Stroke

in
ro l o
Nu
e
gy
EFINITION
TIOLOGY
ATHOPHYSIOLOGY
ANCILLARY AND LABORATORY
LINICAL MANIFESTATION
NTERVENTION
REATMENT
UTCOME
Exam
• Cardio
• Irregularly irregular rhythm
• no murmurs rubs or gallops
• Neck exam
• Normal
• Check for carotid bruit
Exam
• Airways
• To assess airway patient and for potential need for intubation
• Breathing exam
• Assess efficacy of breathing in this acutely alerted patient
• Swallowing
• Circulation exam
• To check for signs of shock
• Pulmonary exam
• Make sure there is no evidence of focal lung sounds concerning for aspiration
Exam
• Neurological Examination
• Somnolent, unable to
follow command
• 2/5 RUE, 3/5 RLE
• Central facial palsy right
• Expressive and receptive
aphasia
• No blink and visual threat
on the right
• Right homonymous
hemianopsia
Cerebrovascul
ar Disease
EFINITION
Cerebrovascular Disease
• sudden focal neurologic syndrome due to cerebrovascular disease

• Cerebrovascular disease designates any abnormality of the brain
resulting from a pathologic process of the blood vessels
• Pathologic process —
* occlusion of the lumen by embolus or thrombus
* rupture of a vessel
* an altered permeability of the vessel wall
* increased viscosity or other change in the quality of the
blood flowing through the cerebral vessels
EFINITION
 one of leading causes of death and disability throughout the world

 affects 20M people in the world every year
 kills 5 M people annually
• is the #2 killer worldwide
• frequently the predominant vascular disease in any given region in

Asia
• is the #1 killer in Asia
• WHO estimates 2.7 M stroke deaths in Asia in
2000
Ten leading causes of MORTALITY in the
Philippines
EFINITION Ischemic
• occlusion of a cerebral
blood vessel and causes

cerebral infarction.
Stroke
Hemorrhagic
• Bleed within the

parenchyma or
subarachnoid space
EFINITION
Vascular Cerebral Subarachnoid Transient
occlusion Hemorrhage Hemorrhage Ischemic Attack

• Embolic- • also abrupt in • Instantaneous • Reverses
sudden peak onset, may be dramatically
onset static or steadily over a period of
• Thrombotic- progressive over minutes to an
saltatory a period of hour
fashion minutes or
hours
ISCHEMIC STROKE
TIOLOGY
• Atherosclerotic Infarction 20%

• Lacunar Infarction 25%
• Cardioembolic Infarction 20%
• Cryptogenic Infarction 30%
• Infarction of other Undetermined Cause 05%
- NINDS Stroke Data Bank

TIOLOGY
TIOLOGY
Atrial Diabetes
Hypertension
Fibrillation Mellitus
Cigarette
Hyperlipidemia OCP use
Smoking
TIOLOGY
Non-Modifiable Risk Factors Modifiable Risk Factors
Age Doubles per decade after age 55 •Hypertension*

Gender Males > Females •Cigarette smoking
•Diabetes
Previous stroke 10x •Heart disease
Race-ethnicity Blacks > Whites •Hypercholesterolemia
•Heavy alcohol intake
Heredity •Obesity
•Physical inactivity/sedentary lifestyle
•Stress
•Heavy snoring
•medical conditions
• result from unhealthy
lifestyle
ATHOPHYSIOLOGY
Two Processes:
1. loss in the supply of oxygen and glucose secondary to
vascular occlusion
2. an array of changes in cellular metabolism consequent to
the collapse of energy-producing processes, ultimately with
disintegration of cell membranes
Note: The effects of ischemia whether functional and reversible or structural and
irreversible, depend on its degree and duration
ATHOPHYSIOLOGY
• Reduction of cerebral blood flow below 10-12 ml/100grams brain/minute leads to

infarction
• Critical level of hypoperfusion that abolishes function that leads to tissue damage:
CBF 12-23 ml/100 grams brain/ minute
• “Ischemic penumbra” – region of marginal perfusion

