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Stroke. 1995;26:392-398

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(Stroke. 1995;26:392-398.)
© 1995 American Heart Association, Inc.

Articles

Early Predictors of Death and Disability After Acute Cerebral Ischemic Event

H. Hénon, MD; O. Godefroy, MD; D. Leys, MD; F. Mounier-Vehier, MD; C. Lucas, MD; P. Rondepierre, MD; A. Duhamel, MD J. P. Pruvo, MD

From the Departments of Neurology (H.H., O.G., D.L., F.M.-V., C.L., P.R.), Statistics (A.D.), and Neuroradiology (J.P.P.), University of Lille, France.

Correspondence to Hilde Hénon, MD, Service de Neurologie B, Hôpital B, F-59037 Lille, France.


*    Abstract
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 *Abstract
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Background and Purpose Many clinical trials are currently being conducted to evaluate the ability of neuroprotectors and thrombolytic agents to improve survival and functional outcome after ischemic stroke. Such trials require early predictors of survival and disability for ethical and methodological reasons. The aim of the study was to determine which variables, of those easily assessable during the first 24 hours after stroke onset, would be predictors of 8-day mortality rate and 3-month clinical outcome.

Methods One hundred fifty-two consecutive patients with an acute ischemic event were evaluated within 24 hours after symptom onset. We determined (1) the 8-day mortality rate and (2) the 3-month functional outcome (Glasgow Outcome Scale). The following potential predictors of outcome were tested by means of a stepwise logistic regression analysis: age, sex, body mass index, atrial fibrillation, previous stroke, existence of headache, Orgogozo score, level of consciousness, swallowing disturbances, hemianopia, pulse rate, mean blood pressure, hematocrit, glycemia, and computed tomographic scan data (cerebral atrophy score, hyperdense middle cerebral artery sign, number of silent infarcts, leukoaraiosis score).

Results The multivariate analysis revealed that the 8-day mortality rate depended only on the level of consciousness at admission (P=.0001); death or dependence at month 3 (scores 3 to 5 on the Glasgow Outcome Scale) depended on the severity of the clinical deficits (P=.0001), previous stroke (P=.0018), and age (P=.0237).

Conclusions In future drug trials, the distribution of patients between "active treatment" and "placebo" groups should be balanced regarding the severity of clinical deficits, history of stroke, and age.


Key Words: cerebral ischemia • mortality • prognosis


*    Introduction
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 up arrowAbstract
 *Introduction
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 down arrowResults
 down arrowDiscussion
 down arrowReferences
 
In ischemic stroke research, many clinical trials are currently being or will be conducted to evaluate the ability of neuroprotectors or thrombolytic agents to improve survival and functional outcome. These trials require early predictors of survival and disability for two reasons: (1) from an ethical point of view, drugs that are potentially effective but also dangerous, such as thrombolytics, should not be administered in patients who are likely to have a good clinical outcome, and (2) potential prognostic factors should be balanced between the active drug group and the placebo group.

Previous studies found no relationship between gender and outcome.1 2 3 4 5 Aging,2 6 7 8 9 10 11 12 13 impaired consciousness,7 9 10 14 15 hemianopia,4 12 and a low functional score4 7 10 12 13 15 16 17 18 are usually found to be predictors of disability or early death. A previous stroke might also be a predictor of disability1 3 9 but not of early death.13 Chronic arterial hypertension13 16 seen as high blood pressure at admission19 does not seem to influence the short-term prognosis. On computed tomographic (CT) scans, even if a hyperdense middle cerebral artery sign has been suggested to predict a poor clinical outcome,20 21 22 one fifth of patients who have this sign have a complete recovery within 2 weeks.23

Other findings are more controversial. Although hemodilution has been proposed in ischemic strokes,24 there is no evidence for an increased short-term mortality rate in patients with a high hematocrit level.25 In diabetic patients, it has been suggested that microcirculatory damage and a higher risk of infections may reduce the likelihood of complete recovery,26 but it has never been proven in clinical studies.13 16 21 However, hyperglycemia at admission in nondiabetic patients is a predictor of early death.13 27 Atrial fibrillation has sometimes been found to be another predictor of poor clinical outcome16 28 but not in all studies.29

