ObjectivesNearly one-third of healthcare costs are potentially avoidable and would not compromise medical care if eliminated. Therefore, we sought to evaluate the financial impact of reduction in use of creatinine kinase (CK)-MB and myoglobin tests after removing them from the cardiac enzyme order set at a community hospital.MethodsGrand rounds were held, and an email notification was sent to de-emphasize the use of CK, CK-MB, myoglobin, SGOT (glutamic-oxaloacetic transaminase), and SGPT (serum glutamic-pyruvic transaminase) in acute coronary syndrome (ACS) work up. The above tests were removed from the pre-checked cardiac enzyme order set in the computerized physician order entry on February 13, 2014. The tests continued to be available, but needed to be ordered individually. The mean monthly volume of cardiac enzyme tests for 12 months after this intervention was compared with the mean monthly volume of 12 months before the change. Total cost savings were calculated.ResultsAfter the intervention, the number of CK, CK-MB, myoglobin, SGOT, and SGPT tests utilized for ACS workup decreased dramatically (p<0.001). The volume of troponin testing remained the same (p=0.283). The total annual savings of billable charges to healthcare payers was $463,744.7.ConclusionsRemoval of CK-MB, myoglobin, CK, SGOT, and SGPT tests from cardiac enzyme order sets can successfully reduce unnecessary laboratory testing for ACS workup, leading to significant cost savings to the healthcare system.
The possible role of infectious and inflammatory states in the pathogenesis of atherosclerotic disease has been a matter of debate in the literature. There are case reports of active cytomegalovirus (CMV) infection unmasking underlying dormant systemic lupus erythematosus (SLE). CMV infection has also been postulated to be associated with atherosclerosis development in the coronaries. We present a unique case where a patient with newly diagnosed SLE and acute myocardial infarction was found to have high anti-CMV titers suggesting concomitant active CMV infection. A literature review has postulated strong affiliation of CMV infection with the development of coronary artery disease, an avenue which has yet to be explored further by ongoing research.
Medications, especially non-steroidal anti-inflammatory drugs and antimicrobials, have been most commonly associated with acute interstitial nephritis (AIN); antiepileptic drugs (AEDs) are rarely known to cause AIN. This is a case of a 27-year-old male who was recently started on treatment with lamotrigine for bipolar disorder and was found to have rapidly progressive renal failure. Renal biopsy features were suggestive of AIN. Lamotrigine-induced AIN was suspected to be the most likely cause. Discontinuation of the drug and treatment with steroids resulted in complete renal recovery. Lamotrigine use has been recently gaining popularity, not only as an AED but also as a mood stabilizer. With the use of this drug becoming more popular, it is important to emphasize that – although rare – AIN is one of its potential complications.
It is well known that cancer and hypercoagulability go hand in hand. Most thromboembolism is venous in nature although arterial thrombosis can occur. Arterial thrombosis secondary to malignancy is usually seen in the lower extremities; however, it can also be seen elsewhere. This is a case of bronchogenic carcinoma with no history of typical atherosclerotic risk factors including smoking, diabetes mellitus, hypertension, or hyperlipidemia presented with chest pain and was found to have an acute ST segment elevation myocardial infection. Coronary angiography showed a large thrombus in the left anterior descending artery in the absence of any atherosclerotic lesions. Malignancy is considered to be the major contributing factor for this myocardial infarction in the absence of both atherosclerotic risk factors and atherosclerotic lesions in the coronary angiography. We will focus on the relationship between cancer and thrombosis with special emphasis on arterial thromboembolism with subsequent development of myocardial infarction.
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