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Cerebral aneurysms

A cerebral aneurysm (also called an intracranial


aneurysm or brain aneurysm) is a bulging, weakened
area in the wall of an artery in the brain, resulting in
an abnormal widening, ballooning, or bleb. Because
there is a weakened spot in the aneurysm wall, there
is a risk for rupture (bursting) of the aneurysm
INCIDENCE

Intracranial aneurysm accounts for half of the cases


of hemorrhagic strokes.
The mortality rate has been reported as high
as 48% at 30 days after an intracranial hemorrhage.
Hemorrhagic strokes account for 15% to 20% of
cerebrovascular disorders and ate primarily caused
by intracranial hemorrhage.
Primary intracerebral hemorrhage from a
spontaneous rupture of small vessels accounts for
approximately 80% of hemorrhagic strokes.
Almost 5,00,000 people die every year due to brain
aneurysms. every year i.e., approximately 0.07% of
the total population .
Brain aneurysms can develop in anyone at any age
but Peak incidence is between 40-60 years old.
Very rare in children.
Women tend to be affected more commonly than
men
Etiology

Congenital theory : A congenital / developmental


defect exists in the medial and adventitial layers of
artey or in the circle of willis.

Degenerative theory : The intima of blood vessel


covered only by the adventia, bulges from a local
weakness. During later midlife, hemodynamic stress
causes ballooning and rupture.
Classification
Based on shape

1. The most common type of cerebral aneurysm is


called a saccular, or berry, aneurysm,
occurring in 90 percent of cerebral aneurysms. This
type of aneurysm looks like a "berry" with a narrow
stem. More than one aneurysm may be present.
2 A fusiform aneurysm bulges out on all sides
(circumferentially), forming a dilated artery.
Fusiform aneurysms are often associated with
atherosclerosis.
3 A dissecting aneurysm results from a tear along
the length of the artery in the inner layer of the
artery wall, causing blood to leak in between the
layers of the wall. This may cause a ballooning out on
one side of the artery wall, or it may block off or
obstruct blood flow through the artery. Dissecting
aneurysms usually occur from traumatic injury, but
they can also happen spontaneously. The shape and
location of the aneurysm may determine which
treatment is recommended.
Mycotic aneurysm. A mycotic aneurysm occurs
as the result of an infection that can sometimes affect
the arteries in the brain. The infection weakens the
artery wall, causing a bulging aneurysm to form.
Traumatic aneurysm resulting from traumatic
head injury
Charcot-Bouchard aneurysm – Microscopic
aneurismal formation associated with hypertension,
involves basal ganglia and brain stem.
Based on Size

Aneurysms are also classified by size: small, large, and


giant.

Small aneurysms are less than 15 millimeters in


diameter (about the size of a large pencil eraser).
Large aneurysms are 15 to 25 millimeters in diameter
Giant aneurysms are 25 to 50 millimeters in diameter
Supergaint aneurysms are larger than 50mm in
diameter
Inherited risk factors

Alpha-glucosidase deficiency.
 Alpha 1-antitrypsin deficiency. A hereditary disease
that may lead to hepatitis and cirrhosis of the liver or
emphysema of the lungs
Arteriovenous malformation (AVM). An abnormal
connection between an artery and a vein.
Coarctation of the aorta. A narrowing of the aorta,
which is the main artery coming from the heart.
Family history of aneurysms
Female gender
Acquired risk factors

Advancing age
Alcohol consumption
Atherosclerosis. A buildup of plaque (made up of deposits
of fatty substances, cholesterol, cellular waste products,
calcium, and fibrin) in the inner lining of an artery
Cigarette smoking
Use of illicit drugs, such as cocaine or amphetamine
Hypertension
Trauma to the head
Infection
Pathophysiology

Rupture of aneurysm

Blood under high pressure is forced into subarachnoid space

Fibrin, platelets and fluid seal off the site of bleeding

Resulting clot occlude the area or interfere with CSF absorption

Released blood irritates the brain tissue

Results in inflammatory response


Cerebral edema
Symptoms of a cerebral aneurysm

The presence of a cerebral aneurysm may not be


known until the time of rupture. However,
occasionally there may be symptoms that occur prior
to an actual rupture due to a small amount of blood
that may leak, called "sentinel hemorrhage" into the
brain. Some aneurysms are symptomatic because
they press on adjacent structures, such as nerves to
the eye. They can cause visual loss or diminished eye
movements, even if the aneurysm has not ruptured.
Unruptured aneurysm

