engleski

Acute stroke therapy

The primary aim of specific treatment is to reduce brain damage, and thus the neurologic deficit caused by ischemia. By decreasing the infarct zone we reduce the risk of premature death, mainly due to cerebral edema and transtentorial herniation. The mechanism of cerebral ischemia is complex, and in general it leads to insufficient nutrition of neurons. In the core of ischemic process, glucose metabolism is reduced and so is the synthesis of adenosine triphosphate and phosphocreatine, which in turn entails a decrease in cell energy. The region surrounding the ischemic core, where partial energy reduction is present, is called ischemic penumbra. This is the critical region in which therapeutic intervention can reduce the damage. In acute stroke, it is necessary to start the treatment early. Optimal time is 3-6 hours from the onset of symptoms. It would be ideal to provide the treatment at specialized units of intensive care for stroke patients. Emergency care includes good respiration, oxygenation, Dehydration, correction of metabolic disturbance, monitoring of bladder and bowel function, and prevention of decubitus. Con-tmon complications such as elevated body temperature caused by infection or deep vein thrombosis, cardiac decompensation, and hypertension (systolic and diastolic blood pressure greater than 185 and 110 mm Hg, respectively) should be treated. For many years, heparin has been used in therapy for acute stroke, especially for progressive stroke, however, its advantage has never been demonstrated, while at the same time indications for its use are still a matter of controversy. Anticoagulant drugs with heparin can stabilize symptoms in patients with developing stroke. Patients with small, nonhemorrhagic infaret caused by embolus can initially be treated with heparin, and then with warfarin for 6e next six months. Use of anticoagulants should be delayed by 5-7 days in patients with large ischeniic stroke due to cardioembolism, and by 2-4 weeks in patients with hemorrhagic infarct of cardioembolic origin. Antiplatelet therapy for atherothrombotic stroke is still a matter of investigation. At present, trials with recombinant tissue plasminogen activator (tPA) have been performed. The agent should be administered within three hours from the onset of symptoms. The dose is 0.9 mg/kg i.v. (maximal dose is 90 mg), 10% given as a bolus over 12 min, and the remaining 90% by infusion over 1 hour. Patients should meet several criteria to be included in the treatment. Results of the use of tPA showed the symptomatic and fatal hemorrhage to be more frequent in this group of patients than in the placebo group, while overall mortality was the same. This therapy can only be used at specialized centers. Vital signs are monitored continuously during the first 24 hours upon the administration of tPA, and any bleeding should be immediately treated. Anticoagulants and antiplatelet drugs should not be taken within 24 hours of the last tPA dose. Cerebral edema is the most common cause of death in patients with stroke. It usually occurs within 28-48 hours and peaks at 96 hours from the onset of stroke. Corticosteroids have been shown to be ineffective in the treatment of patients with edema in acute stroke. Mannitol should be used cautiously and not too aggressively, because it may induce a rebound effect. Vascular surgery is not indicated as an emergency measure in the management of acute stroke.

acute stroke ; therapy

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