Despite the large number of studies, it remains difficult to determine the prognosis at admission to the emergency department because only a few studies involved data from the first hours after stroke onset.13 16 19 Moreover, there are discrepancies between their results30 31 ; several studies were retrospective22 30 and included hemorrhagic as well as ischemic strokes.2 3 7 10 18 These studies cannot be compared because they differed in inclusion criteria and evaluation of outcome. Moreover, most of them evaluated potential predictors of clinical outcome in a univariate fashion.32

The aim of this study was to determine predictors of 8-day death and 3-month death and disability in 152 consecutive patients admitted within 24 hours after ischemic stroke onset, by means of a multivariate analysis, taking into account clinical and radiological factors that may easily be assessed within a few hours in any care center.


*    Subjects and Methods
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During the study period (January 1, 1991, through February 28, 1992), 152 patients with an acute ischemic event were consecutively admitted within 24 hours after symptom onset; those who had a history of neurosurgery (1 patient), severe head trauma (1 patient), or cerebral vascular malformation (1 patient) or who were included in a drug trial (6 patients) were excluded. The study population consisted of 89 men (59%) and 63 women (41%) with a mean age of 62.6 years (range, 24 to 100 years). Thirty patients (20%) were subsequently classified as having had a transient ischemic attack and 122 (80%) as having had a stroke. All patients underwent standard blood and urine tests, 12-lead electrocardiography, chest radiography, and CT scanning within 24 hours after stroke onset.

Medical history was determined from all available records (general practitioner's letter or telephone call) and sources (patient or family) concerning history of stroke, atrial fibrillation, and recent headache. The following data were prospectively collected: age (years), sex, body mass index (weight in kilograms divided by height in meters squared), pulse rate (beats per minute), mean arterial blood pressure (BP; [systolic BP+2 diastolic BP]/3), glucose level (grams per liter), and hematocrit (percent) at admission. The severity of the clinical deficits was scored according to the rating scale of Orgogozo et al.33 The level of consciousness was assessed by the ad hoc subtest of that scale.33 Swallowing disturbances and hemianopia were also recorded in a yes/no fashion. All these data were recorded as soon as possible after onset and always within 24 hours.

CT scans were performed without contrast within the first 24 hours after onset on a Siemens Somatom II machine, according to the procedure reported by Leys et al.23 In a conference, one neuroradiologist and one neurologist blinded to the clinical data determined the type of lesions according to previously reported rules.23 34 The interobserver and intraobserver reliability of this method of assessment of CT data has previously been reported as excellent.35 Leukoaraiosis was defined by the criteria of Inzitari et al36 and scored with the 0- to 3-point rating scale of Blennow et al.37 Leukoaraiosis was assessed on the hemisphere opposite to the unilateral focal vascular lesion, if any was present, and on the right hemisphere in the remaining patients. Cerebral atrophy was scored according to the criteria of Leys et al.38 Presence of a hyperdense middle cerebral artery sign23 and the number of silent infarcts defined according to the criteria of Mounier-Vehier et al34 were also recorded. The main clinical, biological, and CT characteristics in the study group are summarized in Table 1Down.


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  		Table 1. Clinical, Biological, and Computed Tomographic Characteristics of the Study Population (n=152)

All patients were treated by a low dosage of subcutaneous low-molecular-weight heparin within 24 hours after onset to prevent peripheral venous thrombosis. Their previous antidiabetic and antihypertensive treatments, if any, were maintained. Acute arterial hypertension usually was not treated at the acute stage unless it exceeded 240 mm Hg for the systolic BP or 130 mm Hg for the diastolic BP or in the case of cardiac failure. When an antihypertensive treatment was required (3 patients), we used continuous intravenous infusion of nicardipine. All patients were given nimodipine orally or through a nasogastric tube (120 mg daily). Patients began speech and physical rehabilitation as soon as possible.

Follow-up was undertaken by telephone contact 3 months after stroke onset. We studied the 8-day mortality rate. The 3-month functional outcome was evaluated according to the Glasgow Outcome Scale (GOS).39 GOS evaluation was performed by the patient's general practitioner. In a subgroup of the first 65 patients, GOS evaluation was assessed by one of us (H.H.), who was not involved in the patients' care at the acute stage. The interobserver agreement between the general practitioners and the neurologist was perfect ({kappa} value=1). Therefore, evaluation of the subsequent patients was performed by general practitioners only.

