Cerebral Aneurysm


Article Author:
Andrew Jersey


Article Editor:
David Foster


Editors In Chief:
Sherri Murrell


Managing Editors:
Avais Raja
Orawan Chaigasame
Khalid Alsayouri
Kyle Blair
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Navid Mahabadi
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Abbey Smiley
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beenish Sohail
Hajira Basit
Phillip Hynes
Sandeep Sekhon


Updated:
12/16/2018 4:16:35 PM

Introduction

Cerebral aneurysms are defined as dilations that occur at weak points along the arterial circulation within the brain. They can vary in size (small less than 0.5 mm, medium 6 to 25 mm, and large greater than 25 mm).  Most are saccular (berry), which is associated with a thin or absent tunica media, and an absent or severely fragmented internal elastic lamina. However, fusiform (circumferential) and mycotic (infectious) aneurysms are present in a small percentage of cases. The majority of cerebral aneurysms are silent and may be found incidentally on neuroimaging or upon autopsy. Approximately 85% of aneurysms are located in the anterior circulation, predominately at junctions, or bifurcations along the circle of Willis. Subarachnoid hemorrhage (SAH) usually occurs with rupture and is associated with a high rate of morbidity and mortality.[1][2][3]

Etiology

Most cerebral aneurysms are acquired lesions, with an increased incidence in patients with certain risk factors such as advanced age, hypertension, smoking, alcohol abuse, and atherosclerosis. Other causes include cocaine use, tumors, trauma and certain embolic-forming infections like endocarditis. There is also a strong genetic element with the incidence significantly increased in patients with a strong family history of aneurysms (in other words, more than one family member affected). Certain genetic conditions are associated with higher prevalence. This includes, but is not limited to, autosomal dominant polycystic kidney disease, Ehlers-Danlos syndrome, fibromuscular dysplasia, tuberous sclerosis, arteriovenous malformations (AVM), and coarctation of the aorta.[4]

Epidemiology

The worldwide prevalence of cerebral aneurysms is estimated to be approximately 3.2%, with a mean age of 50, and an overall 1:1 gender ratio. This ratio changes significantly after age 50, with an increasing female predominance approaching 2:1, thought to be due to decreased circulating estrogen causing a reduction in collagen content of the vascular tissue. The rate of rupture causing SAH is about 10 per 100,000. This is higher in certain populations such as the Finnish and Japanese. However, this is not due to a higher prevalence of aneurysms in these populations. The overall mortality due to aneurysmal SAH is considered to be 0.4% to 0.6% of all-cause deaths, with an approximate 20% mortality and additional 30% to 40% morbidity in patients with known rupture.[5]

Pathophysiology

It is believed that a multifactorial process leads to the formation of saccular aneurysms. Hemodynamic stress on the internal elastic lamina causes breakdown over time. This is coupled with vibrations from turbulent blood flow causing structural fatigue. There is also evidence that T-cell and macrophage-mediated inflammation causes histologic changes within the vascular wall contributing to aneurysmal formation and growth. The process is expedited and amplified in patients with certain risk factors as described previously. Conversely, fusiform aneurysms are predominantly caused by atherosclerosis and mycotic aneurysms from septic emboli present in infectious endocarditis. [4][6][7]

History and Physical

Unruptured cerebral aneurysms are asymptomatic and are therefore unable to be detected based on history and physical exam alone. However, when ruptured, they commonly present with a sudden onset, severe headache. This is classically described as a “thunderclap headache” or “worse headache of my life.” In 30% of patients, the pain is lateralized to the side of the aneurysm. A headache may be accompanied by a brief loss of consciousness, meningismus, or nausea and vomiting. Seizures are rare, occurring in less than 10% of patients. Sudden death may also occur in 10% to 15% of patients. Interestingly, 30% to 50% of patients with major SAH report a sudden and severe headache 6 to 20 days prior. This is referred to as a “sentinel headache,” which represents a minor hemorrhage or “warning leak.” Physical exam findings may include elevated blood pressure, dilated pupils, visual field and/or cranial nerve deficits, mental status changes such as drowsiness, photophobia, motor or sensory deficits, neck stiffness, and lower back pain with neck flexion.

