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Causes and symptoms
The most common site for an arterial aneurysm is the abdominal aorta. A true aneurysm results from formation of a sac by the arterial wall with at least one unbroken layer. It is most often associated with atherosclerosis. A false aneurysm usually is caused by trauma. In this case, the wall of the blood vessel is ruptured and blood escapes into surrounding tissues and forms a clot. Because of pressure within the clot arising from the heart's contractions, the clot often pulsates against the examiner's hand as does a true aneurysm.
Although atherosclerosis is responsible for most arterial aneurysms, any injury to the middle or muscular layer of the arterial wall (tunica media) can predispose the vessel to stretching of the inner and outer layers of the artery and the formation of a sac. Other diseases that can lead to an aneurysm include syphilis, cystic medionecrosis, certain nonspecific inflammations, and congenital defects in the artery.
It is possible for a person to be unaware of a small aneurysm for years. About 80 per cent of all abdominal aneurysms are palpable and may be noticed on a routine physical examination. One should be particularly alert to the possibility of an aneurysm in persons with a history of cardiovascular disease, hypertension, or peripheral vascular disease.
Aneurysms tend to increase in size, presenting a problem of increasing pressure against adjacent tissues and organs and a danger of rupture. When an aneurysm ruptures, a critical situation ensues. The patient with a ruptured aortic aneurysm exhibits severe pain and blood loss, leading to shock. A ruptured cerebral aneurysm produces neurologic symptoms and can resemble the clinical picture of stroke syndrome.
Treatment of aneurysm depends on the vessel involved, size of the aneurysm, and general health status of the patient.
cerebral aneurysmA dilated and weak segment of a cerebral artery, often located in the circle of Willis at the base of the brain, which is susceptible to rupture; cerebral aneurysms may be birth defects or follow poorly controlled hypertension.
“Thunderclap headache” often associated with nausea, vomiting and reduced consciousness.
cerebral aneurysmBrain aneurysm Neurology A dilated and weakened, rupture-prone segment of a cerebral artery, which may be a birth defect or develop 2º to poorly controlled HTN; ±5% of general population has an aneurysm; rupture occurs in 4/105/yr Clinical-rupture Severe 'thunderclap' headache, weakness, numbness, N&V, neurologic defects, ↓ consciousness. See Aneurysm.
cer·e·bral an·eur·ysm(sĕr-ēbrăl anyūr-izm)
|Mean LOS:||3.6 days|
|Description:||SURGICAL: Craniotomy and Endovascular Intracranial Procedures Without CC or Major CC|
|Mean LOS:||6.8 days|
|Description:||MEDICAL: Nonspecific Cerebrovascular Disorders With Major CC|
Cerebral aneurysm is an outpouching of the wall of a cerebral artery that results from weakening of the wall of the vessel. It is difficult to determine the frequency of cerebral aneurysms because of differences in the definitions of the size of aneurysm and the ways that aneurysms are detected. The prevalence is estimated to range from 5% to 10%; unruptured aneurysms account for approximately 50% of all aneurysms.
Cerebral aneurysms have a variety of sizes, shapes, and causes (Table 1). Most cerebral aneurysms are sacular or berrylike with a stem and a neck. The incidence of cerebral aneurysm has been estimated at 12 cases per 100,000 individuals, with approximately 15% to 25% of patients having multiple aneurysms, often bilaterally in the same location on both sides of the head. Clinical concern arises if an aneurysm ruptures or becomes large enough to exert pressure on surrounding structures. When the vessel wall becomes so thin that it can no longer withstand the surrounding arterial pressure, the cerebral aneurysm ruptures, causing direct hemorrhaging of arterial blood into the subarachnoid space (subarachnoid hemorrhage).