The statistical analysis was performed by means of SAS statistical analysis software.40 The first step consisted of a bivariate analysis comparing the 18 variables listed in Table 1Up between (1) patients who were dead at day 8 and those who were not and (2) patients who were independent at month 3 (defined as those who had a score of 1 or 2 at the GOS) and patients who were dependent or dead (defined as having a score of 3 to 5 at the GOS). We used the odds ratio (OR) method with 95% confidence intervals (CI) to compare qualitative factors between groups and the Mann-Whitney U test to compare quantitative factors. The second step consisted of a multivariate analysis with the same 18 independent variables of age, body mass index, Orgogozo score, consciousness score, pulse rate, mean BP, hematocrit, glycemia, CT data (cerebral atrophy scores, hyperdensity of the middle cerebral artery [present=1, absent=0], number of silent infarcts, leukoaraiosis scores), and the following variables defined as either absent (0) or present (1): male sex, previous stroke, previous or current atrial fibrillation, headache associated with symptom onset, swallowing disturbances, and hemianopia. Factors predicting 8-day mortality and 3-month death or dependence were evaluated by means of a logistic stepwise regression.41 42 Multicolinearity was assessed using the analysis of correlations among the continuous independent variables.41 The third step of analysis consisted of an evaluation of the risk of death at day 8 and dependence or death at month 3 in patients with predictors of poor clinical outcome found in the multivariate analysis, isolated or associated together.


*    Results
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 *Results
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Three months after onset, 80 patients (52.6%) returned to their former functional level even if with a minor focal deficit (GOS score=1); 19 patients (12.5%) were moderately disabled but remained independent (GOS score=2); 10 patients (6.6%) were dependent for their daily living activities (GOS score=3); 21 patients (13.8%) were comatose (GOS score=4). Six patients (3.9%) died within 8 days and 16 patients (10.5%) between day 8 and month 3. The causes of death are detailed in Table 2Down.


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  		Table 2. Causes of Death Within 3 Months After Stroke Onset

Results of the bivariate analysis are reported in Tables 3Down and 4Down. Patients with early death (day 8) had lower Orgogozo scores at admission (P=.0002), lower consciousness scores (P=.0001), and higher rates of atrial fibrillation (OR, 9.68; 95% CI, 1.67 to 56.12) than other patients. Patients with death or dependence at month 3 were older (P=.0008) and had lower Orgogozo (P=.0001) and consciousness scores (P=.0001) and higher mean BP (P=.0057) and serum glucose levels (P=.0063) than other patients; they were also more likely to have had a previous stroke (OR, 4.06; 95% CI, 1.40 to 11.75) and to have swallowing disturbances (OR, 6.06; 95% CI, 2.50 to 14.69).


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  		Table 3. Comparison of Clinical, Biological, and Computed Tomographic Findings Between Patients Who Died Before Day 8 and Survivors


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  		Table 4. Comparison of Clinical, Biological, and Computed Tomographic Findings Between Patients Who Died or Were Dependent at Month 3 and the Survivors

Using the stepwise logistic analysis, only the consciousness subscore was found to be an independent factor of early death ({chi}2, 49.99; P=.0001). Orgogozo score ({chi}2, 54.06; OR, 0.948; P=.0001), previous stroke ({chi}2, 9.69; OR, 6.398; P=.0018), and age ({chi}2, 5.11; OR, 1.032; P=.0237) were found to be predictors of dependence or death at month 3. Assessment of multicolinearity revealed no redundancy between the 18 factors, since none of the correlations reached a value higher than r=.6. The statistical model providing the probability of dependence was P=.7614-(0.0532xOrgogozo score)+(1.8561xprevious stroke)+(0.0314xage).

The risks of death or dependence at month 3 are detailed in Table 5Down.


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  		Table 5. Risk of Death or Dependence at Month 31 in Patients With Combination of Predictors of Poor Outcome2


*    Discussion
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 up arrowAbstract
 up arrowIntroduction
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 up arrowResults
 *Discussion
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Among the factors associated with early death, only the level of consciousness has been established as an independent predictor. Concerning the 3-month outcome, only the severity of clinical deficits, presence of previous stroke, and age have been established as independent predictors. These findings are similar to those of previous studies in which the evaluation was performed later after stroke onset.7 8 9 10 14 15 17 18 They are also consistent with studies conducted within 616 43 or 24 hours44 after stroke onset.

