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91. Toxicology – Colchicine Toxicity
Source
Colchicine is a medication commonly prescribed for gout, pericarditis, and familial Mediterranean fever. It is derived from the autumn crocus plant (Colchicum autumnale) and has a narrow therapeutic index.
Typical Presentation
Patients usually present after an overdose with severe gastrointestinal symptoms that may initially resemble infectious gastroenteritis. Toxicity can rapidly progress to multiorgan failure over the following days.
Clinical Features
Colchicine poisoning classically progresses through three stages:
  • Phase 1 (within hours): Severe nausea, vomiting, diarrhea, abdominal pain, dehydration, tachycardia, hypotension, and early kidney injury.
  • Phase 2 (days later): Multisystem toxicity develops, including bone marrow suppression, low white blood cell counts, kidney and liver failure, rhabdomyolysis, pulmonary edema, ARDS, cardiovascular collapse, and pancytopenia.
  • Phase 3 (recovery phase): Survivors may later develop hair loss (alopecia) and ascending peripheral neuropathy.
Mechanism of Action
Colchicine disrupts microtubule formation and inhibits mitosis, impairing rapidly dividing cells such as those in the gastrointestinal tract and bone marrow.
Management
Treatment is primarily supportive and includes:
  • Aggressive IV fluid resuscitation
  • Airway and hemodynamic support
  • Antiemetics for severe GI symptoms
  • Activated charcoal to reduce enterohepatic recirculation
Granulocyte colony-stimulating factor (G-CSF) may help in severe leukopenia. Hemodialysis is ineffective because colchicine is poorly removed by dialysis.
Key Points
  • Early symptoms may mimic viral gastroenteritis.
  • Toxicity can progress rapidly to fatal multiorgan failure.
  • Bone marrow suppression is a major complication.
  • Dialysis is not useful in colchicine overdose.

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