* increase in K+ levels (efflux from depolarized cells)
* depleted ATP
* reduction in creatine phosphate
ATHOPHYSIOLOGY
• Ischemic Necrosis: CBF 6-8 ml/100 gm/minute

* release of excitatory NT (glutamate, aspartate)
* increase in intracellular calcium levels
* increase in extracellular K+
* depletion in ATP
* reduction in creatine phosphate
* cellular acidosis
* activation of free fatty acids
* accumulation of PGs, leukotrienes, and free radicals
• Pale infarction: tissue are devoid of blood
• Red, Hemorrhagic infarction: due to extravasation of
blood vessels from small vessels in the infarcted
tissue ( due usually to cerebral embolism)
ATHOPHYSIOLOGY
Vascular Anatomy
Anterior Circulation
• From carotid system
• Supplies 80% of brain ACA
Posterior Circulation MCA
• From vertebral system

• Supplies 20% of brain PCA
BASILAR
VERTEBRAL
ANCILLARRY AND
DIAGNOSTICS
Neuroimaging Studies:
- continue to enhance the clinical study of stroke
patients; they allow the demonstration
of both the cerebral lesion and the affected
blood vessel
CT scanning
- demonstrates and accurately localizes even
small hemorrhages, hemorrhagic infarcts,
subarachnoid blood, clots in and around
aneurysms, regions of infarct necrosis and
AVM’s
ANCILLARRY AND
DIAGNOSTICS
Doppler Ultrasound Studies

- demonstrate atheromatous plaques and stenoses of large vessels,
particularly of the carotid but also the vertebrobasilar arteries
Transcranial Doppler
- occlusion or spasm of the main vessels of the circle of Willis can
be seen using ultrasound
Arteriography
- most accurately demonstrates stenoses & occlusions of the larger
vessels as well as aneurysms, vascular malformations, & other
blood vessel diseases (arteritis)
ANCILLARRY AND
DIAGNOSTICS
- conventional dye-injection angiography has been supplanted by

magnetic resonance angiography (MRA) and venography (MRV)
for the visualization of large intracranial arteries and veins
* these have the advantage of safety but do not yet give
refined images of the smaller vessels and are not as
accurate as angiography in measuring the severity of
stenosis of a vessel
- spiral CT angiography now offer images of better resolution,

comparable to conventional arteriograms
CLINICAL MANIFESTATIONS
Stroke Syndromes
Dominant Hemisphere:
• Majority of right handed and most left handed patients have dominance
for speech and language located in the left hemisphere
• Left hemisphere infarction is characterized by aphasia (both motor
[Broca’s] and sensory [Wernicke’s]) and apraxia
Non-dominant Hemisphere:
• Less predictable syndromes
• Attention defects: extinction and neglect
• Behavioral changes: acute confusion and delirium
Case 1
• 70 yr old male
• sudden onset right side hemiplegia, hemianesthesia/sensory
• eyes deviated to left (preferential gaze to left)
• Difficulty with speech/language
Middle Cerebral Artery territory
Embolism from ICA or heart to

MCA is most common cause of
cerebral infarction
MCA Stroke
• Contralateral hemiplegia and hemianesthesia: arm and face
> leg
• Deviation of the head and eyes toward side of infarct “Gaze
preference”
• Global aphasia (in dominant hemisphere)
• Hemianopsia, Hemineglect
Case 2
• 68 yr old female
• woke up with weakness in right leg
• slight right side weakness leg > arm
• family states she has “impaired judgment and insight”
• “seems like a baby: sucking and grasping”
ACA territory Supplies basal and medial aspects
of the cerebral hemispheres and

extends to anterior two thirds of
parietal lobe
ACA Stroke
• weakness of the leg
• +/- proximal muscle weakness in the upper extremities
• affect frontal lobe: impaired judgment and insight, change

in affect
• Presence of primitive grasp and suck reflexes
• Language impairment (common finding)

