Progressive stroke : clinical course and outcome

Abstract

The knowledge about progression of symptoms in acute stroke patients was scanty when this thesis was planned. The aim was therefore to study if the rate and type of progression, had any impact on patient outcome, predictors for progression and effectiveness of heparin treatment. The frequency of progression and its clinical consequences were evaluated in 402 unselected, untreated, consecutive stroke patients cared for in a stroke unit. A marked progression occurred in 25% of the patients. Those with progression became statistically significant more disabled and needed institutional care more often at discharge than patients without.

Progression mostly occurred within the first days of hospitalisation and one third of the patients continued to progress gradually during the hospitalisation. No clinical predictors for progression were found. The validity and reliability of an assessment instrument, the Scandinavian Stroke Supervision Scale, was determined through a study of 50 acute stroke patients. The scale consists of well defined and graded items of consciousness, motor power as well as speech and was based on information obtained from the first report. It had a high predictive validity for patient outcome and was strongly correlated to four more complicated instruments. The reliability was also very high, especially for trained raters. Besides being time saving and easy to use, the scale was able to detect clinically relevant progression to the same degree as the other instruments. Effectiveness of heparin treatment for stroke progression was investigated in a prospective evaluation of 1205 acute stroke patients. They were systematically supervised and those with ischemic lesions and progression were treated with intravenous heparin. Progression rate in this patient group was 21% (n=907). In spite of the heparin regime, patients with progression became disabled and needed institutional care at discharge to the same extent as the untreated ones in the first evaluation and much more often than those without progression. One third of the patients continued to progress while on treatment. No clinically important predictors of progression or continued progression in the course of treatment were found. The impact of severe ipsilateral carotid disease during the clinical course (progression or recurrence) and outcome during the acute stage was studied in 266 acute stroke patients with ischemic lesions or TIA in the carotid territory.

Clinical information at admission and during hospitalisation was prospectively collected, as was the result of a sonography of the carotid arteries. Evidence of severe carotid disease (i.e. stenosis of > 70% or occlusion) was found in 15% of the patients. They had no significant increase in progression or recurrence rate nor were they more disabled or in need of institutional care more often at discharge than patients without severe carotid disease. Acute stroke patients with ischemic lesions have an activated coagulation with low antithrombin activity. Many patients with progression continue to progress while receiving heparin. The importance of antithrombin activity for heparin efficacy was assessed in 42 subjects treated with heparin for progressing ischemic stroke. Nine patients continued to progress. There were no differences in antithrombin activity before treatment between patients who continued to progress and those in whom the progression ceased on account of treatment. Anti-thrombin activity decreased in all patients during the treatment period, with no differences between patients with a more or less favourable clinical course.

Conclusions: Progression of stroke symptoms after admission is common and results in serious consequences for patient outcome. For detection and follow-up of progression the Scandinavian Stroke Supervision Scale is valid, reliable and easy to handle. No clinically important factors have been found that can predict progression. Nor were severe carotid lesions associated with an increased risk for progression. Heparin treatment for progression did not improve patient outcome or reduce the frequency of continued progression. The inadequateness of heparin was not dependent on the level of antithrombin activity.