Friday, April 17, 2015

Prenatal Vitamin Overdose

Case presentation:
A 16 - year - old female intentionally overdosed on an unknown quantity of “ vitamins. ” She
arrives at the emergency department 4 hours after the overdose complaining of nausea, vomiting, and epigastric abdominal pain. Her initial vital signs reveal pulse 123 beats per minute, blood pressure 85/34 mmHg, respiration 24 breaths per minute, and temperature 37.2 ° C. Her examination is signifi cant only for epigastric tenderness on palpation of her abdomen.

Her laboratory studies are signifi cant for the following: iron 567 mg/dL, serum bicarbonate 15 mEq/L, glucose 256 mg/dL, and white blood count 13.2 × 10 9 /L. A radiograph of her abdomen is pictured here.


Question: Which of the following is the next most appropriate management step for this patient?


A. Begin an intravenous infusion of deferoxamine
B. Administer dimercaprol (BAL) intramuscular
C. Infuse calcium disodium ethylenediaminetetraacetate (EDTA)
D. Administer succimer (DMSA) orally
E. Administer d-penicillamine orally

Answer: A
Diagnosis: Iron toxicity
Discussion: Acute iron toxicity occurs from the ingestion of iron supplements. The total elemental iron ingested is dependent upon the type of preparation. Common formulations include ferrous gluconate (containing 12% of elemental iron), ferrous sulfate (20%), and ferrous fumarate
(33%). Studies have shown that most iron poisonings are unintentional due to accidental ingestion of prenatal vitamins, which have a high content of iron about 60 – 65 mg elemental iron (multivitamins usually containing about 15 – 18 mg). Intentional ingestions are most commonly seen in females in their teens and twenties. Mortality from intentional ingestions has been reported to be as high as 10%.
Iron toxicity is dose - dependent. Toxic effects (gastrointestinal symptoms) generally occur at greater than 20 mg/ kg elemental iron. Severe toxicity (shock) generally occurs at doses higher than 60 mg/kg. The primary mechanism of injury is free radical production and lipid peroxidation.


Five classic clinical phases have been described: 
• Phase 1 (30 minutes – 6 hours): Gastrointestinal distress predominates initially due to the direct corrosive effects of the iron. Symptoms include abdominal pain, diarrhea, and emesis. In severe cases, hypovolemic shock may occur, resulting in death. In most individuals with mild - to - moderate toxicity, gastrointestinal  symptoms will resolve within a few hours and will not progress from this phase.

• Phase 2 (6 – 24 hours): A “ latent ” phase may be seen, where gastrointestinal symptoms subside but end - organ toxicity continues. This phase might be absent in patients with severe toxicity. Care should be taken to continuously re - evaluate the patient to determine whether he or she is progressing to the next phase or whether the toxicity has truly resolved.

• Phase 3 (6 – 72 hours): Multisystem organ failure ensues.  Symptoms include hypotension, cardiotoxicity, oliguria,  anuria, coagulopathy, lethargy, seizures, shock, coma, and possibly death.
• Phase 4 (1 – 4 days): Fulminant liver failure may develop. Liver failure is the second most common cause of death.
• Phase 5 (2 – 8 weeks): Initial gastrointestinal corrosive injury obstruction occurs at different levels from luminal scarring.

Evaluation includes a thorough history and physical examination. An iron level should be obtained and a repeat level drawn to assure that iron levels are not increasing. Peak iron concentrations usually occurs 4 – 6 hours after overdose. Serum iron levels over 500 ì g/dL are commonly associated with systemic toxicity. Total iron - binding capacity is unreliable and should not be used to estimate free iron levels. Patient can have an anion gap metabolic acidosis. The iron tablets may be seen on
abdominal X - rays (Figure ).
radioopacity arrow dissolved iron tab in stomach


 A negative X - ray is does not rule out iron ingestion (children ’ s chewable multivitamin products are not radio - opaque). There is limited utility of gastrointestinal decontamination following iron overdose. Ipecac and gastric lavage are generally not recommended. Activated charcoal does not adsorb iron and should not be administered. Whole - bowel irrigation may be useful, especially if tablets are visible on X - ray or levels are rising. Adequate fluid resuscitation and supportive care are the primary initial interventions.



Deferoxamine is the antidote of choice as it chelates free iron and increases its excretion. Indications include signifi cant clinical signs of toxicity (e.g., protracted vomiting or diarrhea), metabolic acidosis, shock, serum iron levels greater than 500 ì g/dL and/or an X - ray positive for multiple pills.

 Deferoxamine infusions are given intravenously at a starting rate of 15 mg/kg per hour and continued for 6 hours. The patient should then be re - evaluated. Deferoxamine - induced hypotension may occur at fast rates due to histamine release, and adequate hydration should be assured before initiation of the infusion.

As iron is chelated and excreted, the urine will develop a characteristic rusty - red ( “ vin rose ” ) appearance (Figure ).
“vin rose” urine Chelated with deferoxamine

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