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Methadone Case Studies

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Methadone Case Studies
Our patient had a history of drug abuse and as such had only one home medication, which is Methadone. Methadone has been associated with thrombocytopenia in patients with hepatitis. She does have hepatitis hence she is at risk for thrombocytopenia because of methadone. This patient has continued this therapy throughout her stay in the hospital, as such not meeting any of the criteria established in the table above plus she has had methadone for years prior to hospitalization.5
This patient was on Enoxaparin 40mg daily at the time she had thrombocytopenia, it was discontinued as well and reintroduced after our patient’s platelet got stable. Furthermore, enoxaparin had not just been newly introduced to her therapy she had been exposed to the
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Since rifampin induced thrombocytopenia usually occurs within a few days (4-6) of therapy.3
Our patients vital sign had stabilized and at that point she did not meet the sepsis criteria rolling out sepsis and consequent organ failure as a cause of the thrombocytopenia.
On the other hand Nafcillin met 3 of the 4 criteria’s in the George Criteria list but for one since the was no re- exposure of nafcillin to our patient, especially since they were other options to help with her treatment other than nafcillin. Our patients IBW was estimated at 50.5kg and her dose was appropriate at 12g/24 hours.

Nafcillin and cefazolin are considered first-line therapy for most infections with methicillin-susceptible Staphylococcus aureus (MSSA).1 Nafcillin is a Beta-lactam antibiotic which is mainly bactericidal, anti-staphylococcal. Due to its side chains, it is penicillinase hydrolysis resistant. Thus, its coverage for MSSA. It Is usually unlikely to experience Drug-induced immune thrombocytopenia (DITP). They can be triggered by a wide range of medications. Although most cases are mild some can be life-threatening. Therefore, a decision to discontinue an implicated medication in a patient show symptoms of having DITP is a clinical Judgment call. Drug induce platelet-reactive antibodies once formed, these antibodies cause platelet destruction following exposure to the drug. The mechanism of how this happens are still poorly

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