Cerebral Hemorrhage associated with antiplatelet drugs

Cerebral Hemorrhage associated with antiplatelet drugs
- Antiplatelet (aspirin and ticlopidine) - aspirin antiplatelet action is intense. At low doses of aspirin does not interfere with the synthesis of prostacyclin is produced by vascular endothelium, which is a benefit of aspirin, confirmed by several randomized clinical trials conducted in recent years. However, some studies have resulted in different aspects, in the sense that some groups there was the same frequency of HC in patients treated with aspirin as in those on placebo, while the other groups studied HC appeared with greater frequency in treatment with aspirin. However we can not say with certainty if long-term aspirin therapy increases the risk of HC or not.

 
- Anticoagulant therapy - heparin and oral preparations induce a percentage of HC. The biggest risk factor for intracranial or systemic bleeding is a prolonged prothrombin time. The coexistence of hypertension also increased bleeding tendency. HC induced by anticoagulants have several characteristics: it often develops insidiously, gradually, within hours or days, are located mainly in the cerebellum, have a high rate of morbidity and mortality, possibly small hemorrhages in 30 cm3 volume have a chance of survival. Cerebellar hemorrhage with anticoagulants is difficult to control.

 
- Medictia thrombolytic - thrombolytic agents are used at more than streptokinase, and rtPA-urokinaza recombinant tissue plasminogen activator. The beneficial effects of thrombolysis are limited but bleeding complications of this therapy, the worst being the HC.

 
Cerebral hemorrhages were reported in large trials, the patients treated with fibrinolytic agents for AMI. To confirm that the use of HC even when appropriate doses of fibrinolytic agent. There have been cerebral hemorrhage occurred within a few hours after administration of streptokinase. Complication occurred in patients with poorly controlled hypertension. In other cases it was found coexisting amyloid angiopathy, which could be a risk factor.

 
Bleeding complications with treatment with rtPA were reported in percentages stronger than those generated by streptokinase. Cerebral haemorrhages were triggered within a few hours after initiating treatment. He noted that the high frequency of HC in some series was correlated with the higher dose of rtPA, age, presence of hypertension and the use of calcium blockers. HC treated with rtPA appeared generally occur early, within hours or within 24 hours after initiation of treatment, are often multiple and sometimes associated with HSA. These hemorrhages have a poor prognosis, with mortality rates between 44% and 80%. Combination thrombolytic therapy with the anticoagulant led to a slight increase in the frequency of HC.
Other factors such as previous brain injury or head injury history were considered factors in the facilitation of intracranial bleeding treated with rtPA. Embolic silent cerebral infarctions also favors the onset of bleeding given their tendency to become hemorrhagic infarcts.

 
The introduction of thrombolytic therapy was observed later than 6 hours of onset increases the risk of bleeding. Thus, the treatment is applied only to patients who present shortly after the onset of HC, respectively in the first 3 hours and who are selected by certain criteria.