Metal Poisoning (Lead, Arsenic, Iron)

Heavy metals poisoning is the toxic accumulation of metals in the body, which can occur due to ingestion or inhalation. These elements are normally found in nature and can have many applications (e.g., agriculture, medicine, industry); however, toxicity is rare. Common metals that the human body absorbs in toxic amounts are lead, arsenic, and iron. Presentation is variable and management involves the use of chelating agents.

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Lead Poisoning

Etiology

Lead poisoning, also known as plumbism, may result from inhalation or ingestion of lead from:

  • Lead paint
  • Food and drinks in lead-soldered cans
  • Contaminated tap water
  • Lead bullets
  • Occupational exposure (e.g., batteries, ammunition, construction, renovation, alcohol distillation with lead soldering)

Pathophysiology

  • Hematologic effects:
    • Contributes to RBC membrane fragility → hemolysis
    • Inhibits ferrochelatase and aminolevulinic acid dehydratase (enzymes in the heme synthesis pathway) → ↓ hemoglobin synthesis
    • Inhibits ribosomal RNA degradation → RBCs retain aggregates of rRNA → basophilic stippling
  • Neurologic effects:
    • Lead displaces calcium ions → ↑ blood-brain barrier permeability → allows lead to cross and contributes to cerebral edema
    • Accumulation in astroglial cells and prevents myelin sheath formation → demyelination

Clinical presentation

Children:

  • Poor appetite
  • Nausea and vomiting
  • Lead lines on gingival border (Burton lines) 
  • Headaches
  • Encephalopathy
    • Somnolence
    • Coma
    • Seizures
  • Developmental delay
  • Behavioral changes

Adults:

  • Nonspecific symptoms:
    • Fatigue
    • Insomnia
    • Arthralgia and myalgia
  • Gl symptoms: 
    • Abdominal pain
    • Constipation
    • Anorexia
  • Neurological manifestations:
    • Headache
    • Short memory loss
    • Cognitive deficits
    • Peripheral neuropathy (e.g., wrist drop, foot drop, sensory neuropathies)
  • Chronic exposure leads to: 
    • Nephropathy
    • Hypertension 
    • ↑ Risk of cardiovascular mortality
Lead line in gingiva - metal poisoning

Clinical findings associated with lead poisoning:
a. lead line along the gingival border (Burton lines)
b. wrist drop as a consequence of peripheral neuropathy

Image: “Radial neuropathy due to occupational lead exposure” by Department of Neurology, National Institute of Mental Health and Neurosciences (NIMHANS), India. License: CC BY 2.0

Diagnosis

  • In children, dense metaphyseal lines can be seen on X-ray (lead concentrates in metaphyses of growing bones):
    • Distal femur
    • Both ends of tibia
    • Distal radius 
  • Initial screening test: capillary (fingerstick) lead measurement
  • Confirmatory test: venous lead measurement
  • Other findings:
    • Normocytic or microcytic anemia
    • Erythrocyte basophilic stippling on peripheral smear
    • ↑ Serum zinc protoporphyrin level
Giemsa stain of coarse basophilic stippling or erythrocytes due to lead poisoning

Wright-Giemsa–stained smear of peripheral blood: coarse basophilic stippling of the erythrocytes

Image: “Wright-Giemsa stained smear” by Yale Cancer Center, Section of Hematology, Yale University School of Medicine, New Haven, CT 06511, USA. License: CC BY 2.0

Management

  • Remove any source of lead exposure.
  • Nutritional interventions 
  • Provide lead education for the family.
  • In a child with acute lead ingestion, consider orogastric or nasogastric tube with whole-bowel irrigation (polyethylene glycol).
  • Chelation therapy:
    • Indicated for: 
      • Asymptomatic children with a blood lead level ≥ 45 μg/dL
      • Asymptomatic adults with a blood lead level ≥ 80 μg/dL
      • Symptomatic patients
    • Options:
      • 1st line: dimercaprol 
      • Calcium disodium edetate

Arsenic Poisoning

Etiology

  • Herbicides (vineyard workers)
  • Insecticides 
  • Metal smelting
  • Contaminated water (often from wells) 
  • Pressure-treated wood

Pathophysiology

  • Arsenic causes glycolysis to produce zero net ATP.
  • Arsenic inhibits lipoic acid (part of pyruvate dehydrogenase complex).
  • Binds to sulfhydryl groups 
  • Disrupts cellular respiration and gluconeogenesis

Clinical presentation

Acute:

  • General:
    • Garlic breath
    • Dehydration 
  • GI:
    • Vomiting
    • Abdominal pain
    • Watery diarrhea 
  • Cardiopulmonary:
    • Hypotension
    • QT prolongation
    • Cardiac arrhythmias
    • Shock
    • ARDS
  • Acute encephalopathy:
    • Delirium
    • Coma
    • Seizures
  • Renal:
    • Proteinuria
    • Acute renal failure

Chronic:

  • Skin manifestations: 
    • Mees lines on fingernails (transverse white bands)
    • Pigmentation (hypo or hyper) 
    • Hyperkeratosis
    • Skin cancer (squamous cell carcinoma)
  • Stocking-glove neuropathy:
    • Burning
    • Painful hypersensitivity
    • Distal weakness
    • Hyporeflexia
  • Liver cancer (angiosarcoma) 
  • Lung cancer
  • Pancytopenia

Diagnosis

  • Suspected through history and physical examination
  • Hemolytic anemia may be seen.
  • Urine arsenic level 
  • Plasma arsenic concentrations (helpful, but rarely available until after the decision to treat is made)

Management

  • Decontamination of the skin and GI tract
  • Supportive care
  • Chelation therapy in symptomatic patients only:
    • Dimercaprol (1st line)
    • Succimer (dimercaptosuccinic acid (DMSA))
    • Unithiol (2,3-Dimercapto-1-propanesulfonic acid (DMPS))
  • Hemodialysis in severe cases

Iron Poisoning

Etiology

  • Accidental ingestion by children (iron tablets may look like candy) 
  • Can be chronic in patients requiring multiple transfusions of RBCs

Epidemiology

Iron toxicity is one of the leading causes of deaths by poisoning in children < 6 years.