The Hunt and Hess grading system can be used by clinicians to predict an outcome based upon initial neurologic status. There are 5 grades, ranging in severity of symptoms that correlate with the overall rate of mortality. Grade 1 includes a mild headache with slight nuchal rigidity. Grade 2 is given for a severe headache with a stiff neck but without neurologic deficit other than cranial nerve palsy. For Grade 3, the patient is drowsy or confused with a mild focal deficit. In Grade 4, the patient is stuporous with moderate to severe hemiparesis. Finally, Grade 5 includes coma with decerebrate posturing.

Evaluation

Most unruptured cerebral aneurysms are identified incidentally when a patient gets neuroimaging for some other reason. However, high-risk individuals may be screened with magnetic resonance imaging (MRI), computerized tomographic angiography (CTA), or conventional angiography. In the case of suspected rupture causing SAH, the diagnosis is traditionally made with a non-contrast CT of the brain, with or without a lumbar puncture (LP). CT alone is considered very sensitive for SAH when the patient presents early, but sensitivity declines over time. Some studies suggest that CT is 100% sensitive if performed within 6 hours of onset of symptoms, but drops to 92% within 24 hours, and 58% at day 5 (14 to 18).

If CT is negative and there is still clinical suspicion for SAH, then an LP should be performed. The classic findings on LP are an elevated opening pressure and an elevated red blood cell count that does not diminish from tube 1 to tube 4. The presence of xanthochromia, a pink or yellow tint of the cerebrospinal fluid (CSF) due to hemoglobin breakdown products, is highly suggestive of SAH. Xanthochromia can be identified by visual inspection or by using spectrophotometry and is considered more than 95% sensitive when performed at least 12 hours after onset of bleed.

Once the diagnosis of SAH is made, the source of bleeding should be identified. This can be done using CTA, MRA, or digital subtraction angiography (DSA). DSA consists of inserting a catheter into the arterial circulation and injecting contrast under fluoroscopy. This is considered the “gold standard” for detection of aneurysmal SAH.[8][1][9]

Treatment / Management

The decision to treat is multifactorial and depends on size, location, age, and comorbidities of the patient, as well as whether or not there is a rupture. The treatment can be divided into 2 categories: surgical and endovascular. The surgical approach is performed under general anesthesia in the operating room and includes placing a tiny metal clip across the neck of an aneurysm preventing blood from entering the aneurysmal sac, thus eliminating the risk of bleeding. The aneurysm is accessed by temporarily removing a small portion of the skull, dissection of the dura, and separation from other blood vessels using a microscope. The clip is then carefully applied, the skull is secured in place with thin metal plates and screws, and the wound is closed. Over time the aneurysm will shrink and scar, however, the clip will usually remain for life.[10][11]

Endovascular coiling is an alternative approach that can be used in certain situations. Although considered minimally invasive, it poses an increased risk of complications such as thromboembolism and intraprocedural aneurysm rupture. The procedure is performed by inserting a catheter through the femoral artery and passing it up into the artery containing the aneurysm. Then, a second, microcatheter is inserted through the initial catheter, which contains the platinum coil. Electric current is used to detach the coil from the catheter within the lumen of the aneurysm. This promotes local clot formation and obliteration of the aneurysmal sac.

In the case of rupture, management also includes treating complications associated with SAH. This usually occurs within an intensive care unit (ICU) setting to monitor for signs of clinical deterioration caused by rebleeding, symptomatic vasospasm, hydrocephalus, seizures, and hyponatremia. Nimodipine, a calcium channel blocker, is frequently used to prevent cerebral ischemia due to vasospasm following SAH.

Complications

  • Recurrent bleeding
  • Vasospasm
  • Seizures
  • SIADH
  • Hydrocephalus
  • Arrhythmias. CHF
  • GI bleeding
  • DVT
  • Neurogenic pulmonary edema

Postoperative and Rehabilitation Care

  • After discharge, most patients require physical, speech and occupational therapy.
  • Patients also need to be prophylaxes against DVT, urinary tract infections, and seizures.
  • Serial imaging is also done to ensure that the aneurysm has been obliterated.

