New Zealand

National Poisons Centre

IRON OVERDOSE
 IRON POISONING

•Naturally aVailable as haemutite, magnatite

•Inborn errors normal iron cause toxic effect
due to accumulation is called as
haemochromatosis
•Iron salts are administered therapeutically
in iron defficiency
 IRON

In healthy adults ~ 2 to 10% of dietary iron absorbed

In iron deficiency states (including children) 80 to 90% is

absorbed

In overdose, there is proportionally less of an ingested dose

absorbed compared to a therapeutic dose, however, damage
to intestinal mucosa can increase absorption

Following absorption iron is bound to transferrin and actively

taken up by the liver during “first pass”. The remaining iron is
transported by transferrin, primarily to the bone marrow.
 TOXIC MECHANISM

In overdose total iron binding capacity is surpassed and free

Ferric iron (Fe+++) is present in the blood:

•Free protons are liberated leading to acidosis

Fe3+ + 3H2O  FE(OH)3 + 3H+

•Fe+++ leads to production of the OH. radical, in turn causing

lipid peroxidation and:
- Local tissue injury – primarily the gut and liver
-Mitochondrial damage with loss of cellular aerobic respiration

•Free iron is a vasodilator

•Direct depression of coagulation factors

 SIGNS AND SYMPTOMS

“Classic” stages of iron poisoning

Stage I
Gastrointestinal 30m to 6 hrs

Stage II
Latent phase 2 to 4 hrs

Stage III
Shock / multiorgan failure / acidosis 2 to 24 hrs

Stage IV
Hepatotoxicity 12 to 24 hrs

Stage V
Gastrointestinal obstruction 1 to 7 wks
 STAGE I – GASTROINTESTINAL

Initial symptoms are secondary to direct irritant and

corrosive effect of iron. In larger overdoses, lipid
peroxidation causes further injury. Complaints include:
Epigastric pain
Nausea / vomiting
Diarrhoea
In more severe cases
Haematemesis
Vasodilation
Hypotension

Metabolic acidosis may also develop during this initial stage

leading to the latent phase being “by-passed”.
 STAGE II – LATENT PHASE

A period where there is a deceptive apparent improvement

in the patient’s gastrointestinal condition. It is often tempting
to discharge such patients.

However, in the seriously poisoned, a metabolic acidosis is

evolving. This may be compounded by a lack of adequate
fluid resuscitation.
STAGE III – SHOCK, MULITORGAN FAILURE, ACIDOSIS

Loss of adequate tissue perfusion and multiorgan

failure: most deaths occur during this stage.

Shock occurs secondary to gastrointestinal

haemorrhage, vomiting,vasodilation, and reduced
cardiac output (due to myocardial toxicity).

Multiorgan failure related to inadequate perfusion and

direct toxicity ensues and results in:
Altered mental status / coma
Seizure
Acute renal failure
Pulmonary oedema
 STAGE IV – HEPATOTOXICITY

Hepatic dysfunction is a poor prognostic sign. Patients

suffer related:
Hypoglycaemia
Coagulopathy and haemorrhage
Jaundice
Hepatic encephalopathy / coma
 STAGE V – GASTROTINESTINAL OBSTRUCTION

mucosal injury may lead to the formation of strictures

& scaring
Though usually occurring at the pylorus, they may be found
throughout the gastrointestinal tract.
 DIAGNOSIS

History of ingestion

Ingestions of 40 to 60 mg/kg should be medically

assessed; those above 60 mg/kg should be
decontaminated.

Investigation

Abdominal x-ray
Serum iron concentration at 2 to 4 hours post-ingestion
 DECONTAMINATION

Activated charcoal will not bind iron, therefore it is necessary

to administer whole bowel irrigation.

Appropriate decontamination is recommended:

-For ingestions greater than 60 mg/kg elemental iron

Follow WBI with AXR to ensure removal of iron

 INTERVENTION CRITERIA

Less than 60 umol/L (335 ug/dL)

Discharge into the care of a responsible guardian if:

- Asymptomatic, and
- Iron not detected on abdominal x-ray, and

Observe and repeat iron serum concentration at 4 to 6 hours

post-ingestion if:
- Patient symptomatic (treatment may be indicated by
severity), or
- Iron detected on abdominal x-ray, or
- Sustained release or enteric-coated formulation ingested
 INTERVENTION CRITERIA

60 to 90 umol/L (335 to 500 ug/dL)

Observe and repeat serum iron concentration at 4 to 6

hours post-ingestion if:
- Asymptomatic, and
- Iron not detected on abdominal x-ray, and

Admit for management if:

- Symptomatic
- Iron detected on abdominal x-ray
 INTERVENTION CRITERIA

Greater than 90 umol/L (500 ug/dL)

Admit regardless of symptoms for management, including

treatment with desferrioxamine
 CHELATION

Indicated in all cases with signs of systemic intoxication and

especially those have metabolic acidosis.

Desferrioxamine
15 mg/kg/hr IV up to 80 mg/kg/d IM
Continue until acidosis reversed and symptoms have resolved
.

Note:
•Hypotension following too rapid infusion
•Renal failure in hypovolaemic patients
•Prolonged (>24 hour) infusion associated with ARDS
•Interference with serum iron measurement
 SUPPORTIVE CARE

Cardiovascular

Hypotension is a significant problem and may be due to

haemorrhage, third spacing, vasodilation and compromised
cardiac output. Initially robust fluid replacement is required.
In severe cases invasive blood pressure monitoring is
warranted to guide management.
 SUPPORTIVE CARE

Acute Renal Failure

Acute renal failure generally occurs secondary to shock.

Haemodialysis should be employed increase removal of
iron-chelate, it will not remove iron itself.

Acute Liver Failure

A poor prognostic sign: requires management of

hypoglycaemia, coagulopathy (factor replacement), and
early consultation with a liver unit.