Cerebral Aneurysms
Deidre A. Buckley
Joanne V. Hickey
OVERVIEW
A cerebral aneurysm is a saccular outpouching of a cerebral artery. Intracranial saccular aneurysms or berry aneurysms account for approximately 80% to 90% of all intracranial aneurysms (IAs) and are the most common cause of nontraumatic subarachnoid hemorrhage (SAH). These small, berry-like projections occur at arterial bifurcations in the circle of Willis, with other shapes such as pedunculated, sessile, and multilobulated aneurysms occasionally seen.1 Rupture of a cerebral aneurysm usually results in an SAH, which is defined as bleeding into the subarachnoid space. The prevalence of unruptured IAs is variable based on current studies. Most recent prospective autopsy and angiographic studies indicate an overall frequency of IAs to be about 2% to 4%, suggesting that unruptured IAs will affect about 6 million individuals in the United States at some point in their lives.2, 3
The authors would like to acknowledge Michael Phillips, BA for his contributions of vignettes, and also his review and suggestions related to content for the chapter.
The mean age of the US population is increasing and IAs seem to become clinically apparent with increasing age. The incidence of SAH from aneurysms also increases with age. Most studies have found an increased occurrence of aneurysms in women compared with men, although in childhood and adolescence the ratio appears to be opposite, with a male-to-female ratio of 2:1.1 The annual incidence of SAH in North America is about 15 cases per 1,00,000 or about one hemorrhage every 18 minutes. About 80% of patients with nontraumatic SAH have ruptured saccular aneurysms, which occur in 30,000 patients annually in the United States.4
SAH is one of the most feared causes of acute headache upon presentation to the emergency department (ED). Headache accounts for 1% to 2% of ED visits and up to 4% of visits to primary care offices. Among the patients who present to the ED with headaches, approximately 1% has SAH. Two prospective studies found that if only patients with “the worst headache” of their lives and a normal neurological exam were considered, 12% of the patients would have SAH.5, 6, 7 Early and accurate diagnosis is critical. The initial hemorrhage may be fatal. For those who survive, patients may have minor to severe neurological deficits. Despite the widespread availability of neuroimaging, misdiagnosis or delays in diagnosis occur in up to 25% of patients with SAH8 when initially presenting for medical treatment. A list of common misdiagnoses is included in Table 24-1.9
CASE STUDY: JP is a 45-year-old male who was in his usual state of health while enjoying a steak dinner and watching the TV show “Gunsmoke” when he experienced the worst headache of his life. JP took aspirin for several days with moderate effect. When his headache returned, he presented to his local ED where he was diagnosed with a migraine headache without a CT scan and was given a prescription for Fioricet. JP had no money to fill his prescription.
Two days later, JP awoke at 4 AM with another severe headache and presented to the same ED. A CT scan was performed demonstrating SAH in the right sylvian fissure. He was transferred to the neurosurgery service of a larger tertiary care center for treatment, where a CTA showed SAH and revealed two 3-mm aneurysms, one on the posterior communicating artery (Pcomm) and one at the basilar artery (BA) apex (Fig. 24-1). Both the aneurysms had wide-based necks, and it was unclear which one had ruptured.
Microsurgical clipping of both aneurysms was deemed the most appropriate treatment because of his younger age, the wide-based nature of the lesions, and the fact they could be clipped in the same approach. JP’s social situation also made endovascular treatment less ideal. He is an unemployed heavy smoker (two packs per day) with a consistent history of heavy drinking (up to a pint of hard alcohol a day). It is feared that he would not be a reliable candidate for the required follow-up required with endovascular treatment. Microsurgical clipping and management of his risk factors would provide a more permanent solution.
The procedure was performed without complication. Post-operatively, JP was extremely agitated and required a psychiatric consult for alcohol withdrawal. His agitation was managed with phenobarbital and antipsychotic medications. He was closely watched in the neuroscience intensive care unit for the development of vasospasm and/or hydrocephalus.
Clinical Pearl: JP is a case of missed and delayed diagnosis. Thankfully, it did not cost him his life. Due to the relative rarity of SAH in patients who present with headaches, many providers do not include SAH as a differential diagnosis. As a nurse, you may encounter patients experiencing the worst headaches of their lives; be sure to consider SAH as a possibility. In many cases, the severity of their headache will be
due to a migraine, not an aneurysm. However, you must evaluate the patient’s headaches in the context of their risk factors and think of radiologic evaluation. JP was a heavy smoker and drinker since 8 years old; in this situation, a CT scan should have been performed on the initial ED encounter to assess for the presence of subarachnoid blood.
due to a migraine, not an aneurysm. However, you must evaluate the patient’s headaches in the context of their risk factors and think of radiologic evaluation. JP was a heavy smoker and drinker since 8 years old; in this situation, a CT scan should have been performed on the initial ED encounter to assess for the presence of subarachnoid blood.
TABLE 24-1 COMMON MISDIAGNOSES OF SUBARACHNOID HEMORRHAGE | ||||||||||
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CLASSIFICATION
Cerebral aneurysms present in a variety of sizes, shapes, and etiologies. When classified by size, the following categories are used.
Small: up 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 includes the following categories.
Berry aneurysm: most common type; berry or saccular shaped with a neck or stem (Fig. 24-2)
Fusiform aneurysm: an outpouching of an arterial wall, without a stem (Fig. 24-2)
Traumatic aneurysm: any aneurysm resulting from a traumatic brain injury (accounts for a small number)
Mycotic (infectious) aneurysm: rare; caused by septic emboli from infections, such as bacterial endocarditis; may lead to aneurysmal formation
Figure 24-1 ▪ Computed tomography angiogram demonstrating basilar apex aneurysm and right posterior communicating artery aneurysm. (Courtesy: Christopher S. Ogilvy, MD, Massachusetts General Hospital, Boston, MA.)
Figure 24-2 ▪ Aneurysms. (A) Saccular (sac-like), with a well-defined neck. (B) Fusiform (spindle shaped) without a distinct neck. (Copyright 2003 American Stroke Association.)
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
LOCATION
Cerebral aneurysms usually occur at the bifurcations and branches of the large arteries at the base of the brain (circle of Willis). Eighty-five percent of aneurysms develop in the anterior part of the circle of Willis. The remaining 15% are found in the posterior circulation, known as the vertebrobasilar system (see Figure 24-3 for distribution of aneurysms).
 Figure 24-3 ▪ Aneurysms located on arteries of the circle of Willis. |
The most common sites of saccular aneurysms are the following.
