Cerebral Aneurysm

Cerebral Aneurysm
INTRODUCTION:
 Blood to the brain is supplied by four major blood
vessels that join together forming Circle of Willis at the
base of the brain, which are: 1. anterior cerebral artery.
2. Posterior cerebral artery. 3. Internal carotid artery.
4. Basilar artery.
 Artery junction points may become weak, causing
ballooning of the blood vessel wall that can form a small
sac or aneurysm.
A cerebral aneurysm is an out pouching of a
cerebral artery.
 Rupture of a cerebral aneurysm usually

results in a subarachnoid hemorrhage (SAH),
which is defined as bleeding into the
subarachnoid space.
 The most common cause of non-traumatic

subarachnoid hemorrhage.
DEFINITIONS:
 A cerebral or intracranial aneurysm is an abnormal focal
dilation of an artery in the brain that results from a
weakening of the inner muscular layer (the intima) of a blood
vessel wall.
 The vessel develops a "blister-like" dilation that can become
thin and rupture without warning.
COMMON MISDIAGNOSES OF
SUBARACHNOID HEMORRHAGE
 Headache (migraine, tension, or cluster headache)
 Trauma
 Meningitis or encephalitis
 Hypertensive crisis
 Neck problems (arthritis or cervical Sinusitis disc disease)
 Alcohol or drug intoxication
 Psychiatric diagnoses
 Transient ischemic attack/ischemic stroke

ETIOLOGY
 Although the precise etiology of cerebral

aneurysms remains unclear.
 The degenerative theory is strongly supported by

current research and describes causation to
hemodynamically induced degenerative vascular
disease.
 According to this theory, the intima, covered only by
the adventitia, bulges from a local weakness.
 By late midlife, stress causes vessel ballooning and

rupture.
 Peak incidence is between 40-60 years old. Very rare
in children. Female predominance in adults.
We do not know why aneurysms develop in a majority of
cases, however the following may play a role:
 Congenital or familial inheritance
 Atherosclerosis
 Hypertension
 Connective tissue disorders
 Sickle cell anemia
 Infections
 Trauma
 Cigarette smoking
 Illicit drug use
 Alcohol
CLASSIFICATION
 When classified by size
• Small: to 10 mm
• Medium: 10 to 15 mm
• Large: 15 to 25 mm
• Giant: 25 to 50 mm
• Super-giant: larger than 50 mm

Classification by shape and etiology:
 Berry aneurysm: most common type; berry or

saccular shaped with a neck or stem.
 Fusiform aneurysm: an out pouching of an arterial

wall, without a stem.
 Mycotic (infectious) aneurysm: rare; caused by septic

emboli from infections, such as bacterial endocarditis;
may lead to aneurysmal formation
 Charcot-Bouchard aneurysm: microscopic aneurysmal
formation associated with hypertension; involves the basal
ganglia and brainstem.
 Dissecting aneurysm: related to atherosclerosis,

inflammation, or trauma; an aneurysm in which the
intimal layer is pulled away from the medial layer and
blood is forced between the layers.
 Traumatic aneurysm: any aneurysm resulting from a

traumatic head injury (accounts for a small number).
LOCATION
 Cerebral aneurysms usually occur at the bifurcations and

branches of the large arteries at the base of the brain
(circle of Willis).
 85% to 95% in the carotid system, with the following

three most common locations:
• A-comm is the single most common: 30%
• ACA are more common in males
• P-comm: 25%
• MCA: 20%
• Artery junction points may become weak,
causing ballooning of the blood vessel wall
that can form a small sac or aneurysm.
 5% to 15% in the posterior circulation (vertebrobasilar
arteries)
• About 10% on BA: basilar bifurcation, known as basilar

tip, most common followed by basilar artery–superior
cerebellar artery (BA-SCA), basilar artery–vertebral
artery (BA-VA) junction, and AICA.
• About 5% on vertebral artery (VA) and posterior inferior

cerebellar artery (PICA) junction is the most common.
SIGNS AND SYMPTOMS
 Unruptured Aneurysms
 Dilated pupil (loss of light reflex; oculomotor nerve

[cranial nerve (CN) III] deficit).
 Extraocular movement deficits of the oculomotor (CN III),

trochlear (CN IV) or abducens (CN VI) cranial nerves.
 Possible ptosis (oculomotor nerve [CN III] deficit).