Pathophysiology

Absorption of excessive quantities of ingested iron can lead to:

  • Cellular toxicity:
    • Impaired oxidative phosphorylation and mitochondrial dysfunction → cellular death
    • The liver is the most affected organ.
    • In chronic overload, iron deposits into myocardial cells → myocardial siderosis and death
  • Corrosive toxicity:
    • Iron is corrosive to GI mucosa.
    • Leads to GI symptoms and potential blood loss

Clinical presentation

  • Stage 1: GI
    • < 6 hours after ingestion
    • Nausea
    • Diarrhea
    • Abdominal pain
    • Hemorrhagic gastroenteritis:
      • Hematemesis
      • Melena
    • Capillary leak/3rd spacing → hypovolemia or shock
  • Stage 2: latent
    • 6–24 hours after ingestion
    • GI symptoms resolve → patient seems to improve and recover
    • Some patients may demonstrate: 
      • Hypotension
      • Metabolic acidosis
      • Oliguria
  • Stage 3: metabolic/cardiovascular
    • 6–72 hours after ingestion
    • Metabolic acidosis
    • Cardiovascular symptoms
      • Tachycardia
      • Hypotension
      • Pallor
      • Shock
    • Central nervous system symptoms:
      • Stupor
      • Coma
    • GI hemorrhage
    • Acute lung injury or ARDS
    • Coagulopathy
    • Renal dysfunction
    • Most deaths occur in this stage.
  • Stage 4: hepatic
    • 12–96  hours after ingestion
    • ↑ Liver enzymes and bilirubin levels 
    • Coagulopathy
    • Hypoglycemia may accompany liver dysfunction.
  • Stage 5: delayed
    • 2–8 weeks after ingestion
    • Scarring of the GI tract → gastric outlet or intestinal obstruction

Diagnosis

  • Suspected by history and physical examination 
  • Serum iron levels will confirm the diagnosis.
  • Supporting studies: 
    • ↑ Anion gap metabolic acidosis
    • Check liver function, CBC, coagulation factors, glucose, and renal function tests.
  • Abdominal imaging may show radiopaque tablets in the stomach.

Management

  • Stabilize the patient.
  • IV fluids
  • Orogastric lavage and/or whole-bowel irrigation is indicated in patients with a significant number of radiopaque pills in the stomach on imaging.
  • Chelation therapy (IV deferoxamine, oral deferasirox) is indicated if any of the following is present: 
    • Severe symptoms (altered mental status, hemodynamic instability, persistent vomiting, and/or diarrhea) 
    • ↑ Anion gap metabolic acidosis 
    • Serum iron concentration > 500 μ/dL  
    • Significant number of pills on abdominal X-ray
  • Dialysis (exchange transfusion or continuous veno-venous hemofiltration) is indicated if chelation therapy fails to improve patient symptoms.

Differential Diagnosis

  • Sideroblastic anemia: microcytic anemia in which the bone marrow produces sideroblasts (ring-shaped RBCs) instead of normal, round-shaped RBCs due to the inability of the body to place iron properly into hemoglobin. Lead poisoning inhibits the conversion of protoporphyrins necessary for heme synthesis, resulting in sideroblastic anemia.
  • Esophagitis: inflammation or irritation of the esophagus. The major types of esophagitis are medication induced, infectious, eosinophilic, corrosive, and acid reflux. Patients typically present with odynophagia, dysphagia, and retrosternal chest pain. Diagnosis is by endoscopy and biopsy. Management depends on the etiology but includes medications and possible surgery.
  • Herbicides: substances used to control the growth of unwanted plants and in the construction industry. Different types of herbicides result in different clinical manifestations. Early management and treatment are important to prevent further intoxication.
    Pesticides: chemical substances used to control pests, including weeds. Important types include organochlorines (dichlorodiphenyltrichloroethane (DDT)) and organophosphates (malathion and parathion). Different types of pesticides result in different clinical manifestations. Early management and treatment are important to prevent further intoxication.

References

  1. Blumenberg, A. (2019). Arsenic Toxicity Clinical Presentation. Emedicine. Retrieved March 14, 2021, from https://emedicine.medscape.com/article/812953-clinical
  2. Buggs, A. (2021). Emergent Management of Lead Toxicity. Emedicine. Retrieved March 15, 2021, from https://emedicine.medscape.com/article/815399-overview#a4
  3. Spanierman, C. (2020). Iron Toxicity. Emedicine. Retrieved March 14, 2021, from https://emedicine.medscape.com/article/815213-overview
  4. Sample, J. (2020). Childhood lead poisoning: Clinical manifestations and diagnosis. UpToDate. Retrieved March 14, 2021, from https://www.uptodate.com/contents/childhood-lead-poisoning-clinical-manifestations-and-diagnosis
  5. Goldman, R. and Hu, H. (2020). Lead exposure and poisoning in adults. UpToDate. Retrieved March 14, 2021, from https://www.uptodate.com/contents/adult-occupational-lead-poisoning
  6. Golfman, R. (2020). Arsenic exposure and poisoning. UpToDate. Retrieved March 13, 2021, from https://www.uptodate.com/contents/arsenic-exposure-and-poisoning
  7. Liebelt, E. (2020). Acute iron poisoning. UpToDate. Retrieved March 13, 2021, from https://www.uptodate.com/contents/acute-iron-poisoning

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