85% to 95% in the carotid system, with the following three most common locations.
Anterior communicating artery (Acomm) is the single most common: 30%
Anterior cerebral artery (ACA) are more common in males
Posterior communicating artery (Pcomm): 25% to 30%
Middle cerebral artery (MCA): 20%
5% to 15% in the posterior circulation (vertebrobasilar arteries)
About 10% on the BA: basilar bifurcation, known as basilar tip, most common followed by basilar artery-superior cerebellar artery (SCA) (BA-SCA), basilar artery-vertebral artery (VA) (BA-VA) junction, and anterior inferior cerebellar artery (AICA)
About 5% on the VA and posterior inferior cerebellar artery (PICA) junction is the most common
Fusiform aneurysms are more common in the vertebrobasilar system
20% to 30% of patients who suffer an aneurysm will have multiple aneurysms
Multiple aneurysms occur in 20% to 25% of patients with saccular aneurysms, with approximately 20% of patients with saccular aneurysms having a family history of IAs or SAH.10 A variety of other pathologic entities have been associated with IAs such as polycystic kidney disease, arteriovenous malformations, coarctation of the aorta, moyamoya disease, Marfan’s syndrome, Ehlers-Danlos syndrome, pituitary tumors, and pseudoxanthoma.3
ETIOLOGY
Although the precise etiology of cerebral aneurysms remains unclear, many extrinsic, congenital, and genetic factors have been implicated in the formation and rupture of IAs. One theory suggests that a congenital/developmental defect exists in the medial and adventitial layers of the artery in the circle of Willis. There is little scientific basis for this theory, because these defects are commonly found post mortem in persons without aneurysms. The degenerative theory is strongly supported by current research and ascribes causation to hemodynamically induced degenerative vascular disease.11 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. There may be a predisposition to aneurysm formation in individuals with hypertension and in those in whom connective tissue disease promotes fragility of the arterial wall.11 Forbus12 suggested that aneurysms were acquired lesions resulting from degeneration of the elastic membrane due to a continued overstretching, combined with an underlying congenital defect in the muscularis portion of the arterial wall. Glynn proposed that the degeneration of the internal elastic lamina, possibly caused by atherosclerosis, was the leading cause in the formation of a saccular aneurysm. He stated that both congenital medial defects and acquired internal elastic defects had to be present before aneurysm formation.13
Phillips et al.14 noted that the distribution of the defects was inconsistent with the frequency of distribution of berry (saccular) aneurysms in humans. He further rationalized that the thinning of the arterial wall occurred early and was associated with the degeneration of the cells in the elastica and of the muscle cells of the intracellular matrix. He also noted that the increased rate of aneurysmal SAHs with increasing age suggests that they are not congenital lesions. This does not preclude congenital predisposition. More recently, research has demonstrated an association between the presence of specific human leukocyte antigen alleles and the genetic role they may play in aneurysm formation.15
Although the etiology of most IAs is as yet unknown, there are types of intracerebral aneurysms in which the etiology has been well demonstrated. Cerebral trauma can result in traumatic IA from localized arterial tear. Bacterial and fungal infections have also been known to cause infectious (mycotic) aneurysms. Infectious aneurysms form when bacteria, usually from septic emboli, break off and invade and destroy the vessel wall. Atherosclerotic aneurysms can form in vessel walls that have been damaged by deposits of atheromatous material, resulting in fusiform aneurysms. Fusiform aneurysms are rarely associated with SAH.
Familial Intracranial Aneurysms
There have been many families with documented IAs. Familial intracranial aneurysms (FIAs) are defined as the presence of two or more family members among first- and second-degree relatives with proven aneurysmal SAH or incidental IAs.16, 17, 18 Incidence of FIAs among SAH patients is 6% to 20%.19, 20 The estimated prevalence of FIAs among patients with SAH is 7% to 10%. Ogilvy21 states that in his experience with patients with ruptured and unruptured aneurysms, approximately 22% will have family members with aneurysms. Leblanc et al.22 reviewed 13 families with IAs and found the occurrence in the same decade in two affected siblings in 10 of 12 cases (83%). Although the usual incidence of morbidity and mortality from initial rupture of hemorrhage is about 40%, when familial patients are reviewed, the incidence of patients who suffered death or disability at the initial hemorrhage is 70%.
The familial occurrence does suggest the possibility of a genetically determined defect of the arterial wall. Several studies report that individuals with FIAs are more likely to have multiple aneurysms, and that these aneurysms are more likely to rupture at
a smaller size than those patients with an isolated aneurysm.23 Therefore, treatment considerations are different for patients with an unruptured isolated aneurysm.
a smaller size than those patients with an isolated aneurysm.23 Therefore, treatment considerations are different for patients with an unruptured isolated aneurysm.
The FIA study recruited a number of families with a goal to identify genes that underlie the development and rupture of IAs. This study was sponsored by the National Institutes for Health (NIH) and the National Institute of Neurological Disorders and Stroke (NINDS); it is the largest genetic linkage study to date. The study includes 26 clinical centers which have broad experience in clinical management and imaging of patients with IAs. Enrollment of 542 families with 2,874 subjects was completed in November, 2011.24 There is evidence suggesting that a genetic component plays an important role in the development of IAs, but specific loci affecting the risk of IAs have not been identified. The primary hypothesis of this study was that there are specific human chromosomal regions that are associated with an increased risk of IAs. The long-term objective is to identify susceptibility genes that are related to the formation of IAs.25
Population-based studies suggest that genetic factors play an important role in IA formation and aneurysm rupture. The risk of unruptured aneurysms, as determined by noninvasive screening such as magnetic resonance angiography (MRA) in unaffected relatives of families with two or more members who have an IA, is about four times greater than the risk among the general public.26 These disorders account for less than 1% of all IAs in the population and hence cannot explain the familial aggregation of IAs.25
Another important aspect of the systematic, genetic study of IA formation is the critical need to consider environmental factors in disease risk such as smoking. Nearly 80% of patients with an IA have a history of smoking at some time in their life.27 Not all individuals who smoke develop IA. Smoking may increase the risk of IA in individuals with specific genotypes at IA susceptibility loci.
