Rosen & Barkin's 5-Minute Emergency Medicine Consult (121 page)

• Transport pill/pill bottles to ED
  
• Calcium for bradycardic/unstable patient with confirmed CCB overdose
  

• ABCs:
  
  • Airway protection, as indicated
    
  • Supplemental oxygen, as needed
    
  • 0.9% NS IV access
    
• Hemodynamic monitoring
  

• HR >60 beats/min
  
• Systolic BP >90 mm Hg
  
• Adequate urine output
  
• Improving level of consciousness
  

• Syrup of ipecac: Contraindicated in the pre-hospital and ED setting
  
• Activated charcoal:
  
  • May be helpful, especially in the presence of coingestants
    

• Usually only transiently effective
  
• Calcium gluconate (10%):
  
  • Contains 0.45 mEq Ca
    ²⁺
    /mL
    
  • Does not cause tissue necrosis as calcium chloride does
    
  • Calcium gluconate: Preferred agent in an acidemic patient
    
• Calcium chloride (10%):
  
  • Contains 1.36 mEq Ca
    ²⁺
    /mL (3 times more calcium than calcium gluconate)
    
  • Can cause tissue necrosis and sloughing with extravasation
    
  • Very irritating to veins
    
• Follow serum calcium levels if repeated doses of calcium administered.
  
• Contraindicated in known digoxin toxicity because calcium may cause serious adverse effects in this setting
  

• IV fluids:
  
  • Administer cautiously in the hypotensive patient.
    
  • Swan-Ganz catheter or central venous pressure (CVP) monitoring to help follow volume status
    
• Atropine usually ineffective
  
• High-dose insulin (HDI):
  
  • CCBs cause myocardial insulin resistance and inhibit insulin release from pancreatic islet cells
    
    • Results in inefficient fatty acid metabolism
      
  • HDI promotes more efficient myocardial carbohydrate metabolism and has been shown to improve hemodynamic function
    
• Vasopressor agents:
  
  • No clear evidence that 1 agent is more effective than another
    
  • Institute invasive monitoring to help guide treatment.
    
  • Dopamine:
    
    • β
      ₁
      -Receptor agonist at low doses, which causes a positive inotropic effect on the myocardium
      
    • α-Receptor agonist at higher doses, which leads to vasoconstriction
      
  • Epinephrine:
    
    • Potent α- and β-receptor agonist
      
• Amrinone:
  
  • Selective phosphodiesterase inhibitor
    
  • Indirectly increases cAMP leading to increased inotropy
    
• Electrical pacing: When other treatment options have failed
  
• Potential future therapies:
  
  • Hypertonic sodium bicarbonate
    
  • IV fat emulsion (20% intralipid)
    

• Amrinone: Loading dose 0.75 mg/kg; maintenance drip 2–20 μg/kg/min; titrate for effect
  
• Atropine: 0.5 mg (peds: 0.02 mg/kg) IV; repeat 0.5–1 mg IV (peds: 0.04 mg/kg)
  
• Calcium chloride: 5–10 mL of 10% solution slow IVP (peds: 0.2–0.25 mL/kg; repeat in 10 min if necessary) followed by infusion 20–50 mg/kg/h
  
• Calcium gluconate: 10–20 mL of 10% solution slow IVP (peds: 1 mL/kg; may repeat in 10 min if necessary)
  
• Dextrose: 50 mL of 50% solution (peds: 0.25 g/kg of 25% solution)
  
• Dopamine: 2–20 μg/kg/min; titrate to effect
  
• Epinephrine: 1–2 μg/min (peds: 0.01 mg/kg or 0.1 mL/kg 1:10,000); titrate to effect
  
• Norepinephrine: Start 2–4 μg/min IV; titrate up to 1–2 μg/kg/min IV
  
• Potassium: 40 mEq PO or IV
  

• Should be considered if response to fluid resuscitation is inadequate
  
• Insulin (regular insulin): 1 IU/kg bolus IV followed by 0.5–1 IU/kg/h titrated up to clinical response
  
• Administer dextrose if blood glucose <200 mg/dL
  
• Administer potassium if serum potassium <2.5 mEq/L
  
• Monitor serum glucose and potassium concentrations every 30 min for the 1st 4 hr
  
• Approximate 24-hr insulin requirement: 1,500 U of regular insulin for adult patient
  

• IV fluids
  
• Calcium
  
• HDI
  
• Vasopressor agents
  

• Amrinone
  
• IV fat emulsion
  

FOLLOW-UP

• Admit symptomatic patients to a monitored bed for hemodynamic monitoring.
  
