Introduction: Contrast-induced nephropathy (CIN), defined as an increase in serum creatinine (SCr) greater than 25% or ≥0.5 mg/dL within 3 days of intravenous (IV) contrast administration in the absence of an alternative cause, is the third most common cause of new acute renal failure in hospitalized patients. It is known to increase in-hospital mortality up to 27%. The purpose of this study was to investigate the rate of outpatient follow up and the occurrence of CIN in patients who presented to the emergency department (ED) and were discharged home after computed tomography (CT) of the abdomen and pelvis (AP) with IV contrast.Methods: We conducted a single center retrospective review of charts for patients who required CT of AP with IV contrast and who were discharged home. Patients' clinical data included the presence of diabetes mellitus, hypertension, chronic kidney disease (CKD) and congestive heart failure (CHF).Results: Five hundred and thirty six patients underwent CT of AP with IV contrast in 2011 and were discharged home. Diabetes mellitus was documented in 96 patients (18%). Hypertension was present in 141 patients (26.3%), and 82 patients (15.3%) were on angiotensin-converting-enzyme inhibitors (ACEI). Five patients (0.9%) had documented CHF and all of them were taking furosemide. Seventy patients (13%) had a baseline SCr >1.2 mg/dL. One hundred fifty patients (28%) followed up in one of the clinics or the ED within one week after discharge, but only 40 patients (7.5%) had laboratory workup. Out of 40 patients who followed up within 1 week after discharge, 9 patients (22.5%) developed CIN. One hundred ninety patients (35.4%) followed up in one of the clinics or the ED after 7 days and within 1 month after discharge, but only 71 patients (13.2%) had laboratory workup completed. Out of 71 patients who followed up within 1 month, 11 patients (15%) developed CIN. The overall incidence of CIN was 15.3% (17 out of 111 patients).Conclusion: There was a poor outpatient follow up after CT of AP with IV contrast and biochemically CIN appears to be present in some patients. Unlike previous reports that CKD is the major risk factor for CIN, our results demonstrated that risk factors such as advanced age, DM and hypertension seem to predispose patients to CIN rather than abnormal baseline SCr. [West J Emerg Med. 2014;15(3):276–281.]
Background. Computerized electrocardiogram (ECG) analysis has been of tremendous help for noncardiologists, but can we rely on it? The importance of ST depression and T wave inversions in lead aVL has not been emphasized and not well recognized across all specialties. Objective. This study's goal was to analyze if there is a discrepancy of interpretation by physicians from different specialties and a computer-generated ECG reading in regard to a TWI in lead aVL. Methods. In this multidisciplinary prospective study, a single ECG with isolated TWI in lead aVL that was interpreted by the computer as normal was given to all participants to interpret in writing. The readings by all physicians were compared by level of education and by specialty to one another and to the computer interpretation. Results. A total of 191 physicians participated in the study. Of the 191 physicians 48 (25.1%) identified and 143 (74.9%) did not identify the isolated TWI in lead aVL. Conclusion. Our study demonstrated that 74.9% did not recognize the abnormality. New and subtle ECG findings should be emphasized in their training so as not to miss significant findings that could cause morbidity and mortality.
Background: Wellens’ sign (WS) has been reported as a sign of critical proximal left anterior descending (PLAD) artery lesion with lumen narrowing greater than 90%. Wellens’ ECG signs for critical PLAD lesion are characterized by two different electrocardiogram (ECG) patterns: 1) Deep T wave inversion in leads V2, V3 (approximately 76% of cases); and 2) Biphasic T wave in leads V2, V3 (approximately 24% of cases). The prevalence of the ECG feature of WS ranges from 14-18%. The prognostic significance of WS in detecting significant coronary artery lesion defined as a luminal narrowing of the coronary vessel by more than 70% has not been well studied. Our study’s goal was to evaluate if WS is present in all patients with critical and significant PLAD lesions and is a sensitive or specific sign for critical and significant (>70% stenosis) PLAD lesions. Methods: All patients that underwent percutaneous coronary intervention (PCI) at an urban community hospital between January 2009 and December 2011 were included in the study. Log books from the cardiac catheterization laboratory were reviewed for all lesion types and corresponding demographics. The ECGs of patients with PLAD lesion were reviewed for T wave changes in precordial leads. Additionally, demographics such as age, gender and cardiovascular risk factors were recorded and analyzed. Descriptive statistics were used to analyze the data. Results: A total of 431 patients underwent PCI [emergent PCI 152 (35.3%), elective PCI 279 (64.7%)]. A total of 78 patients (18.1%) from both groups were found to have PLAD lesion. Fifty eight patients were male and 20 patients were female. The average age was 63.7 years. Critical PLAD lesion was present in 26 patients (33.3%) and 52 patients (66.7%) had PLAD lesion less than 90%. Of the 26 patients, 17 (65.4%) had WS. Wellens’ sign for predicting a critical PLAD had a sensitivity of 65.4%, a specificity of 69.2%, a positive predictive value (PPV) of 51.5% and a negative predictive value (NPV) of 80% (p = 0.0069, two-tailed Fisher’s exact test). Of the 42 patients who had PLAD lesion greater than 70%, 21 patients (50%) had WS. Of the 36 patients who had PLAD lesion less than 70%, 11 patients (30.6%) had WS. Wellens’ sign for predicting significant PLAD lesion in this cohort has a sensitivity of 50%, a specificity of 69.4%, a PPV of 65.6% and a NPV of 54.3% ( p = 0.1074). Conclusion: Our results corroborated prior studies showing that WS predicts the presence of critical (90%) PLAD lesion. Unfortunately, the value of WS for detecting/predicting significant CAD in PLAD was weak. Our results indicated that we were not able to predict the presence of significant (70%) PLAD lesion using WS. However, in appropriate clinical settings such as Non-ST elevation MI (NSTEMI) or unstable angina, Wellens’ sign may indicate the need for a more aggressive treatment strategy with patients proceeding to the cardiac catheterization suite sooner than later.
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