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Cerebral Aneurysm, Emergency Medicine

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Cerebral Aneurysm, Emergency Medicine

Basics

Description

Compression of adjacent structures may cause neurologic symptoms:

Lumbar puncture if suspect aneurysmal leak or rupture with normal head CT

Following initial stabilization, the major goals of early treatment of ruptured or leaking aneurysms are to prevent re-rupture, cerebral vasospasm, and hydrocephalus (see "Subarachnoid Hemorrhage"¯).

  • Abnormal, localized dilation or outpouching of cerebral artery wall:Occurs in 5-10% of population
  • Rupture of saccular aneurysms account for 5-15% of strokes
  • Of those that rupture:40% occur at anterior communicating artery (ACA)30% at internal carotid (IC)20% in middle cerebral artery (MCA)5-10% in vertebrobasilar artery (VBA) system
  • Occurs in 5-10% of population
  • 40% occur at anterior communicating artery (ACA)
  • 30% at internal carotid (IC)
  • 20% in middle cerebral artery (MCA)
  • 5-10% in vertebrobasilar artery (VBA) system

Etiology

  • Asymptomatic in 3.2% of population
  • "Congenital,"¯ saccular, or berry aneurysms most common (90%):Develop at weak points in arterial wall and bifurcations of major cerebral arteriesIncidence increases with ageMultiple in 20-30%Increased incidence:Polycystic kidney diseaseCerebral arteriovenous malformationType III collagen deficiencyFibromuscular dysplasiaEhlers-Danlos syndromeMarfan syndromePseudoxanthoma elasticumNeurofibromatosisMoyamoya syndromeCoarctation of the aortaTuberous sclerosisSickle cell diseaseOsler-Weber-Rendu syndromeĪ±1-Antitrypsin deficiencySystemic lupus erythematosusGlucocorticoid remediable hyperaldosteronism
  • Arteriosclerotic, fusiform, or dolichoectatic (7%):More common in peripheral arteries
  • Inflammatory (mycotic):10% of patients with bacterial endocarditis
  • Traumatic, associated with severe closed head injury
  • Neoplastic, embolized tumor fragments
  • Familial correlation: 1st-degree relative with history of aneurysm essentially doubles lifetime risk
  • Develop at weak points in arterial wall and bifurcations of major cerebral arteries
  • Incidence increases with age
  • Multiple in 20-30%
  • Increased incidence:Polycystic kidney diseaseCerebral arteriovenous malformationType III collagen deficiencyFibromuscular dysplasiaEhlers-Danlos syndromeMarfan syndromePseudoxanthoma elasticumNeurofibromatosisMoyamoya syndromeCoarctation of the aortaTuberous sclerosisSickle cell diseaseOsler-Weber-Rendu syndromeĪ±1-Antitrypsin deficiencySystemic lupus erythematosusGlucocorticoid remediable hyperaldosteronism
  • Polycystic kidney disease
  • Cerebral arteriovenous malformation
  • Type III collagen deficiency
  • Fibromuscular dysplasia
  • Ehlers-Danlos syndrome
  • Marfan syndrome
  • Pseudoxanthoma elasticum
  • Neurofibromatosis
  • Moyamoya syndrome
  • Coarctation of the aorta
  • Tuberous sclerosis
  • Sickle cell disease
  • Osler-Weber-Rendu syndrome
  • Ī±1-Antitrypsin deficiency
  • Systemic lupus erythematosus
  • Glucocorticoid remediable hyperaldosteronism
  • More common in peripheral arteries
  • 10% of patients with bacterial endocarditis
  • Although rare in children, more likely to be giant (>25 mm)
  • Occur in the posterior circulation