• Admit all patients who ingested sustained-release CCBs for 24-hr observation and monitoring owing to the potential delay in symptoms.
  

Discharge asymptomatic patients 8 hr after ingestion of immediate-release preparation.

• Psychiatric evaluation for all suicidal patients
  
• Poison prevention guidance for parents of pediatric accidental ingestion
  

• Consider CCB toxicity in patients presenting hypotensive and bradycardic.
  
• Consider suicidal gesture in patients presenting with CCB toxicity.
  
• Consider HDI with dextrose and potassium if fluid resuscitation not rapidly effective.
  

• Greene SL, Gawarammana I, Wood DM, et al. Relative safety of hyperinsulinaemia/euglycaemia therapy in the management of calcium channel blocker overdose: A prospective observational study.
  Intensive Care Med
  . 2007;33:2019–2024.
  
• Levine M, Boyer EW, Pozner CN, et al. Assessment of hyperglycemia after calcium channel blocker overdoses involving diltiazem or verapamil.
  Crit Care Med
  . 2007;35:2071–2075.
  
• Shepherd G. Treatment of poisoning caused by beta-adrenergic and calcium-channel blockers.
  Am J Health Syst Pharm
  . 2006;63:1828–1835.
  
• Shepherd G, Klein-Schwartz W. High-dose insulin therapy for calcium-channel blocker overdose.
  Ann Pharmacother
  . 2005;39:923–930.
  

See Also (Topic, Algorithm, Electronic Media Element)

β-Blocker, Poisoning

CODES

972.9 Poisoning by other and unspecified agents primarily affecting the cardiovascular system

BASICS

• Infection of oral mucosa with any species of Candida
  
• Up to 80% of isolates are
  Candida albicans
  (most common),
  Candida glabrata, and Candida tropicalis
  .
  
• Candida normally present as oral flora in 60% of the healthy population.
  
• Variations include:
  
  • Pseudomembranous (thrush)
    
  • Chronic and acute atrophic candidiasis
    
  • Angular cheilitis
    
  • Hyperplastic candidiasis
    
• More common in neonates, elderly, and immunosuppressed individuals
  
• Usually benign course in healthy patients
  
• In immunocompromised patients, more likely to be recurrent and a non-
  albicans
  species
  
• May represent an early manifestation of AIDS in HIV-infected patients
  
• Typically localized
  
• Risk factors for systemic infection:
  
  • AIDS
    
  • Diabetes
    
  • Hospitalization
    
  • Immunosuppressive therapy
    
  • Malignancy
    
  • Neutropenia
    
  • Organ transplantation
    
  • Prematurity
    

• Usually overgrowth of
  C. albicans
  from alterations in intraoral environment
  
• May be medication induced—commonly antimicrobials, inhaled or systemic steroids, chemotherapy, immunosuppressive agents
  
• Immunocompromised patients
  
• Alterations or impairment of salivary flow:
  
  • Anticholinergic or psychotropic medications
    
  • Sjögren disease
    
  • Head or neck radiation
    
• Presence of dentures or other orthodontics:
  
  • Occurs in up to 50–65% of denture wearers
    
  • Common etiology for chronic atrophic candidiasis
    
• Interruption of epithelial barrier (cheek biting)
  
• Endocrinopathies (diabetes, hypothyroidism)
  

• Acute pseudomembranous candidiasis (thrush) is common in infancy likely because of immaturity of their immune system and lack of mature oral flora
  
• Initial presentation may be feeding difficulty secondary to dysphagia
  
• May have concurrent Candida diaper rash
  
• Consider maternal treatment if breastfeeding:
  
  • Maternal breast colonization may be cause for persistent thrush. Query maternal nipple pain, burning, itching, or cracked skin