An unruptured brain aneurysm may produce no symptoms,


particularly if it's small. However, a larger unruptured
aneurysm may press on brain tissues and nerves, possibly
causing:

 Pain above and behind one eye


 Oculomotor nerve palsy – Dilated pupil, possible ptosis,
extraocular movement deficits with possible diplopia
 Localized headache
 Extraocular movement deficits of trochlear and abducens nerve
 Numbness of one side of the face
 Small, intermittent blood leakage cause generalized headache,
neck pain, upper back pain, nausea and vomiting.
Ruptured aneurysm

A sudden, severe headache is the key symptom of a ruptured aneurysm. This


headache is often described as the "worst headache" ever experienced.

 Common signs and symptoms of a ruptured aneurysm include:


 Sudden, extremely severe headache
 Nausea and vomiting
 Stiff neck
 Blurred or double vision
 Sensitivity to light
 Seizure
 A drooping eyelid
 Loss of consciousness
 Confusion
'Leaking' aneurysm

In some cases, an aneurysm may leak a slight amount


of blood. This leaking (sentinel bleed) may cause
only a:

Sudden, extremely severe headache


A more severe rupture often follows leaking.
CLINICAL GRADES OF CEREBRAL
ANEURYSMS
- HUNT AND HESS CLASSIFICATION
The Hunt and Hess scale describes the severity of
subarachnoid haemorrhage resulting from the rupture of
an intracerebral aneurysm and is used as a predictor of
survival.
 Grade 1 - Asymptomatic or minimal headache and slight neck
stiffness, 70% survival
 Grade 2 - Moderate to severe headache; neck stiffness; no
neurologic deficit except cranial nerve palsy, 60% survival
 Grade 3- Drowsy; minimal neurologic deficit, 50% survival
 Grade 4 - Stuporous; moderate to severe hemiparesis; possibly
early decerebrate rigidity and vegetative disturbances, 20%
survival
 Grade 5 - Deep coma; decerebrate rigidity; 10% survival
Diagnosis

In addition to a complete medical history and physical examination,


diagnostic procedures for a cerebral aneurysm may include:

 Digital subtraction angiography (DSA). This provides an image of


the blood vessels in the brain to detect a problem with vessels and
blood flow.
 Computed tomography scan
 Magnetic resonance imaging
 Magnetic resonance angiography
 Blood studies : WBC, hematocrit, fibrinogen, platelets, bleeding
time
Electrolytes, Blood gas analysis
Treatment for cerebral aneurysm

Many factors are considered when making treatment decisions


for a cerebral aneurysm.

The size and location of the aneurysm,


The presence or absence of symptoms,
The patient's age and medical condition
The presence or absence of other risk factors for aneurysm
rupture are considered.

In some cases, the aneurysm may not be treated and the patient
will be closely followed by a doctor. In other cases, surgical
treatment may be indicated.
There are two primary surgical treatments for a cerebral
aneurysm:

Open craniotomy (surgical clipping).

This procedure involves the surgical removal of part


of the skull. The doctor exposes the aneurysm and
places a metal clip across the neck of the aneurysm
to prevent blood flow into the aneurysm sac. Once
the clipping is completed, the skull is secured back
together.
Endovascular coiling or coil embolization. -

Endovascular coiling is a minimally invasive technique, a


catheter is advanced from a blood vessel in the groin up into
the blood vessels in the brain. Fluoroscopy will be used to
assist in advancing the catheter into the head and into the
aneurysm.
Once the catheter is in place, very tiny platinum coils are
advanced through the catheter into the aneurysm. These tiny,
soft, platinum coils, which are visible on X-ray, conform to the
shape of the aneurysm. The coiled aneurysm becomes clotted
off (embolization), preventing rupture. This procedure is
performed either under general or local anesthesia
Endovascular Balloon therapy –
Usually poor surgical candidates are selected, mainly
patients with aneurysms that are anatomically
unclippable (having no neck, or thick or sclerotic
neck or a gaint aneurysm), or that are located in
inaccessible areas such as the cavernous sinus or
posterior circulation.
2 types
Balloon occlusion of aneurysm
Balloon occlusion of parent vessel
Other treatments

Other treatments for a ruptured cerebral aneurysm aim to control symptoms and
reduce complications. These treatments include:

