Why must thrombolytic therapy be initiated immediately upon
Why must thrombolytic therapy be initiated immediately upon onset of ischemic stroke?In Canada a stroke occurs every ten minutes, it is the fourth leading cause of death and is the number one cause of long-term disability. Canadians spend a total of 3 million days in hospital because of stroke costing the Canadian economy $2.7 billion a year, with the average acute care stay costing approximately $27,500 per stroke (Heart and Stroke Foundation of Canada, 2002). Currently there are 350,000 Canadians living with the effects of stroke with 50,000 new strokes occurring every year and the incidence is increasing as Canadian's age. Of every 100 people experiencing a stroke in Canada, 10 are so severely disabled they require long-term care, 40 are left with moderate to severe impairment or disability, 25 will have minor impairment or disability, 10 will completely recover and 15 will die. Fewer than 50% of stroke patients ever return to work (Canadian Stroke Network, 2004). This paper will use the pathopysiology concepts of ischemic stroke to answer this question: Why must thrombolytic therapy be initiated immediately upon onset of ischemic stroke? This is a very clinically important question because early identification of strok
Those ischemic strokes caused by emboli occur in patients that have bacterial or nonbacterial endocarditis, cardiac arrhythmia, cardiac disease, diabetes mellitus, hyperlipidemia, obesity, and from postsurgical sequel. By acting on bound plasminogen, TPA reduces systemic fibrinolytic activity and hemorrhagic complications (Vance, 2001). Further injury occurs when the macrophages release toxic oxygen radicals and enzymes. Some other drugs being researched are calcium channel blockers; excitatory amino acid inhibitors that block the effects of glutamate; vitamin E and tirilazad, which inhibit lipid peroxidation and act as free-radical scavengers; and gangliosides that promote regeneration and sprouting of neurons and neuronal survival. Ischemic events caused by thrombi include atherosclerosis of intracranial and extracranial arteries, arteritis caused by bacteria or collagen, cardiovascular disease such as hypertension and congestive heart failure, cerebral venous thrombosis, and hypercoagulation. Cerebral tissue is oxygen-dependent, and ischemia occurs when oxygen delivery to the brain is interrupted, ultimately leading to immediate cell death. When ischemia occurs, the affected brain tissue undergoes a series of complex neurochemical changes known as the "ischemic cascade," which, if uninterrupted, ends in infarction and neurologic disability. This results in smooth muscle proliferation in the vessels that are affected. The National Institute of Neurological Disorders and Stroke (NINDS) study, published in 1995 was concerned with strokes of thrombotic and embolic origin, provided valid evidence that patients treated with TPA within 3 hours of symptom onset achieved greater neurologic recovery and experienced less disability than patients who received a placebo (Gladstone & Black, 2001). Pathophysiology of Thrombolitic Stroke Thrombolitic strokes (cerebral thrombosis) occur when thrombi occlude arteries supplying the brain and intracranial vessels. Without early detection and treatment significant permanent disability of Canadians stricken with stroke will result (Bahouth & LaMonte, 2000). You end up with lipid laden foam cells that gather in large amounts and form a lesion known as a fatty streak. With ischemia aerobic metabolism cannot be maintained and loss of function occurs (Felberg & Naidech, 2003). and infarction (cell death) occurs when cerebral blood flow falls to 17 mL/100 g/min (Kongable, 1997). Thrombolytic drugs may be delivered directly to the area of the blockage and additional neuroprotective agents given so that the patient's symptoms dramatically improve.
Common topics in this essay:
Stroke Thrombolitic,
Felberg Naidech,
Ischemic Stroke,
Currently TPA,
Ingram Sedlack,
Stroke Network,
Synthetic TPA,
Embolotic Stroke,
Stroke Association,
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kongable 1997,
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