CASE 6

ACUTE IRON POISONING

Amahle Mnyamana
Ziyaan Zoutenberg
Siyakha Mbhejwa
Ammaarah Isaacs
Phiwokuhle Zungu
 Case 6
A young child weighing 10kg accidently ingested
approximately 10 tablets of her mother's ferrous
sulphate tablets (each tablet contains 20% elemental
iron). The patient is asymptomatic 2 hours later
when she presents to the hospital
 Pharmacodynamic Effects
Acute iron poisoning refers to the ingestion of a lethal dose of iron, usually most common amongst kids.
Iron poisoning has 3 (or 5 as labelled in some sources) phases that correspond to one another but draw
attention to the different effects of iron toxicity on the body after certain periods of time.

Local effects of iron
poisoning:
corrosion of GIT mucosa
resulting in emesis,
Systemic effects: free iron is toxic at the cellular level as it generates free
radicals when interconverting between its ferrous and ferric form.
Severe overdose causes impaired oxidative phosphorylation and
mitochondrial dysfunction. Iron enters cells and concentrates in the
mitochondria, thus disrupting cell processes ultimately leading to cell death.
- affects liver and CVS, secondary CNS effects, metabolic acidosis, free
protons and coagulopathy.

haematemsis, diarrhoea,
melaena and loss of fluid.
Expected Course of Events without
Treatment
When there is an overload of iron the absorpition shifts internally thus causing the hepatotoxicity and
failure.Heamorragic necrosis , GI bleeds and cellular changes in the CVS and CNS can also be seen.
Iron enters cels and concentrates in the mitochondria thus disrupting cell processes ultimately leading
to cell death

Stage 1 ( 0.5-6hrs )
there is a effect on the GI tract, symptoms of vomiting diarrhea and abdominal pain may occur. It also puts the patient at
risk for hypovolemic shock. Hematemesis and melaena

Stage 2- latent
Between 6 and twelve hour the patient may recover from the GI symptoms as iron is absorbed

Stage 3 – shock and metabolic acidosis ( 12-48 hours )

Shock from vasodilation, anion gap metabolic acidosis and hepatorenal failure Iron-induced coagulopathy, hepatic
dysfunction, cardiomyopathy, and renal failure are also observed in this stage

Stage 4 - hepatoxicity and hepatic necrosis (12-96 hours)

is characterized by an elevation of aminotransferase levels and possible progression to hepatic failure

Stage 5 (2-8 weeks)

This stage represents the consequences of the healing of the injured GI mucosa including pyloric or proximal bowel
scarring and obstruction.
EMERGENCY CARE

[2,3]
What is Desferrioxamine?
• A.K.A Deferoxamine or desferal.
• A molecule produced by the fermentation of Streptomyces pilosus.
• It is a chelating agent that removes excess iron or aluminium from the bloodstream for excretion in urine.
Mechanism of action in acute iron poisoning:

• It binds ferric iron (Fe3+) that is either free, bound to ferritin or haemosiderin.
• It does not remove iron bound to transferrin, haemoglobin or cytochromes.
• The binding of desferrioxamine with Fe3+ forms the water-soluble ferrioxamine, which is excreted in urine and gives it a
characteristic “vin rosé” colour (orange-reddish brown).
• 100 mg of deferoxamine is capable of binding approximately 8.5 mg of ferric iron.
Indications:
• Severe acute iron toxicity
⚬ Systemic toxicity: coagulopathy, cardiomyopathy, and hepatic and renal failure.
⚬ Hemodynamic instability, lethargy, persistent vomiting, metabolic acidosis, OR
⚬ Toxic serum iron levels: >500 mcg/dL
• Iron overload (acute or chronic): ferritin >800-3000 ng/mL
• Aluminium toxicity
Desferrioxamine cont. Safe administration:
• Poor GIT absorption so it must be given intramuscularly, subcutaneously, or intravenously.
• In severe acute iron toxicity: 15 mg/kg/h is given as a 24-hour IV infusion using an indwelling catheter.
• It should not be given for >24 hours as this increases risk of acute respiratory distress syndrome (ARDS)

Adverse effects:

• Hypotension
• Hypersensitivity
• Sensorineural hearing loss, retinopathy and ARDS (if infusions > 24 hours)
• Increased risk of infection (Mucormycosis, Yersinia, and Vibrio)

Contraindications:
• Previous desferrioxamine hypersensitivity
• Renal disease or anuria
 PREVENTION
Primary Prevention
• keep iron supplements locked up and out of children's sight and
reach
• Always replace the safety caps immediately after product use
• Keep products and medications in their original containers to
avoid confusion
• Teach children not to drink or eat anything unless it is given to
them by an adult
• Avoid taking medication in front of small children as childtren
tend to copy adult behaviour
• Discard old and outdated medicines appropriately
• Don't use words such as candy when referring to medicines- Call
it by its name

Seconday Prevention
• Development of poison control centres
• Western Cape: 24 hour Poison Information helpline-0861 555 777
 REFERENCES
• Yuen.H, Becker, W (2022) “ iron toxicity “ . National Library of medicine . Statpearls Available : https://www.ncbi.nlm.nih.gov/books/NBK459224/

Long, N (2020) ‘Iron ingestion” https://litfl.com/iron-ingestion/

2. The Royal Children's hospital melbourne (no date) The Royal Children's Hospital Melbourne. Available at: https://www.rch.org.au/clinicalguide/guideline_index/Iron_poisoning/ (Accessed: January
31, 2023).

3. Ho-Wang Yuen and Wenxia Becker (2019). Iron Toxicity. [online] Nih.gov. Available at: https://www.ncbi.nlm.nih.gov/books/NBK459224/.

4. Velasquez J, Wray AA. (2022). Deferoxamine. [online] National Library of medicine. Available: https://www.ncbi.nlm.nih.gov/books/NBK557654/ (Accessed 26 January 2023)

5. Liebelt EL. (2022). Acute Iron Poisoning. [online] UpToDate. Available:

https://www.uptodate.com/contents/acute-iron-poisoning?source=search_result&search=iron%20poisoning&selectedTitle=1~56#H30 (Accessed 26 January 2023)