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Hypoglycemic Agent Poisoning, Emergency Medicine


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

  • Neonatal hypoglycemia may occur after maternal use of sulfonylureas during labor
  • Ingestion of 1 sulfonylurea tablet may cause hypoglycemia in a child:
    • Death has been reported after ingestion of a single tablet
  • Onset of symptomatic hypoglycemia may be delayed up to 8 hr

History
  • Diagnosis of diabetes in patient
  • Access to diabetic medications:
    • If occurring in a medical setting (hospital, nursing home), consider:
      • Dosing error
      • Malicious intent

Physical Exam
  • Vital signs:
    • Tachycardia (may be blunted if on β-blockers)
  • Neurologic:
    • Confusion, obtundation, coma
    • Ataxia, other cerebellar signs

Essential Workup


  • Diagnosis based on clinical presentation and an accurate history
  • Monitor serum glucose concentration
  • Monitor vital signs and neurologic status
  • Obtain serum electrolytes and lactate for biguanide ingestion
  • Obtain liver function tests for thiazolidinedione ingestion

Diagnosis Tests & Interpretation


Lab
  • Serum glucose before and after treatment
  • Electrolytes:
    • Check for hypokalemia
    • Anion gap acidosis
  • BUN, creatinine:
    • May reveal renal insufficiency, causing drug accumulation
  • CBC
  • Ethanol level
  • Lactate level (especially if biguanide medications involved)
  • Liver function tests
  • Arterial blood gas
  • Assays for immunoreactive insulin and C-peptide levels:
    • Confirms administration of exogenous insulin if insulin level is high and C-peptide is low in the setting of hypoglycemia
    • Do not correlate with severity of clinical symptoms

Imaging
  • ECG: Sinus tachycardia, premature ventricular contractions (PVCs), atrial dysrhythmias
  • EEG: Diffuse slowing without focal abnormalities
  • CT scan: Cerebral edema if prolonged hypoglycemia
  • Chest radiograph: Aspiration pneumonia or pulmonary edema

Differential Diagnosis


  • Addison disease
  • Panhypopituitarism
  • Sepsis
  • Insulinoma
  • Neuroendocrine tumors
  • Cirrhosis
  • Chronic ethanol abuse
  • Ethanol ingestion
  • Salicylate ingestion
  • β-antagonist ingestion
  • Ackee fruit poisoning

Treatment


Pre-Hospital


Transport all medications, pills, and pill bottles involved in overdose for identification in ED �

Initial Stabilization/Therapy


  • ABCs:
    • Airway control essential
    • Administer supplemental oxygen
    • IV access
    • Cardiac monitor and pulse oximetry
  • Naloxone, thiamine, D50 (or Accu-Chek) if altered mental status

Ed Treatment/Procedures


  • Hypoglycemia:
    • D50 bolus, then:
      • IV infusion D5W or D10W to maintain euglycemia or mild hyperglycemia
      • Food (if mental status improves or normalizes)
  • Neuroglycopenia:
    • May persist shortly after serum glucose corrected
    • Persistent symptoms require further dextrose administration
  • Decontamination:
    • Consider administration of activated charcoal for recent or large ingestion of oral agent (sulfonylurea or biguanide)
  • Provide supportive care
  • Hypotension:
    • 0.9% NS IV fluid bolus
    • Pressor support with dopamine or norepinephrine as needed:
      • Pressors may increase lactate production
      • Use cautiously with biguanide-induced lactic acidosis
  • Administer sodium bicarbonate for biguanide-induced lactic acidosis if pH < 7
  • Administer benzodiazepines for seizures
  • Inhibit insulin secretion for sulfonylurea overdose with recurrent hypoglycemia with:
    • Octreotide
    • Diazoxide (watch for hypotension)
  • Early hemodialysis may be beneficial in cases of biguanide-induced lactic acidosis:
    • Corrects acid-base abnormalities
    • Enhances elimination of the drug

