Hemorrhagic stroke treatment

Discuss the various treatment options for acute ischemic stroke and hemorrhagic stroke. 

All patients should have a brain computed tomography scan or magnetic resonance imaging scan to differentiate an ischemic stroke from a hemorrhagic stroke, as the treatment... 

Assessment of risk factors for ischemic stroke as well as for hemorrhagic stroke is an important component of the diagnosis and treatment of patients. A major goal in the long-term treatment of ischemic stroke involves the prevention of a recurrent stroke through the reduction and modification of risk factors. The major focus of primary prevention (prevention of the first stroke) is also reduction and modification of risk factors. Risk factors for ischemic stroke can be divided into modifiable and non-modifiable factors. Every patient should have risk factors assessed and treated, if possible, as management of risk factors can decrease the occurrence and/or recurrence of stroke.4... 

Streptokinase is not indicated for use in acute ischemic stroke treatment. Three large randomized controlled trials evaluating streptokinase were stopped early due to a high incidence of hemorrhage in the streptokinase-treated patients.14-16 At the present time, there is no indication for the use of streptokinase or thrombolytics other than alteplase in the acute treatment of ischemic stroke. 

Perform a CT scan to rule out a hemorrhagic stroke prior to administering any treatment. 

Stroke A stroke occurs when there is an interruption of blood supply to the brain. An ischemic stroke occurs when a clot prevents blood flow in the brain. A hemorrhagic stroke is when there is a rupture of a blood vessel in the brain. In either case, the brain cells in the affected area die. This area is called an infarct. Medical treatment is required to arrest the damage. More effective treatment can be administered within 6 hours of the onset of stroke. A stroke may result in weakness, paralysis, impairment of speech and memory, or even death. Medical treatment includes the use of anticoagulants to treat stroke victims. 

Hypertensive crises are characterized initially by headache, but can evolve to include neck stiffness, chest discomfort, palpitations, confusion, and, ultimately, hemorrhage or stroke. Treatment of MAOI-associated hypertension may include a watch-and-wait stance by the patient if the symptoms are mild. Some patients have the ability to check and monitor their own blood pressure. Others may consult with a physician for blood pressure checks and observation, but if symptoms are severe, the patient may need to go to an emergency room or self-medicate. Standard emergency room treatment is intravenous phentolamine, an a-adrenergic blocker, continuous monitoring and management until blood pressure is normalized without medication. Some doctors will provide patients with small doses of chlorpromazine or nifedipine to treat hypertension if a problem arises. 

In view of the perceived benefit of aspirin in the secondary prevention of stroke and myocardial infarction, two large trials involving physicians as subjects were initiated to study the effect of aspirin in the primary prevention of arterial thrombosis. In the American study, 22,000 volunteers (age 40 to 84 years) were randomly assigned to take 325 mg of aspirin every other day or placebo. The trial was halted early, after a mean follow-up of 5 years, when a 45% reduction in the incidence of myocardial infarction and a 72% reduction in the incidence of fatal myocardial infarction were noted with aspirin treatment. However, total mortality was reduced only 4% in the aspirin group, a difference that was not statistically significant, and there was a trend for a greater risk of hemorrhagic stroke with aspirin. Thus, the prophylactic use of aspirin in an apparently healthy population is not recommended at this time, unless there are risk factors for cardiovascular disease. 

Superior to DSA, MRI can depict arterial flow or lumen as well as the vessel walls. Analysis of plaque morphology was improved in recent years by the development of specific MRI techniques. Plaques can now be characterized in vivo with regard to fibroid or lipid content or hemorrhagic lesions (Fig. 5.8). It can be expected that, in the future, plaque examination will influence stroke treatment protocols if the risk of plaque rupture can be reliably estimated (Cappendijk et al. 2005 Hayes et al. 1996 Trivedi et al. 2004 Yuan et al. 2001). Plaque examinations, however, are not yet clinical routine. Source images of TOF-MRA allow only limited assessment of vascular walls. 

The general treatments described in this chapter are applicable to all patients with acute major stroke regardless of etiology. Specific treatment for ischemic and hemorrhagic stroke is discussed in Chs. 21 and 22, respectively. Therapy for acute stroke can be divided into ... 

Many of the trials of therapy in acute stroke did not distinguish between stroke subtypes other than by division into hemorrhagic and ischemic stroke. Therefore, there is little evidence for different effectiveness for most acute ischemic stroke treatments according to stroke subtype and location. However, stroke subtype determines patient selection for specific secondary preventive strategies. Therefore, better characterization of stroke will aid overall patient management (Ch. 6). 

Hellingman CA, van den Bergh WM, Beijer IS et al. (2007). Risk of rebleeding after treatment of acute hydrocephalus in patients with aneurysmal subarachnoid hemorrhage. Stroke 38 96-99... 

Tyrosine can be decarboxylated to tyramine by aromatic L-amino acid decarboxylase of intestinal bacteria. Tyramine, which is present in large amounts in certain foods (e.g., aged cheeses, red wines), is converted by monoamine oxidase (MAO) to the aldehyde derivatives. However, individuals who are receiving MAO inhibitors for the treatment of depression can accumulate high levels of tyramine, causing release of norepinephrine from sympathetic nerve endings and of epinephrine from the adrenal medulla. This results in peripheral vasoconstriction and increased cardiac output, which lead to hypertensive crises that can cause headaches, palpitations, subdural hemorrhage, stroke, or myocardial infarction. 

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