case study 5
pari123
NeurologicalSystem2021.pptxNeurological System
NUR 41500
Cerebral Blood Supply
Derived from 2 systems:
Internal Carotid Arteries
Vertebral-Basilar Arteries
Circle of Willis The circle of Willis acts 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 pneumoniae infection
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
Photophobia
CLINICAL MANIFESTATIONS
For many- a bleed may be first sign
Visual, motor, sensory disturbances
Signs of meningeal irritation
Positive Kernig’s sign
Positive Brudzinski’s sign
HUNT & HESS GRADING SYSTEM
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
