Rosen & Barkin's 5-Minute Emergency Medicine Consult (26 page)

• Transport all pill bottles/pills involved in overdose for identification in ED.
  
• OTC cold remedies often contain APAP.
  

• Airway, breathing, circulation (ABCs)
  
• Administer supplemental oxygen.
  
• Administer naloxone, thiamine, D
  ₅₀
  (or Accu-Chek) for altered mental status.
  

• Supportive care:
  
  • IV fluids
    
  • Antiemetics
    
• Gastric decontamination:
  
  • Administer a single dose of activated charcoal if recent ingestion.
    

• Administer if toxic level detected as defined by Rumack–Matthew nomogram.
  
• NAC virtually 100% hepatoprotective if initiated within 8 hr of an acute overdose
  
• NAC available in oral form or IV form
  
• <8 hr postingestion:
  
  • Check APAP level.
    
  • Initiate NAC if APAP level will not be available within 8 hr of ingestion and toxic ingestion suspected.
    
  • Discontinue NAC if APAP level nontoxic.
    
• ≥8 hr postingestion:
  
  • Initiate NAC immediately if suspected toxic ingestion.
    
  • Check APAP level.
    
  • Discontinue NAC if APAP level is nontoxic.
    
• >24 hr postingestion or chronic repeated APAP ingestion
  
  • Initiate NAC if:
    
    • Ingestion >150 mg/kg APAP
      
    • Symptomatic
      
    • Abnormal hepatic screening panel
      
    • Discontinue NAC if APAP falls to nondetectable level and no AST elevation occurs by 36 hr postingestion.
      
    • Call poison center ([800] 222-1222) or toxicologist for help.
      

• Oral NAC:
  
  • Poor taste and odor:
    
    • Dilute to 5% with fruit juice or soft drink to increase palatability.
      
  • Use antiemetics (metoclopramide or ondansetron) liberally to facilitate PO administration.
    
  • If the patient vomits NAC within 1 hr of administration, repeat the dose.
    
  • Administer NAC as a drip through nasogastric (NG) tube if vomiting continues.
    
  • Given q4h
    
• IV NAC (2 options):
  
  • Acetadote
    ^®
    infusion given per manufacturer’s instructions
    
  • Oral NAC given by IV route if:
    
    • Oral form not tolerated because of vomiting
      
    • Acetadote
      ^®
      not available
      
    • Contact local poison center or toxicologist for help.
      

• No teratogenicity with NAC
  
• NAC may be effective in protecting fetal liver:
  
  • Fetal liver metabolizes APAP to toxic NAPQI after 14 wk gestation.
    

• NAC: 140 mg/kg PO loading (adult and pediatric) followed by 70 mg/kg q4h for 17 additional doses
  
• Acetadote: 21 hr IV infusion: 150 mg/kg over 60 min, then 50 mg/kg over 4 hr, then 100 mg/kg over 16 hr for total dose 300 mg/kg (see package insert for additional guidance, especially for pediatric infusion dosing)
  
• Activated charcoal: 1–2 g/kg PO
  
• Dextrose: D
  ₅₀
  W 1 amp (50 mL or 25 g; peds: D
  ₂₅
  W 2–4 mL/kg) IV
  
• Metoclopramide: Start with 10 mg (peds: 1 mg/kg) IV (1 mg/kg max.)
  
• Naloxone (Narcan): 0.4–2 mg (peds: 0.1 mg/kg) IV or IM initial dose
  
• Ondansetron: >80 kg, 12 mg; 45–80 kg, 8 mg (peds: 0.15 mg/kg) IV
  
• Thiamine (vitamin B
  ₁
  ): 100 mg (peds: 50 mg) IV or IM
  

Treating the mother maximizes treatment for the fetus. NAC crosses the placenta and is considered safe PO or IV.

FOLLOW-UP

• Hepatotoxic level of APAP requiring full course of NAC therapy (see “Treatment”)
  
• LFT abnormalities in the setting of chronic ingestion or late presentation
  
• Nontoxic suicide attempt requiring psychiatric treatment
  

Asymptomatic patients with nontoxic ingestions not requiring full course of NAC therapy

Evidence of significant hepatotoxicity at time of ED arrival warrants early evaluation by hepatology and/or transplant service.

• Substance abuse referral for patients with oral opiate abuse
  
• Patients with unintentional (accidental) poisoning require poison prevention counseling.
  
• Patients with intentional (e.g., suicide) poisoning require psychiatric evaluation.
  

• Consider occult APAP poisoning in patients evaluated for oral opiate abuse.
  
• Do not use the nomogram for patients with chronic ingestion or late presentation.
  
• Do not stop NAC therapy until nondetectable APAP level
  and
  improvement (or resolution) of laboratory and clinical evidence of hepatotoxicity.
  

• Brok J, Buckley N, Gluud C. Interventions for paracetamol (acetaminophen) overdose.
  Cochrane Database Syst Rev
  . 2006;19(2):CD003328.
  
• Heard K. Acetylcysteine for acetaminophen poisoning.
  N Engl J Med
  . 2008;359(3):285–292.
  
• Larson AM, Polson J, Fontana R, et al. Acetaminophen-induced acute liver failure: results of a United States multicenter, prospective study.
  Hepatology
  . 2005;42(6):1364--1372.
  
• Rumack BH. Acetaminophen misconceptions.
  Hepatology
  . 2004;40(1):10–15.
  
