Hypoglycemia: Difference between revisions

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==Background==
==Background==
*
*Brain depends on glucose as primary source of energy, but is unable to synthesize or store glucose
 
==Clinical Features<ref>Jalili M. Type 2 Diabetes Mellitus In: Tintinalli's Emergency Medicine. 7th ed. McGraw Hill. 2011:1431-1432</ref>==
*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


==Clinical Features==
*


==Differential Diagnosis==
==Differential Diagnosis==
*[[Adrenal insufficiency]]
*[[Adrenal insufficiency]]
*[[Head trauma (adult)|Head trauma ]]
*Hepatic failure
*Hepatic failure
*Insulinoma
*Insulinoma
*Medication-induced
*Medication-induced
*[[Seizure]]
*[[Sepsis]]
*[[Sepsis]]
*Toxin
*[[Stroke (Main)|Stroke]]
*[[Sympathomimetic toxicity]]
*[[Toxic ingestion]]


==Diagnosis==
==Diagnosis<ref>Jalili M. Type 2 Diabetes Mellitus In: Tintinalli's Emergency Medicine. 7th ed. McGraw Hill. 2011:1431-1432</ref>==
*Blood glucose level
*Symptoms consistent with the diagnosis
**See ''Clinical Features''
*Blood glucose level usually <50 mg/dL
**Whole blood glucose approximately 15% less than serum or plasma
*Symptoms resolve with glucose administration
*Symptoms resolve with glucose administration
*Determine etiology of hypoglycemia


==Management==
==Management==
#D50
*If altered mental status
#Oral glucose intake
**Dextrose 50% 50mL bolus (equals "one amp")
#Glucagon<ref>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</ref>
***Contains 25mg glucose
##Efficacy dependent on hepatic glycogen stores
*If awake
##Onset of action slower than IV dextrose (7-10min)
**Oral glucose  
##1mg SC or IM
*Glucagon<ref>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</ref>
**Efficacy dependent on hepatic glycogen stores
**Onset of action slower than IV dextrose (7-10min)
**1mg SC or IM


{{Sulfonylurea Toxicity}}
{{Sulfonylurea Toxicity}}
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===Hypoglycemia from Long Acting Insulin===
===Hypoglycemia from Long Acting Insulin===
*Similar treatment as for Sulfonylureas except no role for Octreotide
*Similar treatment as for Sulfonylureas except no role for Octreotide
*Treatment should include oral PO intake as well as maintenance glucose containing drip either D5 or D10
*Treatment should include oral intake as well as maintenance glucose containing drip either D5 or D10


==Disposition==
==Disposition==

Revision as of 17:09, 27 August 2015

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]

  • Symptoms consistent with the diagnosis
    • See Clinical Features
  • Blood glucose level usually <50 mg/dL
    • Whole blood glucose approximately 15% less than serum or plasma
  • Symptoms resolve with glucose administration
  • Determine etiology of hypoglycemia

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
    • Onset of action slower than IV dextrose (7-10min)
    • 1mg SC or IM

Hypoglycemia from Sulfonylureas[4][5]

Activated charcoal[6]

  • 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[7]

  • 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

  • Admit for refractory hypoglycemia, sulfonylurea-induced hypoglycemia or long acting insulins

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. ↑ Rowden AK, Fasano CJ. Emergency management of oral hypoglycemic drug toxicity. Emerg Med Clin N Am 2007; 25:347-356
  5. ↑ 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
  6. ↑ Tran D et al. Oral Hypoglycemic Agent Toxicity Treatment & Management. Jul 14, 2015. http://emedicine.medscape.com/article/1010629-treatment#showall.
  7. ↑ 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
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