• Pain above and behind eye
• Localized headache
• Nuchal rigidity (neck pain on flexion)
• Possible photophobia
RUPTURED ANEURYSM
 The patient experiences a violent headache, often
described as “explosive” or “the worst headache
of my life.”
 Immediate loss of consciousness may occur, or
the level of consciousness may decrease.
 Vomiting is common.
OTHER SIGNS AND SYMPTOMS
INCLUDE:
 Cranial nerve deficits (especially CNs III, IV, and VI);
non–pupil-sparing CN III palsy produced by expanding
posterior communicating artery aneurysm.
 Those related to meningeal irritation.
 Those related to a stroke syndrome.
 Those related to cerebral edema and increased ICP (mass

effect).
 Those related to pituitary dysfunction secondary to

irritation or edema
HUNT-HESS CLASSIFICATION
I Asymptomatic, or mild headache and slight nuchal
rigidity
II Cranial nerve (CN) palsy (e.g.,CN III, CN VI),
moderate to severe headache, nuchal rigidity
III Mild focal deficit, lethargy, or confusion
IV Stupor, moderate to severe hemiparesis, early
decerebrate rigidity
V Deep coma, decerebrate rigidity, moribund appearance
 Modified classification adds the following:
0 Unruptured aneurysm
1a No acute meningeal/brain reaction, but with fixed
neurological deficit
DIAGNOSIS
 History and results of neurological examination
 CT scan, without contrast media
 If the CT findings are negative, lumbar puncture is used in
selective cases. Red blood cell (RBC) counts usually
exceed 100,000 per mm.
 CTA is now being used in many institutions as the first
radiographic tool.
 MRI is not sensitive within the first 24 to 48 hours.
 Cerebral angiography remains the “gold standard” for
evaluation of cerebral aneurysms.
AIM Allow the brain to
recover from initial
insult ( bleeding)
Prevent or treat
other complication Vasospas
m
MANAGEMENT
The goals of initial medical management include:
 Augmenting cerebral blood flow (CBF) by:
 Increasing cerebral perfusion pressure (CPP)

 Improving blood circulation
 Maintaining euvolemia
 Maintaining normal ICP
 Neuroprotection
 Fluid Volume Control
 Blood Pressure Control
 Drug Therapy
 The calcium channel blocker nimodipine
 Anticonvulsants may be given as prophylaxis
 Stool softeners prevent constipation and straining at stool
 Analgesics (acetaminophen or codeine/morphine)
 Sedatives
 Use of steroids is controversial
 Insulin (regular human) drip sliding scale may be ordered.

SURGICAL APPROACHES
 Wrapping—although this is usually not the goal of
surgery, situations may arise in which little else can be
done (e.g., fusiform aneurysms).
 Endovascular Technique: Coiling

STENTS
NURSING DIAGNOSIS
 Pain (headache, neck/back pain) related to (R/T)
meningeal irritation.
 Sensory/Perceptual Alterations, Visual, R/T photophobia

secondary to meningeal irritation.
 High Risk for Injury R/T seizure activity secondary to

cerebral irritation.
 Anxiety (mild, moderate, or severe) R/T illness and/or
restrictions of aneurysm precautions
 High Risk for Secondary Brain Injury R/T rebleeding or
cerebral vasospasms
NURSING DIAGNOSIS
 Ineffective Airway Clearance related to (R/T)

unconsciousness or ineffective cough reflex.
 Risk of Aspiration R/T inability to protect airway or

unconsciousness.
 Ineffective Tissue Perfusion, cerebral, R/T ischemia,

cerebral edema, or increased intracranial pressure (ICP)
NURSING RESPONSIBILITIES
INCLUDE
 Vital signs with neurological checks every hour
 O2 saturation monitoring
 Bed rest with head of bed (HOB) elevated by 30 degrees
 Low level of external stimulation; restricted visitation
 Strict intake and output (I&O) record
 Thigh-high antiembolic (TED) hose and pneumatic
compression boots
 Indwelling urinary catheter if patient is lethargic,
incontinent, or unable to void
DEFINITION
 Stroke is a heterogeneous, neurological
syndrome characterized by gradual or rapid,
non-convulsive onset of neurological deficits
that fit a known vascular territory and that last
for 24 hours or more.
CLASSIFICATION
RISK FACTORS
CEREBROVASCULAR MALFORMATIONS
 Capillary telangiectases,
 Venous malformations (VMs),
 Arteriovenous malformations (AVMs),
 Dural arteriovenous fistulas (DAVFs), and
 Cavernous malformations (CMs)
PATHOPHYSIOLOGY
For Ischemic Stroke
 A fall in cerebral blood flow to “Zero” causes death of

