Pathophysio Cva Infarct.chicheng

8/3/2019 Pathophysio Cva Infarct.chicheng

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If not managed

Lysed or moved thrombusfrom the vessel

Vascular wall becomesweakened and fragile

Leaking of blood from thefragile vessel wall

Guarded Prognosis

Cerebral Hemorrhage

If managed:Dx: CT scan, MRI, cerebral angiography,arteriography,

lumbar puncture, skull x-ray Tx: chronic hypertensives, surgical

decompression, evacuation and aspiration, administration of fresh frozen

plasma with fibrinogen or cryoprecipitate

If not managed

Hematoma evacuation

Sx: , headache,unconsciousness,nausea/vomiting,

visual disturbances

If managed:

Actual:Dx:Cranial CT scan (6/16/08)Capsuloganglionic bleed Lacunar infarct,Bilateral Internal Carotid

AteriosclerosisDoppler (6/16/08)Mean flow velocities and

pulsatility index of bothanterior and posterior circulation within normal limits

EEG/ECG, skull x-ray,carotid ultrasonography

TX: aspirin within 24 hrs,thrombolytics within 3

hours, carotid stenting,hypothermia,

anticoagulants, surgical decompression

(hemicraniectomy), carotid endartectomy

Possible:Dx: PET scan, MRI,

cerebral angiography,lumbar puncture,

EEG/ECG, skull x-ray,carotid ultrasonography

TX: aspirin within 24hrs, thrombolytics

within 3 hours, carotid stenting, hypothermia,

anticoagulants, surgical decompression

(hemicraniectomy),carotid endartectomy

Formation of cavity surrounded by dense gliosis

Mass of blood forms andgrows

DecreasedICP



Formation of smalland large clots

Vasospasm of tissue and arteries

CEREBRALHYPOPERFUSION

Sx: dizziness,confusion,headache Impaired distribution of

oxygen and glucose

Tissue hypoxia andcellular starvation

Cerebral Ischemia

Initiation of ischemiccascade

Anaerobic metabolism bymitochondria

Production of oxygen freeradicals and other reactive

oxygen speciesGenerates large amountsof lactic acid

Blood seeps into theventricles

Obstruction of CSFpassageway

Accumulation of CSF inthe ventricles

Ventricles dilate behindthe point of obstruction

If not managedIf managed:Ventriculostomy,

VP shunt, ICP

Alternative routefor return of CSFin the circulation

Unrelievedobstruction

Compression of brain tissues will

not occur Guarded

Prognosis

< 30 mlhemorrhage

30-60 mlhemorrhage

> 60 mlhemorrhage

Increased ICP

Lodges untoother cerebral

arteries

Poor prognosisIntermediate

prognosis

Good prognosis

Metabolic Acidosis

Failure production of adenosine triphosphatase

Failure of energy dependentprocess

(ion pumping)



Release of excitatoryneurotransmitter glutamate

Influx of calcium

Damage to the bloodvessel endothelium

Activates enzymes thatdigest cell proteins, lipids

and nuclear material

Failure of mitochondria

Transient Ischemic Attack

If managed:-t-PA (urokinase,

streptokinase)-calcium channel

blockers

If not managed

GuardedPrognosis

Brain sustains an irreversiblecerebral damage

Release of metalloprotrease(zinc and calcium-dependent enzymes)

Break down of collagen, hyaluronic acid andother elements of connective tissue

Structural integrity loss of braintissue and blood vessels

Breakdown of the protectiveBlood Brain Barrier

Further energydepletion



Cerebral edema

Vascular Congestion

Compression of tissue

Increased intracranial

Impaired perfusion andfunction

MiddleCerebral Artery

Anterior cerebralartery

Posterior CerebraI Artery

Internal CarotidArtery

Vertebrobasilar System

Anteroinferior Cerebellar

Posteroinferior cerebellar

Lateral hemisphere,

frontal, parietal and temporal lobes, basal

ganglia

Frontal Lobe Occipital lobe;anterior and

medial portion of temporal lobe

Branches intoophthalmic, PCA,anterior choroidal,

ACA, MCA

Cerebellum and brain stem

Cerebellum Cerebellum



Sx:

Contralateral

hemiparesis or

hemiplegia ,

unilateral

neglect , altered

consciousness

, homonymous

hemianopsia,

inability to turn

eyes toward

affected side,

vision changes,

dyslexia,

dysgraphia,

aphasia ,

agnosia,

memory deficits,

vomiting

Sx:

Contralateral

hemiparesis,

foot and leg

deficits greater

than the arm,

foot drop, gait

disturbances,

contralateral

hemisensory

alterations,

deviation of

eyes toward

affected side,

expressive

aphasia,

confusion,

amnesia, flat

affect, apathy,

shortened

attention span,

loss of mental

acuity, apraxia,

incontinence

Sx:

Mild

contralateral

hemiparesis,

intention

tremor, diffuse

sensory loss,

pupillary

dysfunction,

loss of

conjugate

gaze,

nystagmus,

loss of depth

perception,

cortical

blindness,

homonymous

hemianopsia,

perseveration,

dyslexia,

memory

deficits, visual

hallucinations

Sx:

contralateral

hemiparesis

with facialasymmetry,

contralateral

sensory

alterations,

homonymous

hemianopsia,

ipsilateral

periods of blindness,

aphasia if

dominant

hemisphere is

involved, Mild

Horner’s

syndrome,

carotid bruits

Sx:

Alternating

motor

weaknesses,

ataxic gait,

dysmetria,

contralateral

hemisensory

impairments,

double vision,

homonymous

hemianopsia,

nystagmus,

conjugate

gaze,

paralysis,

dysarthria,

memory loss,

disorientation,

drop attacks,

tinnitus,

hearing loss,

vertigo,

dysphagia,

coma

Sx:

Ipsilateral

ataxia, facial

paralysis,ipsilateral loss

of sensation in

face, sensation

changes on

trunk and

limbs,

nystagmus,

Horner’ssyndrome,

tinnitus,

hearing loss

Sx:

Ataxia,

paralysis of thelarynx and soft

palate,

ipsilateral loss

of sensation in

face,

contralateral on

body,

nystagmus,dysarthria,

Horner’s

syndrome,

hiccups and

coughing,

vertigo, nausea

and vomiting



If managed:Palliative care-Frequent vital sign and

neurovital signs,intubation, mechanical

ventilation,vasodilators, osmotic

diuretics,ventriculostomy, ICP

monitoring

If not managed:

Continued insufficiency of blood

flow

Further compression of tissues

Coma

Cerebral Death

Loss of neural feedback

mechanisms

Cessation of physiologic

functions

Poor cerebral perfusion

Poor improvement

Poor Prognosis





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Pathophysio Cva Infarct.chicheng