Diagnosis

Signs and Symptoms

  • Commonly asymptomatic before rupture
  • Sentinel headaches occur in 30-60% of patients before rupture:Can be unilateral
  • Seizures, syncope, or altered level of consciousness
  • Can be unilateral
  • Onset of headache
  • Family history
  • Altered mental status
  • Focal neurologic deficits
  • Rupture results in subarachnoid hemorrhage:Headache: Severe ("worst headache ever"¯) with sudden onset ("thunderclap"¯)Different from prior headachesClassically without focal deficitsNuchal rigidity (most common sign) secondary to blood in CSF
  • Headache: Severe ("worst headache ever"¯) with sudden onset ("thunderclap"¯)Different from prior headachesClassically without focal deficits
  • Nuchal rigidity (most common sign) secondary to blood in CSF
  • Different from prior headaches
  • Classically without focal deficits
  • ACA aneurysms:Optic tract: Altitudinal field cut or homonymous hemianopsiaOptic chiasm: Bitemporal hemianopsiaOptic nerve: Unilateral amblyopia
  • Aneurysms at IC-posterior communicating artery junction:Oculomotor nerve: Fixed and dilated pupil, ptosis, diplopia, and temporal deviation of eye with inability to turn eye upward, inward, or downward
  • Aneurysms in cerebral cortex may produce focal deficits including:HemiparesisHemisensory lossVisual disturbancesAphasiaSeizures
  • Optic tract: Altitudinal field cut or homonymous hemianopsia
  • Optic chiasm: Bitemporal hemianopsia
  • Optic nerve: Unilateral amblyopia
  • Oculomotor nerve: Fixed and dilated pupil, ptosis, diplopia, and temporal deviation of eye with inability to turn eye upward, inward, or downward
  • Hemiparesis
  • Hemisensory loss
  • Visual disturbances
  • Aphasia
  • Seizures

Essential Workup

  • Complete neurologic examination
  • Emergent noncontrast head CT scan will diagnose 90-95% of subarachnoid hemorrhages
  • Lumbar puncture with CSF analysis if CT scan is negative

Diagnosis Tests & Interpretation

  • Coagulation studies
  • Baseline CBC with platelets and differential
  • Electrolytes
  • Renal and liver function tests
  • Arterial blood gas
  • CXR for pulmonary edema
  • 4-vessel cerebral angiography remains gold standard
  • MRA
  • Helical CT scanning may be useful in detecting aneurysms >3 mm
  • Transcranial Doppler US may be useful in detecting vasospasm.

Differential Diagnosis

  • Neoplasm
  • Arteriovenous malformation
  • Optic neuritis
  • Migraine
  • Meningitis
  • Encephalitis
  • Hypertensive encephalopathy
  • Hyperglycemia or hypoglycemia
  • Temporal arteritis
  • Acute glaucoma
  • Subdural hematoma
  • Epidural hematoma
  • Intracerebral hemorrhage
  • Thromboembolic stroke
  • Air embolism
  • Sinusitis

Treatment

Pre-Hospital

  • Cautions:Neurologic examination in the field can be extremely helpfulAssess:Level of consciousnessGlasgow coma scale scoreGross motor deficitsSpeech abnormalitiesGait disturbanceFacial asymmetryOther focal deficits
  • Patients with subarachnoid hemorrhage may need emergent intubation for rapidly deteriorating level of consciousness
  • Patients must be transported to a hospital with emergent CT scanning and intensive care unit (ICU)-level treatment
  • Neurologic examination in the field can be extremely helpful
  • Assess:Level of consciousnessGlasgow coma scale scoreGross motor deficitsSpeech abnormalitiesGait disturbanceFacial asymmetryOther focal deficits
  • Level of consciousness
  • Glasgow coma scale score
  • Gross motor deficits
  • Speech abnormalities
  • Gait disturbance
  • Facial asymmetry
  • Other focal deficits

Initial Stabilization/Therapy

  • ABCs:Supplemental oxygenRapid-sequence intubation may be required for airway protection or for controlled ventilationContinuous cardiac monitoring and pulse oximetry
  • For altered mental status:Check blood glucose immediately, give D50 (if glucose is low)NaloxoneThiamine
  • Reversal of anticoagulation
  • Prevention of acute increases in intracranial pressure from vomiting should be accomplished with antiemetics
  • Seizures should be managed acutely with IV benzodiazepines and fosphenytoin/phenytoin
  • Seizure prophylaxis is controversial and not recommended
  • Supplemental oxygen
  • Rapid-sequence intubation may be required for airway protection or for controlled ventilation
  • Continuous cardiac monitoring and pulse oximetry
  • Check blood glucose immediately, give D50 (if glucose is low)
  • Naloxone
  • Thiamine

Ed Treatment/Procedures

Surgery/Other Procedures

  • Optimal timing for angiography and surgery remain controversial, but trend is toward early surgery to decrease incidence of rebleeding and cerebral vasospasm
  • Early placement of ventriculostomy in appropriate patients may allow for direct intracranial pressure monitoring and often decreases systemic hypertension

