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We greatly enjoyed reading the recently published review on acute stroke by Davenport and Dennis.1 Their didactic approach and strict compromise to distinguishing between evidence based approaches and their personal beliefs deserve compliment. We would like to contribute by clarifying some information on two topics.
Firstly, the authors make a brief comment on the use of anticoagulants in the treatment of cerebral venous thrombosis (CVT) indicating that a recent randomised trial showed a non-significant favourable effect.2 This may lead to a misinterpretation. Most experts currently agree that anticoagulation should be used in the acute treatment of CVT based on the available evidence. In 1991, Einhaulp et al 3 published the results of their randomised double blind prospective study comparing heparin and placebo. This study was prematurely interrupted after enrolling 20 patients because of the dramatic differences noted in outcome in favour of the heparin group (basically eight patients recovered fully and no deaths occurred in the heparin arm whereas only one patient recovered completely and three others died in the placebo group). Concerns about possible methodological flaws in this German trial fueled some controversy about its results. This led to a new trial by the Cerebral Venous Sinus Study Group3 which randomised 60 patients with CVT to receive nadroparin or placebo for 3 weeks. Poor outcome was defined as death, Barthel index of less than 15 at 3 weeks or Oxford handicap score equal or greater than 3 at 12 weeks. The results showed poor outcome in six of 30 patients (20%) in the nadroparin arm and seven of 29 (24%) in the placebo group at 3 weeks and four of 30 (13%) in the nadroparin treated patients versus six of 29 (21%) in the placebo group (absolute risk reduction of 7% and relative risk reduction of 38% for a non-statistically significant difference). But also very remarkably, there were no new symptomatic cerebral haemorrhages even among the 15 patients treated with anticoagulation who had haemorrhagic lesions on the initial CT. Finally, the same authors performed a meta-analysis combining the results of the two available trials2 3 which showed a “modest but clinically important” (although not statistically significant) benefit in the use of anticoagulation (absolute risk reduction of 14% in mortality and 15% in death or dependency, with relative risk reductions of 70% and 56% respectively). When combined with the proved safety of anticoagulation even in the setting of pre-existent haemorrhagic infarct and the highly unpredictable course of patients with CVT, these results should encourage the use of anticoagulation in the treatment of CVT.
Secondly, Davenport and Dennis mentioned the use of decompressive craniectomy as one of the interventions that may be used in patients with stroke who are rapidly deteriorating from raised intracranial pressure. However, they questioned whether this aggressive approach was associated with “improved survival with acceptable quality of life”.1 Growing experience with our patients as well as the available literature seems to indicate that it does, especially when decompressive surgery is performed early. Schwabet al 4 studied 63 patients with complete middle cerebral artery (MCA) infarctions and evidence of increased intracranial pressure treated with either early (within 24 hours of symptom onset) or late craniectomy. Mortality was 27% (compared with 78% in historical controls) and all suvivors were reported to be able to walk short distances without assistance and none were left with global aphasia. Mean Barthel index scores were 68.8 in the early hemicraniectomy group, 62.6 in the late hemicraniectomy group, and 60 in historical controls (but the very high mortality in this last group may account for a less dramatic difference in functional outcome). Similar favourable results were reported by Carteret al 5 in their a retrospective analysis of 14 patients treated with decompressive surgery after massive non-dominant hemispheric infarctions. Eight of their 11 surviving patients were able to function with minimal to moderate assistance (Barthel index >60) 1 year after the surgery. Depression and failure to reintegrate socially were often found in this group of patients5 as opposed to the experience reported by Schwabet al.4
In conclusion, decompressive craniectomy seems a valuable treatment option in cases of malignant MCA infarction, especially when involving the non-dominant hemisphere. This surgery is potentially lifesaving and reported functional outcomes are encouraging. Therefore, it needs to be considered early in every patient with complete MCA strokes showing incipient signs of increased intracranial pressure.
Davenport and Dennis reply:
We are grateful for Rabinstein's interest and comments. Although our interpretation of the available data may be more conservative, we do indeed consider anticoagulation for CVT, but do not think that it is appropriate in all cases. Similarly, we have considered craniectomy for “malignant” MCA occlusion, but so far we have not thought it appropriate to proceed. We note the good outcomes from the published case series and await the results of randomised trials with interest. However, many of the case series have involved rather younger than average patients, who have a greater capacity for functional recovery than older people (who make up the bulk of our case load), in whom we doubt whether such good functional outcomes are achievable.