brain tissue within 4-10 minutes.
 Values <16-18 mL/100 g brain tissue/min causes

infarction within an hour.
 Values <20 mL/100 g brain tissue/min causes ischemia

without infarction unless prolonged for several hrs or
days.
CON…
CON…
 Focal cerebral infarction occurs via two different
pathways:
1. A necrotic pathway in which cellular cytoskeleton
breakdown is rapid, because of energy failure of the
cell.
2. An apoptotic pathway in which cells becomes

programmed to die.
PATHOPHYSIOLOGY OF ISCHEMIC
STROKE
ACUTE ISCHEMIC STROKE
MANAGEMENT
 To reverse or lessen the amount of tissue infarction and
improve clinical outcome.
Management fall within six categories:
1. Medical support
2. Intravenous thrombolysis
3. Endovascular techniques
4. Antithrombotic treatment
5. Neuroprotection
6. Stroke centers and rehabilitation

 The immediate goal is to optimize cerebral perfusion.
 Maintain blood pressure as per institutional policy

usually ()
 heart rate with beta-1 adrenergic blocker (esmolol).
 Maintain normal body temperature and fever should be

treated with antipyretics and surface cooling.
 Monitor and maintain normal serum glucose (110mg/dl).

CON…
 Start IV mannitol.
 Avoid hypovolemic state (Keep patient in euvolemic

state).
 Prevent common complications such as infection

(pneumonia, urinary tract, skin) and deep vain
thrombosis of bedridden patients.
 Craniectomy
2. INTRAVENOUS THROMBOLYSIS
 Start IV recombinant tissue plasminogen activator (rtPA):
Dose: 0.9mg/kg within 3 hours of stroke onset.
Indications:
 Clinical diagnosis of ischemic stroke
 Onset of symptoms to time of drug administration ≤3

hours
 CT scan showing no hemorrhage or edema of > 1/3 of the
middle cerebral artery.
 Age ≥18 years
 Consent by patients or close relatives (Parents or spouse

or son or daughter)
CON…
 Contraindications:
 Sustained BP>185/110 after treatment
 Platelet counts<1,00,000; Hematocrit<25%
 Serum glucose level<50 or >400 mg/dl
 Use of heparin within 48 hrs and prolonged partial

thromboplastin time (PTT) or increased international
normalized ratio (INR)
CON…
 Prior stroke or intracranial hemorrhage within 3 months.
 Major surgery within last 14 days.
 GI bleeding within last 21 days
 Recent myocardial infarction
 Coma or stupor
 Rapidly improving symptoms

 Administration of rtPA
 IV access with two peripheral IV lines (avoid arterial or

central line placement)
 Review eligibility for rtPA
 Administer 0.9 mg/kg IV (maximum 90 mg) IV as 10%

of total dose bolus, then remainder over 60 minutes.
CON…
 Frequent blood pressure monitoring
 No other antithrombotic treatment for 24hrs
 If neurological status decline or uncontrolled BP,

immediate STOP infusion, give cryoprecipitate. and get
CT scan urgently.
 Avoid urethral catheterization ≥ 2hrs

MANAGEMENT
 Thrombolytics
 Anticoagulants
 Antiplatelets
 Hypothermia
 Symptomatic
 Surgical and Endovascular Interventions

NURSING MANAGEMENT OF PATIENTS WHO HAVE
UNDERGONE CEREBRAL ANGIOGRAPHY/STENT
PLACEMENT
 • Monitor vital signs for hemodynamic instability.

