Stroke Management - Karolinska Stroke Update

Consensus Statement 2004

 

The following Consensus Statement was adopted by the 5th Karolinska Stroke Update meeting on November 15, 2004.

The consensus statement  was proposed by the chairpersons in the session, Professor Michael Brainin, Vienna, and Professor Zoltan Nagy, Budapest, together with the speakers in the session. The statement was then finally approved by the participants of the meeting, after listening to the different presentations.

The speakers in this session were Professor Per Morten Sandset, Oslo, Dr Hanne Christensen, Copenhagen and Professor Didier Leys, Lille

 

Stroke Management

Deep venous thrombosis

After acute ischemic stroke, the risk of deep vein thrombosis (DVT) is dependent on stroke severity and immobilization. In studies using validated methods to detect DVT the risk varies from 28% to 75% in untreated patients.

Treatment with prophylactic subcutaneous unfractionated heparin, low molecular weight or heparinoids reduces the risk of DVT by more than 50%, which is comparable to the 60-80% risk reduction of thromboprophylaxis observed after major surgery (grade A evidence).

Extrapolation of data from thromboprophylaxis in medical patients suggest that a high prophylactic dose might be necessary.

Thromboprophylaxis is probably associated with a very slight increase in the risk of intracerebral hemorrhage.

Aspirin has not been shown to reduce the risk of DVT after stroke, but has a marginal, but questionable effect on the risk of DVT after major surgery (risk reduction of 10-20%).

Elastic compression stockings and intermittent pneumatic compression devices used alone or in combination with medical thromboprophylaxis, reduce the risk of DVT after major surgery. Elastic compression stockings also protect against post-thrombotic syndrome after DVT. Their use after acute stroke remains open and currently is tested in one ongoing large randomized trial.

                                

Dementia

In the absence of evidence - based data, no specific strategy can be recommended at the acute stage of stroke in order to reduce the risk of post stroke dementia. Those that are recommended are to decrease death and dependency.

After stroke or TIA, blood pressure should be lowered, irrespective of its level, with a diuretic and / or an ACE inhibitor, depending on the tolerance of the treatment, to prevent new vascular events (grade A) and cognitive decline (grade B), and dementia in case of stroke recurrence (grade B).

Cholinergic drugs maintain or improve cognition in patients with VaD, or in patients with AD plus vascular lesions of the brain (grade A).

Cholinergic drugs have not been tested in the prevention of PSD.

 

Blood pressure

High blood pressure is common in acute stroke patients on admission to hospital. Increased blood pressure values usually normalise gradually during the first hours and days after hospital admission. There is uncertainty whether systemic blood pressure should be manipulated in the acute phase of stroke and if so, in what subgroups of stroke, at which blood pressure levels and at what duration after ictus intervention should start although one trial (ACCESS) showed an effect of treatment with candesartan.

Treatment of hypertension in the acute phase of stroke should be avoided, but blood pressure values should be closely monitored. In cases of hypertensive encephalopathy, dissecting aortic aneurysm, acute heart failure and unstable angina pectoris/ myocardial ischaemia treatment may be indicated (grade C evidence). In patients with intracerebral hemorrhage blood pressure may be reduced to levels below 180/110 mm Hg before treatment (grade C evidence).

 

Hyperglycaemia consistently aggravates brain injury in ischaemic reperfusion models, acting through accumulation of lactate with acidosis and glutamate increase. Clinical observational findings support the concept of hyperglycaemia-induced cerebral damage, irrespective of whether the patient has previously diagnosed or latent diabetes, or stress hyperglycaemia. Hyperglycaemia is also a predictor of intracerebral haemorrhage during thrombolysis therapy. An ongoing multicentre study is assessing the effect of lowering blood glucose in patients with hyperglycaemia.

It is recommended that blood glucose should be monitored and hyperglycaemia (>10 mmol/l) treated with insulin (grade C evidence).

There is evidence supporting an association between non-diabetic hyperglycaemia in acute stroke and poor outcome independent of stroke severity. When substituting insulin, a glucose-insulin-potassium (GIK)-infusion should be preferred (grade C).

 

Hyperthermia consistently increases brain injury in experimental models, acting through several mechanisms. Observational studies in humans have demonstrated that hyperthermia is independently associated with a worse outcome.

Trials of treating hyperthermia and inducing hypothermia are ongoing.

Until there is randomised evidence, it is recommended that prompt antipyretic therapy (e.g. paracetamol) should be part of routine care in patients with acute stroke and body temperature greater than 37.5 o C (grade C evidence).

 

Hypoxia. No favourable effect was observed from oxygen supplementation in a quasi randomised trial.

It is recommended that in all patients, oxygen tension should be monitored in the acute phase. Supplemental oxygen should not be used unless the patients are hypoxic (grade C evidence).

Further trials of oxygen supplementation (and also hyperbaric oxygen supplementation) are required. 

 

Fluid and electrolyte management. Dehydration may worsen ischaemic injury because of increased blood viscosity and hypotension. Hyper-osmolar dehydration is usually due to decreased fluid intake (or diabetes). Hypo-osmolar dehydration due to inappropriate secretion of antidiuretic hormone is rare and usually transient.

Monitoring and correction of electrolyte and osmotic disturbance is recommended (grade C evidence). Trials of fluid replacement are required.