Consultations

  • Neurosurgeon
  • Neurologist
  • Interventional neuroradiologist
  • Critical care specialist
  • Rehabilitation consultant

Deterrence and Patient Education

Patient education about cerebral aneurysms is critical as 10% die before even reaching the emergency room.

Enhancing Healthcare Team Outcomes

Unruptured cerebral aneurysms are detected more than ever before primarily because of more frequent use of modern imaging tools. The biggest risk of cerebral aneurysm is the risk of rupture and the severe consequences. The majority of patients have no idea that they have an intracranial aneurysm and most often present with a bleed in the brain. Because of the extremely high mortality, it is important to have a systemic approach to these aneurysms once they are detected. [12] (level V)There is expert evidence that the earlier the patient is referred to a neurosurgeon or an interventional neuroradiologist, the outcomes are better than if the patient presents with a rupture. For the most part unruptured aneurysm are managed with clips or coils when possible. However, there are no randomized trials to compare the different treatments. Without any solid evidence, it is difficult to define a strategy. Experts do agree that a multidisciplinary approach is vital and has to take into account patient comorbidity, location of the aneurysm and type of endovascular treatment recommended. (Level E). The nurse should educate the patient on compliance with follow up once an intracranial aneurysm has been detected. The pharmacist should counsel the patient on discontinuing smoking and remaining compliant with blood pressure medications.

Screening

There continue to be debated about screening for cerebral aneurysms because of the expense. Further, there is significant debate on the ideal management of a small intracranial aneurysm. Most experts agree that once an aneurysm reaches 7 mm or more, treatment should be undertaken (Level E).

Outcomes

Once a cerebral aneurysm ruptures, the morbidity, and mortality are very high. Nearly 25 % are dead within the first 24 hours, and 50% will die within the next three months. [13] [14](Level V) Even the following treatment, there is a high mortality rate of nearly 40%. The prognosis is also dependent on the following factors:

  • Age

  • Location of an aneurysm

  • Degree of vasospasm

  • Presence of hypertension and other comorbidities

  • Neurological status on admission

  •  The extent of intraventricular hemorrhage


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Cerebral Aneurysm - Questions

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In a male with anisocoria and a headache, what condition should one suspect?



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A 20-year-old female, 8 days postpartum, presents with a history of headache, seizures, right hemiplegia, and confusion. What is the best first test to make the diagnosis?

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Select the most definitive test to identify intracranial aneurysms.



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A 45-year-old female is transferred to the floor from the neurosurgery intensive care unit after having a craniotomy for clipping of a cerebral aneurysm 6 days ago. What would be the most important thing for the accepting nurse to know?



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What is the most common presentation of a cerebral aneurysm?



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A 65-year-old lady is brought to the emergency department with the complaint of sudden onset unresponsiveness for the past two hours. She has a history of hypertension and type 2 diabetes mellitus. On examination, her blood pressure is 180/110 mm Hg, and her pulse rate is 50 per minute. Her Glasgow coma scale is E2V2M5, and her pupils are bilaterally 4 mm in size, reacting to light. A computed tomogram of the brain is ordered, which shows hemorrhage filling the suprasellar cistern. Vascular abnormality in which of the following blood vessels can be the most likely cause?



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Which of the following is false regarding atherosclerotic fusiform aneurysm?



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A 40-year-old female previously healthy presents to the emergency department with a left-sided headache for the past 9 hours. She describes the headache as sudden and maximal at onset, occurring during exercise. On examination, she has lower back pain with neck flexion but otherwise normal exam. Her vital signs are blood pressure 180/110 mmHg, pulse 90/bpm, temperature 98 F, respiratory rate 20/minute, oxygen saturation 100%. What initial evaluation is recommended at this time?



