Here are some answers corresponding to your questions:
1. You mentioned IV tPA and time-to-presentation was 2.5 hrs. Within that window, the preferred treatment is selective intra-arterial tPA – infuse rPA directly to the vessel leading to the infarct (by neuroradiologist, an emergent procedure as you can see). This way the complication is minimized and the effect of treatment is maximized because there is high concentration of tPA right next to the clot to dissolve it.. IV tPA does have a higher incidence of bleed. Fragments (c-Fn) has been used but mostly for systemic effect but it has a big variation range. So there is no reliable indicator to predict hemorrhagic conversion (that will be nice to have one). The tPA has a short half life indeed. But we do not know for sure when the bleed started. It has to bleed to a certain amount to produce symptom, then MDs are called, then CT is done, and then we know there is bleed on CT.
2. Normal person, CSF (clear water-like fluid) gets reabsorbed by arachnoid granulations, finger-like structures soaked in the veins on the surface of the brain. When there is subarachnoid bleed, the granulations, or some of them are blocked by the sticky blood, and increased intrcranial pressure will develop causing herniation of brain which is very bad. The tube they put in is for this purpose to help to drain those CSF. So there is no CSF vessel. The original strke is caused by blocking of a artery suppling the brain. The tPA will nerve reach the CSF compartment. It does takes time.
3. Her right side will move and responds whenever sedation is light because her left brain is normal (bleed is on the opposite of the symptoms). She should be OK if they can wane her from the respirator.
1. You mentioned IV tPA and time-to-presentation was 2.5 hrs. Within that window, the preferred treatment is selective intra-arterial tPA – infuse rPA directly to the vessel leading to the infarct (by neuroradiologist, an emergent procedure as you can see). This way the complication is minimized and the effect of treatment is maximized because there is high concentration of tPA right next to the clot to dissolve it.. IV tPA does have a higher incidence of bleed. Fragments (c-Fn) has been used but mostly for systemic effect but it has a big variation range. So there is no reliable indicator to predict hemorrhagic conversion (that will be nice to have one). The tPA has a short half life indeed. But we do not know for sure when the bleed started. It has to bleed to a certain amount to produce symptom, then MDs are called, then CT is done, and then we know there is bleed on CT.
2. Normal person, CSF (clear water-like fluid) gets reabsorbed by arachnoid granulations, finger-like structures soaked in the veins on the surface of the brain. When there is subarachnoid bleed, the granulations, or some of them are blocked by the sticky blood, and increased intrcranial pressure will develop causing herniation of brain which is very bad. The tube they put in is for this purpose to help to drain those CSF. So there is no CSF vessel. The original strke is caused by blocking of a artery suppling the brain. The tPA will nerve reach the CSF compartment. It does takes time.
3. Her right side will move and responds whenever sedation is light because her left brain is normal (bleed is on the opposite of the symptoms). She should be OK if they can wane her from the respirator.
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