Posted: June 13th, 2022

case study 5

NURSE write
__________________________Case Study Part 5:Neurological_______________________________
Clinical Course Day 7:The patient was successfully extubated this morning at 0800 and is currently on oxygen via face mask at 2.5L/min. Vital signs are:T 98.3, HR 96, R 21, BP 102/64, O2 Sat 97%. Pt is alert and oriented x 3. Pt able to carry on coherent conversation with medical staff. At 1005, the nurse arrives to discuss medications. The nurse notices that the patient appears to be asleep but when the patient is addressed,it is noted that the left side of her face is drooping and patient is slurring her words. The nurse calls for assistance. Within ten minutes, the patient becomes more alert and her speech becomes less slurred. Within one hour, her sudden onset neuro findings have cleared.
Labs and Diagnostics:
Na 141 meq/LK 3.8 meq/L Cl 118 meq/LHCO3 22 meq/L BUN 58 mg/dL Cr 3.1 mg/dL
WBC 11.0x 103/mm3 Hb 12.8g/dlHct 53% BNP 701 pg/ml Glucose 115
Carotid Ultrasound:
Mild stenosis of the right and left internal carotid artery (<50% stenosis in the range of 15-49%). Based on the above information, answer the following questions: 18.)Define Transient Ischemic attack (TIA) and the likely etiology [2 points].Why is the diagnosis and treatment of TIA important? [2 points]. 19.)Name five risk factors Loretta has for Cerebrovascular Accident [5points]. 20.)In addition to a carotid U/S, name and define 2 other diagnostic tests a cardiologist might order to evaluate Loretta’s neurovascular status? [3 points] 21).List 5 of the guidelines developed by the American Heart Association and American Stroke Association Council on Stroke to reduce stroke risk specifically in women. (5 points) APA 1 point Scholarly Work1 point Total points 19 Neurological System NUR 41500 Cerebral Blood Supply Derived from 2 systems: Internal Carotid Arteries Vertebral-Basilar Arteries Circle of Willis Thecircle of Willisacts to provide collateral blood flow between the anterior and posterior circulations of the brain, protecting against ischemia in the event of vessel disease or damage in one or more areas. Blood flows through the Circle lis to feed the major arteries of the brain Monroe Kellie Principle The intracranial compartment is a rigid container and consists of three components a. brain-80% of total volume b. blood-10% of total volume c. CSF-10% of total volume To maintain a normal ICP, a change in the volume of one compartment must be offset by a reciprocal change in the volume of another compartment Pressure is normally well-controlled through alterations in the volume of blood and CSF Cerebral Hemodynamics CBF, cerebral blood flow CPP, cerebral perfusion pressure CBV, cerebral blood volume Cerebral oxygenation Cerebral Perfusion Pressure- the pressure required to perfuse the cells of the brain Wide range of 60 – 140 mm Hg Normally: 80-100 mm Hg Ischemia:<60 mm Hg Cell death: <30 mm Hg *these numbers may be different according to the source Increased Intracranial Pressure (IICP) Normal 5 to 15 mm Hg Caused by an increase in intracranial content- such as tumor growth, edema, excessive CSF, or hemorrhage Four stages Stages of ICP: Stage 1 Vasoconstriction Venous compression ICP is stable Few symptoms Stages of ICP: Stage 2 ICP exceeds brain’s capacity to adjust Neuronal oxygenation compromised Arterial vasoconstriction occurs to overcome ICP Symptoms subtle and transient Stages of ICP: Stage 3 Hypoxia and hypercapnia of brain tissue Autoregulation is lost Carbon dioxide levels continues to cause vasodilation Brain volume is increasing CPP falls Rapid deterioration of the patient Stages of ICP: Stage 4 Brain tissue shifts from the compartment of greater pressure to the one of lesser pressure Herniating brain tissue is ischemic, hypoxic smaller compartment becomes compromised Hydrocephalus may develop MAP=ICP and cerebral blood flow stops ***can go from stage 1 to stage 4 in minutes** Herniation Syndromes Supratentorial herniation Uncal Uncus or hippocampal gyrus (or both) shifts from the middle fossa through the tentorial notch into the posterior fossa Central Downward shift of the diencephalon through the tentorial notch Cingulate Cingulate gyrus shifts under the falx cerebri Assessment of ^ ICP- Glasgow Coma Scale Eye Opening 4 spontaneous, 3 to loud voice, 2 to pain, 1 none Verbal Response 5 oriented, 4 confused, 3 inappropriate