CEREBRAL ANEURYSM The word aneurysm comes from the Latin word aneurysma, which means dilatation.

Aneurysm is an abnormal local dilatation in the wall of a blood vessel, usually an artery, due to a defect, disease, or injury. Aneurysms can be true or false. A false aneurysm is a cavity lined by blood clot. The 3 major types of true intracranial aneurysms are saccular, fusiform, and dissecting. Aneurysms typically become symptomatic in people aged 40-60 years. Aneurysms commonly arise at the bifurcations of major arteries. Most saccular aneurysms arise on the circle of Willis or the middle cerebral artery (MCA) bifurcation. CAUSES y Atherosclerosis: On aging, a sticky substance called plaque builds up along the inside walls of the arteries and over a period of time excess plaque causes the aorta to harden and narrow the inside of arteries, thus weakening and damaging the arterial walls. This damaged portion of artery can stretch or balloon due to blood pressure inside the artery leading to an aneurysm. Hypertension (high blood pressure) Deep wounds, injuries or infections to blood vessels. High cholesterol content in the blood. Inherited disease such as Marfan syndrome (Marfan syndrome affects the bodys connective tissue causing the people to have long bones and flexible joints). Infections such as untreated Syphilis (a sexually transmitted disease), Vasculitis (inflammation of blood vessels) and Tuberculosis can cause aneurysms. severe traumatic fall or car accident can cause a thoracic aortic aneurysm.

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Risk Factors y y y y y Smoking: A smoker is eight times more at risk as compared to a non-smoker. Overweight or obesity A person with a family history of aortic aneurysm or other arterial disease is at risk of developing aneurysm. Severe and persistent hypertension in people in the age group of 35 to 60 years Usage of stimulant drugs such as cocaine.

SIGNS AND SYMPTOMS: y y y y y y y y y No early symptoms (some aneurysms cause no problems till they rupture) Sudden headache Nausea and Vomiting Vision impairment Loss of Consciousness, Nuchal rigidity, stiff back and legs Seizures, Dysphagia, Pupillary changes

CLASSIFICATION OF INTRACRANIAL ANEURYSM

Saccular aneurysms Fusiform aneurysms Dissecting aneurysms

Saccular Aneurysms (Developmental/Degenerative Aneurysms) - are rounded berrylike outpouchings that arise from arterial bifurcation points, most commonly in the circle of Willis. These are true aneurysms, ie, they are dilatations of a vascular lumen caused by weakness of all vessel wall layers. - The aneurysmal sac itself is usually composed of only intima and adventitia. The intima is typically normal, although subintimal cellular proliferation is common. The internal elastic membrane is reduced or absent, and the media ends at the junction of the aneurysm neck with the parent vessel. Lymphocytes and phagocytes may infiltrate the adventitia. The lumen of the aneurysmal sac often contains thrombotic debris. Atherosclerotic changes in the parent vessel are also common.

Etiology  Congenital (arising from focal defects in the media and gradually developing over a period of years as arterial pressure first weakens and subsequently balloons out the vessel wall.) Hemodynamically induced degenerative vascular injury (occurrence, growth, thrombosis, and even rupture of intracranial saccular aneurysms can be explained by abnormal hemodynamic shear stresses on the walls of large cerebral arteries, particularly at bifurcation points.)

Clinical Manifestations:
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Subarachnoid hemorrhage (most common) Vasospasm (leading cause of disability and death from aneurysm rupture)

Fusiform Aneurysms (Atherosclerotic Aneurysm) These lesions are exaggerated arterial ectasias that occur because of a severe and unusual form of atherosclerosis. Damage to the media results in arterial stretching and elongation that may extend over a considerable length. These ectatic vessels may have more focal areas of fusiform or even saccular enlargement. Intraluminal clots are common, and perforating branches often arise from the entire length of the involved parent vessel. Clinical presentation Fusiform aneurysms usually occur in older patients. The vertebrobasilar system is commonly affected. Fusiform aneurysms may thrombose, producing brainstem infarction as small ostia of perforating vessels that emanate from the aneurysm become occluded. They can also compress the adjacent brain or cause cranial nerve palsies.