The FIA study is powered to detect genes associated with the development of IA rupture and may hopefully determine the complex relationships between genes and the environment that can lead to death.25 The FIA study demonstrated that small unruptured IAs in patients who have a history of hypertension and smoking may have a higher risk of rupture than sporadic unruptured IAs of the same size. This needs to be taken into consideration when counseling a patient about treatment options. The FIA study identified sequence variants on chromosome 9p21.3, 8q11.12-12.1, and 2q33.1 which are associated with IAs.24
Various genetically determined conditions have been associated with IA; a definite link has only been associated with autosomal dominant polycystic kidney disease. The percentage of these patients that have IA varies from 10% to 40%. There is no identified definitive pattern of inheritance. Other diseases frequently mentioned such as Marfan’s syndrome, Ehlers-Danlos syndrome type 4, neurofibromatosis, and pseudoxanthoma elasticum are more often associated with carotid cavernous fistulas than with aneurysms.21 The current recommendation for screening is that each family member should undergo magnetic resonance imaging (MRI), MRA, or computed tomography angiography (CTA). It is recommended that family members be screened in their 20s and every 5 to 10 years thereafter. It is thought that patients who have a family history of IA may develop symptoms at a younger age than those with spurious aneurysms, although there is no conclusive study.21
After an IA is identified in a patient with a family history of aneurysms, treatment is often recommended. Endovascular, surgical, or combined options are considered, and the treatment with the lowest risk and highest efficacy of obliterating the IA is recommended to the individual.21
Intracranial Aneurysms in the Pediatric Population
IAs in children (younger than 18 years old) are rare, with a reported prevalence ranging from 0.5% to 4.6%;26 their epidemiology is poorly understood. Pediatric IAs occur more often in male patients and have a predilection for the terminal ICA bifurcation.
A total of 706 aneurysms have been reported in the pediatric population in English-language literature since 1939. Male-to-female occurrence is 1.8:1. SAH was the presentation in 80% of the children. The most common overall location was the ICA terminus which was the location in 26% of the cases. Only 17% of IAs occurred in the posterior circulation, and one fifth were giant lesions. Surgical treatment was performed in 79% of the cases. There was an overall good outcome in 60% of the cases, with mortality in 28%.28 The gender predominance (male-to-female ratio 1.8:1) may suggest the existence of differences in pathogenesis of IA formation in the pediatric patient. One interpretation is that congenital factors present in all IA patients may be expressed more in boys, but environmental factors may contribute to the increased incidence in girls.28
Pediatric aneurysms are likely to be pathologically distinct from adult saccular aneurysms.29 The characteristic abrupt termination of the internal elastic lamina and muscularis media at the entrance to adult saccular aneurysms at arterial bifurcations thought to be susceptible to sheer stress or to hypertensive and atherosclerotic deterioration was not found in the autopsy series of pediatric aneurysm specimens.28 Other theories for aneurysm formation in children include a connective tissue abnormality, an infectious process, a congenital anomaly causing an internal or medial elastic membrane defect, or head injury including birth trauma.30 More studies are necessary to better understand the differences in aneurysm formation in children versus adults. The male dominance and distinct anatomic location suggest the expression of a yet undetermined pathologic mechanism of aneurysm formation in children.28
RUPTURED ANEURYSMS
Aneurysm Hemodynamics
The occurrence, growth, thrombosis, and rupture of intracranial saccular aneurysms can be directly related to the effect of hemodynamic forces. Strong evidence favors the idea that IAs of this nature occur because of hemodynamically induced degenerative vascular injury.11 Despite in vitro studies over the last decade, the exact mechanisms of action of these stresses remain to be completely understood, and guidelines for determining the likelihood that a particular IA will grow, rupture, regress, or thrombose do not exist.
Evolving and improved imaging techniques that depict accurate vascular morphology as well as quantification of particular aspects of cerebral hemodynamics provides an opportunity to add to the understanding of the natural history of saccular aneurysms.31 An assessment of the chance of rupture of an asymptomatic saccular aneurysm is almost entirely based on a statistical analysis of the natural history of “similar lesions.” Several factors combine to influence the magnitude of this risk (e.g., history of smoking, age, gender, number of aneurysms), and they all play a role in formulating techniques that would allow a more objective and individual estimation of risk. Research directed at the use of
several evolving techniques in angiography, magnetic resonance, and ultrasound aimed at the improved imaging of hemodynamic stresses that affect IAs may better define the relationship between the stresses and the vascular remodeling seen in aneurysm wall degeneration and healing.31
several evolving techniques in angiography, magnetic resonance, and ultrasound aimed at the improved imaging of hemodynamic stresses that affect IAs may better define the relationship between the stresses and the vascular remodeling seen in aneurysm wall degeneration and healing.31
Aneurysm growth is a dynamic process that results from complex and incompletely understood interactions between hemodynamic forces and production of structural components that compose an aneurysm’s wall. Due to physical limitations in the collagen present at the site where IAs form, it would be expected that a growth much larger than 8 mm in diameter would result in rupture. However, in most instances, this does not occur. Changes in various hemodynamic factors (e.g., shear stress, pressure, and impingement force) as well as the presence of several humoral factors (e.g., inflammatory mediators and adhesion molecules) are potential signs of arterial injury. Sensing these signs, endothelium has the capacity to regulate the activity of substances that act to either promote or inhibit the repair of an aneurysm wall.31 Combinations of CT, CTA, MRI, MRA, and ultrasound can, in some instances, measure both geometric relationships and physiologic parameters such as shear stress, pulse pressure, and compliance before and after a given intervention. As these techniques evolve, improve, and become more widely used, they will provide data that will be valuable in both the laboratory and in a clinical setting.31
Pathophysiology
At the time of aneurysmal rupture, blood under high pressure is forced into the subarachnoid space at the base of the brain (circle of Willis), spreading by way of the sylvian fissures into the basal cisterns (Fig. 24-4). Less often, the aneurysm ruptures into one of the following areas of the brain, resulting in the formation of a hematoma: the brain parenchymal tissue (intracerebral hematoma); the ventricles (intraventricular hematoma); the subarachnoid space (subarachnoid hematoma); or the subdural space (subdural hematoma). When rupture occurs, it usually occurs at the thin-walled dome of the aneurysm, causing blood to enter into the subarachnoid space. Tissue pressure surrounding the aneurysm stops the bleeding and fibrin, platelets, and fluid form a plug that seals off the site of bleeding. The resulting clot can occlude the area or interfere with cerebrospinal fluid (CSF) absorption. The blood released irritates the brain tissue, setting up an inflammatory response that enhances cerebral edema.