 Complete bed rest


 Initiate aneurysm precautions
 Apply elastic stockings or sequential compression boots
 Maintain normal fluid volume
 Control of B.P
 Drug therapy – Anticonvulsants, Stool softners, Steroids, Analgesics
 Fluid volume control : Dehydration can increase the hemoconcentration which
can increase the incidence of cerebral vasospasm
 B.P control medications : Anticonvulsants, stool softners, steroids, analgesics,
sedatives.
 Monitor for complications : Re-bleeding, cerebral vasospasm,
hydrocephalous
 Antiseizure drugs (anticonvulsants). These drugs may be used to
prevent seizures related to a ruptured aneurysm. (Phenytoin)

 Calcium channel-blocking drugs. Risk of stroke by vasospasm can be


reduced with calcium channel-blocking drugs. (Nimodipine,Verapamil
(Isoptin)

 Osmotic diuretic (Mannitol 20%)


 Antihypertensives (Nitropruside)

 If surgery is delayed or contraindicated (antifibrinolytic agents)


 Analgesics (acetaminophen)
 Laxatives to prevent straining to avoid BP
 In addition to elastic stocking to prevent DVT
Aneurysm Precautions

Assessment Upon admission of the patient to the


intensive care unit Hourly neurologic exam checks
(including a complete neurologic exam, Glasgow
Coma Scale, and hemodynamic monitoring)
Airway and oxygenation Intubation and mechanical
ventilation may be indicated for patients with
decreased mental status, compromised airways, or
acute lung injuries from subarachnoid hemorrhage
 Hourly monitoring of breath sounds and frequent
deep breathing should be encouraged.
Coughing is discouraged in the SAH patient before
aneurysm securement because of the increased risk of
aneurysm rupture with the increased ICP and BP that
occurs during coughing.
BP management - BP control is achieved before aneurysm
securement
Intracranial pressure monitoring
Laboratory data - basic metabolic chemistry and
electrolytes, cardiac troponin, creatine phosphokinase
(CPK), coagulation studies , complete blood count , type
and screen, urine toxicology and chemistry,Arterial blood
gases ,12-lead electrocardiogram and a chest X ray.
 9 . Intravenous fluids
 10. Activity is limited in patients with an unsecured aneurysm.
All activities that increase BP (and, therefore, ICP) are limited
to prevent rebleed. The patient should be maintained in a quiet
environment with limited visitors until after aneurysm
securement
 11. Deep vein thrombosis prophylaxis Because of limited
mobility, patients with an unsecured aneurysm are at risk for
deep vein thrombosis (DVT). In these patients, thigh-high
stockings and pneumatic (sequential) compression devices
should be implemented as soon as possible
 12. Anticoagulants (e.g., heparin) should be avoided until after
aneurysm securement
 Medications
a. Seizure prophylaxis The administration of prophylactic
anticonvulsants
b. Stool softeners Stool softeners are initiated.. For patients able to take
oral nutrition, a high-fiber diet is instituted.
c. Pain management- Headache pain is usually intense after a SAH.
Analgesics are administered as needed for pain.
d.Antiemetics Vomiting increases ICP and can cause aneurysmal
rebleed.
f. Gastrointestinal hemorrhage prophylaxis - Histamine-receptor
antagonists or proton pump inhibitors are instituted to prevent ulcer
formation and gastrointestinal hemorrhage.
g. Psychosocial Alleviate anxiety by explaining procedures and ICU
routine to patients and families.
Rehabilitative therapy.

Individuals who have suffered a subarachnoid


hemorrhage often need physical, speech, and
occupational therapy to regain lost function and
learn to cope with any permanent disability
Complications that can develop after the
rupture of an aneurysm include :
Aneurysm re-bleeding
Highest incidence occurs in the first 2 weeks after initial
hemorrhage.

Clinical features - Sudden severe headache, severe nausea and


vomiting, decreased LOC, new neurological deficits.

Treatment - Systolic B.P is maintained at 150mm Hg or below


Antifibrinolytics are used – Amicar, Tranexamic acid

Early surgery – clipping of aneurysm


Vasospasm.
Narrowing of the cerebral blood vessel leading to
decreased cerebral perfusion and ischemia. Usually
develops 4-14 days after initial hemorrhage.
Clinical features -
Gradual neurological deterioration, paresis paralysis
of one side, cranial nerve deficit, aphasia.
Treatment - Increase the cerebral perfusion pressure
Administer crystalloids and colloids
 Communicating hydrocephalous
Problem with reabsorption of CSF

 Acute – occurs within first 24 hrs after hemorrhage characterized


by onset of stupor. Treated by immediate venticulostomy.

