Usefulness of the Neutrophil-to-Lymphocyte Ratio as a Predictor of Pneumonia and Urinary Tract Infection Within the First Week After Acute Ischemic Stroke.

Background: A high Neutrophil-to-Lymphocyte ratio (NLR) in patients with acute ischemic stroke (AIS) has been associated with post-stroke infections, but it's role as an early predictive biomarker for post-stroke pneumonia (PSP) and urinary tract infection (UTI) is not clear. Aim: To investigate the usefulness of NLR obtained within 24 h after AIS for predicting PSP and UTI in the first week. Methods: Clinical and laboratory data were retrieved from the University Hospital Brussels stroke database/electronic record system. Patients were divided into those who developed PSP or UTI within the first week after stroke onset and those who didn't. Receiver operating characteristics (ROC) curves and logistic regression analysis were used to identify independent predictors. Results: Five hundred and fourteen patients were included, of which 15.4% (n = 79) developed PSP and 22% (n = 115) UTI. In univariate analysis, NLR was significantly higher in patients who developed PSP (4.1 vs. 2.8, p < 0.001) but not in those who developed UTI (3.3 vs. 2.9, p = 0.074). Multiple logistic regression analysis for PSP showed that NLR, male gender, dysphagia, and stroke severity measured by the National Institutes of Health Stroke Scale (NIHSS), were independent predictors of PSP. For NLR alone, the area under the curve (AUC) in the ROC curve was 0.66 (95% CI = 0.59-0.73). When combining NLR ≥ 4.7 with age >75 years, male gender, NIHSS > 7, and dysphagia, the AUC increased to 0.84 (95% CI = 0.79-0.89). Conclusion: The NLR within 24 h after AIS appears to have no predictive value for post-stroke UTI, and is only a weak predictor for identifying patients at high risk for PSP. Its predictive value for PSP appears to be much stronger when incorporated in a prediction model including age, gender, NIHSS score, and dysphagia.

Quantitation of phosphatidylethanol in dried blood after volumetric absorptive microsampling.

BACKGROUND: Stimulated by the increased recognition of phosphatidylethanol (PEth) as sensitive direct marker of alcohol intake, the Ghent University's Laboratory of Toxicology and the National Institute of Criminalistics and Criminology combined their efforts to develop a quantitative method. To facilitate implementation the focus was on the use of a sampling technique which allows quick and easy blood collection, without the need of dedicated personnel at any place/any time. In the meantime the cooperation of the two labs should also allow to initiate a Belgian network of laboratories capable of quantifying PEth. METHODS: Dried blood microsamples were collected via volumetric absorptive microsampling (VAMS). PEth 16:0/18:1 was quantified after liquid-liquid extraction using two independent isotope dilution - liquid chromatography - tandem mass spectrometry methods. A systematic review of the entire process at both sites was performed before the final method comparison using samples from 59 routine toxicology cases collected within a one-year time interval. RESULTS: Initial differences between both laboratories were solved by focusing on important methodological aspects: (i) trueness verification of the calibration protocol focusing on the primary material, preparation of the stock solutions and adequate equilibration of calibrators and QCs, and (ii) verification of comparability of results obtained with different m/z transitions. Several of these aspects could only be verified by critically assessing spiked and native samples. After a final validation good average comparability of the two methods was observed. The average bias was -0.4%, with 85% of the differences within 20%. Moreover, the methods proved to be reproducible and robust within a one-year time interval. CONCLUSION: This study is the first to develop a quantitative volumetric absorptive microsampling based method for PEth measurements, in addition it is the first to perform a systematic comparison of PEth measurements between two laboratories. From the discussion on the encountered pitfalls it is clear that also on a global scale, more efforts are needed to improve interlaboratory agreement.

Role of infarct location and pre-existing depression on cardiac baroreceptor sensitivity in subacute ischemic stroke.

Reduced cardiac baroreceptor sensitivity (BRS) after acute stroke is associated with worse outcome. The underlying mechanisms of reduced BRS are unclear. We evaluated cross correlation BRS (xBRS) in 184 patients with suspected acute ischemic stroke within 72 h of symptom onset. Among these patients, 22 had a transient ischemic attack (TIA) and 27 had a stroke mimic. Sixty-four age- and sex-matched ambulant control subjects without stroke were included. Compared with controls, xBRS was significantly lower in patients with ischemic stroke, TIA, and stroke mimics (4.6, 4.7, and 4.4, respectively, vs 6.6, p < 0.01). There was no difference in xBRS between right and left hemispheric infarctions (4.3 vs 4.9, p = 0.144), right and left insular infarctions (4.5 vs 5.3, p = 0.286), and insular infarction vs non-insular infarctions (4.7 vs 4.5, p = 0.996). Stroke patients with pre-existing depression/use of antidepressant medication had lower xBRS values than stroke patients with normal mental health (2.9 vs 4.8, p < 0.05). Control patients with depression also had lower xBRS compared to controls without depression (3.4 vs 5.9, p < 0.01). Our results suggest that decreased xBRS in the subacute phase after stroke is not associated with infarct localization. We found preliminary evidence for an association between pre-existing depression and use of antidepressant medication, and decreased BRS.

High natural killer cell number might identify stroke patients at risk of developing infections.

OBJECTIVE: To investigate early changes in leukocyte subsets and autonomic function as predictors of the development of poststroke infections. METHODS: We assessed the time course of leukocyte subsets in the blood of 59 patients with acute ischemic stroke. We divided the patients into 2 groups: those who developed infections during the first 7 days after stroke onset and those who did not. We measured urinary norepinephrine and epinephrine concentrations and pulse rate variability indices within 24 hours of admission. RESULTS: We found that the number of circulating natural killer (NK) cells within the first hours after stroke was higher in stroke patients who developed infections (mean 435 cells/mL; 95% confidence interval [CI] 321-588) than in stroke patients who did not develop infections (mean 236 cells/mL; 95% CI 186-300; p = 0.001). This was followed by a decrease in all lymphocyte subsets from admission to day 1, varying between 22% and 40%, which was not seen in patients without poststroke infection (mean increase varied between 2% and 23%; all p < 0.005). In the group that developed infections, pulse rate variability revealed a decreased high frequency component. These findings all remained significant after adjustment for age and stroke volume. CONCLUSIONS: High circulating NK cell count within the first hours after ischemic stroke onset followed by a drop in all lymphocyte subsets identified patients who developed infections and may be caused by a sympathovagal imbalance with sympathetic overweight. These findings need to be validated in larger studies.

Autonomic dysfunction in acute ischemic stroke: an underexplored therapeutic area?

Impaired autonomic function, characterized by a predominance of sympathetic activity, is common in patients with acute ischemic stroke. This review describes methods to measure autonomic dysfunction in stroke patients. It summarizes a potential relationship between ischemic stroke-associated autonomic dysfunction and factors that have been associated with worse outcome, including cardiac complications, blood pressure variability changes, hyperglycemia, immune depression, sleep disordered breathing, thrombotic effects, and malignant edema. Involvement of the insular cortex has been suspected to play an important role in causing sympathovagal imbalance, but its exact role and that of other brain regions remain unclear. Although sympathetic overactivity in patients with ischemic stroke appears to be a negative prognostic factor, it remains to be seen whether therapeutic strategies that reduce sympathetic activity or increase parasympathetic activity might improve outcome.