Cerebral Infarction Management

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THE ACUTE STROKE

Clinical history, examination and investigation will separate infarction and haemorrhage. Once the nature of the 'stroke' has been confidently defined, treatment should be instigated.

Treatment aims

- Prevent progression of present event

- Prevent immediate complication

- Prevent the development of subsequent events

- To rehabilitate the patient.

General measures

Around the edge of an infarct, ischaemic tissue is at risk, but is potentially recoverable. This compromised but viable tissue must be protected by ensuring a good supply of glucose and oxygen. Factors which might adversely affect this must be maintained - hydration, oxygenation, blood pressure. To / this end, treat chest infections and cardiac failure/dysrhythmias.

Infarction

Specific measures

The following are generally ineffective, or are as yet inadequately evaluated.

Anticoagulant therapy

The role of antithrombotic therapy (heparin) in patients with acute infarction is uncertain and currently under evaluation (1ST - International Stroke Trial).

In patients with a known cardiac source of emboli, the risk of recurrent embolic infarction is high and anticoagulant therapy should be commenced once CT scan has ruled out haemorrhagic infarction. In chronic valvular disease, treatment is long term; following myocardial infarction (with mural thrombus) - 6 months. With mitral valve prolapse, antiplatelet drugs will suffice. In atrial fibrillation the overall annual risk of stroke is 5%. Several recent trials show highly significant benefit from long term oral anticoagulation with warfarin (target INR 1.2-2.0)

Heparin is often used in the management of 'stroke in evolution'. The neurological deficit fluctuates but gradually worsens over some hours. The gradual progression is considered due to increasing thrombus formation with progressive 'silting' of collateral vessels. Studies of anticoagulant therapy produce conflicting results probably because of other potential mechanisms, e.g. collateral perfusion failure.

Thrombolytic agents

Recent experience with thrombolytic agents, especially recombinant tissue plasminogen activator (rTPA) suggests a sustained, significant neurological improvement when initiated within a few hours of infarction. Such agents are associated with rapid recanalisation of occluded vessels. Randomised clinical trials of rTPA and other thrombolytics are currently underway. Experience with streptokinase shows unacceptable risk of intracranial haemorrhage and studies have been suspended.

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