|Year : 2019 | Volume
| Issue : 4 | Page : 774-778
Association of stroke severity, leukocytosis, and infarction size with early neurological deterioration in acute ischemic stroke
Jehan Saeed1, Ghada M Samir1, Ahmed F El-Said2
1 Department of Internal Medicine, Zagazig University, Zagazig, Egypt
2 Department of Public Health and Community Medicine, Zagazig University, Zagazig, Egypt
|Date of Submission||01-Feb-2019|
|Date of Acceptance||17-Feb-2019|
|Date of Web Publication||18-Aug-2020|
MD Jehan Saeed
Department of Internal Medicine, Zagazig University, Zagazig, 44519
Source of Support: None, Conflict of Interest: None
Background About one-third of patients with acute ischemic stroke will endure early neurological deterioration (END), which leads to increased mortality and functional disability. A better understanding of risk factors for END is still required.
Objective The aim of this study was to determine the risk factors of END in ischemic stroke patients.
Patients and methods One hundred and twenty patients with first ever ischemic stroke were included in this study. All patients were clinically evaluated to determine the risk factors. END was assessed using the National Institute of Health Stroke Scale (NIHSS) after acute ischemic stroke. Laboratory and radiological investigations were done for all patients.
Results In all, 35% patients showed clinical END after stroke onset and 65% patients were stable or improved. END patients had statistically significant high body temperature, increased leukocyte count, serum blood glucose, triglycerides, NIHSS at admission, high-sensitivity C-reactive protein, and infarction size. Multivariable logistic regression analysis for different variables showed that leukocyte count, stroke severity using NIHSS, and lesion size were independent factors associated with neurological deterioration.
Conclusion Stroke severity, white blood cell, and lesion size of infarction were the only independent factors associated with END.
Keywords: early neurological deterioration, ischemic stroke, National Institute of Health Stroke Scale, white blood cell
|How to cite this article:|
Saeed J, Samir GM, El-Said AF. Association of stroke severity, leukocytosis, and infarction size with early neurological deterioration in acute ischemic stroke. Egypt J Intern Med 2019;31:774-8
|How to cite this URL:|
Saeed J, Samir GM, El-Said AF. Association of stroke severity, leukocytosis, and infarction size with early neurological deterioration in acute ischemic stroke. Egypt J Intern Med [serial online] 2019 [cited 2020 Sep 28];31:774-8. Available from: http://www.esim.eg.net/text.asp?2019/31/4/774/292195
| Introduction|| |
Approximately one-third of ischemic stroke patients will clinically deteriorate following hospital admission. This is called early neurological deterioration (END) .
END commonly occurs as a result of microglia activation and inflammation in the brain . Inflammatory response is due to the activation of resident cells, production of cytokines, and inflammatory cellular infiltrate in the infarcted area .
Studies tried to recognize the predictive factors for END to clarify its occurrence. Demographic variables, risk factors, clinical examination, laboratory tests, and imaging studies affect the outcome ,.
Acute inflammatory response was associated with ischemic stroke including elevation of C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), total peripheral white blood cell count, and body temperature . An increase in leukocyte count as well as hyperthermia in the acute phase of cerebral ischemia was significant independent predictors of poor initial stroke severity and clinical outcome ,. Leukocytic infiltration of the penumbra that leads to excitotoxic neuronal death is thought to contribute to END .
CRP is a prognostic factor and an independent predictor of death and recurrent vascular events in acute ischemic stroke. Moreover, higher CRP levels were associated with larger infarct volumes and these results may serve as a marker for severity of acute ischemic stroke ,.
| Patients and methods|| |
This study was conducted on 120 ischemic stroke patients who were admitted in the Intensive Care Unit of Internal Medicine Department, Zagazig University Hospitals during the period from January 2018 to November 2018. Informed consent was obtained from the patients or their relatives regarding the study.
Patients were selected according to the following criteria; patients with first ever ischemic stroke and admitted within 24 h of symptom onset.
We excluded patients with hemorrhagic stroke and patients with hemorrhagic transformation on follow computed tomography (CT), pre-existing and poststroke infectious disease, trauma, burns, surgery, chronic inflammatory disease and patients with anti-inflammatory treatment, neoplasm, hepatic or renal impairment, hematological disorders, and recent myocardial infarction.
All patients were subjected to the following: detailed medical history taking plus complete general and neurological examination with particular stress on National Institute of Health Stroke Scale (NIHSS). stroke severity was classified into mild, moderate, and severe stroke . END was defined as an increase by at least two points in the NIHSS between admission and day 5 . Patients were categorized into two groups, with END and without END.
CT scan of the brain was performed to all patients to confirm the diagnosis of ischemic stroke and to evaluate the early signs of infarction. To assess the size of the infracted area, follow-up CT was done after 72 h. Stroke lesions were classified according to their size of infarction into small (<1.5 cm), moderate (1.5–3 cm), and large (>3 cm) . Laboratory investigations were done for all patients including complete blood count, random blood sugars, lipid profile (cholesterol, low-density lipoprotein, high-density lipoprotein, and triglycerides), liver and renal function tests and high-sensitivity C-reactive protein (HS-CRP).
