Makindo Medical Notes

Related Subjects: |Drug Toxicity - clinical assessment |Metabolic acidosis |Aspirin or Salicylates toxicity |Ethylene glycol toxicity |Ethanol toxicity |Methanol toxicity |Ricin toxicity |Carbon Tetrachloride Toxicity |Renal Tubular Acidosis |Lactic acidosis |Iron Toxicity |Tricyclic Antidepressant Toxicity |Opiate Toxicity |Carbon monoxide Toxicity |Benzodiazepine Toxicity |Paracetamol (Acetaminophen) toxicity |Amphetamine toxicity |Beta Blocker toxicity |Calcium channel blockers toxicity |Cannabis toxicity |Cyanide toxicity |Digoxin Toxicity |Lithium Toxicity |NSAIDS Toxicity |Ecstasy toxicity |Paraquat toxicity |Quinine toxicity |SSRI Toxicity |Theophylline Toxicity |Organophosphate (OP) Toxicity |Toxin elimination by dialysis |Drug Toxicity with Specific Antidotes

Ricin is a type 2 ribosome-inactivating protein, which has a heterodimeric structure consisting of an A-chain linked by a disulfide bond to a B-chain. The B-chain facilitates internalization of the A-chain, which then exerts its toxic effects by inhibiting protein synthesis, leading to cell death.

About

• Ricin is a highly toxic extract derived from the castor bean (Ricinus communis), and poses a significant bioterrorism threat. A dose as small as 500 micrograms can be lethal.
• The process for extracting ricin has been widely known and described, with details even included in a patent.
• The patent detailing ricin extraction was removed from the United States Patent and Trademark Office (USPTO) database in 2004, but it is still available through various online sources.
• Ricin can be delivered in various forms: inhalation, ingestion, or injection, all of which are fatal if not treated quickly.
• It is classified as a "Category B" bioterrorism agent by the Centers for Disease Control and Prevention (CDC), indicating it is moderately easy to disseminate and can cause significant morbidity and mortality.

Aetiology

• Ricin is a naturally occurring lectin that disrupts cellular function by inactivating ribosomes, halting protein synthesis, and triggering apoptosis (cell death).
• It is a type 2 ribosome-inactivating protein (RIP), meaning it consists of two subunits:
  • A-chain: Exerts toxic effects by inhibiting protein synthesis inside the cell.
  • B-chain: Facilitates the internalization of the A-chain by binding to cell surface receptors.
• Ricin damages endothelial cells, leading to vascular leak syndrome, where fluid and proteins leak from blood vessels, causing severe tissue oedema and organ dysfunction.
• It causes direct damage to tissues such as the lungs, gastrointestinal tract, and kidneys, depending on the route of exposure.

Clinical Features

• Inhaled ricin:
  • Initial symptoms appear 4-8 hours after exposure and include fever, chest tightness, cough, and shortness of breath.
  • Progresses to severe respiratory distress, pulmonary oedema, and hypoxia.
  • In severe cases, death can occur within 36-72 hours due to respiratory failure.
• Ingested ricin:
  • Early symptoms include nausea, vomiting, diarrhoea, and abdominal pain, typically within 6 hours of ingestion.
  • Leads to severe dehydration, multi-organ failure, and circulatory collapse due to fluid loss and vascular damage.
  • Death typically occurs within 3-5 days if untreated.
• Injected ricin:
  • Localized pain and swelling at the injection site, followed by systemic effects like organ failure.
  • Symptoms may progress more rapidly due to direct introduction into the bloodstream.
• General symptoms across exposure types include weakness, hypotension, and multi-organ dysfunction.

Investigations

• FBC, U&E, and LFTs: Monitor for organ dysfunction, including liver and kidney damage.
• CXR or CT scan: Evaluate for signs of pulmonary oedema or lung damage in inhalation cases.
• Urinalysis: May show evidence of renal damage or failure.
• ELISA and other immunoassays: Can detect ricin in blood, urine, or tissue samples, though availability is limited.
• Ricin-specific PCR: Used for identifying ricin exposure in environmental samples or body fluids, but not routinely available.
• Postmortem findings often reveal haemorrhage, necrosis, and oedema in affected organs, depending on the route of exposure.

Management

• No specific antidote exists for ricin poisoning, and death typically occurs within 36-72 hours after exposure.
• Supportive care is the mainstay of treatment and includes:
  • Ventilatory support for respiratory failure.
  • Intravenous fluids for dehydration and shock.
  • Electrolyte management and renal support for acute kidney injury.
  • Vasopressors to maintain blood pressure in the case of severe hypotension.
• Decontamination:
  • Remove ricin from the skin using soap and water to prevent further absorption.
  • Rinse the eyes thoroughly with water or saline if exposed.
  • Use activated charcoal for recent ingestions to prevent absorption.
• Experimental vaccines and antibodies against ricin are in development, but none are currently available for widespread use.

Prognosis

• The prognosis for ricin poisoning is poor without immediate supportive care, particularly in cases of inhalation or injection.
• Survival depends on the dose and route of exposure, with lower doses and ingestion providing a slightly better chance of recovery.
• Death is typically due to multi-organ failure or circulatory collapse.