When we started our study (January 1, 1991), we knew of the results of studies by Gelmers et al45 46 suggesting a beneficial effect in patients treated with oral nimodipine during the first 24 hours after stroke onset. Other trials47 48 suggested that nimodipine might be a useful agent at least in subgroups of patients with acute stroke. The TRUST study49 and the study of Bogousslavsky et al50 found no benefit from oral nimodipine; however, the TRUST study49 entered all possible "strokes" and may have included hemorrhagic strokes, and the study by Bogousslavsky et al50 included only a small number of patients. Therefore, all our patients were given nimodipine orally. After our patient recruitment ended, negative results concerning nimodipine trials51 52 53 were published, and we no longer administer oral nimodipine to our patients.

We chose our 18 independent variables because they have been considered to be of prognostic value1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 25 27 28 29 or because it is probable that they could be of prognostic value. We chose variables that are easily assessable in any care center; if a drug is proven to affect stroke prognosis, it will have to be used in many patients, not only in specialized stroke units. We have explored these variables within 24 hours after stroke onset. When we started our study, data concerning the duration of the therapeutic window were not as clear as now: one hypothesis was to open the time window based on evidence that clinical worsening could occur over a 48-hour period,54 and many therapeutic trials published around 1990 included patients up to 24 or even 48 hours after stroke onset.46 47 49 50 53 The aim of our study was to obtain data potentially useful for such trials; thus, we decided to include patients within 24 hours after stroke onset. However, it became obvious that drug trials must be started within the first 6 to 8 hours. Of course, the results of our study can only be generalized to patients seen within 24 hours after stroke onset. However, our conclusions give indications as to which variables should be of interest in further studies conducted within the first 6 hours. Moreover, early inclusion will allow CT scan data to be taken into account because of a lower degree of heterogeneity in the delay between stroke onset and CT scans.

In our study, we have mixed infratentorial and hemispheric strokes: if a neuroprotector is recognized as effective, neuroprotective treatments will become largely diffused, even in nonspecialized units and before admission. Moreover, in emergency cases, in patients without cranial nerve palsy or cognitive impairment (pure motor hemiplegia, for instance), it may be difficult to determine the location of the infarct. Our study population is therefore reasonably representative of the ischemic strokes seen in general practice.

We decided to use a single scale for supratentorial and infratentorial infarcts. The rating scale of Orgogozo et al was constructed to assess patients with hemiplegia due to middle cerebral artery infarction. However, it is a widely distributed and easily applied scale, largely used in many centers. Moreover, all the rating scales that are currently used (Orgogozo scale, Scandinavian Rating Scale, Canadian Neurological Scale, etc) have been assessed only in hemispheric infarcts, indeed in middle cerebral artery infarcts, and there is no reliable and currently used rating scale for infratentorial strokes.

The use of a stroke scale as a surrogate measure of neurological status has many detractors; however, it has the undeniable advantage of summarizing a multifactorial impairment in a single score. As an alternative, all subscores may be included in the multivariate model, but using an evaluation scale considerably increases sensitivity compared with analysis of any individual item.55 Therefore, we decided to enter the Orgogozo score rather than a score for each item in the multivariate analysis. We did include the consciousness subscore in the analysis because it is a well-established predictor of stroke outcome in the literature. However, the consciousness score accounts for only 15% of the Orgogozo score, and assessment of multicolinearity in the statistical analysis showed no redundancy between the independent variables. Perhaps more weight should be given to the level of consciousness in scales designed to evaluate the severity of stroke.

We chose 8-day mortality rate and 3-month functional outcome as end points, instead of improvement in functional status56 or status at discharge,57 because they have been suggested to be more reliable12 and because most of the improvement usually occurs within 3 months.57 Although it was originally designed for the evaluation of outcome in patients with head trauma, we used the GOS for the 3-month evaluation because this outcome scale is simple, valid, and reliable39 and easily can be administered by telephone.