Dissecting Aneurysms In arterial dissections, blood accumulates within the vessel wall through a tear in the intima and internal elastic lamina. The consequences of this intramural hemorrhage vary. If blood dissects subintimally, it causes luminal narrowing or even occlusion. If the intramural hematoma extends into the subadventitial plane, a saclike outpouching may be formed. Do not confuse these focal aneurysmal dilatations with the pseudoaneurysms that result from arterial rupture and subsequent encapsulation of the perivascular hematoma. Uncomplicated dissections do not project beyond the lumen of the parent vessel, and dissections with saclike outpouchings are termed dissecting aneurysms. The term false saccular aneurysm, or pseudoaneurysm, should be used for encapsulated, cavitated, paravascular hematomas that communicate with the arterial lumen. Etiology Dissecting aneurysms may arise spontaneously. More commonly, trauma or an underlying vasculopathy such as FMD is implicated. Location Most dissecting aneurysms that involve the craniocerebral vessels affect the extracranial segments; intracranial dissections are rare and usually occur only with severe head trauma. Although the common carotid artery (CCA) can be involved by cephalad extension of an aortic arch dissection, the CCA and carotid bulb are usually spared. The ICA is commonly affected. Most dissections involve the midcervical ICA segment and terminate at the extracranial opening of the petrous carotid canal. The VA is also a common site of arterial dissection. The common location is between the VA exit from C2 and the skull base. Involvement of the first segment, which extends from the VA origin to its entry into the foramen transversarium (usually at the C6 level), is relatively rare.

DIAGNOSTIC EXAMINATIONS: Catheter-Based Angiography Catheter-based angiography or digital subtraction angiography (DSA) continues to be the criterion standard for revealing and delineating the features of an intracranial aneurysm Computed Tomography Scan Aneurysms that are large enough (usually at least 10 mm) or that contain calcium may be visualized on a noncontrast CT scan and should be sought on any CT scan as a hint to the diagnosis in a patient with an atraumatic SAH Patent aneurysms On noncontrast CT scan, the typical nonthrombosed aneurysm appears as a welldelineated isodensetoslightly hyperdense mass located somewhat eccentrically in the suprasellar subarachnoid space or sylvian fissure. Patent aneurysms enhance intensely and quite uniformly following administration of intravenous contrast material.

Computed Tomographic Angiography Angiographiclike images of the cerebral vasculature can be obtained using rapid contrast infusion and thin-section dynamic CT scanning (CTA). Various 3-dimensional display techniques, including shaded surface display, volume rendering, and maximal intensity projection, are used to complement the conventional transaxial images. Such studies provide multiple projections of anatomically complex vascular lesions and delineate their relationships to adjacent structures Magnetic Resonance Imaging Aneurysm appearance on MRI is highly variable and may be quite complex. The signal depends on the presence, direction, and rate of flow. Magnetic Resonance Angiography The macroscopic motion of the moving spins in flowing blood, together with background suppression of stationary tissue, can be used to create images of the cerebral vasculature. MANAGEMENT: Surgical clipping Goal- to place a clip across the neck of the aneurysm to exclude the aneurysm from the circulation When the aneurysm cannot be clipped because of the nature of the aneurysm or poor medical condition of the patient, the following alternatives may be considered:
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Wrapping: Although this should never be the goal of surgery, situations may arise in which little else is possible (eg, fusiform basilar trunk aneurysms). Plastic resins may be slightly better than muscle or gauze for this purpose. Wrapping can be performed with cotton or muslin, with muscle, or with plastic or other polymer. Some studies demonstrate benefit with plastic or other polymer, but others show no difference from natural course. In one study with long-term follow-up, the protection from rebleeding during the first month was unchanged, but, thereafter, the risk was slightly lower than for the natural history. Trapping: Effective treatment requires both distal and proximal arterial interruption with direct surgery (ligation or occlusion with a clip). Treatment may also incorporate extracranial-intracranial (EC-IC) bypass to maintain flow distal to the trapped segment. Proximal (hunterian) ligation: Proximal ligation has been used with some success for giant aneurysms, particularly of the vertebrobasilar circulation. Advanced endovascular techniques, however, now offer better alternatives for such lesions.