• Williamson K, Wahl MS, Mycyk MB. Direct Comparison of 20-Hour IV, 36-Hour Oral, and 72-Hour Oral Acetylcysteine for Treatment of Acute Acetaminophen Poisoning.
  Am J Ther
  . 2013;20(1):37--40.
  

CODES

965.4 Poisoning by aromatic analgesics, not elsewhere classified

BASICS

Respiratory acidosis.

• Reduced pH owing to alveolar hypoventilation with elevated PaCO
  ₂
  
• Defined as PaCO
  ₂
  >45 mm Hg or higher than expected for calculated respiratory compensation for metabolic acidosis
  
• Divided into 3 broad categories:
  
  • Primary failure in CNS drive to ventilate:
    
    • Sleep apnea
      
    • Anesthesia
      
    • Sedative overdose
      
  • Primary failure in transport of CO
    ₂
    from alveolar space:
    
    • COPD
      
    • Myasthenic crisis
      
    • Severe hypokalemia
      
    • Guillain–Barré syndrome
      
  • Primary failure in transport of CO
    ₂
    from tissue to alveoli:
    
    • Severe heart failure/pulmonary edema
      

Metabolic acidosis

• Process that reduces serum pH by decreasing plasma bicarbonate levels
  
• Primarily caused by:
  
  • Accumulation of a strong acid through ingestion or metabolism
    
  • Loss of bicarbonate from the body
    
• Metabolic acidosis is clinically evaluated by dividing into 2 main groups:
  
  • Elevated anion gap metabolic acidosis:
    
    • Bicarbonate reduced through buffering of added strong acid
      
    • Anion gap is increased due to retention of the unmeasured anion from the titrated strong acid.
      
  • Normal anion gap metabolic acidosis due to:
    
    • Kidneys fail to reabsorb or regenerate bicarbonate.
      
    • Losses of bicarbonate from GI tract (diarrhea)
      
    • Ingestion or infusion of substances that release hydrochloric acid
      
  • No anion gap is observed owing to the absence of any unmeasured anion of a titrated acid and secondary chloride retention with HCO
    ₃
    ⁻
    loss.
    

• Respiratory acidosis:
  
  • Inhibition of respiratory center:
    
    • Cardiac arrest
      
    • Drugs (opiates, benzodiazepines, etc.)
      
    • Meningitis/encephalitis
      
    • CNS lesions (mass, CVA)
      
  • Impaired gas exchange:
    
    • Pulmonary edema
      
    • Asthma/COPD
      
    • Pneumonia
      
    • Interstitial lung disease
      
    • Obesity
      
    • Pulmonary contusion
      
  • Neuromuscular disease:
    
    • Diaphragmatic paralysis
      
    • Guillain–Barré syndrome
      
    • Myasthenia gravis
      
    • Muscular dystrophy
      
    • Spinal cord injury
      
    • Hypokalemia/hypophosphatemia
      
    • MS
      
  • Obstructive:
    
    • Congenital lesions (laryngomalacia)
      
    • Foreign body aspiration
      
    • Vascular ring
      
    • Infectious (epiglottitis, croup, abscess)
      
• Anion gap acidosis: Mnemonic
  A CAT PILES MUD
  :
  
  • Alcohol ketoacidosis
    
  • Carbon monoxide or cyanide
    
  • Aspirin
    
  • Toluene
    
  • Paraldehyde
    
  • Iron/isoniazid
    
  • Lactic acidosis
    
  • Ethylene glycol
    
  • Starvation
    
  • Methanol
    
  • Uremia
    
  • Diabetic ketoacidosis
    
• Increased osmolar gap: Mnemonic
  ME DIE
  :
  
  • Methanol
    
  • Ethylene glycol
    
  • Diuretics (mannitol; no acidosis)
    
  • Isopropyl alcohol (no acidosis)
    
  • Ethanol
    
• Nonanion gap metabolic acidosis:
  
  • GI losses of bicarbonate:
    
    • Diarrhea
      
    • Villous adenoma
      
    • Removal of small bowel, pancreatic or biliary secretions
      
    • Tube drainage
      
    • Small bowel/pancreatic fistula
      
  • Anion exchange resins (i.e., cholestyramine)
    
  • Ingestion of calcium chloride or magnesium chloride
    
  • Type I renal tubular acidosis (distal): Hypokalemic hyperchloremic metabolic acidosis:
    
    • Decreased ability to secrete hydrogen
      
    • Serum HCO
      ₃
      <15 mEq/L when untreated
      
    • Potassium low
      
    • Renal stones common
      
  • Type II renal tubular acidosis (proximal): Hypokalemic hyperchloremic metabolic acidosis:
    
    • Decreased proximal reabsorption of HCO
      ₃
      ⁻
      
    • Acidosis limited by reabsorptive capacity of proximal tubule for HCO
      ₃
      ⁻
      
    • Serum HCO
      ₃
      typically 14–18 mEq/L
      
    • Low/normal potassium
      
  • Type IV renal tubular acidosis (hypoaldosteronism): Hyperkalemic hyperchloremic acidosis:
    
    • Aldosterone deficiency or resistance causing decreased H
      ⁺
      secretion
      
    • Serum bicarb >15 mEq/L
      
    • Normal/elevated potassium
      
  • Carbonic anhydrase inhibitors
    
  • Tubulointerstitial renal disease
    
  • Hypoaldosteronism
    
  • Addition of hydrochloric acid such as:
    
    • Ammonium chloride
      
    • Arginine hydrogen chloride
      
    • Lysine hydrogen chloride