The Post-Resuscitative Urinalysis Associate the Survival of Patients with Non-Traumatic Out-of-Hospital Cardiac Arrest

Abstract

ObjectiveTo analyze whether urine output and urinalysis results are predictive of survival and neurologic outcomes in patients with non-traumatic out-of-hospital cardiac arrest (OHCA).MethodsInformation was obtained from 1,340 patients with non-traumatic OHCA who had achieved a sustained return of spontaneous circulation (ROSC). Factors that were associated with survival in the post-resuscitative period were evaluated. The association between urine output and fluid challenge in the early resuscitative period was analyzed and compared between the survivors and the non-survivors. The results of the initial urinalysis, including the presence of proteinuria and other findings, were used to evaluate the severity of vascular protein leakage and survival. The association between proteinuria and the neurologic outcomes of the survivors was also analyzed. The clinical features of capillary leakage were examined during the post-resuscitative period.ResultsOf the 1,340 patients, 312 survived. A greater urine output was associated with a higher chance of survival. The initial urine output increased in proportion to the amount of fluid that was administered during early resuscitation in the emergency department for the survivors but not for the non-survivors (p<0.05). In the initial urinalysis, proteinuria was strongly associated with survival, and severe proteinuria indicated significantly poorer neurologic outcomes (p<0.05 for both comparisons). Proteinuria was associated with a risk of developing signs of capillary leakage, including body mass index gain and pitting edema (both p<0.001).ConclusionThe severity of proteinuria during the early post-resuscitative period was predictive of survival.

Acute kidney injury after cardiac arrest

“…A study by Chang et al . suggests that glomerular barrier dysfunction and vascular hyperpermeability may also play an important role in the pathogenesis of post-CA renal dysfunction [ 28 ]. Patients with AKI also received greater cumulative epinephrine doses than others; vasoconstrictors can induce alterations in intra-renal hemodynamics [ 29 ] and epinephrine may worsen the function of all organs, as suggested by alterations in cerebral microcirculation and lung exchange or increased post-resuscitation myocardial dysfunction observed in porcine models of CA [ 30 ].…”

“…Moreover, rhabdomyolysis could be associated with marked creatinine release from skeletal muscle, which may theoretically influence the course of sCr. Fourth, we did not record other findings from urine analysis, such as proteinuria or specific gravity, although these have been associated with patient outcome after CA [ 28 ]. Also, we did not use the standard UO criteria for AKI stage 1 (that is <0.5 mL/kg/h for 6 h) and this may have underestimated the occurrence of AKI stage 2 and/or stage 3 in our population.…”

Acute kidney injury after cardiac arrest

“…Acute tubular necrosis is uncommon in postmortem studies of patients dying of shock [27]. A study by Chang et al suggests that glomerular barrier dysfunction and vascular hyperpermeability may also play an important role in the pathogenesis of post-CA renal dysfunction [28]. Patients with AKI also received greater cumulative epinephrine doses than others; vasoconstrictors can induce alterations in intrarenal hemodynamics [29] and epinephrine may worsen the function of all organs, as suggested by alterations in cerebral microcirculation and lung exchange or increased post-resuscitation myocardial dysfunction observed in porcine models of CA [30].…”

Accumulated Epinephrine Dose is Associated With Acute Kidney Injury Following Resuscitation in Adult Cardiac Arrest Patients

“…We believe the pathophysiological process related to AKI development after resuscitation was multi-factorial. In addition to myocardial dysfunction and insufficient tissue perfusion, systemic inflammatory response ( Adrie et al, 2002 ), extensive subcapsular hemorrhages ( Hutchens et al, 2010 ), glomerular barrier dysfunction, and vascular hyperpermeability contributed to AKI ( Chang et al, 2013 ). All of these changes might be directly or indirectly related to epinephrine administration, which was supported by the present study.…”