Secondary central nervous system to pathological processes involving blood vessels disorders are very common on the top of the fifth decade of life. Any sudden focal neurologic deficit no seizure can be called "coup". Vascular disorders are usually characterized by his sudden appearance. Strokes in general terms are divided in ischemic and hemorrhagic lesions. When the blood supply to the brain is interfered with, develop infarction and ischemic necrosis. Blockage of an artery can be by thrombus or embolus. Sometimes rough by the impairment of the cerebral circulation due to hypotension produced by heart failure or shock may also lead to cerebral ischemia.
The location and size of the stroke or hemorrhage determined neurological dficit. Stroke is the most frequent presentation mode. The course of developing neurological events often gives the clue for the type of stroke. Cerebral embolism, deficit begins suddenly, reaching its maximum in minutes. Cerebral thrombosis has a rough start but involves slowly over a period of several minutes, hours or days in a series of steps, instead of a smooth course. In cerebral hemorrhage, deficit starts from their time of onset and continually progresses over a period of minutes or hours. Although these patterns are recognizable in most cases, a considerable overlap occurs that clinical events can be misleading at the time.
Transient ischaemic (AIT)
This is cuased focal neurologic deficit by vascular insufficiency, but symptoms resolved within 24 hours. Sometimes, many patients experience more than one episode of TIA and they may take a few days up to three weeks to recover. These are called neurological deficit reversible ischemic (BARK).
Ischemic stroke
The net effects of arterial occlusion in brain tissue depends of the available amount of blood flow collateral to the affected area. The circle of Willis normally provides suitable in case of any vessel proximal occlusion her blood flow. If the internal carotid artery occlusion can have a retrograde anastomotic artery flow external carotid of the ophthalmic artery. Addition of the permeability of the collateral vessels, occlusion speed also influences the provision of collateral. Gradual narrowing of a vessel da collateral channels opening time.
Presence of hypotention or hypoxia at a critical moment can make ineffective anastomosis channels.
Risk factors: multi-factor predisposes to the development of ischemic stroke. Hypertension is perhaps the most important risk factor for cerebral infarction and intracerebral hemorrhage. Both systolic and disastolic pressures play a role.
Diabetes mellitus is an important factor of predisposition that accelerates the process of atherosclerotic seteries of large and small. Other factors such as smoking, obesity, hyper-lipidemia, Polycythemia, and the use of oral contraceptives in women that increase the risk are known. Embolic strokes are usually secondary to cardiac valvular disease, ischemic heart disease, infectious endocarditis, congenital lesions and arrhythmias, especially atrial fibrillation artrial disorders. In atherosclerosis affecting extracranial internal carotid and platelets of arteries during ateromas plates and vertebral thrombi can get separated to be embolized.
Management of ischemic stroke: stroke prevention assumes great importance because there is no known therapeutic method that can invest fully established infarction. In the acute phase, the objective is to ensure adequate cerebral perfusion and t avoid all factors that interfere with cerebral blood flow. The patient is raised in the posture recumbent, carefully avoidi8ng upright posture. Coexistent disorders such as Polycythemia anemia must be corrected. If the diastolic blood pressure is over 110 mm Hg, are administered antihypertensive. A short course of dexamethasone is given by injection at a dose of 4 mg, 6 hours. It is useful to reduce cerebral edema.
The use of anticoagulants is controversial, since the majority of patients is clinically indistinguishable from ischemic and hemorrhagic stroke. Anticoagulants have no role in stroke completed. It is important to exclude the intracranial hemorrhage preferably tomography, or at least by CSF examination before start anticoagulants. Absence of erythrocytes in the CSF almost excluded cerebral hemorrhage. Hypertension is not a serious contraindication.
Anticoagulants are considered in patients with recurrent AIT or stroke in evolution, halt more thrombosis. When stroke is obvious, are clearly these drugs. As usual is starting heparin 5000 units of 4 hours for 1-2 weeks and after that, replace it with oral anticoagulants such as Coumadin for 8-16 weeks.
Antiplatelet drugs have shown great promise in preventing thrombotic attacks. (150 Mg) in a single daily dose aspirin inhibits platelet aggregation. Dipyridamole 75 mg three times daily administered by mouth is also equally effective. Antiplatelet drugs are of special value in preventing the progression of carotid AIT.
Surgical treatment: always recurring TIAs are associated with demonstrable stenosis due to atheroma or recommended plates on the vessels of the neck or the aortic arch indicates surgical intervention. Thromnoendarterectomy graft or derivation of carotid, innominate or subclavian arteries have been beneficial in control of the TIA.
Completed strokes, drug therapy is unsuccessful. Physical therapy is started early to facilitate movement and rehabilitation. Advocates early ambulation since this helps to prevent contractures, peri-artritis and decubitus.
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