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| {{Navbox
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| | name = Clinically Relevant Bacteria
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| | title = [[Microbiology (Main)|Disease-Causing Bacteria]]
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| | state = {{{state|autocollapse}}}
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| |listclass = hlist
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| | groupstyle = background:PowderBlue;
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| |group1 = [[Gram Negatives]]
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| |list1 = {{Navbox subgroup
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| }}
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| }}
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| ==Clinical Features==
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| *Absence of GI symptoms within 6hr of ingestion excludes significant iron ingestion (exception: enteric coated tablets)
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| *Significant iron toxicity can result in a severe [[lactic acidosis]] from hypoperfusion due to volume loss, vasodilation and negative inotropin effects.
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| {| class="wikitable"
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| |+ Iron Toxicity Stages
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| |-
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| ! scope="col" | '''Staging'''
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| ! scope="col" | '''Clinical Effect'''
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| ! scope="col" | '''Time Frame'''
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| |-
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| | Stage 1||GI irritation: nausea and vomiting, abdominal pain, diarrhea||30 mins-6 hours
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| |-
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| | Stage 2: Latent||Reduced GI symptoms||6-24 hours
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| |-
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| | Stage 3: Shock and metabolic acidosis||Metabolic acidosis, lactic acidosis, dehydration||6-72 hours
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| |-
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| | Stage 4: Hepatotoxicity/ Hepatic necrosis||Hepatic failure||12-96 hours
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| |-
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| | Stage 5: Bowel obstruction||GI mucosa healing leads to scarring||2-8 weeks
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| |}
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| *Stage I: GI toxicity: nausea, vomiting, diarrhea, GI bleeding from local corrosive effects of iron on the gastric and intestinal mucosa
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| *Stage II: Quiescent phase with resolution of GI symptoms and apparent clinical improvement
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| **controversy between toxicologists whether this stage exists in significant poisonings
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| *Stage III: Systemic toxicity: shock and hypoperfusion
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| **Primarily hypovolemic shock and acidosis, myocardial dysfunction also contributes
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| **GI fluid losses, increase capillary permeability, decreased venous tone
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| **Severe anion gap acidosis
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| **Free radical damage to mitochondria disrupt oxidative phosphorylation which leads to lactic acidosis
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| **Hepatotoxicity from iron delivery via portal blood flow
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| *Stage IV: Clinical recovery, resolution of shock and acidosis usually by days 3-4
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| *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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| {| class="wikitable"
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| |+ CDC management guidelines for children with elevated blood levels<ref name="Kosnett06-242">[[#CITEREFKosnett06Pois|Kosnett (2006)]] p. 242</ref>
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| ! scope="col" | '''Blood lead level (μg/dL)'''
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| ! scope="col" | '''Treatment'''
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| |-
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| | 10–14
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| | Education, repeat screening
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| |-
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| | 15–19
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| | Repeat screening, case management to abate sources
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| |-
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| | 20–44
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| | Medical evaluation, case management
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| |-
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| | 45–69
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| | Medical evaluation, chelation, case management
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| |-
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| | >69
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| | Hospitalization, immediate chelation, case management
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| |}
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| [https://curbsidehealth.com/pathways/275/edit?uuid=79a30f97-97aa-5daa-847f-95cd64f7e8ea Test MIS-C pathway] | | [https://curbsidehealth.com/pathways/275/edit?uuid=79a30f97-97aa-5daa-847f-95cd64f7e8ea Test MIS-C pathway] |
