Thrombolytic Agent for Stroke - Oren Zarif - TPA Stroke
Since its first use in 1996, tPA stroke treatment has been proven effective. In fact, the American College of Emergency Physicians and the Academy of Neurology have created a joint development panel to produce an evidence-based guideline on the use of tPA after stroke. The panel's findings have already been incorporated into clinical decision-making by stroke specialists and other hospitals. Here, we'll review some of the most important information about tPA treatment for stroke.
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The study was a pivotal milestone in the development of tPA. It supported the early studies of tPA and led pivotal clinical trials that ultimately led to FDA approval. NINDS scientists understood the importance of rapid stroke treatment and pioneered protocols for assessment and treatment of patients with unprecedented speed. These studies are important because they provide important insight into the risks and benefits of tPA treatment. To learn more about the efficacy of tPA for stroke, read our latest blog posts.
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The study was conducted in two cohorts. The first group included 2,317 stroke patients. In the second, 1,016 patients were randomized to receive tPA or a placebo. Interestingly, only 25% of patients receiving tPA received the treatment within three hours. The study included patients with higher severity of stroke at the time of stroke and more medical comorbidities. As a result, this study may have missed some of the benefits of tPA.
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A third group of patients were excluded from thrombolytic therapy. These patients had an ischemic stroke, a common cause of death. In addition, physicians who disincline to use thrombolytic therapy may also be at risk of malpractice lawsuits. Despite these benefits, however, there is a lack of systematic reviews of malpractice cases involving tPA and ischemic stroke. We will focus on malpractice cases reported in the most widely used medical databases.
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The results of the NINDS part II trial showed that tPA treatment improved outcomes while reducing mortality. But, the study also noted that the "enough time" concept may lead to delays in tPA administration. However, the earliest tPA administration is best. This approach improves outcomes and ensures the safety of clinical evaluation and brain imaging. Although this study was funded by the National Institutes of Health, it is not yet clear how effective tPA treatment is for a particular type of stroke.
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Neuroprotective agents have anti-inflammatory and anti-oxidant properties and are effective in preventing brain injury. They are also thought to increase the release of certain neurotransmitters, including glutamate and cytokines. Both neuroprotectants may increase the rate of reperfusion in stroke patients and reduce the risk of ischemic stroke. And if all this is true, tPA could be an effective treatment for stroke patients.
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The most common indication for tPA is acute ischemic stroke. This treatment must be given within three to four hours to minimize brain damage. It is not recommended for those with subarachnoid hemorrhage or active internal bleeding. Patients with active internal bleeding should undergo regular neurologic assessments. This includes checking for major bleeding. The interprofessional team should use the tPA-based therapy as part of their stroke management.
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Rapid treatment protocols can dramatically improve acute stroke care in the U.S. and many hospitals have begun developing specialized stroke teams and resources to become primary tPA stroke centers. Once tPA was approved for stroke treatment, the National Institute of Neurological Disorders and Stroke (NINDS) launched a public awareness campaign, known as Know Stroke, to inform the public about the symptoms and the importance of getting to the hospital as quickly as possible. This campaign has been widely spread across the media and even has Spanish-speaking populations.
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The only FDA-approved treatment for acute ischemic stroke, tPA is an effective and safe drug. However, delays in tPA administration have been linked to increased incidence of HT, ICH, and edema. In addition, delayed administration of tPA can lead to reperfusion injury, thereby increasing the risk of death. In addition, the drug activates matrix metalloproteases, which further damage the BBB.
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The plaintiffs in the tPA lawsuit have argued that the treatment failed to meet the legal standard of care. However, their expert witnesses argued that the tPA treatment had a fifty-one percent chance of improving the patient compared to a patient without the treatment. This argument does not hold much water, because the plaintiffs must show that the failure of the tPA treatment did not result in any improvement in the patient's condition.
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