Case 3
• 77 yr old male
• sudden onset of dizziness
• double vision
• On examination, has pain and temperature deficit on half of
face and on opposite side of body
Vertebrobasilar System
• Heterogeneous syndromes and

presentations
• Cranial nerve deficits and
involvement of cerebellum and
neurosensory tracts
• Diplopia, dysphagia, dysarthria,
dizziness, vertigo, ataxia
• Pain and temperature deficits in
Pontine Infarct face occur on opposite side of body
Case 4
• 85 yr old male
• diabetic, hypertension
• sudden onset of being unable to move left side of body
• able to talk
• sensation intact
Lacunar Infarction
• Lesion of small penetrating branch arteries into BG,

thalamus, pons, internal capsule
• “Pure” strokes
* motor, sensory, ataxic hemiparesis
• Usually result in hemiparesis of face,
arm and leg
• Lack of impairment of
consciousness, aphasia, or visual
disturbances
• More common in blacks & history of
HTN, DM
• 60% of patients with lacunar
infarctions will be independent at 1
year following stroke
Case 5
• 85 yr old female
• In ICU, post repair or ruptured abdominal artery aneurysm
• GCS 15
• Complaining of difficulty moving her leg and that it feels numb
Watershed Infarction
• Occurs in vulnerable areas supplied by distal

distribution cerebral arteries during periods of
hypotension
• Infarction between the ACA and MCA presents with
hemiparesis & hemianesthesia, predominantly in the leg
• Dominant hemisphere infarctions: decrease in verbal
ability with preserved comprehension
• Infarction involving the posterior
watershed area presents with
homonymous hemianopia +/-
hypoesthesia in the face and legs
REATMENT
Medical
IV fluids, bed rest
(Thrombolysis, Antithrombotics,
antihypertensives, etc)
Close monitoring Surgery, decompressive Hemicraniectomy

REATMENT
• Stroke Unit admission
• Anti-thrombotic Agents:
• Anti-platelets (ASA, Clopidogrel, Cilostazol, etc)
• Anticoagulant (Heparin, Warfarin, LMWH)
• Thrombolytic therapy (r-TPA)
• Neuroprotectants
• Hemicraniectomy (surgery)- last option
REATMENT
Neuroprotection
AVOID the following:
• Hypotension
• (treat only if MAP >130 mm Hg)
• Hypoxemia
• Hyperglycemia
• Hyponatremia
• Fever
REATMENT
Decompressive Hemicraniectomy
Large MCA Infarction SYNDROME:
• Clinical ---
Changes in sensorium Heminanopsia
Dense Hemiparesis/plegia Neglect
Hemisensory loss Gaze preference
Aphasia - if dominant
• CT scan ---
Dense MCA sign
Hypodensity >1/3 MCA territory
Effacement of sulci
HEMORRHAGIC STROKE
Types of Hemorrhagic STROKE
• Hemorrhage ---
rupture of an artery
Intracerebral Subarachnoid
EFINITION
• Intracerebral Hemorrhage
EFINITION
Most common sites:

• putamen & internal capsule - 50%
• thalamus
• lobar (central white matter of the temporal, parietal, or frontal
lobes)
• cerebellar hemisphere
• pons
Most common sites and sources of ICH
Thalamogeniculate
branches off the PCA

are the source of
thalamic hemorrhage
ICH involving the cerebral

lobes most commonly
originates from cortical
branches of ACA, MCA, & Lenticulostriate branches
PCAs of the MCA are the
common source of basal
ganglia hemorrhage
Charcot-Bouchard aneurysms
(miliary aneurysms)
Paramedian branches
Penetrating branches of posterior inferior,
from the basilar artery are
anterior inferior, & superior cerebellar arteries
the source of hemorrhage
the source of cerebellar hemorrhage
in the pons
ATHOPHYSIOLOGY
• vascular lesion that leads to arterial rupture in some cases