Medication


  • Activated charcoal: 1 g/kg PO
  • Dextrose: 50-100 mL D50 (peds: 2 mL/kg of D25 over 1 min) IV; repeat if necessary
  • Diazepam: 5-10 mg (peds: 0.2-0.5 mg/kg) IV q10-15min
  • Diazoxide: 200 mg PO or 1-3 mg/kg IV (infant: 8-15 mg/kg/24 h q8-12hPO/IV; child: 3-8 mg/kg/24 h q8h PO/IV)
  • Glucagon: 1-2 mg (peds: 0.03-0.1 mg/kg) IM/SC/IV
  • Lorazepam: 2-4 mg (peds: 0.03-0.05 mg/kg) IV q10-15min
  • Octreotide: 50-100 μg q8-12h SC/IV
  • Thiamine (vitamin B1): 100 mg (peds: 50 mg) IV or IM

Follow-Up


Disposition


Admission Criteria
  • Hypoglycemia owing to sulfonylurea agents (may require several days of monitoring) or long-acting insulin preparations
  • Any patient requiring a constant infusion of dextrose to maintain euglycemia
  • Intentional overdose or self-injection of insulin warrants admission for 24 hr glucose monitoring
  • All children with accidental ingestion of sulfonylureas
  • Metabolic alterations owing to biguanide ingestion or accumulation

Discharge Criteria
  • Accidental hypoglycemia owing to short-acting insulin injection in the setting of dietary insufficiency:
    • Must be tolerating oral intake
    • Ensure return to baseline mental status
  • Discharge after glucose correction and a 4 hr period of observation

Issues for Referral
  • Patients with unintentional (accidental) poisoning require poison prevention counseling
  • Patients with intentional (e.g., suicide) poisoning require psychiatric evaluation

Followup Recommendations


Close primary care follow-up to help monitor blood sugar and adjust medication dosages �

Pearls and Pitfalls


  • Sulfonylureas can have markedly prolonged half-lives and long elimination times:
    • Delayed hypoglycemia and refractory hypoglycemia are common
    • Admit for observation, at a minimum
  • Metformin must be held for 48 hr after any study requiring IV contrast media:
    • IV contrast can prolong renal clearance of biguanides
    • Can induce metformin-associated lactic acidosis

Additional Reading


  • Bosse �GM. Chapter 48. Antidiabetics and hypoglycemics. In: Hoffman �RS, Nelson �LS, Goldfrank �LR, et al., eds. Goldfranks Toxicologic Emergencies. 9th ed. New York, NY: McGraw-Hill; 2011.
  • Dougherty �PP, Klein-Schwartz �W. Octreotide's role in the management of sulfonylurea-induced hypoglycemia. J Med Toxicol.  2010;6(2):199-206.
  • Glatstein �M, Scolnik �D, Bentur �Y. Octreotide for the treatment of sulfonylurea poisoning. Clin Toxicol (Phila).  2012;50(9):795-804.
  • Kopek �KT, Kowalski �MJ. Metformin-associated lactic acidosis (MALA): Case files of the Einstein Medical Center medical toxicology fellowship. J Med Toxicol.  2013;9(1):61-66.
  • Kruse �JA. Metformin-associated lactic acidosis. J Emerg Med.  2001;20(3):267-272.
  • Little �GL, Boniface �KS. Are one or two dangerous? Sulfonylurea exposure in toddlers. J Emerg Med.  2005;28(3):305-310.
  • Rowden �AK, Fasano �CJ. Emergency management of oral hypoglycemic drug toxicity. Emerg Med Clin North Am.  2007;25:347-356.

See Also (Topic, Algorithm, Electronic Media Element)


Hypoglycemia �

Codes


ICD9


962.3 Poisoning by insulins and antidiabetic agents �

ICD10


T38.3X1A Poisoning by insulin and oral hypoglycemic drugs, acc, init �

SNOMED


  • 212545006 Poisoning by antidiabetic agent (disorder)
  • 21445009 Poisoning by oral sulfonylurea derivative (disorder)
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