Markers of cardiogenic shock predict persistent acute kidney injury after out of hospital cardiac arrest

Abstract

Objective: Ischemia and reperfusion injury (IRI) in cardiac arrest patients after return to spontaneous circulation causes dysfunctions in multiple organs. Kidney injury is generally transient but in some patients persists and contributes both to mortality and increased resource utilisation. Ongoing shock may compound renal injury from IRI, resulting in persistent dysfunction. We tested whether cardiac dysfunction was associated with the development of persistent acute kidney injury (PAKI) in the first 72 hours after cardiac arrest. Methods: We performed an observational retrospective study from January 2013 to April 2017. We included consecutive patients treated after out-of-hospital cardiac arrest at a single academic medical center with renal function measured and immediately and for 48 hours post arrest. We also recorded each patient's pre arrest baseline creatinine, demographic and clinical characteristics. Our primary outcome of interest was PAKI, defined as acute kidney injury (AKI) on at least 2 measurements 24 hours apart. We compared demographics and outcomes between patients with PAKI and those without, and used logistic regression to identify independent predictors of PAKI. Results: Of 98 consecutive patients, we excluded 24 for missing data. AKI was present in 75% of subjects on arrival. PAKI developed in 35% of patients. PAKI patients had a longer hospital length of stay (median 21 vs 11 days) and lower hospital survival (47% vs 71%). Serum lactate levels, dosage of adrenaline during resuscitation and days of dobutamine infusion strongly predicted PAKI. Conclusions: Among patient who survive cardiac arrest, acute AKI is common and PAKI occurs in more than one third. PAKI is associated both with survival and with length of stay at the hospital. High doses of adrenaline, high serial serum lactate levels, and dose of dobutamine predict

Renal function after out-of-hospital cardiac arrest; the influence of temperature management and coronary angiography, a post hoc study of the target temperature management trial

“…An increasing time from CA to ROSC, an indicator of ischaemic burden, was independently associated with a higher risk of AKI, as was a higher serum creatinine on admission. The association of the intensity of ischaemia/reperfusion injury after CA (whether assessed as amount of epinephrine administered, time to ROSC, lactate concentration or the early presence of shock) and AKI has been noted in several studies [3–5, 19, 21]. Increased serum creatinine concentrations on admission and risk of AKI are also well described [4, 5, 19].…”

“…The post cardiac arrest syndrome is characterised by multi-organ dysfunction as a result of an acute inflammatory response and persistent haemodynamic instability. Ischaemia-reperfusion injury and on-going shock may aggravate renal injury [1–3]. Acute kidney injury (AKI) is common in these circumstances, affecting 12–81% of patients depending on definition and patient selection [1, 2, 4, 5].…”

Cardiogenic shock and acute kidney injury: the rule rather than the exception

“…In these two scenarios, clinicians should initiate a low PEEP regimen (3–5 cmH 2 O) only when euvolemic state is achieved, with a view to up-titration. Close evaluations of blood gas analysis can help to adjust the ventilatory strategy, as well as to evaluate lactates, whose high levels were found to predict persistent AKI [ 42 ].…”

The adaptive immune response in cardiac arrest resuscitation induced ischemia reperfusion renal injury

“…ATN after ischemic shock has a mortality rate of 30% and many survivors are subject to dialysis [ 2 ]. Among patients surviving cardiac arrest (CA), the onset of acute kidney injury (AKI) is also common (> 75%) and persistent AKI (PAKI) occurs in more than one-third of the patients [ 3 ]. A plethora of renal diseases, but also renal transplant rejection [ 4 ] are due to AKI resulting from ischemic shock [ 5 ].…”