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Transcript of stroke
sign and symptoms
Non Pharmacological Therapy
Primary Prevention of acute ischemic stroke
Secondary Prevention of acute ischemic stroke
surgical decompression can be lifesaving in cases of significant swelling associated with cerebral infarction.
interdisciplinary approach to stroke care that includes early rehabilitation is very effective in reducing longterm disability.
In subarachnoid hemorrhage due to a ruptured intracranial aneurysm , surgical intervention to clip or ablate the vascular abnormality substantially reduces mortality from rebleeding.
Understand the types of strokes.
Understand the pathophysiology of cerebral ischemia and cerebral hemorrhage.
Identify the modifiable and non-modifiable risk factors associated with ischemic stroke and hemorrhagic stroke.
Discuss the various treatment options for acute ischemic stroke and hemorrhagic stroke.
Determine whether thrombolytic therapy is indicated in a patient with acute ischemic stroke.
are focal ischemic neurologic deficits lasting less than 24 hours and usually less than 30 minutes.
is a term used to describe an abrupt onset of focal neurologic deficit that lasts at least 24 hours and is presumed to be of vascular origin.
Transient ischemic attacks (TIAs) :
1- local thrombus formation
2- emboli that occlude a cerebral artery
Ischemic stroke :
Hemorrhagic stroke :
1- subarachnoid hemorrhage : trauma
2- Intracerebral hemorrhage : ruptured blood vessel within the brain parenchyma
Sudden weakness, numbness, or paralysis of the face, arm, or leg
(especially on one side of the body "Hemiparesis or monoparesis")
Loss of speech or trouble talking or understanding language
Sudden loss of vision
Sudden severe headache
Unexplained dizziness or loss of balance or coordination
1- thrombus formation :
( carotid atherosclerosis) plaques may rupture, resulting in collagen exposure, platelet aggregation, and thrombus formation. eventually occluding a cerebral vessel.
presence of blood in the brain tissue and/or surrounding spaces resulting in compression.
hematoma is associated with a poor outcome.
Brain tissue swelling and injury is a result of inflammation caused by thrombin and other blood products.
This can lead to increased intracranial pressure
2- embolism :
stasis of blood flow in the atria or ventricles leads to formation of local clots that can dislodge and travel through the aorta to the cerebral circulation.
race (African American, Asian, Hispanic)
family history of stroke, and low
2- modifiable risk factors
cardiac disease (especially atrial fibrillation).
3- Other major risk factors include
lab tests :
Protein C, protein S, antithrombin III are best and Antiphospholipid antibodies
Other Diagnostic Tests :
• A computed tomography (CT) scan of the head
• Magnetic resonance imaging (MRI) of the head ( within minutes.)
• Carotid Doppler studies will determine whether the patient has a high degree of stenosis
• The electrocardiogram will determine whether the patient has atrial fibrillation or not
• A transthoracic echocardiogram will identify whether there are heart valve abnormalities
(1) reduce the ongoing neurologic injury and decrease mortality and long-term disability
(2) prevent complications secondary to immobility and neurologic dysfunction
(3) prevent stroke recurrence.
Inclusion Criteria :
Age 18 years or older
Clinical diagnosis of ischemic stroke
Time of symptom onset well established to be less than 180 minutes before treatment would begin
Exclusion Criteria :
Evidence of intracranial hemorrhage on noncontrast head CT
Active internal bleeding (e.g., GI/GU bleeding within 21 days)
Patient has received heparin within 48 hours and had an elevated aPTT
Recent use of anticoagulant (e.g., warfarin) and elevated PT (>15 seconds)/INR
Intracranial surgery, serious head trauma, or previous stroke within 3 months
Lumbar puncture within 7 days
Recent acute myocardial infarction
SBP >185 mm Hg or DBP >110 mm Hg at time of treatment
Inclusion and Exclusion Criteria for Alteplase
Aspirin 325 mg per day begun within 48 h of stroke onset decreases morbidity & mortality (may begin 24 h after t-PA) and should be continued for at least 2 week
Aspirin is typically considered to be the first-line secondary prevention agent for ischemic stroke and decreases the risk of subsequent stroke by approximately 25% in both men and women with previous transient ischemic attacks or stroke.
A wide range of doses have been used (30 to 1500 mg per day); however, enteric-coated aspirin 325 mg orally once daily is the most widely used and recommended regimen
Warfarin is the antithrombotic agent of first choice for secondary prevention in patients with atrial fibrillation and a presumed cardiac source of embolism
The goal International NormalizedRatio (INR) for this indication is 2 to 3.
Elevated blood pressure is common after ischemic stroke, and its treatment is associated with a decreased risk of stroke recurrence.
The Joint National Committee and AHA/ASA guidelines recommend an angiotensin- converting enzyme inhibitor and a diuretic for reduction of blood pressure in patients with stroke or TIA after the acute period (first 7 days).