Medication

  • Labetalol: 20-30 mg/min IV bolus, then 40-80 mg q10min max. 300 mg; follow with continuous infusion 0.5-2 mg/min
  • Nimodipine: 60 mg PO/nasogastric q4h
  • Ondansetron: 4 mg PO/SL/IV q4h PRN (peds: 0.1 mg/kg IV; max. 4 mg/dose)
  • Prochlorperazine: 5-10 g IV/IM q6-8h (peds: 0.2 mg/kg/d IM in 3 or 4 div. doses); max. 40 mg/d
  • Diazepam: 5-10 mg IV q10-15min max., 30 mg (peds: 0.2-0.3 mg/kg q5-10min max. 10 mg)
  • Docusate sodium: 100 mg PO BID
  • Fosphenytoin: 15-20 mg/kg phenytoin equivalents (PE) at rate of 100-150 mg/min IV/IM
  • Hydralazine: 10-20 mg IV q30min
  • Lorazepam: 2-4 mg IV q15min PRN (peds: 0.03-0.05 mg/kg/dose; max. 4 mg/dose)
  • Nicardipine: 5 mg/h IV infusion, increase by 2.5 mg/h q5-15min max. 15 mg/h (peds: Dosing unavailable)
  • Phenytoin: 15-20 mg/kg IV load at max. 50 mg/min; max. 1.5 g (adult and peds); maintenance 4-6 mg/kg/d IV/IM

Follow-Up

Disposition

  • Any patient with acute aneurysmal subarachnoid hemorrhage should be admitted, preferably to ICU
  • Any patient with symptomatic unruptured aneurysm should receive admission and urgent neurosurgical consultation, given high rate of rupture
  • Patients with incidentally discovered asymptomatic intracranial aneurysms may be discharged with close neurosurgical follow-up
  • Note that overall risk of rupture is 1-2%/yr and that critical size at which risk for rupture outweighs risk for surgery is controversial (classically 10 mm, but probably in the 4-8-mm range).

Follow-Up Recommendations

  • Neurosurgery
  • Neurology
  • Primary care

Pearls and Pitfalls

  • CT scan alone is not sufficient to exclude subarachnoid hemorrhage
  • Vasospasm is typically seen on day 3 after bleed or surgery
  • Nimodipine can prevent or treat vasospasm but should never be administered IV
  • Nitroprusside and nitroglycerine should be avoided due to tendency to increase cerebral blood volume and thereby intracranial pressure

Additional Reading

  • Backes D, Rinkel GJ, Kemperman H, et al. Time-dependent test characteristics of head computed tomography in patients suspected of nontraumatic subarachnoid hemorrhage. Stroke. 2012;43:2115-2119.
  • Bederson JB, Connolly ES Jr, Batjer HH, et al. Guidelines for management of aneurysmal subarachnoid hemorrhage: A statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association. Stroke. 2009;40:994-1025.
  • Menke J, Larsen J, Kallenberg K. Diagnosing cerebral aneurysms by computed tomographic angiography: Meta-analysis. Ann Neurol. 2011;69:646-654.
  • Naval NS, Stevens RD, Mirski MA, et al. Controversies in the management of aneurysmal subarachnoid hemorrhage. Crit Care Med. 2006;34:511-524.
  • Raymond J, Guillemin F, Proust F, et al. Unruptured intracranial aneurysms: A critical review of the International Study of Unruptured Aneurysms (ISUIA) and of appropriate methods to address the clinical problem. Interv Neuroradiol. 2008;14:85-96.
  • Seibert B, Tummala RP, Chow R, et al. Intracranial aneurysms: Review of current treatment options and outcomes. Front Neurol. 2011;2:45.
  • Swadron SP. Pitfalls in the management of headache in the emergency department. Emerg Med Clin North Am. 2010;28:127-147.
  • Vlak MH, Rinkel GJ, Greebe P, et al. Trigger factors for rupture of intracranial aneurysms in relation to patient and aneurysm characteristics. J Neurol. 2012;259:1298-1302.

See Also (Topic, Algorithm, Electronic Media Element)

Codes

ICD9

  • 430 Subarachnoid hemorrhage
  • 437.3 Cerebral aneurysm, nonruptured
  • 747.81 Anomalies of cerebrovascular system

ICD10

  • I60.7 Nontraumatic subarachnoid hemorrhage from unspecified intracranial artery
  • I67.1 Cerebral aneurysm, nonruptured
  • Q28.3 Other malformations of cerebral vessels

SNOMED

  • 128609009 Intracranial aneurysm (disorder)
  • 233983001 Ruptured cerebral aneurysm
  • 590005 Congenital aneurysm of anterior communicating artery (disorder)
  • 277196008 Berry aneurysm
  • 128608001 cerebral arterial aneurysm (disorder)
  • 42994005 Nonruptured cerebral aneurysm