 Subacute – occurs within first few days to 7 days after hemorrhage


characterized by drowsiness. Treated by venticulostomy.

 Delayed – Occurs 10 or more days after hemorrhage associated


with blood in CSF. Treated using ventriculoperitoneal shunt.
Hyponatremia.
A drop in blood-sodium levels (hyponatremia) can
lead to swelling of brain cells and permanent damage
Nursing Management
 All patients should be monitored in the intensive care unit after an
intracerebral aneurysm.
Nursing Assessment
 A complete neurologic assessment is performed initially and
includes evaluation for the following:
 Altered level of consciousness.
 Sluggish pupillary reaction.
 Motor and sensory dysfunction.
 Cranial nerve deficits (extraocular eye movements, facial droop,
presence of ptosis).
 Speech difficulties and visual disturbance.
 Headache and nuchal rigidity or other neurologic deficits.
Nursing Diagnosis
Based on the assessment data, the patient’s major nursing diagnoses
may include the following:

 Ineffective cerebral tissue perfusion related to bleeding or vasospasm.


 Pain related to meningeal irritation
 Sensory perceptual alteration, visual related to photophobia secondary
to meningeal irritation
 Anxiety related to illness and/or medically imposed restrictions
(aneurysm precautions).
 High risk for injury related to seizure activity secondary to cerebral
irritation
 High risk for neurological deterioration related to re-bleeding or
vasospasm.
The goals for the patient may include:

Improve cerebral tissue perfusion.


Relief of sensory and perceptual deprivation.
Relief of anxiety.
Absence of complications
Nursing Interventions
All patients should be monitored in the intensive care unit after an intracerebral
hemorrhage.

Improving Cerebral Tissue Perfusion

 Monitor closely for neurologic deterioration, and maintain a neurologic flow record.
 Check blood pressure, pulse, level of consciousness, pupillary responses, and motor function
hourly; monitor respiratory status and report changes immediately.
 Implement aneurysm precautions (immediate and absolute bed rest in a quiet, non stressful
setting; restrict visitors, except for family).
 Elevate the head of bed 15 to 30 degrees or as ordered.
 Avoid any activity that suddenly increases blood pressure or obstructs venous return (eg,
Valsalva maneuver, straining), instruct patient to exhale during voiding or defecation to
decrease strain, eliminate caffeine, administer all personal care, and minimize
external stimuli.
 Apply antiembolism stockings or sequential compression devices. Observe legs for signs and
symptoms of deep vein thrombosis tenderness, redness, swelling, warmth, and edema.
Relieving Sensory Deprivation
 Keep sensory stimulation to a minimum.
Explain restrictions to help reduce patient’s sense
of isolation.
Relieving Anxiety
Inform patient of plan of care.
Provide support and appropriate reassurance to
patient and family
Monitoring and Managing Potential Complications

 Assess for and immediately report signs of possible vasospasm, which may occur
several days after surgery or on the initiation of treatment (intensified
headaches, decreased level of responsiveness, or evidence of aphasia or partial
paralysis). Also administer calcium channel blockers or fluid volume expanders
as prescribed.
 Maintain seizure precautions. Also maintain airway and prevent injury if
a seizure occurs. Administer antiseizure medications as prescribed
(phenytoin [Dilantin] is medication of choice).
 Monitor for onset of symptoms of hydrocephalus. Report symptoms
immediately: acute hydrocephalus is characterized by sudden stupor or coma;
subacute or delayed is characterized by gradual onset of drowsiness,
behavioral changes, and ataxic gait.
 Monitor for and report symptoms of aneurysm rebleeding. Rebleeding occurs
most often in the first 2 weeks.
Symptoms include sudden severe headache, nausea,
vomiting, decreased level of consciousness, and neurologic
deficit.
Administer medications as ordered.

Hyponatremia: monitor laboratory data often


because hyponatremia (serum sodium level under 135
mEq/L) affects up to 30% of patients. Report low levels
persisting for 24 hours, as syndrome of
inappropriate antidiuretic hormone (SIADH) or cerebral
salt wasting syndrome (kidneys cannot conserve sodium)
ay develop.

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