Rosen & Barkin's 5-Minute Emergency Medicine Consult (378 page)

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Authors: Jeffrey J. Schaider,Adam Z. Barkin,Roger M. Barkin,Philip Shayne,Richard E. Wolfe,Stephen R. Hayden,Peter Rosen

Tags: #Medical, #Emergency Medicine

BOOK: Rosen & Barkin's 5-Minute Emergency Medicine Consult
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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)
  • Altered
  • Mental
  • Status
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

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