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Colchicine poisoning occurs due to the ingestion of colchicine, a drug derived from the plant colchicum autumnale, and can be life-threatening.
Pathophysiology
Colchicine's toxicity arises primarily from its mechanism of action, which involves binding to tubulin and disrupting microtubule formation, leading to impaired cellular processes. This disruption affects rapidly dividing cells, particularly in the gastrointestinal tract and bone marrow, resulting in significant gastrointestinal symptoms such as nausea, vomiting, and diarrhea due to rapid turnover of intestinal mucosal cells. The drug is metabolized in the liver, primarily by cytochrome P450 enzymes, leading to the formation of several metabolites, including 3-demethylcolchicine (3DMC) and 2-demethylcolchicine (2DMC). These metabolites can exhibit increased toxicity compared to the parent compound, contributing to hepatic injury and other systemic effects. As colchicine inhibits mitosis by preventing spindle formation, it leads to multi-organ dysfunction. The early phase (10-24 hours post-ingestion) is characterized by gastrointestinal distress and initial leukocytosis. In the subsequent phase (2 to 7 days), patients may experience severe complications including renal failure, disseminated intravascular coagulation (DIC), and cardiac issues due to direct toxicity on cardiac myocytes. The high affinity of colchicine for tissues like the liver and kidneys contributes to its rapid accumulation in these organs, leading to further complications.
Symptoms
Symptoms typically manifest in three phases:
Phase 1 (10-24 hours)
This initial phase is characterized primarily by gastrointestinal symptoms, which can be severe and debilitating. The most common early symptoms include nausea, vomiting, and abdominal pain, often intense and persistent. Diarrhea is another hallmark symptom, potentially becoming profuse and even bloody in severe cases. These symptoms can lead to significant dehydration due to excessive fluid loss. patients may develop peripheral leukocytosis, an early increase in white blood cell count. This is often accompanied by electrolyte imbalances, including hyponatremia, hypocalcemia, and hypokalemia. The severe fluid loss and electrolyte disturbances can result in metabolic acidosis. Cardiovascular symptoms may also manifest during this phase. Hypotension can occur as a result of the severe vomiting and diarrhea, often accompanied by tachycardia as a compensatory mechanism. Some patients may develop a fever.
In more severe cases of colchicine poisoning, additional symptoms may appear during this initial phase. These can include scleral icterus (yellowing of the whites of the eyes), oliguria (decreased urine output), and peripheral cyanosis (bluish discoloration of extremities). Some may experience hypothermia. It's crucial to note that even if symptoms appear mild during this initial phase, patients should be closely monitored. The onset of severe toxicity can be delayed, and the progression to subsequent phases can occur rapidly. Therefore, any suspected case of colchicine poisoning should be treated as a medical emergency, regardless of the initial presentation's severity.
Phase 2 (2-7 days)
Phase 2 of colchicine poisoning is characterized by multi-organ dysfunction and potentially life-threatening complications. This phase is associated with a high mortality risk due to the potential for multi-organ failure and severe systemic effects.
One of the primary features of this phase is bone marrow suppression, which can lead to pancytopenia, including neutropenia, thrombocytopenia, and anemia. This hematopoietic inhibition increases the risk of severe infections and bleeding tendencies. Cardiovascular complications are common during this phase. Patients may experience cardiac arrhythmias, hypotension, and in severe cases, cardiogenic shock or cardiac arrest. Respiratory complications can also occur, with some patients developing acute respiratory distress syndrome (ARDS) that may necessitate mechanical ventilation. Renal dysfunction is another hallmark of this phase, with oliguric renal failure being a common occurrence. This often requires renal replacement therapy, such as continuous kidney replacement therapy (CKRT). Hepatic dysfunction may also develop, contributing to coagulopathy and metabolic disturbances. Neurological effects can manifest as changes in mental status, ranging from confusion to coma. Rhabdomyolysis, the breakdown of muscle tissue, can occur during this phase, exacerbating renal failure. The combination of these multi-system effects often results in a clinical picture of multiple organ failure, which may include hepatic, renal, respiratory, and circulatory failure.