Data were analyzed using SPSS version statistics 20.0 (IBM corporation, Armonk, New York, USA) software package. Data were expressed as percentage for discrete variables and mean±SD for continuous variables. Student’s t-tests, χ2, correlation, and multivariable logistic regression analysis were done when appropriate. P value of up to 0.05 was considered significant and a P value less than 0.001 was considered highly significant.
| Results|| |
This study included 120 ischemic stroke patients. They were divided into two main groups: with END [42 (35%) patients] and without END [78 (65%) patients]. Characteristics of the patients are shown in [Table 1]. There was no statistically significant difference between the END group and without END as regards sex and age. According to the history of risk factors, patients with END had a statistically significant history of diabetes mellitus and hyperlipidemia more than patients without END.
|Table 1 Demographic data of early neurological deterioration and nonearly neurological deterioration patients|
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Concerning severity of stroke using NIHSS (mean±SD), the END group has statistically significant higher level than without the END group at admission and on the fifth day. Also, temperature was significantly higher in the END group. Patients with END have significantly larger infarct size than the without END group. The laboratory results of both groups are shown in [Table 2]. END patients had significant elevation in leukocytes, HS-CRP, serum blood glucose, and triglyceride levels than without END patients.
|Table 2 Comparison between early neurological deterioration group and nonearly neurological deterioration regarding laboratory data at admission|
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Univariate analysis showed significant correlations between END and leukocyte count, serum blood glucose, body temperature, NIHSS at admission, HS-CRP, and infarction size as shown in [Table 3]. Multivariable logistic regression analysis ([Table 4]) for different variables showed that leukocyte count, stroke severity using NIHSS and lesion size were independent predictors of neurological deterioration.
|Table 4 Multivariate logistic regression analysis of risk factors associated with neurological deterioration|
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| Discussion|| |
Stroke patients are at high risk of END which is often happened early after cerebral infarction . It was reported that the frequency of END ranged from 15 to 40% ,,. This study included 120 ischemic stroke patients, 35% patients showed clinical END after stroke onset, and 65% patients were stable or improved. This result was in accordance with Siegler et al. , who reported a deterioration of 36.9% in their study.
There was no age difference between END and without END which was similar to other studies that found no association between age and the occurrence of neurological deterioration ,; however, other studies established old age as a risk factor for END ,,.
Our result found significant association between diabetes and hyperlipidemia with the END group compared with without END. This was similar to that observed by Hansson  and Tanaka et al. . Regarding history of hypertension, cardiac diseases, smoking, and transient ischemic attack, there was no significant difference between both groups. This results were in accordance with other studies ,.
The role of hyperthermia in neurological deterioration was supported by its association with higher plasma levels of proinflammatory markers in acute ischemic stroke . Our results found a significant association between temperature and END which was supported by other studies ,. Moreover, there was significant correlation between temperature and size of infarction. Our finding was in accordance with the results of Karaszewski et al. . Saini et al.  realized that increased temperature might have a possible suggested cascade of events through opening the blood–brain barrier that leads to increased extracellular edema, more infarct enlargement, more limited capillary flow in the ischemic tissue with decreases reperfusion which leads to more ischemic damage and larger infarction size.
Elevated leukocyte count in this study was associated with END. Excitotoxic neuronal death which could be due to leukocytic infiltration of the penumbra gives an explanation for END . This was in agreement with Nardi et al. , Miyoamoto et al. , and Kumar et al. . Moreover, this elevated leukocyte count was significantly correlated with stroke severity which was supported by the results of Buck et al.  and Nardi et al.  studies.
The correlation of CRP with ischemic stroke is tortuous, while most studies have found that increased levels of CRP were associated with END and poor outcome in patients after ischemic stroke ,. Di Napoli  and Toyoda et al.  studies could not realize that CRP can predict the outcome after stroke. In this study, a significant higher level of CRP was detected in patients with END. In addition, our study found significant correlation between CRP neurological deterioration and these results were supported by the results of Seo et al. , Abubakar et al.  and, Luo et al. .
Another significant factor of END in our study is the lesion size. We found that patients with large-sized infarctions on follow-up CT were more likely to deteriorate than patients with medium or small infarctions. This was supported by the result of Dohmen et al. , who found that the most common etiology of ND was the extension of the initial infarction.
Multivariable logistic regression analysis for different variables showed that leukocyte count, stroke severity using NIHSS, and lesion size were independent factors associated with neurological deterioration. Our result was in agreement with the studies of Siegler et al. , Siegler et al. , and Schonewille et al. . This findings showed that increased susceptibility of stroke patients for END can be attributed to patients’ characteristics, stroke-induced inflammation, and imaging data. Careful attention should be paid to patients with elevated total leukocyte count with severe stroke and large volume size. Finally, it can be concluded that stroke severity, white blood cell, and lesion size of infarctions were the only independent factors associated with END. Further large, randomized studies are needed to stratify risk factors for END.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Table 1], [Table 2], [Table 3], [Table 4]