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A 54-year-old female with past medical history significant for polycystic kidney disease presents to the emergency department by ambulance after developing sudden onset severe headache and neck stiffness that started 2 hours ago. On exam, the patient is awake and alert but uncomfortable due to pain. She is noted to have a Cranial nerve III palsy on the left but otherwise normal neurologic exam. Vitals are blood pressure 170/106 mmHg, pulse 100 bpm, temperature 97.6 F, respiratory rate 18/minute, oxygen saturation 100% on room air. CT scan reveals subarachnoid hemorrhage. Based on the Hunt and Hess classification system, what grade of subarachnoid hemorrhage does this patient have?



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Cerebral Aneurysm - References

References

Malhotra A,Wu X,Gandhi D,Sanelli P, The Patient with Thunderclap Headache. Neuroimaging clinics of North America. 2018 Aug     [PubMed]
Toth G,Cerejo R, Intracranial aneurysms: Review of current science and management. Vascular medicine (London, England). 2018 Jun     [PubMed]
Wilkinson DA,Heung M,Deol A,Chaudhary N,Gemmete JJ,Thompson BG,Pandey AS, Cerebral Aneurysms in Autosomal Dominant Polycystic Kidney Disease: A Comparison of Management Approaches. Neurosurgery. 2018 Jul 27     [PubMed]
Lee KS,Shim JJ,Shim JH,Oh JS,Yoon SM, Cerebral Aneurysms in Judicial Precedents. Journal of Korean Neurosurgical Society. 2018 Jul     [PubMed]
Revilla-Pacheco F,Escalante-Seyffert MC,Herrada-Pineda T,Manrique-Guzman S,Perez-Zuniga I,Rangel-Suarez S,Rubalcava-Ortega J,Loyo-Varela M, Prevalence of Incidental Clinoid Segment Saccular Aneurysms. World neurosurgery. 2018 Jul     [PubMed]
Diagbouga MR,Morel S,Bijlenga P,Kwak BR, Role of hemodynamics in initiation/growth of intracranial aneurysms. European journal of clinical investigation. 2018 Jul 1     [PubMed]
Zhou S,Dion PA,Rouleau GA, Genetics of Intracranial Aneurysms. Stroke. 2018 Mar     [PubMed]
Mastantuono JM,Combescure C,Elia N,Tramèr MR,Lysakowski C, Transcranial Doppler in the Diagnosis of Cerebral Vasospasm: An Updated Meta-Analysis. Critical care medicine. 2018 Aug 3     [PubMed]
Wang X,Zhu C,Li J,Degnan AJ,Jiang T,Lu J, Knowledge-based iterative model reconstruction: Comparative image quality with low tube voltage cerebral CT angiography. Medicine. 2018 Jul     [PubMed]
Abi-Aad KR,Aoun RJN,Rahme RJ,Ward JD,Kniss J,Kwasny MJ,Sattur MG,Welz ME,Bendok BR, New generation Hydrogel Endovascular Aneurysm Treatment Trial (HEAT): a study protocol for a multicenter randomized controlled trial. Neuroradiology. 2018 Aug 17     [PubMed]
Lindgren A,Vergouwen MD,van der Schaaf I,Algra A,Wermer M,Clarke MJ,Rinkel GJ, Endovascular coiling versus neurosurgical clipping for people with aneurysmal subarachnoid haemorrhage. The Cochrane database of systematic reviews. 2018 Aug 15     [PubMed]
Pierot L,Gawlitza M,Soize S, Unruptured intracranial aneurysms: It is not a bomb! Revue neurologique. 2017 Nov     [PubMed]
Ajiboye N,Chalouhi N,Starke RM,Zanaty M,Bell R, Unruptured Cerebral Aneurysms: Evaluation and Management. TheScientificWorldJournal. 2015     [PubMed]
Brinjikji W,Kallmes DF,Cloft HJ,Lanzino G, Age-related outcomes following intracranial aneurysm treatment with the Pipeline Embolization Device: a subgroup analysis of the IntrePED registry. Journal of neurosurgery. 2016 Jun     [PubMed]

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