** Other studies (not normally done in ED): insulin, C-peptide, pro-insulin, glucagon, growth hormone, cortisol, B-OH, insulin antibodies | **Other studies (not normally done in ED): insulin, C-peptide, pro-insulin, glucagon, growth hormone, cortisol, B-OH, insulin antibodies | ||
===Evaluation<ref>Jalili M. Type 2 Diabetes Mellitus In: Tintinalli's Emergency Medicine. 7th ed. McGraw Hill. 2011:1431-1432</ref>=== | ===Evaluation<ref>Jalili M. Type 2 Diabetes Mellitus In: Tintinalli's Emergency Medicine. 7th ed. McGraw Hill. 2011:1431-1432</ref>=== | ||
"Whipple's Triad" | "Whipple's Triad" | ||
* Symptoms suggestive of hypoglycemia | *Symptoms suggestive of hypoglycemia | ||
**See ''Clinical Features'' | **See ''Clinical Features'' | ||
* Low glucose | *Low glucose | ||
** Serum glucose <60mg/dL | **Serum glucose <60mg/dL | ||
** 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 | ||
==Management== | ==Management== | ||
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==Disposition== | ==Disposition== | ||
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> | 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 | *Hypoglycemia fully and rapidly reversed without continuous infusion of dextrose | ||
* Tolerated a full meal in ED | *Tolerated a full meal in ED | ||
* Clear and innocuous cause identified with recurrence unlikely | *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 | *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 08:52, 9 July 2016
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
Drugs
- Anti-hyperglycemic
- Insulin
- Oral secretagogue
- Other
Systemic Illness
- Critical Illness
- Organ Failure
- Hepatic failure
- Renal failure
- Endocrinopathy
- Seizure
Malignancy
- Insulinoma
- Non-islet cell
- Insulin/receptor autoantibodies
- High tumor burden
Other
- Artifactual
- Specimen collection
- Consumption
- Leukemia
- Erythrocytosis
- Hemolytic disease
- Post-surgical
- Gastric bypass
- Gastrectomy
- Pyloroplasty
- Starvation
Precipitants of anti-hyperglycemic induced hypoglycemia
- Decreased glucose
- Missed meal
- Consumption (exercise, illness)
- Increased drug
- Error (patient, provider)
- Intentional overdose
- Increased availability
- Hepatic failure
- Renal failure
- Drug interaction
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.
