Cerebral Aneurysm.

Aneurysm is an abnormal local dilatation in the wall of a blood vessel, usually an artery, due to a defect, disease, or injury. The 3 major types of true intracranial aneurysms are saccular, fusiform, and dissecting.

 ETIOLOGY/ PATHOGENESIS

  • Saccular, berry, or congenital aneurysms constitute 90% of all cerebral aneurysms and are located at the major branch points of large arteries.
  • Saccular aneurysms are situated in the anterior circulation in 85-95% of cases, whereas dolichoectatic aneurysms affect predominantly the vertebrobasilar system. Multiple saccular aneurysms are noted in 20-30% of patients with cerebral aneurysms.
  • Saccular aneurysms frequently rupture into the subarachnoid space, accounting for 70-80% of spontaneous subarachnoid hemorrhages (SAH). Aneurysmal rupture also may result in intraparenchymal, intraventricular, or subdural hemorrhage. Aneurysmal SAH is a catastrophic condition and Most of these individuals (60%) either die or suffer permanent disability.
  • Giant saccular aneurysms, defined as greater than 25 mm in diameter, represent 3-5% of all intracranial aneurysms. Giant aneurysms are 3 times more common in women than men.
  • Prevalence ranges from 5-10%, with unruptured aneurysms accounting for 50% of all aneurysms. Pediatric aneurysms account for only 2% of all cerebral aneurysms.
  • Higher incidence has been noted in African Americans, with an odds ratio of 2.1.
  • Cerebral aneurysms affect equal numbers of women and men younger than 40 years, although women are affected more frequently in older age groups.
  • Saccular aneurysms are most common in the anterior communicating artery (ACoA) or anterior cerebral artery (ACA) in men, whereas the junction of the ICA with the posterior communicating artery (PCoA) is the most common site for saccular aneurysms in women. Cerebral aneurysms are rarely apparent in infants and children.

PERTINENT HISTORICAL FINDINGS/ CLINICAL SYMPTOMS

  • The clinical presentation of cerebral aneurysms includes symptoms associated with major aneurysmal rupture (eg, SAH), minor aneurysmal hemorrhage (eg, warning leak or sentinel bleed), nonhemorrhagic manifestations (eg, mass effects or cerebral ischemia), and asymptomatic scenarios (eg, incidental aneurysm detection or identification through screening).
  • Although aneurysmal SAH has characteristic historical features, the constellation of symptoms may vary with location, size, shape, and direction of the aneurysm.
  • Headache: acute onset subacute, unilateral, periorbital headache, which patients often describe as “the worst headache of my life.”
  • Alterations in consciousness: The sudden elevation of intracranial pressure associated with aneurysmal rupture may lead to a precipitous decline in cerebral perfusion pressure, causing syncope (50% of cases). Confusion or mild impairment in alertness also may be noted.
  • Seizures: Focal or generalized seizures are present in 25% of aneurysmal SAH cases, with most events occurring within 24 hours of onset.
  • Manifestations of meningeal irritation: Neck pain or stiffness, photophobia, sonophobia, or other hyperesthesia may be noted with SAH.
  • Autonomic disturbances: Subarachnoid accumulation of products of blood degradation may elicit fever. Nausea or vomiting, sweating, chills, and cardiac arrhythmias also may be present.
  • Focal neurological complaints: Hemorrhage or ischemia may manifest with focal deficits including weakness, hemisensory loss, language disturbances, neglect, memory loss, or olfactory disturbances. Focal symptoms are more common with giant aneurysms.
  • Visual symptoms: Blurring of vision, diplopia, or visual field defects may be present.
  • Respiratory dysfunction or cardiovascular instability: These are ominous signs of brainstem compression.

PERTINENT PHYSICAL EXAM FINDINGS

  • The general examination occasionally reveals manifestations of associated conditions such as subacute bacterial endocarditis, trauma, or collagen-vascular disease.
  • Specific physical examination findings may include prominent scalp veins, signs of congestive heart failure (eg, vein of Galen aneurysms), or orbital bruits (eg, cavernous carotid aneurysms).
  • Aneurysmal SAH may be accompanied by nuchal rigidity, decreased level of consciousness, subhyaloid hemorrhages, pupillary abnormalities (ie, typically dilated), ophthalmoplegia, cranial neuropathies, and other focal deficits.
  • Anterior communicating artery: This is the most common site of aneurysmal SAH (34%). Usually, are silent until they rupture.
  • Anterior cerebral artery: Most are asymptomatic until they rupture, although frontal lobe syndromes, anosmia, or motor deficits may be noted.
  • Middle cerebral artery: Aneurysms of the MCA account for about 20% of aneurysms. Aphasia, hemiparesis, hemisensory loss, anosognosia, or visual field defects may be noted.
  • Posterior communicating artery: Pupillary dilatation, ophthalmoplegia, ptosis, mydriasis, and hemiparesis may result.
  • Basilar artery: Clinical findings usually are those associated with SAH, although bitemporal hemianopsia or an oculomotor palsy may occur. Dolichoectatic aneurysms may cause bulbar dysfunction, respiratory difficulties, or neurogenic pulmonary edema.

