Published online Feb 21, 2019. doi: 10.5492/wjccm.v8.i2.9
Peer-review started: December 13, 2018
First decision: January 5, 2019
Revised: January 24, 2019
Accepted: January 29, 2019
Article in press: January 30, 2019
Published online: February 21, 2019
Processing time: 70 Days and 9.4 Hours
Mortality and morbidity after having an in hospital cardiac arrest (IHCA) event are high. Despite the advent of therapeutic modalities such as target temperature management and increased access to rapid response and code blue teams, the survival rates after IHCA are dismal. Markers of poor survival after IHCA have been evaluated and include S-100 and serum neuron-specific enolase concentrations. However, this and many other markers are often analyzed at specialized laboratories and may have a time delay in response. Their routine use is therefore limited.
The main motivation for the study was to evaluate whether neutrophil-lymphocyte ratio (NLR), an easy to obtain marker can be used to gain prognostic information after IHCA patients achieve return of spontaneous circulation (ROSC). Previously, NLR has been evaluated as a marker of poor prognosis for several cardiovascular and non-cardiovascular conditions. Interestingly, a high NLR in patients with out of hospital cardiac arrest (OHCA) has been shown to have increased mortality. It is essential to investigate whether NLR provides any prognostic information in IHCA patients as they are often sicker, older and have poor survival compared to patients with OHCA.
The main objective was to determine the value of an elevated NLR in predicting survival to discharge in patients with IHCA. Furthermore, we evaluated whether a high adrenergic drive or inflammation may be associated with the mechanism associated with IHCA. As a result, we looked at the initial cardiac rhythm and other laboratory values such as potassium, lactate, glucose and platelet level as this may be evaluated in future research as therapeutic targets for improving survival after IHCA.
A retrospective chart review was conducted at our institution of all patients over 18 years of age who has sustained ROSC after IHCA events. Medical records were reviewed for demographics, history and physical examination, laboratory and imaging findings as well as initial cardiac rhythm and outcomes were collected. Of note, the laboratory data was collected during 24 h of the IHCA being recorded.
The main finding out this study was that a NLR cut-off of 4.55 derived from receiver operating characteristic analysis (area under the curve = 0.66), provided 73% positive predictive value, 82% sensitivity, 42% specificity predicting in-hospital death. Multivariable logistic regression analysis yielded an NLR ≥ 4.55 [odds ratio (OR) = 5.2, confidence interval (CI): 1.5-18.3, P = 0.01], older age (OR = 1.03, CI: 1.00-1.07, P = 0.05), and an elevated serum lactate level (OR = 1.2, CI: 1.03-1.4, P = 0.02) as independent predictors of death. Older individuals, or those with pulseless electrical activity and/or asystole as the initial cardiac rhythm were more likely to have died from IHCA despite achieving ROSC. A limitation of this paper is that it did not evaluate the prognostic significance of other biomarkers such as S-100, serum neuron-specific enolase amongst others compared to NLR. Our study was also a single center retrospective study with modest number of cases and as results our findings should be considered as hypothesis-generating.
The new findings of our study are that an increased NLR may be a marker of decreased survival in patients with ROSC after IHCA. NLR may have some utility in improving clinical decision making and family’s understanding of risk of death after IHCA. This study proposes that modulating inflammation may improve mortality in patients after an IHCA event.
The authors suggest using NLR as a tool to further assist in prognosticating patients with ROSC after IHCA. Future investigations may look to compare NLR values and survival before and after currently accepted interventions such as target temperature management or even after modulation of inflammation, a cascade which is less well understood but likely plays a detrimental role in the outcome after IHCA.