 Figure 24-4 ▪ Cross section of the brain with subarachnoid and intracerebral hemorrhage. Asset provided by Anatomical Chart Co. |
Concurrent with rupture, significant SAH occurs, raising intracranial pressure (ICP) toward the mean arterial pressure and lowering cerebral perfusion pressure (CPP). These hemodynamic changes probably account for the transient loss of or altered level of consciousness. Clinically, a stroke syndrome with associated increased ICP develops. The specific signs and symptoms associated with the event depend on the location of the hemorrhage and the degree of ICP.
Natural History and Incidence of Subarachnoid Hemorrhage
Many questions regarding natural history of SAH can be answered from available data. SAH of any cause represents from 4.5% to 13% of all strokes. Age-adjusted incidence rates of SAH are available from numerous studies, with reported rates from 7.9 per 1,00,000 persons per year in Oxfordshire, England. In China, there are 2 cases per 1,00,000 compared to 22.5 cases per 1,00,000 in Finland. In Japan, there has been higher incident rates reported—21 to 25 per 1,00,000. Long-term trends are only available from Rochester, Minnesota, in population-based studies, which demonstrate that there was no change in the incidence rate of SAH through 1989. There are some gender-related differences, with female incidence higher than male in some population-based studies.32, 33
The incidence of aneurysmal SAH is higher than most other neurological diseases such as brain tumor, multiple sclerosis, and bacterial meningitis. The incidence of other types of stroke (intracerebral hemorrhage and cerebral infarction) has declined over the years, while the incidence of aneurysmal SAH remains the same.34 There is a possible reduced occurrence of SAH in some premenopausal women, especially those without a smoking history. In the same study, hormone replacement reduced the risk in postmenopausal women who had never smoked.35 Racial differences have been infrequently studied, although there are data that indicate that the incidence rate in the African American population is twice that of whites.36 Age-related differences are detected, with increasing incidence of SAH with age.
SAH is a type of intracranial hemorrhage in which bleeding occurs into the subarachnoid space. It accounts for 6% to 8% of all strokes and continues to be a significant cause of morbidity and mortality. Approximately 12% of patients die before receiving medical attention.23 SAH is associated with mortality rates between 25% and 50% from the consequences of the initial rupture. Approximately half of the untreated survivors will rebleed within the next 6 months, and among this group, morbidity and mortality are even higher.37 Approximately 30% of people die within the first 2 weeks following the acute event, and many survivors have persistent long-term deficits. Although advanced imaging techniques have allowed the noninvasive detection of an aneurysm or AVM as the potential source of a bleed, most aneurysms are detected following rupture. After SAH has occurred, medical complications are aggressively treated, but morbidity from factors other than rebleeding is still common.
CASE STUDY: TS is a 31-year-old man with a history of cigarette smoking, alcohol, and cocaine abuse. After an altercation with his girlfriend, TS fell forward, striking his head against the ground. When EMS arrived, he was noted to be belligerent; he was hemiplegic on his left side. At a local hospital, a CT scan revealed a large intraparenchymal hemorrhage (Fig. 24-5), TS was transported to a large tertiary care center where a CTA further characterized his hemorrhage and revealed a ruptured 1.1-cm right side bi-lobed MCA aneurysm, distal to the bifurcation (Fig. 24-6).
The hemorrhage was determined to be mainly intraparenchymal; however, the scans confirmed the presence of SAH. TS was classified on the Hunt-Hess scale as grade IV. Because of the presence of an intraparenchymal hematoma and SAH, he was determined to be a grade IV on the Fisher scale. The hematoma had enlarged since his initial scan ˜1.5 hours earlier and required emergent evacuation given the presence of significant midline shift, brainstem compression, and clinical obtundation (Fig. 24-7).
The patient underwent a right-sided hemicraniectomy with emergent evacuation of the hematoma and clip obliteration of the right MCA aneurysm without complications. The bone flap was sent to the bone bank. The patient was transferred to the Neurologic ICU (NICU) for monitoring. The NICU team monitored TS closely; he did not develop vasospasm, as predicted, based on his hemorrhage being primarily intrapraenchymal with minimal subarachnoid blood. His NICU stay was complicated by his poly-substance abuse, which required that the neurologists, neurosurgeons, and nurses to monitor for signs and symptoms of alcohol withdrawal. TS was prophylactically managed with lorazepam.
 Figure 24-5 ▪ Axial CT scan demonstrating large intraparenchymal hemorrhage within the right temporal lobe. (Courtesy: Christopher S. Ogilvy, MD, Massachusetts General Hospital, Boston, MA.) |
 Figure 24-6 ▪ Computed tomography angiography with 3D reconstruction of large 11-mm bi-lobed aneurysm arising from the distal right M1 segment. (Courtesy: Christopher S. Ogilvy, MD, Massachusetts General Hospital, Boston, MA.) |
Clinical Pearl: SAH is often associated with a ruptured IA. However, some ruptured aneurysms, in particular a ruptured MCA aneurysm, may present with an intracerebral hematoma along with SAH. The treatment of choice in this situation is open surgery, rather than embolization, in order to evacuate the hematoma and also to surgically obliterate the aneurysm. As the patient recovers, the bone flap can be replaced in approximately 6 weeks.
 Figure 24-7 ▪ Axial CT scan demonstrating increase in size of large intraparenchymal hemorrhage within right temporal lobe with 15 mm of leftward midline shift, right uncal herniation, right subfalcine herniation, and compression and displacement of the midbrain. (Courtesy: Christopher S. Ogilvy, MD, Massachusetts General Hospital, Boston, MA.) |
SIGNS AND SYMPTOMS
Signs and symptoms arising from an IA can be divided into two categories: those presenting before rupture or bleeding (unruptured), and those appearing after rupture or bleeding (ruptured).
Unruptured Aneurysms
Most patients are completely asymptomatic until the time of bleeding. A recent publication of the American Heart Association outlines the recommendations for management of patients with unruptured IAs.38 In approximately 40% of cases, there are warning signs, often called prodromal signs, which are either ignored or attributed to other causes. Prodromal signs may suggest the location of the aneurysm or enlargement of the lesion. Localizing signs and symptoms include the following.
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
Small intermittent aneurysmal leakage of blood may result in generalized headache, neck pain, upper back pain, nausea, and vomiting.