 DIFFERENTIAL DIAGNOSIS

  • Arteriovenous Malformations
  • Basilar Artery Thrombosis
  • Cerebellar Hemorrhage
  • Cluster Headache
  • Dissection Syndromes
  • Head Injury
  • Hydrocephalus
  • Intracranial Hemorrhage
  • Migraine Headache
  • Neurofibromatosis, Type 1
  • Pituitary Tumors
  • Stroke
  • Subarachnoid Hemorrhage
  • Subdural Hematoma
  • Systemic Lupus Erythematosus
  • Tonic-Clonic Seizures
  • Trigeminal Neuralgia
  • Tuberous Sclerosis

DIAGNOSTIC EVALUATIONS

  • CBC with platelets: Monitor for infection, evaluate anemia, and identify bleeding risk.
  • Prothrombin time (PT)/activated partial thromboplastin time (aPTT): Identify a coagulopathy that increases bleeding risk.
  • Serum chemistries, including electrolytes and osmolarity: Obtain baseline studies to monitor hyponatremia, address arrhythmogenic abnormalities, assess blood glucose, and monitor hyperosmolar therapy for elevated intracranial pressure.
  • Liver function tests: Identify hepatic dysfunction that may complicate clinical course.
  • Arterial blood gases: Assess blood oxygenation.
  • CT scan: Aneurysmal SAH may be detected in 90-95% of cases. If CT scan result is negative and SAH is suspected, perform lumbar puncture (LP).Noncontrast CT scan should be performed, as contrast may obscure detection of SAH.
  • CTA may detect aneurysms greater than 3 mm, providing detailed evaluation of morphology such as relationship to the parent vessel and neck width.
  • MRI:  Fluid-attenuated inversion recovery (FLAIR) sequences are very sensitive for SAH, although the comparison of CT scan and MRI in detection of SAH is controversial.
  • Angiography: Conventional angiography is the definitive procedure for the detection and characterization of cerebral aneurysms. Aneurysm location, size, and morphology may be evaluated in the acute or chronic setting with this modality.
  • Transcranial Doppler ultrasonography: TCD facilitates the diagnosis of vasospasm and serial monitoring of cerebral blood flow at the bedside.
  • Single-photon emission computed tomography (SPECT), positron emission tomography (PET), xenon-CT (XeCT)
  • Cervical spine imaging: Radiographic assessment of the cervical spine should be performed in all comatose patients with an unwitnessed loss of consciousness.
  • ECG: Cardiac arrhythmias and myocardial ischemia may be evident. Aneurysmal SAH may be associated with several ECG changes, including peaked P waves, prolonged QT interval, and tall T waves.
  • Echocardiography: Cardiac sources of embolism, including endocarditis and myxomas, may be visualized in cases of infectious or neoplastic aneurysms.
  • Evoked potentials and EEG: These functional neurophysiologic studies may be used to monitor cerebral aneurysm surgery or patients critically ill with aneurysmal SAH.

 MEDICAL MANAGEMENT

  • Prehospital care should include assessment of vital signs and neurological status. Airway, breathing, and circulation should be addressed with endotracheal intubation, if necessary, and establishment of intravenous access.
  • Medical therapy of cerebral aneurysms involves general supportive measures and prevention of complications for individuals who are in the periprocedural period or are poor surgical candidates. Treatment decisions should be based on the clinical status of the patient, vascular anatomy of the aneurysm, and surgical or endovascular considerations.
  • Prior to definitive aneurysm treatment, medical approaches involve control of hypertension, administration of calcium channel blockers, and prevention of seizures.
  • Induced hypertension, hypervolemia, and hemodilution (ie, “triple-H therapy”) aims to maintain adequate cerebral perfusion pressure in the setting of impaired cerebrovascular autoregulation.
  • The management of unruptured intracranial aneurysms is highly controversial. The International Study of Unruptured Intracranial Aneurysms (ISUIA) indicated a relatively low risk of rupture in small aneurysms without history of SAH.

 SURGICAL MANAGEMENT (when applicable)

  • Treatment decisions for ruptured aneurysms differ significantly from those for unruptured aneurysms. Ruptured aneurysms should be treated urgently (within 72 h of hemorrhage) to prevent rebleeding and to permit aggressive management of vasospasm.
  • Unruptured aneurysms are generally treated electively. The following are 3 options for treating intracranial aneurysms: Observation, Craniotomy and clipping, Endovascular coiling.
  • Microsurgical techniques focus on exclusion of the aneurysm from the cerebral circulation and reduction of mass effects on adjacent structures.

 EMERGENCY MANAGEMENT (when applicable)

  • Initial Evaluation for Ruptured Aneurysms: Administer calcium channel blockers to all patients; this has been shown to improve outcomes after subarachnoid hemorrhage.
  • Treat all patients aggressively with hypertension, hypervolemia, and hemodilution (HHH) therapy if vasospasm is suspected. HHH therapy remains the most important aspect of the medical management of vasospasm, but, in refractory cases in which medical management fails, use endovascular methods.

 PATIENT EDUCATION/ MAINTENANCE – PREVENTION

  • Advise bed rest in a quiet dark environment during the initial week following aneurysmal SAH.
  • Perform passive range of motion exercises and frequent turning.
  • Assist patients with self-care activities, followed by slow advancement in activity as tolerated.
  • Educate regarding the warning signs and symptoms of SAH.
  • Educate regarding potential risk factors for aneurysmal SAH, including the following: Hypertension, Cigarette smoking, Illicit drug use, Alcohol

article-new-thumbnail-ehow-images-a04-su-8i-types-aneurysms-800x800  ei_2385

Wikipedia_intracranial_aneurysms_-_inferior_view_-_heat_map  02b5b1699126f94a31b5eac7867162

http://cardiac-surgery.med.nyu.edu/conditions-we-treat/aortic-aneurysm

Dr. Zachary Lahlou

 

 

 

 

 

One thought on “Cerebral Aneurysm.

  1. Pingback: Cerebral Aneurysm. | Dr. Zachary Lahlou

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out /  Change )

Google+ photo

You are commenting using your Google+ account. Log Out /  Change )

Twitter picture

You are commenting using your Twitter account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

w

Connecting to %s