Hyperthermia is a potential factor for an unfavorable functional neurologic recovery after successful cardiopulmonary resuscitation.

We analyzed the medical records of patients with an established diagnosis of acute renal infarction to identify predictive parameters of this rare disease. Seventeen patients (8 male) who were admitted to our emergency department between May 1994 and January 1998 were diagnosed by contrast-enhanced computed tomography (CT) as having acute renal infarction (0.007% of all patients). We screened the records of the 17 patients for a history with increased risk for thromboembolism, clinical symptoms, and urine and blood laboratory results known to be associated with acute renal infarction. A history with increased risk for thromboembolism with 1 or more risk factors was found in 14 of 17 patients (82%); risk factors were atrial fibrillation (n = 11), previous embolism (n = 6), mitral stenosis (n = 6), hypertension (n = 9), and ischemic cardiac disease (n = 7). All patients reported persisting pain predominantly from the flank (n = 11), abdomen (n = 4), and lower back (n = 2). On admission, elevated serum lactate dehydrogenase was found in 16 (94%) patients, and hematuria was found in 12 (71%) of 17 patients. After 24 hours all patients showed an elevated serum lactate dehydrogenase, and 14 (82%) had a positive test for hematuria. Our findings suggest that in all patients presenting with the triad--high risk of a thromboembolic event, persisting flank/abdominal/lower back pain, elevated serum levels of lactate dehydrogenase and/or hematuria within 24 hours after pain onset--contrast-enhanced CT should be performed as soon as possible to rule out or to prove acute renal infarction.

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Background-Platelet activation is a hallmark of acute coronary syndromes. Numerous lines of evidence suggest a mechanistic link between von Willebrand factor or platelet hyperfunction and myocardial damage in patients with acute coronary syndromes. Thus, we assessed whether platelet function under high shear rates (collagen adenosine diphosphate closure times [CADP-CTs]) measured with the platelet function analyzer (PFA-100) may be enhanced in patients with myocardial infarction (MI) and whether it may predict the extent of myocardial damage as measured by creatine kinase (CK-MB) or troponin T (TnT) levels. Methods and Results-Patients with acute chest pain or symptoms suggestive of acute coronary syndromes (nϭ216) were prospectively examined at an emergency department. CADP-CT was significantly shorter in patients with MI, particularly in those with an ST-segment-elevation MI (STEMI) compared with the other patient groups (unstable angina, stable coronary artery disease, or controls). Furthermore, CADP-CT and collagen epinephrine-CT at presentation were independent predictors of myocardial damage as measured by CK-MB or TnT. Patients with MI whose CADP-CT values fell in the first quartile had 3-fold higher CK-MB and TnT levels than those in the fourth quartile. Conclusions-Patients with STEMI have significantly enhanced platelet function when measured under high shear rates.CADP-CT is an independent predictor of the severity of MI, as measured by markers of cardiac necrosis. Measurement of platelet function with the PFA-100 may help in the risk stratification of patients presenting with MI. (Circulation.

We investigated the relationship between lactate clearance and outcome in patients surviving the first 48 hours after cardiac arrest. We conducted the study in the emergency department of an urban tertiary care hospital. We analyzed the data for all 48-hour survivors after successful resuscitation from cardiac arrest during a 10-year period. Serial lactate measurements, demographic data, and key cardiac arrest data were correlated to survival and best neurologic outcome within 6 months after cardiac arrest. Parameters showing significant results in univariate analysis were tested for significance in a logistic regression model. Of 1502 screened patients, 394 were analyzed. Survivors (n = 194, 49%) had lower lactate levels on admission (median, 7.8 [interquartile range, 5.4-10.8] vs 9 [6.6-11.9] mmol/L), after 24 hours (1.4 [1-2.5] vs 1.7 [1.1-3] mmol/L), and after 48 hours (1.2 [0.9-1.6] vs 1.5 [1.1-2.3] mmol/L). Patients with favorable neurologic outcome (n = 186, 47%) showed lower levels on admission (7.6 [5.4-10.3] vs 9.2 [6.7-12.1] mmol/L) and after 48 hours (1.2 [0.9-1.6] vs 1.5 [1-2.2] mmol/L). In multivariate analysis, lactate levels at 48 hours were an independent predictor for mortality (odds ratio [OR]: 1.49 increase per mmol/L, 95% confidence interval [CI]: 1.17-1.89) and unfavorable neurologic outcome (OR: 1.28 increase per mmol/L, 95% CI: 1.08-1.51). Lactate levels higher than 2 mmol/L after 48 hours predicted mortality with a specificity of 86% and poor neurologic outcome with a specificity of 87%. Sensitivity for both end points was 31%. Lactate at 48 hours after cardiac arrest is an independent predictor of mortality and unfavorable neurologic outcome. Persisting hyperlactatemia over 48 hours predicts a poor prognosis.