appears to arise from an arterial wall altered by the effects of
hypertension
*segmental lipohyalinosis and the false aneurysm
(microaneurysm) of Charcot-Bouchard
charcot-bouchard aneurysms are microaneurysms
that are formed due to the weakening of the vessel
wall from lipohyalinosis
• breaks in the elastic lamina at multiple sites, almost always at
bifurcations of the small vessels --possibly these represent
sites of secondary rupture from tearing of small vessels by
the expanding hematoma
NCILARY AND
DIAGNOSTICS
•
Cranial CT scan
• has proved totally reliable in the detection of hemorrhages that are
1.0 cm or more in diameter
• smaller pontine hemorrhages are visualized with less certainty
• coexisting hydrocephalus, tumor, cerebral swelling, and
displacement of the intracranial contents are readily appreciated
NCILARY AND
DIAGNOSTICS
•Cranial MRI
• useful for demonstrating brainstem hemorrhages and residual
hemorrhages, which remain visible long after they can no longer be
seen by the CT scan (after 4 - 5 weeks)
• Lumbar Puncture - is NOT advised
• WBC count in the peripheral blood may rise transiently to
15,000/mm3
• ESR is mildly elevated in some patients
• Acute reactive hypertension - far exceeding the patient’s chronic

hypertensive level; seen with moderate and large clots situated
in deep regions
• Vomiting - at the onset of ICH
• Severe headache
• Nuchal rigidity - disappears as coma deepens
• Seizures - usually focal, occur in the first few days (10% of cases
of supratentorial hemorrhage); rarely at the time of the ictus but
more commonly as a delayed event, months or even years after
the hemorrhage, in association with subcortical slit hemorrhages
• FUNDI - show hypertensive changes in the arterioles

* Roth Spots - white-centered retinal hemorrhages
* Subhyaloid hemorrhages - fresh preretinal hemorrhages, common with
ruptured aneurysm, arteriovenous malformation, or severe trauma
Headache, acute hypertension, and vomiting with a focal

neurologic deficit are the cardinal features and serve most
dependably to distinguish hemorrhage from ischemic stroke.
Putaminal Hemorrhage with extension to Internal Capsule

• most common syndrome
• Hemiplegia - from interruption of the capsule; is a consistent
feature of medium-sized and large clots
• Vomiting
• Headache
• Depressed level of sensorium – with large hemorrhages
Thalamic Hemorrhage
• Severe Sensory Loss - entire contralateral body
• Hemiplegia or hemiparesis - by compression or destruction of the
adjacent internal capsule
• Fluent Aphasia - may be present with lesions of the dominant
side (transient)
• Amorphosynthesis and contralateral neglect - with
lesions of the nondominant side
• Homonymous field defect - if present, usually clears in a few
days
Thalamic Hemorrhages
• OCULAR disturbances —
• pseudo-abducens palsies with one or both eyes turned asymmetrically inward and
slightly downward
• palsies of vertical and lateral gaze
• forced deviation of the eyes downward
• inequality of pupils with absence of light reaction
• skew deviation with the eye ipsilateral to the hemorrhage assuming a higher
position than the contralateral eye
• ipsilateral ptosis and miosis (Horner syndrome)
• absence of convergence
• retraction nystagmus
• tucking in (retraction) of the upper eyelids
Pontine Hemorrhage
• Deep coma usually ensues in a few minutes, & the clinical picture
is dominated by total paralysis, decerebrate rigidity, and small,
reactive (1-mm) pupils. Lateral eye movements, evoked by head
turning or caloric testing, are impaired or absent. DEATH usually
occurs within a few hours.
• Rare exceptions - consciousness is retained; smaller lesion in the