words, 2 incomprehensible sounds, 1 none Best Motor Response 6 obeys command, 5 localizes, 4 withdraw, 3 flexion posturing, 2 extension posturing, 1 none GCS: Posturing Cushing’s Triad-Response to continued increased pressure Decrease in heart rate Decrease in respirations Systolic hypertension Cerebral Vascular Accident: Stroke Syndromes A sudden, severe episode of neurologic symptoms caused by a deficit in blood supply to the brain Leading cause of disability, 3rd cause of death in women and 5th leading cause of death in men 75% occur in patients older than 65 Incidence 150% greater in blacks than whites Four times the incidence and eight times the mortality in patients with both HTN and DM Cerebrovascular Accidents: Risk Factors Poorly or uncontrolled arterial hypertension •Smoking, which increases the risk of stroke by 50% •Insulin resistance and diabetes mellitus •Polycythemia and thrombocythemia •High total cholesterol or low HDL cholesterol, elevated LDL •Congestive heart disease and peripheral vascular disease •Hyperhomocysteinemia •Atrial fibrillation •Chlamydia pneumoniaeinfection Types of CVA’s Thrombotic Arterial occlusion caused by thrombi formation in the arteries supplying the brain or intracranial vessels Most often caused by atherosclerosis Increased coagulation Occur when clot detaches, travels upstream causing obstruction of blood flow and acute ischemia Embolic Fragments that break from a thrombus formed outside the brain Heart, aorta, common carotid artery Usually these fragments obstruct at a narrow bifurcation causing ischemia Risk factors are Afib, left heart thrombus, recent MI, endocarditis, rheumatic valve disease, valve prosthesis Often followed by a second stroke because the source of clot still exists Types of CVAs, cont Hemorrhagic Intracranial hemorrhage Hypertension, ruptured aneurysm or AVM, bleeding into a tumor, anticoagulants, head trauma, illicit drugs (cocaine) The mass of blood displaces and compresses brain tissue Lacunar Small vessel disease Caused by occlusion of a single deep perforating artery supplying small subcortical vessels Pure motor and sensory deficits are classic Smaller area of infarct Ischemic Stroke: TIA Brief episode of neurologic dysfunction Caused by a focal disturbance of the brain or retinal ischemia—usually vessel spasm “Angina of the brain” Intermittent blockage Develops suddenly Gone in <24 hours, usually less than 1 hour No evidence of infarction Patients make a complete recovery 80% have a recurrence in 1 year and have higher incidence of stroke Therapeutic Time Window The time during which treatment, aimed at interrupting the ischemic cascade, can reverse damage to the ischemic penumbra. 3 hours max, sooner the better TREATMENT:Ischemic Stroke Bp Control Cardiac Support Antiplatelet/Antithrombotic Rx Isotonic Fluids Prevent DVT Nutrition Infection Prevention Endarterectomy TREATMENT: Hemorrhagic Stroke Refer Refer to neurosurgery Prevent Prevent ICP Prevent Prevent Rebleed Prevent Prevent Vasospasm CEREBRAL ANEURYSM About 4 million Americans harbor asymptomatic aneurysms Caused from atherosclerosis, congenital abnormality, trauma, inflammation, cocaine abuse Most are located at bifurcations or in the Circle of Willis Cause of rupture unknown: peak incidence is age 50-59 with women greater than men 26,00 bleeds/year Less than 1/3 resume normal lives CLINICAL MANIFESTATIONS May be asymptomatic: 40% have warning symptoms “The worse headache of my life” Lethargy>>coma
Neck pain
Nausea, vomiting
Cranial nerve dysfunction
For many- a bleed may be first sign
Visual, motor, sensory disturbances
Signs of meningeal irritation
Positive Kernig’s sign
Positive Brudzinski’s sign
Grade I
Neurologic status intact; mild headache, slight nuchal rigidity
Grade II
Neurologic deficit evidenced by CN involvement; moderate to severe h/a with more pronounced meningeal signs
Grade III
Drowsiness and confusion with or without focal neurologic deficits; pronounced meningeal signs
Grade IV
Stuporous with pronounced neurologic deficits; nuchal rigidity
Grade V
Deep coma state with decerebrate posturing and other brain stem functioning
Evaluation and Treatment
Diagnosis before a bleed is through arteriography
After a bleed diagnosis is made by clinical manifestations, history, CT and MRI
Surgical management
Endovascular embolization if applicable

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