The only predictor of death at day 8 was the level of consciousness. Benedetti et al13 found that age and intensity of motor deficits also predict early death; however, their evaluation was made 30 days after onset, and age and intensity of motor deficits may have led to nonspecific complications in bedridden patients. Moreover, they used a univariate statistical analysis method.

A low Orgogozo score, previous stroke, and age predicted a poor 3-month outcome. As previously found by Censori et al,16 level of consciousness was not an independent predictor of 3-month functional outcome, which may appear to be a discrepancy with previous studies7 9 14 15 that assessed the level of consciousness later after stroke onset. However, an impaired consciousness may have different meanings, whether it occurs within a few hours or several days later.16 The duration of impairment of consciousness could also be of prognostic value.9 However, in our study, as in that of Censori et al,16 only 10 patients (6.6%) were obnubilated, 7 (4.6%) were stuporous, and none were comatose. In our study, hemianopia and swallowing disturbances were not predictors of outcome. Discrepancies with other studies4 12 may be due to differences in the date of evaluation or in the inclusion criteria, since we included both carotid and vertebrobasilar artery infarctions; in infratentorial stroke, absence of hemianopia or swallowing disturbances due to cranial nerve palsies do not always relate to the severity of the infarct. According to Carlberg et al,19 acute arterial hypertension at admission did not influence early death and 3-month outcome; the mechanism of acute arterial hypertension at the early stage of acute stroke remains unknown. It has been suggested that increased arterial hypertension may be beneficial to increase blood flow in the ischemic penumbra area.58 However, there is usually no time relation between symptom onset and BP in most stroke patients, suggesting that a nonspecific stress due to illness and hospitalization may be an important causative factor.59 Hyperglycemia at admission was not selected as an independent prognostic factor in our study. Results of experimental studies of the influence of hyperglycemia on infarct size are controversial.60 61 62 As previously suggested,63 hyperglycemia might also be due to the nonspecific stress induced by stroke and hospitalization. Atrial fibrillation was not selected as an independent predictor of outcome in our study. Previous studies64 65 have found a significant reduction in basal cerebral blood flow in patients with atrial fibrillation. Moreover, collaterals may be less developed in patients with cardioembolism than in patients with a chronic atherosclerosis.16 These factors may contribute to a poor functional recovery in cardioembolic strokes. However, we included cardioembolic as well as thrombotic stroke. Moreover, patients with history of atrial fibrillation and patients with an episode of atrial fibrillation associated with symptom onset have been classified in the same group; we may have minimized the influence of atrial fibrillation. In our study, we did not take into account CT signs of infarct because of the variable delay (1 to 24 hours) between stroke onset and CT scan. Despite the results of several studies,20 21 22 66 67 we did not identify the hyperdense middle cerebral artery sign as an independent factor of poor outcome, as previously suggested.23 However, unlike Ricci et al,21 we did not select patients according to the severity of stroke; moreover, previous studies did not take into account other important prognostic factors.

The risk of death or dependence after 3 months in young patients admitted with a moderate deficit and with no history of stroke is only 6.77%. In patients over 70 years of age, with previous stroke, and with a severe focal deficit, the risk is 75%. However, these results have been obtained in one group of patients and have now to be validated in another population sample. If further analysis validates this model, results should be taken into account in future therapeutic trials. Patients who are likely to have a poor clinical outcome are the best candidates for therapeutic trials that have dangerous side effects. In further drug trials, patient distribution should be balanced between the "active treatment group" and the "placebo group" regarding the severity of clinical deficit, history of previous stroke, and age. Randomization and stratification are probably the best ways to achieve this goal. Stratifications according to other variables are probably less valuable to ensure a balance of prognostic factors between groups. However, because treatments could be beneficial only when given within the first 6 hours after stroke onset, further studies to find very early predictors of survival among variables that are easily assessed during those first 6 hours may be valuable.


*    Acknowledgments
 
The authors are grateful to Marc Hommel (Grenoble, France) for his helpful comments and critical review of this manuscript and to the general practitioners involved in this study.

Received August 17, 1994; revision received December 15, 1994; accepted December 20, 1994.


*    References
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 up arrowIntroduction
 up arrowSubjects and Methods
 up arrowResults
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 *References
 

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