tegmentum of the pons (disturbances of lateral ocular movements,
crossed sensory or motor disturbances, small pupils, and cranial nerve
palsies) in addition to signs of bilateral corticospinal tract involvement.
Cerebellar Hemorrhage
• repeated vomiting, occipital headache, vertigo, and inability to sit,
stand, or walk (ataxia)
• nystagmus or cerebellar ataxia of the limbs
• mild ipsilateral facial weakness & a diminished corneal reflex
• dysarthria & dysphagia
• Ocular signs:
• paresis of conjugate lateral gaze to the side of the hemorrhage, forced
deviation of the eyes to the opposite side, or an ipsilateral 6th nerve
weakness
• Cerebellar Hemorrhage
• CLINICAL FEATURES
• Occasionally, at the onset, there is a spastic paraparesis or a quadriparesis
with preservation of consciousness
• Patients with vermian clots & hydrocephalus were at the highest risk for
deterioration
• as the hours pass, patient becomes stuporous and then comatose or
suddenly apneic as a result of brainstem compression
Lobar Hemorrhages
• CAUSES:
• hypertension
• anticoagulation or thrombolytic therapy
• ruptured aneurysm
• ruptured arteriovenous malformation
• cavernous angioma
• tumoral bleed
• trauma
• amyloidosis of the cerebral vessels - in the elderly
• hematologic disorders - leukemia, aplastic anemia, etc
• illicit drug use - cocaine, methamphetamine
• Occipital Lobe:
• pain around the ipsilateral eye and a dense homonymous hemianopia
• Temporal Lobe:
• pain in or anterior to the ear, partial hemianopia, and fluent aphasia
• Frontal Lobe:
• frontal headache and contralateral hemiplegia, mainly of the arm
• Parietal Lobe:
• anterior temporal headache and hemisensory deficit contralaterally
REATMENT
• The management of patients with large ICH and coma

includes ---
• maintenance of adequate ventilation
• use of controlled hyperventilation to a PCO2 of 25 to 30 mmHg
• monitoring of ICP in some cases and its control by the use of
tissue-dehydrating agents such as mannitol (osmolality kept at 295
to 305 mosmol/L and Na at 145 to 150meq)
• limiting intravenous infusions to normal saline
REATMENT
• Virtually all patients with ICH are hypertensive immediately after the
stroke because of a generalized sympathoadrenal response
• Natural trend is for the BP to diminish over several days --- active
treatment in the acute stages has been a matter of controversy
• Rapid reduction in BP, in the hope of reducing further bleeding,
is not recommended, since it risks compromising cerebral perfusion
in cases of ICP
• Sustained MAP ≥110 mmHg may exaggerate cerebral edema & risk
extension of the clot
• use of betablocking drugs (esmolol, labetalol) or ACE- inhibitors is
recommended; CCB with adverse effects on ICP
UTCOME
• Immediate prognosis for large & medium-sized cerebral clots

is grave
• 30 - 35% of patients die in 1 - 30 days
• CT scan volume of ≤30 mL, predicted a generally favorable
outcome
• Patients with clots of ≥60 mL and an initial GCS score of 8 or
less --- mortality was 90%
UTCOME
• The location of the hematoma, not simply its size, that

determines the clinical effects
• A clot 60 mL in volume is almost uniformly fatal if situated in the
basal ganglia but may be more benign if located in the frontal or
occipital lobe
• Hydrocephalus is also an important predictor of poor

outcome
EFINITION
Cerebral Aneurysms
EFINITION
• Saccular or “berry” aneurysms take the form of small, thin-

walled blisters protruding from arteries of the circle of Willis or
its major branches
EFINITION
• Aneurysms are located at vessels bifurcations &

branchings and are generally presumed to result from
developmental defects in the media and elastica
• An alternate theory holds that the aneurysmal process is
initiated by focal destruction of the internal elastic
membrane, which is produced by hemodynamic forces at the
apices of bifurcations
• As a result of the local weakness  intima bulges outward,
covered only by adventitia  the sac gradually enlarges 
finally rupture
ATHOPHYSIOLOGY
• Saccular aneurysms vary in size from 2 mm to 2 or