The National Cholesterol Education Program considers ischemic stroke or TIA to be a coronary risk equivalent and recommends the use of statins in ischemic stroke patients to achieve a low-density lipoprotein cholesterol concentration of less than 100 mg/dL.
Low-molecular-weight heparin or low-dose subcutaneous unfractionated heparin (5,000 units twice daily) is recommended for prevention of deep venous thrombosis in hospitalized patients with decreased mobility due to stroke and should be used in all but the most minor strokes.
Evaluation of patient outcome :
The most common reasons for clinical deterioration in stroke patients are:
(1) extension of the original lesion in the brain
(2) development of cerebral edema and raised intracranial pressure
(3) hypertensive emergency
(4) infection (e.g., urinary and respiratory tract)
(5) venous thromboembolism
(6) electrolyte abnormalities and rhythm disturbances
(7) recurrent stroke.
• Patients with acute stroke should be monitored intensely for the development of neurologic worsening, complications, and adverse effects from treatments.
DiPiro, Joseph T. Pharmacotherapy: A Pathophysiologic Approach. New York: McGraw-Hill Medical, 2008. Print.
Chisholm-Burns, Marie A. Pharmacotherapy Principles & Practice. New York: McGraw-Hill, 2010. Print
Seemant Chaturvedi, Mark A. Creager, Antonio Culebras, Robert H. Eckel, Robert G. Hart, Larry B. Goldstein, Cheryl D. Bushnell, Robert J. Adams, Lawrence J. Appel, Lynne T. Braun. "Guideline for Healthcare Professionals From the American Heart Association/American Guidelines for the Early Management of Patients With Acute Ischemic Stroke." (2010): n. pag. Web. 7 Jan. 2014.: A
Sahar A. Alkhalifah , PharmD. Candidate 2014
Princess Norh Bint Abullrahman University
internal medicine Rotation -PSMMC
I. Triage–10 min
Review t-PA criteria
Page acute stroke team
Draw pre t-PA labs*
II. Medical Care–25 min
Place O2 , 2 NS IVs
Obtain BP, weight
Obtain 12-lead ECG
Send patient to CT
III. CT & Labs–45 min
Obtain lab results
Return pt to ED
IV. Treatment–60 min
Start IV t-PA
Monitor for ICH
N/V, neuro status
ED stroke care
CBC, platelets, PT/INR, PTT, cardiac panel
Insufficient evidence to recommend routine use of high-dose IV heparin, LMW heparin, or heparinoid as for AIS
other AIS treatment
Recombinant human tissue-type plasminogen activator (t-PA); produces local fibrinolysis
Promotes thrombolysis by converting plasminogen to plasmin; plasmin degrades fibrin and fibrinogen
0.9 mg/kg IV infused over 1 hour; administer 10% of total dose as initial bolus over 1 minute; not to exceed total dose of 90 mg
Bruising and Bleeding
Mechanism of Action
Coronary thrombolysis occurs in 30 min; reaches peak response at 60 min
Peak plasma time: 20-40 min
alteplase, prothrombin complex concentrate, human. pharmacodynamic synergism. Contraindicated.
alteplase and apixaban both increase anticoagulation. Serious - Use Alternative
prothrombin complex concentrate, human
Recent major surgery, cerebrovascular disease, HTN, hemostatic defects, severe thrombophlebitis, severe hepatic/renal dysfunction
Despite an increased incidence of symptomatic intracerebral hemorrhage, treatment with intravenous t-PA within three hours of the onset of ischemic stroke improved clinical outcome at three months.
The use of aspirin in patients with no history of stroke or ischemic heart disease reduced the incidence of non-fatal myocardial infarction (MI) but not of stroke.
A meta-analysis of eight trials found that the risk of stroke was slightly increased with aspirin use, especially hemorrhagic stroke.
Aspirin is beneficial in the primary prevention of MI, but not for primary stroke prevention
Hyperlipidemia has not clearly been established as a risk factor for stroke
although it is a modifiable risk factor for coronary heart disease.
Recent studies show that statin use may reduce the incidence of a first stroke in high-risk patients
Lowering blood pressure in patients who are hypertensive has been shown to reduce the relative risk of stroke, both ischemic and hemorrhagic, by 35% to 45%.
no one agent has been clearly shown to be more beneficial than any other for preventing stroke.
Aspiration and Oxgen
Maintain HOB > 30°
Maintain O2 sat > 92 or 95%
Stroke patient should be on ventilator
however, even patients with normal lipid levels however, may benefit from treatment.
mangment of blood pressure
perindopril alone resulted in a 28% reduction in recurrent stroke compared to placebo. With the addition of the diuretic indapamide a 43% reduction in stroke recurrence was seen
Clopidogrel is slightly more effective than aspirin with a relativerisk reduction of 7.3% more than that provided by aspirin. The usual dose is 75 mg orally taken on a daily basis