Colchicine diarrhea with

Discuss important points the nurse should consider when administering colchicine to a patient with an acute attack of diarrhea. 

Oral colchicine causes dose-dependent GI adverse effects (nausea, vomiting, and diarrhea) in 50% to 80% of patients before relief of the attack. Non-GI adverse effects include neutropenia and axonal neuromyopathy, which may be worsened in patients taking other myopathic drugs (e.g., statins) or in those with renal insufficiency. Colchicine should not be used concurrently with macrolide antibiotics (especially clarithromycin) because reduced biliary excretion may lead to increased plasma colchicine levels and agranulocytosis. 

Gi effects Vomiting, diarrhea, abdominal pain, and nausea may occur, especially with maximum doses. These may be particularly troublesome in the presence of peptic ulcer or spastic colon. At toxic doses, colchicine may cause severe diarrhea, generalized vascular damage, and renal damage with hematuria and oliguria. To avoid more serious toxicity, discontinue use when these symptoms appear, regardless of whether joint pain has been relieved. 

Although colchicine is more specific in gout than the NSAIDs, NSAIDs (eg, indomethacin and other NSAIDs [except aspirin]) have replaced it in the treatment of acute gout because of the troublesome diarrhea sometimes associated with colchicine therapy. Colchicine is now used for the prophylaxis of recurrent episodes of gouty arthritis, is effective in preventing attacks of acute Mediterranean fever, and may have a mild beneficial effect in sarcoid arthritis and in hepatic cirrhosis. Although it can be given intravenously, this route should be used cautiously because of increased bone marrow toxicity. 

Colchicine often causes diarrhea and may occasionally cause nausea, vomiting, and abdominal pain. Hepatic necrosis, acute renal failure, disseminated intravascular coagulation, and seizures have also been observed. Colchicine may rarely cause hair loss and bone marrow depression as well as peripheral neuritis, myopathy, and in some cases death. The more severe adverse events have been associated with the intravenous administration of colchicine. 

As with allopurinol, prophylactic treatment with colchicine or NSAIDs should start at the beginning of treatment to avoid gout flares. The most frequent treatment-related adverse events are liver function abnormalities, diarrhea, headache, and nausea. Febuxostat appears to be well tolerated in patients with a history of allopurinol intolerance. 

Colchicine can cause diarrhea as the result of mucosal damage and it has been established that colchiane interferes with the absorption of vitamin Bu. 

Transient diabetes and hyperlipidemia have been reported. Metabolic acidosis is probably a consequence of heavy, cholera-like diarrhea. Progressive reduction of libido was attributed to colchicine in patients with familial Mediterranean fever (312). 

Most common adverse effects include nausea, vomiting, diarrhea, abdominal pain, bone marrow depression with agranulocytosis, thrombocytopenia, and aplastic anemia. Cumulative toxicity is possible in elderly patients, hence it should be used cautiously. Care also should be exercised in patients with cardiac, hepatic, and renal dysfunctions. Colchicine causes teratogenicity in animals, and there are evidences of the risk of fetal chromosomal damage in humans. Colchicine should not be administered by the parenteral route as it causes severe local irritation. 

Adverse effects Colchicine treatment may cause nausea, vomiting, abdominal pain, and diarrhea (Figure 39.15). Chronic administration may lead to myopathy, agranulocytosis, aplastic anemia, and alopecia. The drug should not be used in pregnancy, and should be used with caution in patients with hepatic, renal or cardiovascular disease. 

Colchicine is an antimitotic agent, highly effective in the treatment of gout, but associated with considerable toxicity. Diarrhea is used as a criterion for adequate dosage. Accidental overdosage occurs relatively often and can be dangerous. For these reasons, NSAIDs (except aspirin) are often used in acute gout instead of colchicine. 

Acute reversible ciclosporin toxicity occurred in a renal transplant patient a few days after colchicine was administered for an acute attack of gout (SEDA-16, 115). Other potential adverse effects of combining colchicine with ciclosporin include diarrhea, increases in serum liver enzymes, bilirubin, and creatinine, and less often severe myalgia (SEDA-19, 101). Acute myopathy, associated with neuropathy in one case, has been observed in two young renal transplant recipients (SEDA-22, 119). 

Proresid (mitopodozide), a mixture of more than 20 derivatives of Podophyllum emodi, has been used for many years in some countries as a disease-modifying agent in rheumatoid arthritis. A microtubuhn antagonist, it is comparable with colchicine and griseofulvin. Its use has been limited because treatment is often comphcated by severe diarrhea, abdominal pain, nausea, and vomiting. Leukopenia and thrombocytopenia have been reported (3,4). 

Colchicine Colchicine would be a reasonable choice for patients with contraindications or who are intolerant to NSAIDs. The gastrointestinal side effects of colchicine (including severe diarrhea) may make it difficult for patients who are having difficulty accessing the bathroom quickly. 

Animal toxicity is primarily related to ingestion of the plant C. autumnale. Colchicine is available as a pesticide for burrowing animals. The estimated toxic dose for cows is lOgkg with fresh leaves or 2 or 3gkg with dried leaves. Symptoms may include gait disorders, hypersalivation, bloody vomitus, and diarrhea. Death within 72 h has occurred secondary to shock. It is only slightly toxic to cold-blooded and hibernating animals. 

Colchicine can be given orally or parenterally. Unless contraindications exist or the patient has renal insufficiency, the usual oral dose is 1 mg initially, followed by 0.5 mg every 2 hours until the joint symptoms subside, until the patient develops abdominal discomfort or diarrhea, or until a total dose of 8 mg has been administered. " About 75% to 95% of patients with acute gouty arthritis respond favorably to colchicine when ingestion of the drug is begun within 24 to 48 hours of the onset of joint symptoms. If the initiation of colchicine is delayed longer than 48 hours after the onset of acute symptoms, the probability of success with the drug diminishes substantiahy. 

Three treatments are available for patients with acute gouty arthritis. Colchicine is less favored now than in the past because its onset of action is slow and it invariably causes diarrhea. Nonsteroidal antiinflammatory drugs, which are currently favored, are rapidly effective but may have serious side effects. Corticosteroids, administered either intraarticularly or parenterally, are used increasingly in patients with monarticular gout, especially if oral drug therapy is not feasible. 

A. After an acute overdose, symptoms are typically delayed for 2-12 hours and include nausea, vomiting, abdominal pain, and severe bloody diarrhea. Shook results from depressed cardiac contractility and fluid loss into the gastrointestinal tract and other tissues. Delirium, seizures, or coma may occur. Lactic acidosis related to shock and inhibition of cellular metabolism is common. Other manifestations of acute colchicine poisoning include acute myocardial injury, rhabdomyolysis with myoglobinuria, disseminated intravascular coagulation, and acute renal failure. 

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