3 cm in diameter (averaging 7.5mm)
• Those that rupture usually have a diameter of 10
mm or more (by angiography)
• Aneurysms vary greatly in form ----
• Some are round & connected to the parent artery
by a narrow stalk
• others are broad-based w/o a stalk
• others take the form of narrow cylinders
The site of rupture is usually at the dome of the
aneurysm, which may have 1 or more
secondary sacculations
ATHOPHYSIOLOGY
• ~90-95% of saccular aneurysms lie on the

anterior part of the circle of Willis --- most
common sites are:
• (1) the proximal portions of the anterior
communicating artery
• (2) at the origin of the posterior communicating
artery from the stem of the ICA
• (3) at the first major bifurcation of the MCA
• (4) at the bifurcation of the ICA into MCA and
ACAs
ATHOPHYSIOLOGY
• Other sites: ICA in the cavernous sinus, at the origin of the ophthalmic
artery, the junction of the posterior communicating and posterior
cerebral arteries, the bifurcation of the basilar artery, and the origins of
the three cerebellar arteries
Aneurysms that rupture in the cavernous sinus may give rise to an
arteriovenous fistula.
NCILARY AND
DIAGNOSTICS
•
Benefits of CT scan
• Detects blood locally or diffusely in the subarachnoid spaces
or within the brain or ventricular system in more than 90% of
cases and in practically all cases in which the hemorrhage has
been severe enough to cause momentary or persistent loss of
consciousness.
• Coexistent hydrocephalus also is demonstrable.
NCILARY AND
DIAGNOSTICS
•MRI
• Can also detect blood in the proton density sequence; after a day
has passed, this can also be done with the fluid attenuated inversion
recovery (FLAIR) technique
• If SAH is suspected but not apparent on imaging studies, a
lumbar puncture should be done
• Usually the CSF becomes grossly bloody within 30 min of the
hemorrhage
• Xanthochromia is found after centrifugation if several hours or
more have elapsed from the moment of the ictus
NCILARY AND
DIAGNOSTICS
•
Carotid and vertebral angiography is the only certain means
of demonstrating an aneurysm and does so in over 90% of
patients in whom the correct diagnosis of spontaneous SAH
is made on clinical grounds
Conventional angiogram,
anteroposterior view,
showing a 7-mm left
middle cerebral artery
bifurcation aneurysm
(arrow) after a left
internal carotid artery
injection
NCILARY AND
DIAGNOSTICS
• MRI with modern scanners detects most aneurysms of the basal vessels
and of their first branches but may not yet be of sufficient sensitivity to
replace conventional angiography in cases where an aneurysm is
strongly suspected but too small to be detected
by MRA
• With the development of SAH, the resulting clinical events assume 1 of

3 patterns:
• (1) the patient is stricken with an excruciating generalized headache and
vomiting and falls unconscious almost immediately
• (2) headache develops in the same manner but the patient remains
relatively lucid—the most common syndrome
• (3) rarely, consciousness is lost quickly without any preceding
complaint
• Decerebrate rigidity and brief clonic jerking of the limbs may occur at
the onset of the hemorrhage, in association with unconsciousness
• If the hemorrhage is massive, death may ensue in a matter of

minutes or hours, so that ruptured aneurysm must be considered in
the differential diagnosis of sudden death
• Persistent deep coma is accompanied by irregular respirations, attacks
of extensor rigidity, and finally respiratory arrest and circulatory collapse
• In these rapidly fatal cases, the subarachnoid blood has greatly
increased the intracranial pressure to a level that approaches
arterial pressure and caused a marked reduction in cerebral
perfusion
• Rupture - occurs while the patient is active rather than during sleep,
and in a few instances during sexual intercourse, straining at stool,
lifting heavy objects, or other sustained exertion
• momentary Valsalva maneuvers, as in coughing or sneezing, have
generally not caused aneurysmal rupture (they may cause arterial
dissection)
• In patients who survive the initial rupture, the most feared
complication is RERUPTURE, an event that may occur at any time
from minutes up to 2 or 3 weeks
• Convulsive seizures, usually brief and generalized, occur in 10-25% of
cases, in relation to acute bleeding or rebleeding
• VASOSPASM - delayed hemiplegia and other focal deficits usually appear 3

