Iron Poisoning
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þ Suspect iron poisoning if:
 - Vomiting and diarrhea (especially hemorrhagic)
 - Hyperglycemia with metabolic acidosis during or following episodes of
   abdominal pain and gastroenteritis

þ  Iron poisoning is often classified into 4 distinct stages. Understanding
   the course of poisoning is important, especially the second (recovery)
   stage, which may lure the physician into a false sense of security and
   result in premature and inappropriate discharge of a patient.
    * Stage 1: GI
          o Nausea and diarrhea, often accompanied by abdominal pain,
          o If severe, GI hemorrhagic
          o fluid and blood loss, with additional third-spacing:
            hypovolemia or shock.
          o Sometimes fatal
    * Stage 2: Silent Phase
          o resolution of GI symptoms.
          o The patient appears to improve and recover.
          o Deceptive, usually occurs 6-12 hours postingestion and may last
            as long as 24 hours.
          o Metabolic abnormalities during this phase may include hypotension,
            metabolic acidosis, and coagulopathy.
          o Some patients skip this phase and progress directly to stage 3.
    * Stage 3:  Metabolic Acidosis.
          o high iron concentrations produce venous pooling and third-spacing of fluids.
          o Elevated liver enzymes and bilirubin, coagulopathy,
          o Hypoglycemia may accompany liver dysfunction.
          o The acidosis may indicate failure of other organs, such as the
            heart and kidneys.
    * Stage 4: scarring of the healing GI tract.
          o The stomach and/or intestines may be affected, resulting in gastric
            outlet or intestinal obstruction.
          o weeks after a severe poisoning.

þ Factors that influence iron toxicity are:
    * Copper Level
    * Phosphorus Level
    * Vitamin E level

þ Factors that enhance iron absorption are:
    * Valine and Histidine
    * Ascorbic Acids, with or without Vitamin E
    * Succinate
    * Pyruvic Acid
    * Citric Acid

þ Mortality much decreased from 1980 to 1990, probably due to deferoxamine
  treatment.

þ Iron is insoluble, not excreted by liver or kidneys in significant amounts,
  and excretion not increased by charcoal, diuresis, or
  dialysis/hemoperfusion.

þ Deferoxamine chelates iron and forms ferrioxamine which is renally excreted.
  Unlike EDTA, deferoxamine does not chelate other important metal ions.
  Dose: 1 gm IV not to exceed 15 mg/kg/hr (to prevent hypotension), maximum of
  6 gm in 24 hours.  Oral use not recommended.  IM not as effective due to
  iron-induced hypotension.  Endpoint is clinical improvement (asymptomatic
  for 24 hours) or normal iron levels; if iron levels not readily available,
  can watch urine; ferrioxamine imparts an orange-pink (vin-rose') color to
  urine; after urine normal color, can stop deferoxamine.  In significant
  exposure, probably safe to use deferoxamine in pregnancy. [Curry SC, et al.
  An ovine model of materinal iron poisoning in pregnancy. Ann Emerg Med
  1990;19:632-638.]

þ Massive OD:
 - Vin rose urine