PRE HOSPITAL
- Diagnosis with finger stick glucose
- IV dextrose preferred
- Oral glucose–containing fluids in awake patient if unable to obtain IV
- Glucagon if unable to give IV glucose or oral glucose
INITIAL STABILIZATION/THERAPY
- ABCs with aspiration and seizure precautions
- Glucose:
- Dextrose IV push (IVP)—this should always be given if possible.
- Oral glucose in awake patient (with no IV) without risk of aspiration
- Glucagon IM if unable to establish IV access
ED TREATMENT/PROCEDURES
- Administer D
50
W 50 mL for decreased level of consciousness:
- 2nd or 3rd amp may be necessary.
- Complications include volume overload and hypokalemia.
- Administer octreotide:
- If hypoglycemia refractory to glucose administration
- If hypoglycemia secondary to sulfonylureas
- Initiate continuous IV infusion of 5–20% glucose solution for persistent mild hypoglycemia or if patient cannot eat.
- Administer glucagon:
- If hypoglycemia refractory to glucose
- If IV access delayed
- Ineffective in alcohol-induced hypoglycemia and significant liver disease
- May repeat twice q20–30min
- Administer hydrocortisone with glucagon for adrenal insufficiency.
- Effective in 10–20 min
Geriatric Considerations
Elderly patients often have less hypoglycemic awareness and require significant time for resolution of symptoms, even after appropriate treatment of hypoglycemia.
MEDICATION
First Line
- D
50
W: 1–2 amps (25 g) of 50% dextrose IVP
- Zimmerman rule of 50: Adult 1 mL/kg of D
50
W; child: 2 mL/kg D
25
W; infants: 5 mL/kg D
10
W)
Second Line
- Octreotide: 50 μg IV bolus then 50 μg IV/hr drip or 50 μg q12hSC/IV
- Glucagon: 0.5–2 mg IV/IM/SC:
- Child: 0.03–0.1 mg/kg IV/IM/SC
- Infant: 0.3 mg/kg IV/IM/SC
- May repeat in 4 hr
- Hydrocortisone: 100 mg (peds: 1–2 mg/kg) IV
- Oral glucose: 20 g orally equals ∼12 oz nondiet fruit juice, 14 oz nondiet cola
- Carbohydrate without fat or protein preferred
FOLLOW-UP
DISPOSITION
Admission Criteria
- Overdose of long-acting oral hypoglycemic agent (e.g., sulfonylureas) or long-acting insulin mandate observation for at least 24 hr.
- Failure of neuroglycopenic symptoms to improve with glucose administration suggests neurologic injury, pre-existing neurologic condition, or another cause for these symptoms.
- Recurrent hypoglycemic state in ED
- Patients unable to tolerate oral fluids or food
- Suicidal intentions
- Older patients may require several days for complete recovery from severe or prolonged hypoglycemia.
Discharge Criteria
- Discharge mild unintentional insulin overusage or failure to take oral calories if blood glucose normal, symptoms resolved, tolerating oral intake, and can be observed.
- Families of patient with recurrent hypoglycemia should be instructed in IM glucagon administration.
- Monitor blood glucose for at least 3 hr prior to discharge.
Issues for Referral
Refer to primary physician for consideration of medication or diet changes if recurrent hypoglycemic episodes.
FOLLOW-UP RECOMMENDATIONS
PMD follow-up for medication re-evaluation within 48 hr
PEARLS AND PITFALLS
- Administration of PO glucose or food may initially further decrease glucose level; therefore, IV dextrose always preferred if possible
- Multiple amps of D
50
W commonly required
- Do not over rely on D10/D20 as even these concentrations contain relatively small amounts of glucose.
- Hypoglycemia should be in the differential for all neurologic and psychiatric presentations.
- Recurrent hypoglycemia patients often require hours to days for full neurologic recovery
ADDITIONAL READING
- McCall AL. Insulin therapy and hypoglycemia.
Endocniol Metab Clin North Am.
2012;41(1):57–87.
- Service FJ. Hypoglycemia.
Med Clin North Am
. 1995;79(1):1–8.
- Stanley CA, Baker L. The causes of neonatal hypoglycemia.
N Engl J Med
. 1999;340:1200–1201.
See Also (Topic, Algorithm, Electronic Media Element)
CODES
ICD9
- 251.1 Other specified hypoglycemia
- 251.2 Hypoglycemia, unspecified
- 775.1 Neonatal diabetes mellitus
ICD10
- E16.1 Other hypoglycemia
- E16.2 Hypoglycemia, unspecified
- P70.2 Neonatal diabetes mellitus
HYPOGLYCEMIC AGENT POISONING
Timothy J. Meehan
BASICS
DESCRIPTION
- Oral or parenteral agents that may cause hypoglycemia or other metabolic imbalances
- Hypoglycemic poisoning may be intentional or unintentional (accidental)
ETIOLOGY
- Insulin:
- Enhances glucose uptake into cells
- Limits glucose availability to the brain (most sensitive to hypoglycemia)
- Influences potassium redistribution (hypokalemia)
- Sulfonylurea and Meglitinide agents:
- Enhance insulin release from pancreatic β cells, reduce hepatic glucose production, and increase peripheral insulin sensitivity
- Hypoglycemic effect enhanced by:
- Polypharmacy (drug interactions)
- Alcohol use and hepatic dysfunction (poor nutritional stores)
- Renal insufficiency (decreased clearance)
- GLP1 modulators:
- Exenatide is an analog of glucagon-like peptide 1 (GLP1)
- Gliptins (sitagliptin and saxagliptin) inhibit DDP4 which normally inactivates GLP1
- Net effects: Enhanced insulin secretion, delayed gastric emptying, and increased satiety
- Unclear effects on glucose metabolism in overdose (data are lacking at this time)
- Biguanide agents (metformin):
- Antihyperglycemic agents:
- Decrease elevated serum glucose concentrations
- Generally do not cause hypoglycemia in isolation.
- In the presence of insulin, biguanides do the following:
- Increase glucose uptake into cells
- Limit glucose availability to the brain (most sensitive to hypoglycemia)
- Influence potassium redistribution (hypokalemia)
- Decrease GI glucose absorption
- Decrease hepatic gluconeogenesis
- Metabolize glucose to lactate in intestinal cells, which may accumulate and lead to profound lactic acidosis
- Thiazolidinediones:
- In the presence of insulin, thiazolidinediones increase glucose uptake and use and decrease gluconeogenesis
- α-glucosidase inhibitors:
- Lower systemic glucose by decreasing GI absorption of carbohydrates
DIAGNOSIS
SIGNS AND SYMPTOMS
- Insulin or sulfonylureas:
- Overdose causes hypoglycemia
- Symptoms most often occur when glucose <40–60 mg/dL (may occur at higher levels in diabetics)
- Symptoms blunted by β-antagonists
- Facial flushing, diaphoresis, pallor, piloerection
- Hunger, nausea, abdominal cramping
- Labored respirations, apnea
- Headache, blurred vision
- Paresthesias, weakness, incoordination, tremor
- Anxiety, irritability, bizarre behavior, confusion, stupor, coma, seizures
- Palpitations, tachycardia, bradycardia (late)
- Hypertension
- Hypothermia
- Biguanides:
- Toxicity primarily owing to lactic acid accumulation
- Nausea, vomiting, abdominal pain
- Agitation, confusion, lethargy, coma
- Kussmaul respirations
- Hypotension, tachycardia