Rosen & Barkin's 5-Minute Emergency Medicine Consult (400 page)

• Peak concentrations are 2–4 hr postingestion
  
• Serum concentrations not reliable if obtained >4–6 hr after ingestion:
  
  • Enteric coated or sustained release—warrants serial levels
    
• Postabsorption: Iron redistributes into tissues, and fall in serum iron occurs as free iron shifts intracellularly resulting in cellular injury
  
• Injury patterns:
  
  • Corrosive injury to intestinal mucosa may result in profound fluid loss (shock), hemorrhage, and perforation
    
  • Liver receives largest load of iron because of portal venous circulation—(hemorrhagic periportal necrosis)
    
• Free iron:
  
  • Concentrates in mitochondria, disrupting oxidative phosphorylation; catalyzes lipid peroxidation and free radical formation, resulting in cell death; increases anaerobic metabolism and acidosis
    
  • Causes myocardial depression, venodilation, and cerebral edema
    
• Hydration of ferric form liberates 3 protons, resulting in acidemia
  

Elemental iron ingestion:

• Nontoxic <20 mg/kg
  
• Moderate to severe >40 mg/kg
  
• Lethality possible >60 mg/kg
  
• Elemental iron equivalents:
  
  • Ferrous sulfate, 20% (325 mg = 65 mg Fe)
    
  • Ferrous gluconate, 12%
    
  • Ferrous fumarate, 33%
    
• Prenatal vitamins vary from 60–90 mg elemental iron per tablet
  
• Children’s vitamins may contain 5–18 mg elemental iron per tablet
  

• Historically notorious for the highest mortality rate among pediatric accidental exposures (adult iron products)
  
• Children’s chewable iron products have been shown to be safe
  

DIAGNOSIS

• Classically divided into 5 stages:
  
  • Stage 1: GI
    (0.5–6 hr):
    
    • Abdominal pain
      
    • Vomiting
      
    • Diarrhea
      
    • Hematemesis
      
    • Hematochezia
      
  • Stage 2: Latent/quiescent
    (6–24 hr):
    
    • Resolution of GI symptoms
      
    • Deceptive phase (ongoing injury?)
      
    • Possible hypotension and acidosis
      
  • Stage 3: Shock and organ failure
    (6–72 hr):
    
    • Hypoperfusion
      
    • Metabolic acidosis
      
    • Coma
      
    • Coagulopathy
      
  • Stage 4: Hepatic failure
    (2–3 days):
    
    • Coagulopathy
      
    • Hypoglycemia
      
    • Jaundice
      
    • Elevated LFTs (transaminases) and bilirubin
      
  • Stage 5: Obstruction
    (2–4 wk):
    
    • Gastric outlet and small bowel obstruction
      
    • Abdominal pain, vomiting
      
• Patient may present in or skip any of the 5 stages
  
• If onset of stage 1 does not occur within 6 hr, likely not significant ingestion
  

Acute iron poisoning is a clinical diagnosis, regardless of lab results

• Serum iron levels (mg/dL):
  
  • Peak absorption 2–6 hr
    
  • 4 hr is most common time for peak
    
  • Delayed peak with enteric coated/sustained release
    
• Electrolytes, BUN/creatinine, glucose:
  
  • Anion gap metabolic acidosis
    
  • Hyperglycemia early
    
  • Hypoglycemia late
    
• Arterial blood gas:
  
  • Metabolic acidosis
    
• CBC:
  
  • Anemia with significant hemorrhage
    
  • Leukocytosis
    
• Liver function
  
• Coagulation profile
  
• Lactate
  
• Type and screen if hemorrhage
  
• Total iron-binding capacity is not useful and not recommended
  

Abdominal radiograph check for:

• Tablets (children’s chewables rarely visible)
  
• Absence of pill fragment interpretation:
  
  • Patient did not ingest iron
    
  • Iron was in solution or has already dissolved
    
  • Patient ingested pediatric multivitamin product
    
  • Absence of radiopacities does not rule out significant or lethal ingestion
    
• Perforation
  

• Sepsis
  
• Acetaminophen toxicity
  
• Toxic ingestions causing anion gap acidosis:
  
  • Salicylate
    
  • Cyanide
    
  • Methanol
    
  • Ethylene glycol
    
• Mushrooms
  
• Heavy metals
  
• Theophylline toxicity
  
• GI bleed from other causes (alcoholic liver disease)
  

TREATMENT

Collect prescription bottles/medications for identification in the ED

• ABCs:
  
  • Intubate if profoundly unstable
    
  • Venous access and fluids for hypotension
    
  • Cardiac monitor and pulse oximetry
    
• Naloxone, thiamine, dextrose (or Accu-Chek) as indicated for altered mental status
  

• Decontamination:
  
  • Poorly adsorbed by activated charcoal
    
  • Gastric lavage has not been shown to change outcome
    
  • NaHCO
    ₃
    , phospho soda, and oral deferoxamine are not recommended
    
  • If pill fragments are visualized on x-ray, or history of significant ingestion:
    
    • Consider whole bowel irrigation (with NG GoLytely: Peds: 10–15 mL/kg/h; adult: 1–2 L/h) while monitoring progression with radiograph (KUB).
      
