Hypoglycemia: Difference between revisions

(Added algorithm for differential diagnosis.)
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[[File:Hypoglycemia Differential Diagnosis.png|thumb|Differential diagnosis of hypoglycemia]]
[[File:Hypoglycemia Differential Diagnosis.png|thumb|Differential diagnosis of hypoglycemia]]


*[[Adrenal insufficiency]]
===Drugs===
*[[Head trauma (adult)|Head trauma ]]
* Anti-hyperglycemic
*Hepatic failure
** Insulin
*[[Insulinoma]]
** Oral secretagogue
*Medication-induced
* Other
*Self-induced insulin overdose
** EtOH
*[[Seizure]]
** B-blocker
*[[Sepsis]]
** ACE
*[[Stroke (Main)|Stroke]]
** Acetaminophen (OD)
*[[Sympathomimetic toxicity]]
===Systemic Illness===
*[[Toxic ingestion]]
* Critical Illness
** Sepsis
** MI
* Organ Failure
** Hepatic failure
** Renal failure
* Endocrinopathy
** Adrenal insufficiency
* 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
** Anorexia nervosa


===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==
==Diagnosis==
===Workup===
===Workup===

Revision as of 17:09, 10 June 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

  • Aspart (Novolog)
  • Lispro (Humalog)
 15-30min 1-2h 3-5h
Short-acting insulin

  • Regular
 30-60min 2-4h 6-10h
Intermediate-acting insulin

  • NPH (Humulin, Novolin)
 1-3h 4-12h 18-24h
Long-acting insulin

  • Glargine (Lantus)
 2-4h None 24h
Sulfonylurea

  • Glimepiride
  • Glipizide (Glucotrol)
  • Glyburide (Glycron, Micronase)
 – 2-6h 12-24h

See also GLP-1 agonists

Clinical Features[1]

Neuroglycopenic

Autonomic

Differential Diagnosis

Differential diagnosis of hypoglycemia

Drugs

  • Anti-hyperglycemic
    • Insulin
    • Oral secretagogue
  • Other
    • EtOH
    • B-blocker
    • ACE
    • Acetaminophen (OD)

Systemic Illness

  • Critical Illness
    • Sepsis
    • MI
  • Organ Failure
    • Hepatic failure
    • Renal failure
  • Endocrinopathy
    • Adrenal insufficiency
  • 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
    • Anorexia nervosa

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:
    • BMP
    • LFT
    • EtOH
    • Infectious workup: CXR, UA, urine and blood cultures
    • ECG, troponin
    • Other studies (not normally done in ED): insulin, C-peptide, pro-insulin, glucagon, growth hormone, cortisol, B-OH, insulin antibodies

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

Algorithm for the management of hypoglycemia
  • 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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