For the last 20 years, efforts have focused an improving survival from out‐of‐hospital cardiac arrest and multiorgan failure. Given the many known nephrotoxic insults of postresuscitation care, it is a common belief that renal function is a contributor to mortality and morbidity postresuscitation; however, this has been poorly studied. The focus of this study was to evaluate changes in renal function in patients surviving out‐of‐hospital cardiac arrest and to identify the predictors of renal function change postarrest.
We conducted a retrospective chart review of all patients presenting to a major academic teaching hospital with out‐of‐hospital, nontraumatic cardiac arrest. We included all consecutive patients who were treated at our center following cardiac arrest since March 30, 2004. Acute renal failure was defined as worsening of calculated creatinine (Cr) by 30% or by a Cr > 2.0 mg/dL. Data were collected according to a standardized protocol following the Utstein style. Continuous data are presented as the median and interquartile range or as the mean and standard deviation. Percentages were calculated for dicholomous variables. Clinical significance was assessed using the chi‐square test, t lest, or ANOVA as appropriate.
We studied 66 consecutive, out‐of‐hospital, nontraumatic cardiac arrest patients who survived to hospital admission. Of these patients, 19 patients survived to hospital discharge. The mean age of survivors was 64.1 ± 9.2 years, 53% were male, and all were smokers. Prearrest Cr was known in 79% of patients and was normal in 17 patients, with a mean of 1.26 ± 0.24 mg/dL (all mean ± SD). Only 2 patients had abnormal baseline Cr (2.5 and 3.2 mg/dL). Twenty‐one percent of survivors underwent therapeutic hypothermia for 24 hours. Mean time to resumption of spontaneous circulation in survivors was 15.5 ± 14.9 minutes (range 4–57 minutes; 75th percentile, 24.5 minutes), and the mean dose of epinephrine administered during resuscitation was 2.9 ± 2.8 mg. Following resuscitation, 15.8% of survivors required pressor support for more than 24 hours, and 32% had contrast imaging studies within 72 hours. Despite these experiences, mean Cr within the first 24 hours was 1.49 ± 0.77, changing to only 1.46 ± 0.99 and 1.44 ± 0.01 mg/dL on days 2 and 3, respectively, Peak Cr was 2.88 ± 2.66 mg/dL, with the peak occurring 7.04 ± 5.86 days postarrest. Mean Cr on discharge was normal (1.6 ± 1.2), with only 3 patients with abnormal Cr. All P > 0.05 when mean Cr at discharge was compared with Cr at baseline and after 24, 48, and 72 hours.
Notwithstanding intrinsic vascular disease, prolonged resuscitation, vasopressors, and contrast media insult, renal function appears to be rather impervious and usually withstands deterioration following cardiac arrest. As such renal function does not appear to signifcantly contribute to the morbidity in the post‐cardiac arrest survivor.
S. Eid, none; K. Stewart, none; S. Carey, none; N. Chandra‐Strobos, none.
To cite this abstract:Eid S, Stewart K, Carey S, Chandra‐Strobos N. Renal Function Trends in Patients with Out‐of‐Hospital Cardiac Arrest. Abstract published at Hospital Medicine 2010, April 8-11, Washington, D.C. Abstract 48. Journal of Hospital Medicine. 2010; 5 (suppl 1). https://www.shmabstracts.com/abstract/renal-function-trends-in-patients-with-outofhospital-cardiac-arrest/. Accessed January 26, 2020.