 • Monitor for bleeding at catheter site; bleeding may also
be noted in urine, stool, GI tract, or mouth.
• Monitor neurological signs for evidence of
intracerebral hemorrhage and reperfusion injury.*
 • Monitor coagulation studies and maintain in
therapeutic range using international normalizing ratio
(INR) parameters.
NURSING MANAGEMENT OF PATIENTS WHO HAVE
UNDERGONE A CAROTID ENDARTERECTOMY
 • Monitor blood pressure and rigorously maintain within

set parameters.
 • Monitor for cardiac arrhythmias and evidence of

myocardial ischemia (myocardial infarction is not
uncommon).
 Monitor neurological signs frequently and observe for
early signs of deterioration.
 • Monitor for cranial nerve deficits (especially facial and

vagal) as a result of surgery.
 • Monitor for signs of intracerebral hemorrhage

(increased ICP, new onset of neurological deficits).
 • Monitor for vascular headache and seizures

(hyperperfusion syndrome).
NURSING DIAGNOSIS
 Ineffective Airway Clearance
 Risk of Aspiration
 Ineffective Tissue Perfusion, (cerebral)
 Risk of Infection
 Impaired Verbal Communication
 Impaired Physical Mobility
 High risk for deep venous thrombosis (DVT)

REHABILITATION
 COMMON MOTOR DEFICITS
 COMMON SENSORY DEFICITS
 LANGUAGE DEFICITS
 INTELLECTUAL DEFICITS
 EMOTIONAL DEFICITS
 BOWEL AND BLADDER DYSFUNCTION

Cerebral Aneurysm

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Cerebral Aneurysm

 Rupture of a cerebral aneurysm usually

 The most common cause of non-traumatic

 Neck problems (arthritis or cervical Sinusitis disc disease)

 Alcohol or drug intoxication

 Transient ischemic attack/ischemic stroke

 Although the precise etiology of cerebral

 The degenerative theory is strongly supported by

 By late midlife, stress causes vessel ballooning and

 Connective tissue disorders

 Sickle cell anemia

 Illicit drug use

• Super-giant: larger than 50 mm

 Berry aneurysm: most common type; berry or

 Fusiform aneurysm: an out pouching of an arterial

 Mycotic (infectious) aneurysm: rare; caused by septic

 Dissecting aneurysm: related to atherosclerosis,

 Traumatic aneurysm: any aneurysm resulting from a

 Cerebral aneurysms usually occur at the bifurcations and

 85% to 95% in the carotid system, with the following

• A-comm is the single most common: 30%

• ACA are more common in males

• About 10% on BA: basilar bifurcation, known as basilar

• About 5% on vertebral artery (VA) and posterior inferior

 Dilated pupil (loss of light reflex; oculomotor nerve

 Extraocular movement deficits of the oculomotor (CN III),

 Possible ptosis (oculomotor nerve [CN III] deficit).

• Nuchal rigidity (neck pain on flexion)

 Those related to meningeal irritation.

 Those related to a stroke syndrome.

 Those related to cerebral edema and increased ICP (mass

 Those related to pituitary dysfunction secondary to

 Increasing cerebral perfusion pressure (CPP)

 The calcium channel blocker nimodipine

 Anticonvulsants may be given as prophylaxis

 Stool softeners prevent constipation and straining at stool

 Analgesics (acetaminophen or codeine/morphine)

 Use of steroids is controversial

 Insulin (regular human) drip sliding scale may be ordered.

 Endovascular Technique: Coiling

 Sensory/Perceptual Alterations, Visual, R/T photophobia

 High Risk for Injury R/T seizure activity secondary to

 Ineffective Airway Clearance related to (R/T)

 Risk of Aspiration R/T inability to protect airway or

 Ineffective Tissue Perfusion, cerebral, R/T ischemia,

 A fall in cerebral blood flow to “Zero” causes death of

 Values <16-18 mL/100 g brain tissue/min causes

 Values <20 mL/100 g brain tissue/min causes ischemia

2. An apoptotic pathway in which cells becomes

Management fall within six categories:

6. Stroke centers and rehabilitation

 Maintain blood pressure as per institutional policy

 heart rate with beta-1 adrenergic blocker (esmolol).

 Maintain normal body temperature and fever should be

 Monitor and maintain normal serum glucose (110mg/dl).

 Avoid hypovolemic state (Keep patient in euvolemic

 Prevent common complications such as infection

Dose: 0.9mg/kg within 3 hours of stroke onset.

 Onset of symptoms to time of drug administration ≤3