    • Caution with GI bleed
      
  • Endoscopy or gastrotomy can remove bezoar formation after massive ingestions (>240 mg/kg)
    
• Chelation with deferoxamine (DFO):
  
  • DFO is a highly specific chelator of parenteral iron
    
  • IV infusion results in more constant DFO levels and is route of choice:
    
    • Administer as soon as possible (<24 hr)
      
  • Administration techniques:
    
    • Increase IV infusion rate to 15 mg/kg/h over 20 min, monitoring for hypotension
      
    • Decrease infusion rate if hypotension
      
    • Infusion rates as high as 45 mg/kg/h have been tolerated
      
    • Disregard manufacturer’s recommendation of max. daily doses of 6 g in serious iron exposures
      
  • IM DFO challenge test is not advocated
    
  • Interpret serum levels cautiously:
    
    • Time since ingestion must be considered: Treatment may be indicated in patient who presents late, after distribution stage (>8 hr postingestion), with serum iron level <350 mg/dL
      
  • If serum iron levels are not readily available, base treatment decisions on clinical status
    
  • Length of infusion (controversial):
    
    • DFO–iron complex causes urine to turn
      vin rose
      color; this suggests continuing infusion until urine returns to normal
      
    • Resolution of signs and symptoms of significant toxicity is criterion for discontinuing DFO
      
    • Prolonged DFO therapy >24–48 hr may precipitate adult respiratory distress syndrome
      
    • In severe cases with continued signs and symptoms, infusion may be continued cautiously at lower dose
      
  • Controversies:
    
    • Safety of DFO infusions given for >24 hr
      
    • Maximal infusion rates and total amount
      
    • Serum iron concentration warranting treatment
      
    • Endpoint of treatment (best endpoint is resolution of poisoning, i.e., acidemia)
      
    • Role of extracorporeal elimination
      
  • Contact regional poison center for moderate to severe iron exposures
    
    • (1-800-222-1222)
      

• Dextrose: D
  ₅₀
  W 1 amp (50 mL or 25 g; peds: D
  ₂₅
  W 2–4 mL/kg) IV
  
• Naloxone (Narcan): 2 mg (peds: 0.1 mg/kg) IV or IM initial dose
  
• Thiamine (vitamin B
  ₁
  ): 100 mg (peds: 50 mg) IV or IM
  

FOLLOW-UP

• GI symptoms or dehydration
  
• Altered mental status
  
• Hypotension, lethargy, metabolic acidosis, or shock
  
• Serum iron >500 mg/dL
  
• Serum iron >350 mg/dL
  and
  pills seen on KUB
  
• Rising serum iron levels
  
• Patients treated with deferoxamine
  
• ICU admission for coma, shock, metabolic acidosis, or iron levels >1,000 mg/dL
  

• Asymptomatic with negative radiograph
  
• Minimal to no symptoms after 6-hr observation
  
• Mild GI symptoms that have resolved without evidence of metabolic acidosis and serum iron <350 mg/dL
  

Contact regional poison center for mild to moderate toxicity

• Follow-up after discharge may be indicated in patients who are at risk of developing gastric outlet obstruction
  
• Psychiatric referral for patients with intentional overdose
  

• DFO may be indicated in patients who present late, after distribution stage (>8 hr postingestion), or with serum iron level <350 mg/dL and signs of intracellular poisoning (e.g., anion gap metabolic acidosis)
  
• Resolution of GI symptoms does not indicate that there is no ongoing toxicity that may progress over time
  

• Bryant SM, Leikin J. Iron. In: Brent J, Wallace KL, Burkhart KK, et al., eds.
  Critical Care Toxicology
  . St. Louis, MO: Mosby; 2005.
  
• Chang TP, Rangan C. Iron poisoning: A literature-based review of epidemiology, diagnosis, and management.
  Pediatr Emerg Care.
  2011;27:978–985.
  
• Tenenbein M. Unit-dose packaging of iron supplements and reduction of iron poisoning in young children.
  Arch Pediatr Adolesc Med
  . 2005;159:557–560.