Whether all unruptured IAs should be treated has been debated for years. Clinical outcomes depend on various factors and require balancing early and delayed risks. There is minimal information available in the literature regarding the natural history of unruptured IAs. A study of the natural history of IA studies observed 130 patients for a follow-up that lasted 8.3 years. None of the IAs smaller than 1 cm in maximal diameter at discovery ruptured during the follow-up whereas 15 of 51 aneurysms 1 cm or larger ruptured during the follow-up. In a review of 142 patients harboring 181 unruptured IAs (some had multiple aneurysms), 27 hemorrhages occurred during 1,944 patient-years of follow-up (mean 13.9 years) with an annual rupture rate of 1.4%. The size of the IA was a predictor of hemorrhage. Other studies have suggested that there was not an insignificant risk of hemorrhage in small IAs and in others, selected locations, such as anterior communicating artery aneurysms, had been associated with increased rupture rate.1
International Study of Unruptured Intracranial Aneurysms
A landmark study has been foundational in providing the evidence for understanding unruptured IAs. In 1998, the investigators of the International Study of Unruptured Intracranial Aneurysms (ISUIA) reported results from the initial aspects of the international collaborative study of unruptured IAs. The retrospective cohort study included patients with unruptured IAs diagnosed among 53 participating centers from 1970 to 1991. Patients with and without SAH were included, but analysis was conducted based on the following categories.
Group 1: patients without SAH
Group 2: patients with an earlier SAH from an aneurysm, but with that ruptured aneurysm definitively treated, and having had another unruptured aneurysm
Patients with traumatic, mycotic, or fusiform aneurysms were excluded from the study. A prospective component including those with and without surgical or endovascular treatment was also conducted, and the surgical results were reported in 1998. Hard copies of cerebral angiograms from all patients were reviewed at the Mayo Clinic. Long-term follow-up was conducted in both prospective and retrospective groups. In the retrospective cohort, 1,449 patients with 1,937 unruptured IAs (727 group 1 and 722 group 2) were observed during follow-up. There were 1,085 (75%) who had a single unruptured IA and 364 had multiple unruptured IAs. Signs and symptoms leading to the diagnosis of unruptured IAs included ischemic cerebrovascular disease, headaches, cranial nerve deficits, aneurysmal mass effect, ill-defined spells, and convulsive disorders.1
Several aneurysm characteristics were analyzed, including site, size, presence of daughter sac, and presence of multiple lobes. During the follow-up period, 32 of the 1,449 patients had an aneurysm rupture, with 28 of 32 ruptures within the first 7.5 years of follow-up. Among group 1 patients with SAH, 1 of 12 was smaller than 10 mm in diameter whereas 17 of 20 patients in group 2 with ruptures had aneurysms smaller than 10 mm in diameter.1
In group 1 patients, the only significant predictors of rupture were size and location of aneurysm. Aneurysms that were smaller than 10 mm were less likely to rupture than those 10 to 24 mm. There were other selected sites—basilar tip, vertebrobasilar and posterior communicating—that were at increased risk of rupture. In group 2, the relative risk of rupture was 5.1 (p = 0.004) for aneurysms at the basilar tip and 1.31 (p = 0.04) for older age. Size of aneurysm did not predict rupture in group 2 patients.
The cumulative rates of rupture for patients were the following.
Group 1 patients (no previous SAH) with aneurysms smaller than 10 mm in diameter were 0.05% per year.
Group 1 patients with aneurysms larger than 10 mm in diameter were 20 times higher—approaching 1% per year.
Group 2 patients—smaller aneurysms (i.e., smaller than 10 mm) were 11 times more likely to rupture as aneurysms of the same size in group 1, at about 0.5% per year.
The rupture rate of larger aneurysms (i.e., larger than 10 mm) was similar in group 2 patients compared with those in group 1, at about 1% per year.
Mortality for SAH was 66%. The paper also reported surgical intervention-related morbidity and mortality of the prospective cohort. At 1 month, group 1 patients’ surgical mortality was 2.3%. Overall morbidity and mortality for all patients in group 1 were 17.5% at 1 month and 15.7% at 1 year.1 A meta-analysis was performed in 1997 that reviewed 23 studies of prevalence and risk of rupture of intracranial saccular aneurysms. For adults without specific risk factors, the prevalence of intracranial saccular aneurysm was 2.3%, which increased with age. Nine studies were used to analyze risk of rupture, totaling 3,907 patient-years. The highest risk per year was 1.9%. For aneurysms equal to 10 mm, the annual risk was 0.7% per year. The risk was slightly higher in women. The risk was also higher for those aneurysms larger than 10 mm in diameter, those that were symptomatic, and those in the posterior circulation.39
Since the publication of phase I of the ISUIA data in 1998, an expert panel concluded that “in consideration of the apparent low risk of hemorrhage from incidental small (<10 mm) aneurysms in patients without previous SAH, treatment rather than observation cannot be generally advocated.”38 The newest ISUIA
information supports a more individualized and sophisticated assessment of the risks of natural history versus the risk of treatment (either surgical or endovascular) on the basis of much more than aneurysm size. With the group 1 patients with aneurysms smaller than 7 mm in size, it is unlikely that the natural history of these lesions can be improved, particularly with older patients and those with anterior circulation aneurysms. Current natural history studies including ISUIA include very few symptomatic patients with small unruptured IAs. An important element in decision making is age of the patient, as age has a major effect on operative morbidity and mortality and very little effect on natural history. It is also important to consider the long-term effects of the efficacy and durability of treatment of both surgical and endovascular procedures and to re-enforce the need for long-term follow-up in these patients.3
information supports a more individualized and sophisticated assessment of the risks of natural history versus the risk of treatment (either surgical or endovascular) on the basis of much more than aneurysm size. With the group 1 patients with aneurysms smaller than 7 mm in size, it is unlikely that the natural history of these lesions can be improved, particularly with older patients and those with anterior circulation aneurysms. Current natural history studies including ISUIA include very few symptomatic patients with small unruptured IAs. An important element in decision making is age of the patient, as age has a major effect on operative morbidity and mortality and very little effect on natural history. It is also important to consider the long-term effects of the efficacy and durability of treatment of both surgical and endovascular procedures and to re-enforce the need for long-term follow-up in these patients.3