to 12 days after rupture and rarely before or after this period, due to
focal narrowing of a large artery or arteries, seen on angiography
• spasm is most frequent in arteries surrounded by the largest collections of
clotted subarachnoid blood
• vasospasm appears to be a direct effect of blood or some blood product,
possibly hematin or a platelet product, on the adventitia of the artery
• Areas of ischemic infarction in the territory of the vessel bearing the
aneurysm, without thrombosis or other changes in the vessel, is the
usual finding in such cases
• HYDROCEPHALUS - If a large amount of blood ruptures into the

ventricular system or floods the basal subarachnoid space, it may find
its way into the ventricles through the foramina of Luschka and
Magendie
• As a result, the patient then may become confused or unconscious
• The clinical signs are greatly improved by draining the ventricles, either
by external ventriculostomy or, in selected cases, by lumbar puncture
• A subacute hydrocephalus due to blockage of the CSF pathways by
blood may appear after 2 to 4 weeks.
REATMENT
• Influenced by the neurologic & general medical state of the

patient as well as by the location and morphology of the
aneurysm
• Ideally, all patients should have the aneurysmal sac
obliterated, but the mortality is high if the patient is
stuporous or comatose (poor grade)
REATMENT
• General medical management in the acute stage ---

• bed rest, fluid administration to maintain above-normal circulating blood volume and
central venous pressure, use of elastic stockings and stool softeners; administration
of BB, CCB, IV nitroprusside, to reduce greatly elevated BP and then maintain
systolic BP at 150 mmHg or less; and pain-relieving medication for headache
• Prevention of systemic venous thrombosis is critical, usually
accomplished by the use of cyclically inflated whole-leg compression
boots
• Use of anticonvulsants is controversial - generally avoided them unless
a seizure has occurred
• CCB (Nimodipine) are being used extensively to reduce the incidence of
stroke from vasospasm
REATMENT
• The most notable advances have been in the techniques for

the obliteration of aneurysms, particularly the operating
microscope and endovascular approaches, and in the
management of ciculatory volume
• Both the risk of rerupture of the aneurysm and some of the
secondary problems that arise because of the massive
amount of blood in the subarachnoid space can be obviated
by early obliteration of the aneurysm
Exam
• Neurological Examination
• NIHSS – for stroke suspects
• Somnolent, unable to
follow command
• 2/5 RUE, 3/5 RLE
• Central facial palsy right
• Expressive and receptive
aphasia
• No blink and visual threat
on the right
TOTAL= 17
• Right homonymous
hemianopsia Why the need to know the NIHSS?
• Management implications
Exam
• Cardio
• Irregularly irregular rhythm Possible arrhythmia
• no murmurs rubs or gallops

• Neck exam
• Normal
• Check for carotid bruit
Exam
• Airways Remember,
patient has
• To assess airway patient and for potential need for intubation altered
sensorium
• Breathing exam
• Assess efficacy of breathing in this acutely alerted patient
• Swallowing if impaired, NGT must be inserted to
prevent aspiration
• Circulation exam
• To check for signs of shock
• Pulmonary exam
• Make sure there is no evidence of focal lung sounds concerning for aspiration
Stabilize
• Insert IV
Permissive hypertension
• Hook to monitor: elevated BP MAP 110-130
• NSS Bolus
• IVF: NSS NO D5 containing fluids
• Check for CBG: 4.7 mmol/L – normal

• Second IV line
• Additional IV accesses in this critical in patient is important to anticipate
multiple infusions and the potential displacement of a line
Stabilize
• Ensure neuroprotection at all times
• MAP 110-130, with SBP <180 mmHg and DBP <110 mmHg
• O2 saturation: =/> 94%
• CBG: 120-180 mg/dL
• Normal temperature
Differential
• Neurologic
• Stroke: ischemic vs hemorrhagic
• How can we differentiate infract
from hemorrhage?
Investigate
The stroke must be HYPERACUTE

