Summary of Admission History and Progress Notes: 67-year-old male has a history of non-ischemic cardiomyopathy with ejection factor of 24%, chronic left ventricle thrombus on anticoagulant, hypertension, metastasis of prostate cancer, chronic kidney disease stage 3. Patient was admitted to UCSD emergency department on 08/20 after falling down stairs. Patient presented confused but conscious. Upon presentation in the ED he had left face, left arm, and left leg weakness. After MRI and cerebral angiogram, findings were conclusive to a right-sided embolic CVA. Echocardiogram revealed apical ventricular thrombus.
Patient presented to ED on Coumadin therapy with INR at 3.1.
Patient was not a candidate for thrombolytic therapy. He continued on Coumadin and aspirin 81 milligrams was added. Left-sided weakness resolved within one to two days. Cardiologist at UCSD recommends Cardiac Thrombectomy to prevent further strokes. Neurologist recommends endovascular intervention to prevent future embolic strokes though not during an acute episode. Patient was held at UCSD ED for permissive hypertension during acute stroke. Patient complained of cough with green phlegm over the past few days; chest x-ray findings of no local infiltrate.
Embolic cerebral vascular accident (CVA); stroke Etiology/Risk factors: Risk factors include a history of transient ischemic attack, hypertension, elevated serum cholesterol, diabetes mellitus, smoking, cardiac valve diseases, anticoagulant therapy, oral contraceptive use, methamphetamine use, aneurysm, or previous stroke (Swearinger, 2012).
Pathophysiology: A stroke is caused by disruption of oxygen supply to the brain by either thrombotic occlusion, embolic occlusion or cerebral hemorrhage. Most thrombotic strokes are the result of atherosclerosis. Plaque formation builds to the point of blockage in the large blood vessels that deliver blood to the brain.
Most embolic strokes are caused by a cardiac emboli resulting from cardiac valve disease or atrial fibrillation. The carotid artery feeds the main blood vessels of the brain, therefore cardiogenic emboli have a direct path to the brain (Swearinger, 2012).
S&S: Signs and symptoms vary depending on severity and side of brain affected. Symptoms may improve within 2 to 3 days as cerebral edema decreases. Patient may appear apathetic, irritable, disoriented, drowsy or comatose; incontinence may occur; unilateral weakness or paralysis may occur; headache, neck stiffness or rigidity may be present. The patient may have difficulty chewing or swallowing and may present with unequal or fixated pupils (Swearinger, 2012).
Diagnostics: Time is critical in diagnosing the type of stroke a patient has experienced. A patient is no longer eligible for rTPA if the critical window of 3 hours from last seen normal has expired. CBC, electrolytes, blood glucose and clotting factors should be drawn immediately in order to determine eligibility for rTPA. An MRI will reveal the site of infarction and other brain structure abnormalities related to cause and effect of the CVA. An MRI may take as long as an hour to complete. While a CT scan is generally a diagnostic tool of choice in many emergency situations due to the rapid process, ischemic areas will not show in the CT imaging until they start to necrose 24 – 48 hours after the CVA (Swearinger, 2012).
Complications: Complications include recurrence of CVA, paralysis, aspiration, depression, falls, and coma.
Chronic left ventricle thrombus on anticoagulant: Anticoagulant therapy is prescribed to prevent increased formation of existing thrombi. Outside of the hospital environment, the anticoagulant of choice is usually warfarin because it may be taken PO. When the therapeutic range of warfarin is achieved patient’s INR will be 2.5-3.5. Cardiogenic trombi are the result of the heart’s inability to effectively ejecting blood after managed daily living, therefore the blood becomes stagnant and begins to clot (Deglin , Sanoski , & Vallerand, 2013).
Chronic kidney disease (CKD) stage 3 is marked by a GFR 30-59 mL per minute (Bladh, et. al., 2013). CKD is a progressive and irreversible disorder. Aggressive management of Hypertension and Diabetes Mellitus, both of which are common contributing risk factors, may slow progression. Eventually CKD can progress to end-stage renal failure (ESRD). Before development of ESRD, a person with CKD can still manage normal daily living through diet and medication (Swearinger, 2012).
Diagnostic Tests, Results and Rationales:
Several areas of restricted diffusion within right MCA region; consistent with acute embolic infarcts MRI images differentiate between acute and chronic lesions. Ischemic strokes can be identified early. Site of infection, hematoma, and cerebral edema can be viewed through MRI
(Swearinger, 2012) Cerebral angiogram
Right MCA stroke, right internal artery non-flow limiting dissection with associated pseudo-aneurysm; right superior trunk M3 occlusion Identify presence of hematoma in stasis of blood vessels after a rupture (Swearinger, 2012) Chest x-ray
Negative for infiltrate
A presence of infiltrate could indicate pneumonia or heart failure (Swearinger, 2012) Echocardiogram Severely depressed left ventricular ejection factor; apical ventricular thrombus Assess ventricular and valvular function of the heart, ejection fraction, and hemodynamic measurements (Swearinger, 2012) Cerebrovascular carotid duplex
Low flow right ICA; bilateral proximal ICA right 9.5 mm, left 5.5 mm; no significant stenosis; vertebral arteries patent with antegrade flow Evaluation of carotid arteries to detect occlusions three-dimensional visualization providing information on circumference, length, and thickness of plaque volume (Swearinger, 2012)
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