After performing a craniotomy, use microsurgical techniques with the operative microscope to dissect the aneurysm neck free from the feeding vessels without rupturing the aneurysm. Final treatment involves the placement of a surgical aneurysm clip around the neck of the aneurysm, thereby obliterating the flow into the aneurysm. The goal at surgery is to obliterate the aneurysm from the normal circulation without compromising any of the adjacent vessels or small perforating branches of these vessels. The clips are manufactured in various types, shapes, sizes, and lengths and are currently manufactured to be MRI compatible. POST OP CARE
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Angiogram is necessary after surgery to confirm good clip placement with total obliteration of the aneurysm and patency of the surrounding vessels.

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Patient remains at significant risk for vasospasm, hydrocephalus, and medical complications (including hyponatremia, venous thromboembolism, infections, cardiac stun) and remains in an intensive care setting for at least 7-10 days. Vasospasm is diagnosed as deterioration in mental status or focal neurologic deficits, most commonly hemiparesis or dysphasia. TCD is frequently used as a noninvasive diagnostic tool and is sensitive to changes in the vessel caliber of the larger vessels of the circle of Willis. A trained technician should perform TCDs daily or every other day during the vasospasm period (day #3-12 postSAH, with some flexibility based on the extent of the hemorrhage). If the patient's condition deteriorates excluding all other causes of neurologic deterioration is important. If in doubt, cerebral angiography is indicated to confirm the diagnosis. Triple "H" therapy (hypertension, hemodilution, and hypervolemia) remains the most important aspect of the medical management of vasospasm, but, in refractory cases in which medical management fails, use endovascular methods. Transluminal balloon angioplasty is the primary method of choice, but intra-arterial papaverine may be used for vasospasm in the distal vasculature, where balloons may not be able to access. Intra-arterial papaverine may be used to temporarily open vessels to permit passage of a balloon, which can then be used to treat the vasospasm.

Endovascular Surgery - This procedure was soon followed by direct obliteration of the aneurysmal lumen, first by detachable balloons and later by microcoils. These coils are soft and can be detached from the stainless steel guide by passing a very small direct current that causes electrolysis at the solder junction. Separation usually occurs within 2-10 minutes after satisfactory coil placement. The Hydrocoil -A newer biologically active coil associated with a small incidence of aseptic meningitis and hydrocephalus. -Neuroform stent which has made endovascular therapy of many aneurysms, requires the use of clopidogrel bisulfate (Plavix) for 6-12 weeks postprocedure and associated with an instent stenosis rate of 5.8% in short term follow-up. Guglielmi detachable coils (GDC) y y Induce thrombosis at the site of deployment via electrothrombosis. Enhance permanency of the thrombus within the coiled aneurysm by permitting a denser packing or engendering a tissue response at the neck of the aneurysm that decreases blood flow into the aneurysm and subsequent recanalization.

Embolization procedure y A guide catheter is placed in the cervical internal carotid or VA.

Microcatheters y y Contains 2 radiopaque markers is advanced into the aneurysm cavity Coils of decreasing sizes are delivered into the aneurysm cavity and electrolytically detached (although some newer generation coils involve detachment strategies that do not involve electrolysis). Angiograms are obtained before each coil is detached to ensure preservation of the parent vessel. This process is continued until maximal angiographic obliteration of the aneurysm cavity is achieved.

Nursing Interventions: Cerebral Aneurysm y y y y y y y y y y y y y y y y Establish and maintain a patent airway as needed. Administer supplemental oxygen as ordered. Position the patient to promote pulmonary drainage and prevent upper airway obstruction. Avoid placing the patient in the prone position as well as hyperextending his neck. Suction secretions from the airway as necessary to prevent hypoxia and vasodilation from carbon dioxide accumulation. Monitor pulse oximetry levels and arterial blood gas level as ordered. Use these levels as a guide to determine appropriate needs for supplemental oxygen. Prepare the patient for emergency craniotomy, if indicated. If surgery cant be performed immediately, institute aneurysm precautions to minimize the risk of rebleeding and to avoid increasing the patients intracranial pressure. Administer hydralazine or another antihypertensive agent as ordered. Turn the patient often. Encourage deep breathing and leg movement. Apply elastic stockings or compression boots to the patients legs to reduce the risk of deep vein thrombosis. Give fluids as ordered and monitor I.V. infusions to avoid overhydration, which may increase ICP. If the patient has facial weakness, assist him during meals; assess his gag reflex and place the food in the unaffected side of his mouth. Implement a bowel elimination program based on previous habits. Raise the beds side rails to protect the patient from injury. Provide emotional support to the patient and his family.