2. Arsenic poisoning

PK

Step	Detail
Absorption	Excellent via GIT and lungs; limited via intact skin
Distribution	Systemic circulation → liver (methylation) → skin, nails, hair (keratin-binding)
Metabolism	Methylated in liver to MMA (monomethylarsonic acid) and DMA (dimethylarsinic acid)
Excretion	Mainly via urine over a few days (but in chronic or massive doses, it stays longer)
Half-life	Normally ~10 hours, but longer if dose is massive or if arsenic is less soluble
Storage	Hair, nails, skin (keratin-bound, like mercury) → used in forensic tests even long after poisoning

PD OF ARSENIC

Mechanism	What It Does
Trivalent arsenic binds -SH	Inhibits enzymes in energy metabolism (e.g. PDH)
Pentavalent arsenic mimics phosphate	Interrupts ATP production by substituting phosphate
Methylated arsenicals (e.g. MMA³⁺)	More toxic than inorganic forms; oxidative stress, gene disruption
Arsine gas (AsH₃)	Causes hemolysis and affects respiration
Arsenobetane	Non-toxic, excreted unchanged
Arsenosugars	Partially metabolized, minimal toxicity

Clinical Features of Acute Inorganic Arsenic Poisoning

Early (within minutes to hours):

• GIT symptoms: Nausea, vomiting, severe watery diarrhea, abdominal pain

• Capillary leak: Leads to hypotension, shock, fluid loss

• Metabolic acidosis: Due to lactic acid buildup from impaired cellular respiration

Cardiopulmonary:

• Cardiotoxicity: Congestive cardiomyopathy

• Pulmonary edema: Cardiogenic and non-cardiogenic

• Arrhythmias: Can appear early or be delayed

Hematologic:

• Pancytopenia: Within 1 week (anemia, leukopenia, thrombocytopenia)

• Basophilic stippling of RBCs

Neurologic:

• Early: Delirium, encephalopathy, coma

• Later (2–6 weeks): Ascending sensorimotor peripheral neuropathy
  

  • May progress to involve respiratory muscles

Skin/Nails:

• Aldrich-Mees lines (transverse white lines on nails): Seen after weeks/months

3. Diagnostic Clue

• Abrupt GI symptoms + hypotension + acidosis
  

  • Think acute arsenic poisoning

• Confirmation: Urinary arsenic and metabolites
  

  • Typically in the thousands of µg/L during the first 2–3 days

Treatment of acute poisoning

Great summary, Salma! Here’s a clear, high-yield breakdown of the treatment of acute arsenic poisoning:

Treatment of Acute Inorganic Arsenic Poisoning

1. Immediate Steps

• Gut Decontamination:
  

  • If ingestion was recent (within 1 hour): gastric lavage may be considered

  • Activated charcoal may help bind any remaining arsenic in the gut

• Supportive Care:
  

  • Fluids + electrolytes: To manage dehydration and shock from GIT losses

  • Correction of acidosis: Often needed due to lactic acidosis

  • Monitor cardiac rhythm, renal function, hematology, and neurologic status

2. Chelation Therapy

• Most effective if started within minutes to hours of exposure:

a) Unithiol (DMPS)

–

1st choice if available

• Route: IV

• Dose: Every 4–6 hours

• Benefit: Effective + safer than dimercaprol

b) Dimercaprol (BAL)

–

Alternative if unithiol not available

• Route: IM

• Interval: Every 4–6 hours

• Caution: More side effects; less safe, especially in patients with peanut allergy (in oil-based prep)

c) Succimer (DMSA)

• Route: Oral or parenteral

• Note: High therapeutic index

• Use: For mild to moderate cases or as follow-up after initial parenteral chelation

Key Point

• Early chelation = better prognosis

• Monitor urine arsenic levels during treatment to guide response

Chronic arsenic poisoning

Chronic Inorganic Arsenic Poisoning – Summary

Carcinogenicity Clarification

• Chronic arsenic exposure is carcinogenic — it is associated with:
  

  • Skin cancer

  • Lung cancer

  • Bladder cancer

• Acute arsenic poisoning is not carcinogenic — its effects are immediate and toxic, but not associated with cancer development.

Clinical Features of Chronic Arsenic Poisoning

Occurs after prolonged exposure to >500–1000 μg/day (dose and individual tolerance vary):

Constitutional Symptoms

• Fatigue

• Weight loss

• General weakness

• Anemia

• Nonspecific GIT symptoms

Neurological

• Symmetric peripheral neuropathy:
  

  • “Stocking and glove” pattern

  • Dysesthesias

  • Sensory > motor involvement (may resemble that seen in acute poisoning)

Dermatological (Pathognomonic)

• “Raindrop” hyperpigmentation (spotted areas of dark skin)

• Hyperkeratosis of palms and soles (rough, thickened skin)

Cardiovascular

• Peripheral vascular disease

• Non-cirrhotic portal hypertension

• Rarely: torsades de pointes (malignant arrhythmia)

Diagnosis of chronic arsenic poisoning

• Clinical suspicion + confirmation of exposure via:
  

  • Urinary arsenic levels:
    

    • Normal: <30 μg/L or <50 μg/24h

    • Can normalize within days–weeks after stopping exposure

    • Avoid seafood for 3 days before testing: marine arsenicals (e.g., arsenobetaine) can falsely elevate levels

  • Hair/nail arsenic:
    

    • Reflect past exposure (binds to keratin)

    • Normal: <1 ppm

Arsenic gas poisoning

Yes, exactly right — here’s a clear summary of arsine gas poisoning to tie it all together:

Arsine Gas Poisoning – Summary

Key Feature

• Profound intravascular hemolytic anemia
  (Typically within 2–24 hours post-inhalation)

Clinical Presentation

Initial nonspecific symptoms (due to hemolysis):

• Malaise

• Headache

• Dyspnea

• Weakness

• Nausea & vomiting

• Abdominal pain

Signs of hemolysis & complications:

• Jaundice

• Hemoglobinuria (dark/red urine)

• Oliguric renal failure (1–3 days post-exposure)

• In massive exposure: death may occur before renal failure develops

Treatment

• Intensive supportive care

• Vigorous IV hydration (prevents renal tubular damage from hemoglobin)

• Exchange transfusion (for severe hemolysis)

• Hemodialysis if renal failure occurs

Let me know if you’d like to compare arsine gas vs inorganic arsenic poisoning side by side!