Asymptomatic Aneurysms
During the last two decades, detection of unruptured IAs has increased because of new and improved diagnostic tests (MRA, digital subtraction angiography, and three-dimensional [3D] CTA) and a more active treatment approach for patients with ruptured IAs. In addition, older patients are more likely to be treated than in the past. The natural history of unruptured IAs is poorly understood, as are the risk factors. The current knowledge of the natural history of unruptured aneurysm is based on only a few studies, with the risk factors being even more controversial because of the differing results published from these studies. Therefore, treatment decisions for unruptured aneurysms vary.10, 40, 41, 42
In a long-term cohort study of 142 patients with unruptured aneurysms, Juvela et al.42 conducted follow-up of 2,575 personyears. They found an approximate rupture rate of 1.3% per year for an unruptured aneurysm. This overall rupture rate is similar to earlier observations of 1% to 2% per year40 but somewhat lower than those reported in another study (2.3% per year),41 and it is higher than that in the ISUIA study (0.3% per year).10
The results of the studies conducted by Juvela et al. suggest that unruptured aneurysms should be treated regardless of size, at least in patients younger than 50 years old.42, 43 In older patients with small aneurysms, smoking cessation alone may be treatment enough. In North America and Europe, the prevalence of smoking in patients who suffer SAH ranges from 45% to 75% whereas in the general adult population the range is 20% to 35%.44 These studies concluded that unruptured IAs should be surgically treated, regardless of size, if technically possible, and that patient age and concurrent diseases do not increase surgical risk. Although cigarette smoking seems to increase the risk of aneurysm rupture, surgery should not be withheld in these cases because of the devastation that can result from aneurysmal rupture compared with the success rates attained in surgical treatment of unruptured aneurysms.42
Studies have determined chronic inflammation may play a role in the deterioration of the aneurysmal arterial wall, thereby risking possible rupture of the aneurysm. Physicians from the ISUIA study reviewed the data collected for the prospective arm of ISUIA to assess the hypothesis of the possible protective mechanism of aspirin on the risk of rupture in the unruptured IA. The results of the study suggested aspirin could possibly reduce the risk of rupture. More studies are needed to confirm the important role aspirin may have in reducing incidence of aneurysmal SAH.45
 Figure 24-8 ▪ Initial MRA demonstrating only 9-mm L MCA aneurysm without anatomic detail. (Courtesy: Christopher S. Ogilvy, MD, Massachusetts General Hospital, Boston, MA.) |
CASE STUDY: BL is a 58-year-old woman with a past medical history of polycystic kidney disease and chronic smoking. She was experiencing headaches and an MRI was ordered to further investigate. The MRI revealed an 8-mm left MCA aneurysm at the trifurcation (Fig. 24-8). BL was referred to a neurosurgeon for further evaluation and treatment. The neurosurgeon needed more detailed imaging of the aneurysm in order to provide her with the proper recommendation for treatment. Typically, a CTA or angiogram would be the next evaluation tool. However, BL had an elevated BUN and creatinine, manifestations of her polycystic kidney disease, making it unsafe and dangerous to proceed with CTA or angiogram because the dye could trigger kidney failure.
The neurosurgeon suggested BL undergo a more detailed imaging study using a new MRI/MRA protocol. The subsequent study provided excellent imaging of the 8-mm left MCA trifurcation aneurysm and a 7-mm left paraclinoid ICA aneurysm, without any damage to her kidneys (Fig. 24-9). A smaller aneurysm was also detected at the right MCA trifurcation measuring approximately 3 mm.
The surgery was performed without complication, and after a short stay in the NICU, the patient was discharged home on day 3.
Clinical Pearl: As clinicians, in order to provide optimum care for our patients, we must sometimes be creative. In this situation, it was necessary to find the best tool to evaluate a cerebral aneurysm in a patient who is a smoker and has polycystic kidney disease with an elevated BUN and creatinine. As nurses, we can reassure our patients about new technologies. In BL’s situation, the neurosurgeon at a busy tertiary care center was able to offer a high-resolution MRI/MRA that would serve as a suitable diagnostic tool which ultimately guided the surgeon to successfully clip the aneurysm.
 Figure 24-9 ▪ “Special protocol” MRI/MRA 3D reconstruction of 9-mm left MCA aneurysm and 7-mm L paraclinoid ICA aneurysm. (Courtesy: Christopher S. Ogilvy, MD, Massachusetts General Hospital, Boston, MA.) |
Ruptured Aneurysm
The most frequent presentation of aneurysms is rupture, which most often produces SAH. Intracerebral hemorrhage occurs in 20% to 40% of cases (more common in those with aneurysms distal to the circle of Willis, e.g., MCA). Intraventricular bleeding occurs in 13% to 28% (most common in Acomm aneurysm; prognosis is worse with about 64% mortality) whereas subdural blood is present in 2% to 5% of cases. At the time of rupture, blood is forced into the subarachnoid space. 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 the following.
Cranial nerve deficits (especially CNs III, IV, and VI); non-pupil-sparing CN III palsy produced by expanding Pcomm aneurysm.
Meningeal irritation including nausea, vomiting, stiff neck, pain in the neck and back, and possible blurred vision or photophobia. Signs of meningeal irritation usually appear 4 to 8 hours after the SAH. Mild temperature elevation may accompany SAH.
Stroke syndromes related to the vascular territory involved and intracerebral hemorrhage (e.g., hemiparesis, hemiplegia, aphasia, cognitive deficits).
Cerebral edema and increased ICP resulting in mass effect including seizures, hypertension, bradycardia, and widening pulse pressure.
Pituitary dysfunction (e.g., diabetes insipidus, hyponatremia) secondary to irritation (from blood) or edema resulting from the proximity of the pituitary gland to common locations of aneurysms.
Hunt-Hess Scale
Many different SAH grading systems have been proposed; the most widely used is the Hunt-Hess scale. This system was initially designed for patients with SAH. It is a helpful tool to guide the physician in diagnosing the severity of SAH secondary to aneurysmal bleeding, as well as in timing surgical intervention if surgery is an option. The patient is assigned to a category on admission to the hospital using the Hunt-Hess scale (Table 24-2). Changes in the patient’s condition are then monitored according to the baseline score. In the description of the scale, there is no consideration of the patients’ age, site of aneurysm, or time since hemorrhage.