Ischemia = Intracerebral hemorrhage = Subarachnoid hemorrhage =
HYPODENSITY/DARK HYPERDENSITY/BRIGHT HYPERDENSITY/BRIGHT
WHY NOT MRI?
• Time bound
management
Investigate
Arrhythmia confirmed!!!
Investigate
• CBC
• Coagulation panel
Investigate
• CXR
Investigate
• Fingerstick blood sugar
• To rule out hypoglycemia: stroke mimicker
• Blood type and screen
• Make sure there is blood bank sample in case this patient needs blood
products after definitive treatment
HOWEVER, plain cranial
We don’t what CT scan does not show
time is the onset any signs of acute
since the patient infarct (hypodensities),
was found by his so we can assume that
wife lying on the the onset is very acute,
floor. probably <6 hrs
After r-TPA
Dose: 0.9mg/kg (other uses 0.6mg/kg)
Bolus: 10% of total dose
1 hour infusion: remaining 90% of total dose
There was neurologic

improvement on the
patient.
Intervene
• r-TPA
• Secondary stroke prevention
• Statins Thrombotic: antiplatelet
• Anti-platelets Depending on the etiology
• Anti-coagulation of the cerebral infarction
• Control of comorbidities embolic: anticoagulant
• DM
• Dyslipidemia
• Hypertension Depending on the etiology
of the cerebral infarction
• etc
Investigation
• 2D echo
• Carotid duplex studies
• Transcranial doppler
Communication
• Neurology
• Talk to the relative

• They may have critical information that will enable definitive treatment

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ANCILLARY AND LABORATORY

• sudden focal neurologic syndrome due to cerebrovascular disease

 one of leading causes of death and disability throughout the world

• frequently the predominant vascular disease in any given region in

blood vessel and causes

• Bleed within the

occlusion Hemorrhage Hemorrhage Ischemic Attack

• Atherosclerotic Infarction 20%

- NINDS Stroke Data Bank

Age Doubles per decade after age 55 •Hypertension*

• Reduction of cerebral blood flow below 10-12 ml/100grams brain/minute leads to

• “Ischemic penumbra” – region of marginal perfusion

• Ischemic Necrosis: CBF 6-8 ml/100 gm/minute

Posterior Circulation MCA

• From vertebral system

Doppler Ultrasound Studies

- conventional dye-injection angiography has been supplanted by

- spiral CT angiography now offer images of better resolution,

Embolism from ICA or heart to

of the cerebral hemispheres and

• affect frontal lobe: impaired judgment and insight, change

• Presence of primitive grasp and suck reflexes

• Language impairment (common finding)

• Heterogeneous syndromes and

• Lesion of small penetrating branch arteries into BG,

• Occurs in vulnerable areas supplied by distal

Close monitoring Surgery, decompressive Hemicraniectomy

• Stroke Unit admission

Most common sites:

branches off the PCA

ICH involving the cerebral

• vascular lesion that leads to arterial rupture in some cases

• Acute reactive hypertension - far exceeding the patient’s chronic

• FUNDI - show hypertensive changes in the arterioles

Headache, acute hypertension, and vomiting with a focal

Putaminal Hemorrhage with extension to Internal Capsule

• Rare exceptions - consciousness is retained; smaller lesion in the

• The management of patients with large ICH and coma

• Immediate prognosis for large & medium-sized cerebral clots

• The location of the hematoma, not simply its size, that

• Hydrocephalus is also an important predictor of poor

• Saccular or “berry” aneurysms take the form of small, thin-

• Aneurysms are located at vessels bifurcations &

• Saccular aneurysms vary in size from 2 mm to 2 or

• ~90-95% of saccular aneurysms lie on the

• With the development of SAH, the resulting clinical events assume 1 of

• If the hemorrhage is massive, death may ensue in a matter of

• VASOSPASM - delayed hemiplegia and other focal deficits usually appear 3

• HYDROCEPHALUS - If a large amount of blood ruptures into the

• Influenced by the neurologic & general medical state of the

• General medical management in the acute stage ---

• The most notable advances have been in the techniques for

• no murmurs rubs or gallops

• Check for CBG: 4.7 mmol/L – normal

The stroke must be HYPERACUTE

There was neurologic

• Talk to the relative

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