|Size||Small, < 15 mm|
|Large, 15–25 mm|
|Giant, 25–50 mm|
|Supergiant, 50 mm|
|Shape||Berry: Most common (95%); berry-shaped aneurysm with a neck or stem|
|Sacular: Any aneurysm with a sacular outpouching|
|Fusiform: Outpouching of an arterial wall but with no stem|
|Etiology||Traumatic: Aneurysm that results from traumatic head injury|
|Charcot-Bouchard: Microscopic aneurysmal formation associated with hypertension; involves the basal ganglia and brainstem|
|Dissecting: Related to atherosclerosis, inflammation, or trauma; aneurysm in which the intimal layer is pulled away from the medial layer and blood is forced between the layers|
Complications of a ruptured cerebral aneurysm can be fatal if bleeding is excessive. Subarachnoid hemorrhage can lead to cerebral vasospasm, cerebral infarction, and death. Rebleeding often occurs in the first 48 hours after the initial bleed but can occur any time within the first 6 months. Other complications include meningeal irritation and hydrocephalus.
Possible causes are congenital structural defects in the inner muscular or elastic layer of the vessel wall; incomplete involution of embryonic vessels; and secondary factors such as arterial hypertension, atherosclerotic changes, hemodynamic disturbances, and polycystic disease. Cerebral aneurysms also may be caused by shearing forces during traumatic head injuries.
Several different genetic loci have been associated with an increased susceptibility to cerebral aneurysm, but specific genes have not yet been implicated. Some researchers have identified 19 single nucleotide polymorphisms (SNPs) on chromosome 9, chromosome 8, and chromosome 4. There are no phenotypic differences between familial and sporadic forms. In one study of familial inheritance patterns, the autosomal recessive pattern was seen in slightly more than half of the population and autosomal dominance was seen in just over one-third, with about 5% showing incomplete penetrance. The autosomal dominantly transmitted disorder polycystic kidney disease has been associated with an increased incidence of intracerebral aneurysm.
Gender, ethnic/racial, and life span considerations
The peak incidence of cerebral aneurysm occurs between ages 35 and 60. Women in their late 40s through mid-50s are affected slightly more than men. The prognosis of subarachnoid hemorrhage resulting from an aneurysm is worse for women than for men. Cerebral aneurysms rarely occur in children and adolescents, but when they occur, they are often larger than those found in adults; pediatric aneurysms account for approximately 2% of all cerebral aneurysms. The odds of African Americans having a cerebral aneurysm are approximately twice that of whites. The prognosis of aneurysmal subarachnoid hemorrhage is worse for women than for men.
Global health considerations
The estimated frequency of cerebral aneurysm globally is approximately 10 (a range of 4 to 20) per 100,000 individuals, but it is dependent on location. The highest rates are reported in Japan, China, Sweden, and Finland.
Prior to rupture, cerebral aneurysms are usually asymptomatic. The patient is usually seen initially after subarachnoid hemorrhage (SAH). Ask about one or more incidences of sudden headache with vomiting in the weeks preceding a major SAH. Other relevant symptoms are a stiff neck, back or leg pain, or photophobia, as well as hearing noises or throbbing (bruits) in the head. “Warning leaks” of the aneurysm, in which small amounts of blood ooze from the aneurysm into the subarachnoid space, can cause such symptoms. These small warning leaks are rarely detected because the condition is not severe enough for the patient to seek medical attention.
Identify risk factors such as familial predisposition, hypertension, cigarette smoking, or use of over-the-counter medications (e.g., nasal sprays or antihistamines) that have vasoconstrictive properties. Ask about the patient’s occupation, because if the patient’s job involves strenuous activity, there may be a significant delay in going back to work or the need to change occupations entirely.
Common symptoms include headache, facial pain, alterations in consciousness, and seizures. In most patients, the neurological examination does not point to the exact site of the aneurysm, but in many instances, it can provide clues to the localization. Signs and symptoms can be divided into two phases: those presenting before rupture or bleeding and those presenting after rupture or bleeding. In the phase before rupture or bleeding, observe for oculomotor nerve (cranial nerve III) palsy—dilated pupils (loss of light reflex), possible drooping eyelids (ptosis), extraocular movement deficits with possible double vision—as well as pain above and behind the eye, localized headache, or extraocular movement deficits of the trochlear (IV) or abducens (VI) cranial nerves. Small, intermittent, aneurysmal leakage of blood may result in generalized headache, neck pain, upper back pain, nausea, and vomiting. Note if the patient appears confused or drowsy.