TABLE 24-2 HUNT-HESS SCALE CLASSIFICATION OF SUBARACHNOID HEMORRHAGES | ||||||||||||||||||
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DIAGNOSIS
Variations in Presentation
Misdiagnosis often results from three diagnostic reasoning errors: failure to understand limitations of computed tomography (CT), failure to appreciate the spectrum of clinical symptoms, and failure to correctly interpret data from lumbar puncture (LP). There are between 20% and 50% of patients with documented SAH who report a distinct, severe headache (known as a thunderclap headache) days to weeks before the aneurysmal hemorrhage. These prehemorrhage headaches are considered warning headaches.5 Thunderclap headaches develop in seconds, achieve maximal intensity in minutes, and can last hours to days. The differential diagnoses include SAH, acute expansion of an existing aneurysm, dissections or thrombosis of an unruptured aneurysm, cerebral venous thrombosis, and benign thunderclap headaches. All patients who present with thunderclap headaches should be evaluated immediately for SAH.5
Almost half of the patients with SAH have episodes of minor bleeding. In one series of 500 patients with SAH, 34% had bleeding during nonstrenuous exercise and 12% during sleep. The headache may be in any location, may be localized or generalized, may be mild, may resolve spontaneously, or may be alleviated by analgesics. Patients with less severe headaches may be diagnosed with more common conditions such as sinusitis, tension headache, or migraine headache.5, 46 When vomiting is present, especially with a low-grade fever, diagnoses such as viral syndrome, viral meningitis, flu, or gastroenteritis may be made. Patients with significant neck pain may be diagnosed with arthritis or cervical
neck pain. Presenting symptoms such as confusion or agitation may lead to a diagnosis of a primary psychiatric disorder. Most patients who present with SAH will have an abrupt onset of severe, unique headache or neck pain. Some will have abnormal findings on neurological examinations, such as subtle meningismus or ocular findings. An understanding of the wide presentation of symptoms along with careful history taking and physical examination is the best strategy for identifying patients who should be evaluated for possible SAH.
neck pain. Presenting symptoms such as confusion or agitation may lead to a diagnosis of a primary psychiatric disorder. Most patients who present with SAH will have an abrupt onset of severe, unique headache or neck pain. Some will have abnormal findings on neurological examinations, such as subtle meningismus or ocular findings. An understanding of the wide presentation of symptoms along with careful history taking and physical examination is the best strategy for identifying patients who should be evaluated for possible SAH.
Diagnostics
The first diagnostic test ordered is a noncontrast CT scan. Very thin cuts (3 mm in thickness) through the base of the brain are suggested because the thicker cuts (10 mm) may miss small collections of blood. The sensitivity of CT decreases over time from the onset of symptoms. The dynamics of the CSF and spontaneous clot lysis can result in rapid clearing of old subarachnoid blood.5, 4, 47 Four studies have evaluated modern, third-generation CT scanners for sensitivity to identifying IAs and SAH.5, 7, 48, 49, 50 In retrospective studies of patients admitted to the hospital with SAH, 100% of patients who underwent scanning within the first 12 hours49 and 93% of patients who had a CT scan within the first 24 hours48 after onset of headache had positive findings on CT scanning. Prospective outpatient studies reported a sensitivity of 98% (117 of 119)50 and of 93% (14 of 15) for scans performed in the first 12 hours. Although MRI continues to advance and detects aneurysms, standard MRI is inferior to CT for the detection of acute SAH. CT remains the imaging method of choice because of its wider availability, lower cost, greater convenience for sick patients, and greater provider experience with interpretation.
An LP is performed in a patient whose clinical presentation suggests SAH, but whose CT scan is negative. “Traumatic taps” occur in up to 20% of LPs and must be differentiated from true hemorrhages. Most practitioners agree that the presence of xanthochromia is the primary criterion for SAH in patients with negative CT scans.47 Some believe that the presence of erythrocytes, even in the absence of xanthochromia, is more accurate. This difference can be explained by the various methods of detecting xanthochromia. Those who believed that xanthochromia is most important used spectrophotometry, and those who believed that erythrocytes are most important used visual inspection, which can miss discoloration in CSF in up to 50% of patients.5
Most warning headaches are indications of unrecognized SAHs and can be diagnosed by appropriate methods. Properly performed and interpreted CT scan and LP in patients with acute severe headaches will identify the majority of patients with SAH. Some patients whose diagnostic test results are inconclusive or who are at unusually high risk for an aneurysm should undergo neurological evaluation and vascular imaging MRA, CT, CTA, or conventional cerebral angiography. The diagnosis of an IA is based on the following.
History and results of the neurological examination.
CT scan, without contrast media; a good-quality fourth-generation CT will detect SAH in 95% or more of cases if scans are done within 48 hours of SAH. Blood appears as high density (i.e., appears white) within the subarachnoid space.
If the CT findings are negative, LP is used in selective cases. RBC counts usually exceed 1,00,000 per mm if a hemorrhage has occurred.
CTA is now being used in many institutions as the first radiographic tool. It is a more recent development than MRA, and its role is being refined, with a reported sensitivity of 95% and specificity of 83%. Unlike conventional angiography, CTA provides a 3D image of the vasculature and demonstrates the relationship to nearby bony structures. With improved techniques in CT scanning, a scan can be completed in a matter of minutes to provide the data necessary to complete 3D imaging of IAs.
MRI is not sensitive within the first 24 to 48 hours, especially with thin layers of blood; it is useful after 4 to 7 days. MRA is also used.
Cerebral angiography remains the “gold standard” for evaluation of cerebral aneurysms. It demonstrates a source of the aneurysm in about 80% to 85% of cases and radiologic vasospasm (i.e., a narrowing of the cerebral blood vessels as seen on radiographic films).
Imaging Studies
Computed Tomography
CT remains the mainstay of initial detection of SAH, with 90% or better sensitivity in detecting a clinically significant SAH in the first 2 days after the event. It is important to realize that a negative CT scan never excludes SAH and that clinical findings suggestive of an SAH, even in the face of a negative CT scan, still requires an LP.51
A plain (without contrast) CT scan obtained within 48 hours of aneurysmal rupture is usually the initial diagnostic procedure ordered. If the scan is performed within 24 hours of the initial SAH, a high-density clot in the subarachnoid space can be demonstrated in 92% to 95% of cases; if done within 48 hours, the clot can be demonstrated in 75% to 85% of cases.4, 40 A CT scan also aids in establishing the extent and location of subarachnoid bleeding and is useful for identifying patients at high risk for the development of vasospasm and for pinpointing the potential vascular territory of the vasospasm.
The Fisher grading scale (Table 24-3) is used to assist in prediction of the patient’s clinical outcome. The amount of blood on CT scan correlates with the severity of cerebral vasospasm.
If an angiogram is ordered and multiple aneurysms are seen, the CT scan is helpful in identifying which aneurysm bled, based on the presence of a clot.
