Diferencia entre revisiones de «Copper toxicity»

Revisión del 21:05 6 ago 2018

Background

Widely available metal
Obtained from various foods including nuts, fish, green vegetables
Numerous poisonings from copper pipes
- Occurs from storage of acidic substances (lemon/orange juice), pipes exposed to carbon dioxide from carbonation process, stagnant, and hot water which leach out copper from pipes
Uses
- Pipes
- Cookware
- Electrical wire
- Medical devices (copper IUD)
- Dietary supplements
- Bordeaux solution (used as a pesticide)
Seen in Wilson disease

Toxicokinetics

Absorbed in the GI tract
- Bound by ceruoplasmin
Elimination via biliary system
- Minimal renal elimination
V_D : 2L/kg
Toxicity is caused through redox reactions
- Fenton reaction
- Haber-Weiss cycle
- Generates oxidative stress, inhibiting key metabolic enzymes, particularly in cell membranes and mitochondria
Organ specific damage
- Erythrocytes
  - Membran dysfunction resulting in hemolysis
  - Occurs within the first 24 hours
- Hepatic
  - Excess copper not bound by metallothionein participates in redox reactions and cause lipid peroxidation
  - Centrilobular necrosis
  - After necrosis there is a release of massive amounts of copper into the blood causing a secondary hemolysis
- Renal
  - ATN with hemoglobin casts, likely from hemolysis

Clinical Features

Acute
- Copper sulfate
  - Most common acute poisoning
  - Lethal dose is 0.15-0.3g/kg
- GI irritation
  - Emesis (may be blue based on copper compound, but is not pathognomonic)
  - Abdominal pain
  - Gastroduodenal hemorrhage, ulceration, and perforation
  - Metallic taste
- Hepatic
  - Jaundice
- Hematologic
  - Hemolysis
  - May see methemoglobinemia
- Renal
  - Renal failure uncommon
- Hypotension and CV collapse
  - Likely multifactorial
Chronic
- Wilson disease
- CNS
  - Ataxia
  - Tremor
  - Parkinsonism
  - Dysphagia
  - Dystonia
- Behavioral
  - Mood changes
- Occular
  - Kayser-Fleischer rings

Differential Diagnosis

Heavy metal toxicity

Evaluation

Clinical diagnosis,as copper levels will likely take days to result
BMP
Hepatic function tests
CBC
PT/PTT/INR
Copper level
- No set number that establishes a prognosis ^[1]
Ceruloplasmin level
Abdominal films to assess for foreign bodies

Management

Supportive care
- Antiemetics
- Fluid and electrolyte repletion
- GI decontamination unlikely to benefit
- Activated charcoal contraindicated
Chelation

Disposition

Consult Toxicology or Poison Control Center

References

↑ Gulliver JM. A fatal copper sulfate poisoning. J Anal Toxicol. 1991;15: 341-342.

Nelson, L. Gold. In: Goldfrank's Toxicologic Emergencies. 9th Ed. New York: McGraw-Hill; 2011: 1256-1265

Authors:

[1] Gulliver JM. A fatal copper sulfate poisoning. J Anal Toxicol. 1991;15: 341-342.

[1]

@@ Línea 1: / Línea 1: @@
 ==Background==
+*Widely available metal
+*Obtained from various foods including nuts, fish, green vegetables
+*Numerous poisonings from copper pipes
+**Occurs from storage of acidic substances (lemon/orange juice), pipes exposed to carbon dioxide from carbonation process, stagnant, and hot water which leach out copper from pipes
+*Uses
+**Pipes
+**Cookware
+**Electrical wire
+**Medical devices (copper IUD)
+**Dietary supplements
+**Bordeaux solution (used as a pesticide)
+*Seen in [[Wilson disease]]
 ==Toxicokinetics==
+*Absorbed in the GI tract
+**Bound by ceruoplasmin
+*Elimination via biliary system
+**Minimal renal elimination
+*V<sub>D</sub> : 2L/kg
+*Toxicity is caused through redox reactions
+**Fenton reaction
+**Haber-Weiss cycle
+**Generates oxidative stress, inhibiting key metabolic enzymes, particularly in cell membranes and mitochondria
+*Organ specific damage
+**Erythrocytes
+***Membran dysfunction resulting in hemolysis
+***Occurs within the first 24 hours
+**Hepatic
+***Excess copper not bound by metallothionein participates in redox reactions and cause lipid peroxidation
+***Centrilobular necrosis
+***After necrosis there is a release of massive amounts of copper into the blood causing a secondary hemolysis
+**Renal
+***ATN with hemoglobin casts, likely from hemolysis
 ==Clinical Features==
+*'''Acute'''
+**Copper sulfate
+***Most common acute poisoning
+***Lethal dose is 0.15-0.3g/kg
+**GI irritation
+***Emesis (may be blue based on copper compound, but is not pathognomonic)
+***Abdominal pain
+***Gastroduodenal hemorrhage, ulceration, and perforation
+***Metallic taste
+**Hepatic
+***Jaundice
+**Hematologic
+***Hemolysis
+***May see methemoglobinemia
+**Renal
+***Renal failure uncommon
+**Hypotension and CV collapse
+***Likely multifactorial
+*'''Chronic'''
+**[[Wilson disease]]
+**CNS
+***Ataxia
+***Tremor
+***Parkinsonism
+***Dysphagia
+***Dystonia
+**Behavioral
+***Mood changes
+**Occular
+***Kayser-Fleischer rings
 ==Differential Diagnosis==
 ===[[Heavy metal]] toxicity===
@@ Línea 31: / Línea 89: @@
 *[[Zinc toxicity]]
 ==Evaluation==
+*Clinical diagnosis,as copper levels will likely take days to result
 *BMP
+*Hepatic function tests
 *CBC
+*PT/PTT/INR
 *Copper level
+**No set number that establishes a prognosis <ref> Gulliver JM. A fatal copper sulfate poisoning. J Anal Toxicol. 1991;15: 341-342. </ref>
 *Ceruloplasmin level
 *Abdominal films to assess for foreign bodies
 ==Management==
+*Supportive care
+**Antiemetics
+**Fluid and electrolyte repletion
+**GI decontamination unlikely to benefit
+**Activated charcoal contraindicated
+*Chelation
+**
 ==Disposition==
 *Consult Toxicology or Poison Control Center