The patient has to cope not only with an unexpected, sudden illness but also with the fear that the aneurysm may rupture at any time. Assess the patient’s ability to cope with a sudden illness and the change in roles that a sudden illness demands. In addition, assess the patient’s degree of anxiety about the illness and potential complications.
|Test||Normal Result||Abnormality With Condition||Explanation|
|Cerebral angiogram||Symmetrical, intact pattern of cerebral vessels||Pooling of contract medium, indicating bleeding or aneurysm||Radiographic views of cerebral circulation show interruptions to circulation or changes in vessel wall appearance|
|Computed tomography||Intact cerebral anatomy||Identification of size and location of site of hemorrhage||Shows anterior to posterior slices of the brain to highlight abnormalities|
Other Tests: Noninvasive angiographic methods (computed tomographic angiography and magnetic resonance angiography) allow for detection of aneurysms; postprocessing techniques allow for three-dimensional evaluation of the aneurysm; lumbar puncture (for patients not at risk for increased intracranial pressure [ICP]), skull x-rays, electroencephalography, transcranial Doppler ultrasonography, single-photon emission computed tomography, positron emission tomography, xenon-CT, cervical spine imaging.
Primary nursing diagnosis
DiagnosisAlteration in tissue perfusion (cerebral) related to interruption in cerebral blood flow or increased ICP
OutcomesCirculation status; Cognitive ability; Neurological status; Tissue perfusion: Peripheral; Communication: Expressive ability; Communication: Receptive ability
InterventionsCerebral perfusion promotion; Circulatory care; Intracranial pressure monitoring; Neurological monitoring; Peripheral sensation management; Circulatory precautions; Hypovolemia management; Vital signs monitoring; Emergency care; Medication management
Planning and implementation
The first priority is to evaluate and support airway, breathing, and circulation. For patients unable to maintain these functions independently, assist with endotracheal intubation, ventilation, and oxygenation, as prescribed. Monitor neurological status carefully every hour and immediately notify the physician of any changes in the patient’s condition.
Microsurgery is indicated to prevent rupture or rebleeding of the cerebral artery. The decision to operate depends on the clinical status of the patient, including the level of consciousness and severity of neurological dysfunction, the accessibility of the aneurysm to surgical intervention, and the presence of vasospasm. Surgical procedures used to treat cerebral aneurysms include direct clipping or ligation of the neck of the aneurysm to enable circulation to bypass the pathology. Endovascular coiling of cerebral aneurysms may also be used in some situations, particularly in aneurysms with a small neck size (< 4 mm), a luminal diameter < 25 mm, and those that are distinct from the parent vessel. An inoperable cerebral aneurysm may be reinforced by applying to the aneurysmal sac such materials as acrylic resins or other plastics. Postoperatively, monitor the patient closely for signs and symptoms of increasing ICP or bleeding, such as headache, unequal pupils or pupil enlargement, onset or worsening of sensory or motor deficits, or speech alterations.
|Medication or Drug Class||Dosage||Description||Rationale|
|Calcium channel blockers||Varies with drugs such as nimodipine, verapamil||Inhibits calcium entry across cell membranes in vascular smooth muscles||Prevent vasospasm and hypertension|
|Corticosteroids||Varies with drugs such as methylprednisolone, hydrocortisone||Inhibits inflammatory processes such as edema and capillary dilation||Reduce swelling|
Other Drugs: Antihypertensives may be prescribed for patients with high blood pressure. Antiepileptics are administered for treatment and prevention of seizures. Sedatives may be prescribed to promote rest and relaxation, and aminocaproic acid, a fibrinolytic inhibitor, may be given to minimize the risk of rebleeding by delaying blood clot lysis. The patient may receive colloids such as albumin or plasmanate to decrease blood viscosity and expand the intravascular volume.