Spiral Computed Tomography Angiography
Spiral CTA using the slip ring technology allows visualization of arterial anatomy after intravenous (IV) administration of a timed bolus of contrast material and can provide images in a very short time. This new technique is often used as a first step in evaluation
of patients with a diagnosis of SAH who are being transferred to a tertiary care facility for further evaluation and treatment. The imaging time takes about 30 to 40 seconds and can provide immediate confirmation of IA so that treatment decisions can be made rapidly. One disadvantage of the technique is the load of contrast material that is administered which can affect kidney function.
of patients with a diagnosis of SAH who are being transferred to a tertiary care facility for further evaluation and treatment. The imaging time takes about 30 to 40 seconds and can provide immediate confirmation of IA so that treatment decisions can be made rapidly. One disadvantage of the technique is the load of contrast material that is administered which can affect kidney function.
TABLE 24-3 FISHER GRADING SCALE (AMOUNT OF BLOOD ON CT SCAN IS A PREDICTOR OF VASOSPASM) | ||||||||||
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The examination begins in the location of interest, either the circle of Willis or the carotid bifurcation, using contiguous unenhanced 5-mm thick axial sections. After the area of interest is determined, nonionic contrast is injected intravenously via an automated power injector into an 18-gauge angiocatheter in the antecubital vein at a rate of 5 mL/sec for a total of 120-mL volume, with a 25-second delay between the injection and the onset of data acquisition.52
Two-dimensional (2D) maximum intensity projection (MIP) views and 3D surface-rendered and volume-rendered reconstructions are reformatted from the raw image data. For example, by using this new technology, the Massachusetts General Hospital (MGH) neurovascular group has been able to diagnose and manage approximately 80% of aneurysm patients using CTA alone. This is true for both ruptured and unruptured aneurysms.52
Another advantage of CTA is its rapidity. For patients presenting in the ED with presumed diagnosis of SAH, the data can be acquired and analyzed within 15 to 20 minutes and provided to clinicians for treatment decisions. The films can be expeditiously reviewed, and a decision can be made to treat the aneurysm with either a surgical or an endovascular approach. This technology has greatly facilitated the care of some critically ill patients who can forgo angiography prior to aneurysm treatment.52
In summary, the advantages of CTA are noninvasive, quick scanning time, requires fewer resources (equipment, staffing, and cost), no sedation required, painless, and suitable for critically ill patients. CTA can detail the anatomy of branch vessels in relation to the aneurysm (Fig. 24-10). It can also detail the bony anatomy in relationship to the aneurysm. Images can also be rotated in any direction to view the aneurysm from a variety of angles. These details give the physician an excellent idea of what the surgery or endovascular treatment may involve before undergoing the procedure. This minimizes risk because the potential pitfalls of surgery can be anticipated prior to initiation of treatment. Thus, CTA has proven to be a useful tool in the diagnosis and management of aneurysms.52
 Figure 24-10 ▪ Computed tomography angiogram demonstrating 11-mm anterior communicating artery aneurysm. (Courtesy: Christopher S. Ogilvy, MD, Massachusetts General Hospital, Boston, MA.) |
CTA is a reliable alternative to MRA in evaluating the circle of Willis and carotid bifurcation. At some institutions, specific applications include triaging patients for possible superselective thrombolysis, following patients with carotid stents, and evaluating multiperspective approaches to IAs. In addition, CTA may ultimately demonstrate advantages in the screening of aneurysms in the appropriate patient population.
Angiography
Cerebral angiography (Figs. 24-11 and 24-12) is still the mainstay of diagnosis for cerebral aneurysms in most centers, but with the advent of CTA, this appears to be changing. Angiography provides visualization of all four major cerebral vessels and their branches. Angiography is commonly scheduled immediately following diagnosis of SAH by CT scan or CTA in patients who are deemed clinically stable. If not clinically stable, the CTA often provides enough information to offer complete treatment of the aneurysm. Early angiography or CTA allows for definitive diagnosis and enables the cerebrovascular physician team (e.g., neurosurgeon, interventional neuroradiologist, and neurologist) to recommend a treatment plan. In addition to the specific location of the aneurysm, the following can be identified using angiography.
The particular characteristics of the aneurysm (e.g., shape, size, presence of daughter sac).
Any anomalies of cerebral vasculature (e.g., involving the circle of Willis) that will affect treatment decisions.
The presence of vasospasm, which may influence the urgency to obliterate the aneurysm either surgically or endovascularly, so that triple H (hypervolemic, hemodilution, and hypertensive) therapy or some combination, such as hypervolemic hypertensive management, can be initiated (Dankbaar, Slooter, Rinkel, & van der Schaaf, 2010).
 Figure 24-11 ▪ Conventional cerebral angiogram demonstrating 11-mm anterior communicating artery aneurysm. (Courtesy: Christopher S. Ogilvy, MD, Massachusetts General Hospital, Boston, MA.). |
 Figure 24-12 ▪ Conventional angiogram with 3D reconstruction demonstrating an anterior communicating artery aneurysm pointing inferiorly with a smaller daughter projection pointing superiorly. (Courtesy: Christopher S. Ogilvy, MD, Massachusetts General Hospital, Boston, MA.) |
Repeat Cerebral Angiography. Repeat angiography may be ordered for the following reasons.
Confirmation of diagnosis when no aneurysm is found on early angiography (small aneurysms can be missed, particularly in the posterior circulation). Angiogram is usually repeated 10 to 14 days after the initial study.
Identification of reversal of previously observed vasospasm.
Detection and treatment of vasospasm when there is deterioration of neurological function such as change in level of consciousness.
Negative Angiogram and Subarachnoid Hemorrhage. In approximately 5% of patients with a documented SAH and IA, the IA is not found on cerebral angiogram. Explanations range from transient thrombosis of the IA to vasospasm, technical error, or ruptured pial vascular malformation. A repeat angiography in conjunction with a CTA is recommended in 7 to 10 days. Some physicians recommended a third angiogram, 3 months after the initial angiogram to ensure normal cerebral vasculature. Currently, some physicians are comfortable with two negative angiograms and CTAs if the hemorrhage pattern on the CT scan is perimesencephalic (defined as the presence of blood restricted to the cisterns surrounding the brainstem and the suprasellar cistern). Others recommend that the patient undergo a CTA rather than a conventional angiography at 3 months to further confirm normal vasculature of the brain and spine.
Perimesencephalic nonaneurysmal SAH is a distinct entity and considered a benign condition with a good outcome. This group has less risk of rebleeding and vasospasm than patients with SAH of unknown etiology. The actual etiology is yet to be determined, but it may be secondary to the rupture of a small perimesencephalic vein or artery. Small aneurysms may obliterate themselves after rupture, leaving no IA to be found on angiography. This type of IA may be referred to as a cryptic aneurysm.
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