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*Stage IV: Clinical recovery, resolution of shock and acidosis usually by days 3-4 | *Stage IV: Clinical recovery, resolution of shock and acidosis usually by days 3-4 | ||
*Stage V: Late onset of gastric and pyloric strictures (2-8 week later) <ref> Fine, J. Iron Poisoning. Curr Probl Pediatr, Vol 30, Iss 3, p 71-90, March 2000 </ref> | *Stage V: Late onset of gastric and pyloric strictures (2-8 week later) <ref> Fine, J. Iron Poisoning. Curr Probl Pediatr, Vol 30, Iss 3, p 71-90, March 2000 </ref> | ||
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|+ CDC management guidelines for children with elevated blood levels<ref name="Kosnett06-242">[[#CITEREFKosnett06Pois|Kosnett (2006)]] p. 242</ref> | |||
! Blood lead<br /> level (μg/dL) !! Treatment | |||
|- | |||
! 10–14 | |||
| Education,<br /> repeat screening | |||
|- | |||
! 15–19 | |||
| Repeat screening, case<br /> management to abate sources | |||
|- | |||
! 20–44 | |||
| Medical evaluation,<br /> case management | |||
|- | |||
! 45–69 | |||
| Medical evaluation,<br /> chelation, case management | |||
|- | |||
! >69 | |||
| Hospitalization, immediate<br /> chelation, case management | |||
|} | |||
Revision as of 20:23, 27 July 2022
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Clinical Features
- Absence of GI symptoms within 6hr of ingestion excludes significant iron ingestion (exception: enteric coated tablets)
- Significant iron toxicity can result in a severe lactic acidosis from hypoperfusion due to volume loss, vasodilation and negative inotropin effects.
| Staging | Clinical Effect | Time Frame |
|---|---|---|
| Stage 1 | GI irritation: nausea and vomiting, abdominal pain, diarrhea | 30 mins-6 hours |
| Stage 2: Latent | Reduced GI symptoms | 6-24 hours |
| Stage 3: Shock and metabolic acidosis | Metabolic acidosis, lactic acidosis, dehydration | 6-72 hours |
| Stage 4: Hepatotoxicity/ Hepatic necrosis | Hepatic failure | 12-96 hours |
| Stage 5: Bowel obstruction | GI mucosa healing leads to scarring | 2-8 weeks |
- Stage I: GI toxicity: nausea, vomiting, diarrhea, GI bleeding from local corrosive effects of iron on the gastric and intestinal mucosa
- Stage II: Quiescent phase with resolution of GI symptoms and apparent clinical improvement
- controversy between toxicologists whether this stage exists in significant poisonings
- Stage III: Systemic toxicity: shock and hypoperfusion
- Primarily hypovolemic shock and acidosis, myocardial dysfunction also contributes
- GI fluid losses, increase capillary permeability, decreased venous tone
- Severe anion gap acidosis
- Free radical damage to mitochondria disrupt oxidative phosphorylation which leads to lactic acidosis
- Hepatotoxicity from iron delivery via portal blood flow
- Stage IV: Clinical recovery, resolution of shock and acidosis usually by days 3-4
- Stage V: Late onset of gastric and pyloric strictures (2-8 week later) [1]
| Blood lead level (μg/dL) |
Treatment |
|---|---|
| 10–14 | Education, repeat screening |
| 15–19 | Repeat screening, case management to abate sources |
| 20–44 | Medical evaluation, case management |
| 45–69 | Medical evaluation, chelation, case management |
| >69 | Hospitalization, immediate chelation, case management |
- ↑ Fine, J. Iron Poisoning. Curr Probl Pediatr, Vol 30, Iss 3, p 71-90, March 2000
- ↑ Kosnett (2006) p. 242