The environment should be as quiet as possible, with minimal physiological and psychological stress. Maintain the patient on bedrest. Limit visitors to immediate family and significant others. Apply thigh-high elastic stockings and intermittent external compression boots. Discourage and control any measure that initiates Valsalva’s maneuver, such as coughing, straining at stool, pushing up in bed with the elbows, and turning with the mouth closed. Assist with hygienic care as necessary. If the patient has a facial weakness, assist her or him during meals.
Preoperatively, provide teaching and emotional support for the patient and family. Position the patient to maintain a patent airway by elevating the head of the bed 30 to 45 degrees to promote pulmonary drainage and limit upper airway obstruction. Suction the patient’s mouth and, if needed, the nasopharynx and trachea. Before suctioning, oxygenate the patient well, and to minimize ICP increases, limit suctioning to 20 to 30 seconds at a time. If the patient has facial nerve palsy, apply artificial tears to both eyes. Take appropriate measures to prevent skin breakdown from immobility. Postoperatively, promote venous drainage by elevating the head of the bed 20 to 30 degrees. Emotional support of the patient and family is also important. The patient may be dealing with a neurological deficit, such as paralysis on one side of the body or loss of speech. If the patient cannot speak, establish a simple means of communication such as using a slate to write messages or using cards. Encourage the patient to verbalize fears of dependency and of becoming a burden.
Evidence-Based Practice and Health Policy
Fargen, K.M., Rahman, M., Neal, D., & Hoh, B.L. (2013). Prevalence of patient safety indicators and hospital-acquired conditions in those treated for unruptured cerebral aneurysms: Establishing standard performance measures using the Nationwide Inpatient Sample database. Journal of Neurosurgery, 119(4), 966–973.
- A national review was conducted among patients with cerebral aneurysm to determine their rates of patient safety indicators (PSIs), including postoperative respiratory failure, deep vein thrombosis, sepsis, and postoperative hemorrhage, as well as hospital-acquired conditions (HACs), including falls resulting in intracranial injury, fracture, or other trauma injury.
- Among 54,589 separate admissions of patients diagnosed with an unruptured cerebral aneurysm, 66% of patients did not receive any treatment for their aneurysm during hospitalization, 18.2% underwent endovascular coiling, 15.2% underwent surgical clipping, and 0.6% underwent both coiling and clipping.
- Investigators estimated a national rate of 170 PSIs (95% CI, 162 to 178) and a rate of 10.6 HACs (95% CI, 8.6 to 13.1) for every 1,000 patients with a clipped unruptured aneurysm. Among patients who received endovascular coiling, investigators estimated a national rate of 127 PSIs (95% CI, 120 to 133) and a rate of 10.7 HACs (95% CI, 8.8 to 12.3) for every 1,000 patients.
- In patients who received treatment for their aneurysm, developing one or more PSIs during hospitalization increased the length of stay by more than 11 days (p < 0.0001) when compared to treated patients without any PSIs during hospitalization.
- Neurological findings: Level of consciousness; pupillary size, shape, and reaction to light; motor function of extremities; other cranial nerve deficits (blurred vision, extraocular movement deficits, ptosis, facial weakness); aphasia; headache and facial pain; and nuchal rigidity (stiff neck, pain in the neck or back, pain with flexion of the neck, photophobia); deterioration of neurological status
- Response to pain medications and comfort measures
Discharge and home healthcare guidelines
Prepare the patient and family for the possible need for rehabilitation after the acute care phase of hospitalization. Instruct the patient to report any deterioration in neurological status to the physician. Stress the importance of follow-up visits with the physicians. Be sure the patient understands all medications, including dosage, route, action and adverse effects, and the need for routine laboratory monitoring if anticonvulsants have been prescribed.