Subarachnoid hemorrhage extravasation of blood into the subarachnoid space between the pial and arachnoid membranes

Etiologies Trauma Spontaneous MOST COMMON cause of SAH Ruptured aneurysms (75-80%) Cerebral AVMs CNS vasculitides Cerebral artery dissection Coagulation disorders Dural sinus thrombosis No cause determined

Risk Factors Hypertension OCPs Substance abuse—cigarette smoking, cocaine abuse, alcohol consumption Diurnal variation ins BP Pregnancy and parturition During LT or cerebral angiography in those with aneurysms Advancing age

Cerebral Aneurysms Cerebral VS extracranial blood vessels Less elasticity of tunica media and adventitia Tunica media has less muscle Adventitia is thinner More prominent internal elastic lamina Subarachnoid space has very little supportive tissue

Cerebral Aneurysms Early precursors of aneurysms are small outpouchings through defects in the media of the arteries These defects are thought to expand as a result of hydrostatic pressure from pulsatile blood flow and blood turbulence, which is greatest at the arterial bifurcations

Cerebral Aneurysms Etiology Congenital (Medial gap: defect in muscular layer of arterial wall) Atherosclerotic or hypertensive Embolic (atrial myxoma) Infectious (mycotic aneurysms) Traumatic Associated with other conditions

Cerebral Aneurysms LOCATION Saccular aneurysms (berry aneurysms) Located on major arteries at the apex of branch points (site of maximum hemodynamic stress on a vessel) Fusiform aneurysms More common in the vertebrobasilar system

Cerebral Aneurysms Saccular aneurysms location 85-95% in carotid system, with the ff most common locations ACoA: 30% P-comm: 25% MCA: 20% 5-15% in the posterior circulation (vertebro-basilar) 20-30% would have multiple aneurysms

Clinical Features SYMPTOMS Headache Vomiting Syncope Photophobia MAJOR RUPTURE IS THE MOST FREQUENT PRESENTATION SYMPTOMS Headache Most common, present in 97% of cases “Worst headache of my life” Severe and sudden Vomiting Syncope Photophobia Neck pain Focal cranial nerve deficits (diplopia, ptosis)

Clinical Features SIGNS (+) Kernig’s or Brudzinksi’s Coma Increased ICP Damage to brain tissue Hydrocpehalus Diffuse ischemia Seizure Low blood flow Ocular hemorrhage Due to compression of the central retinal vein and the retinochoroidal anastomoses by elevated CSF pressure causing venoud HPN and disruption of retinal veins

Aneurysmal Rupture The probability of rupture is related to the tension on the aneurysm wall Law of La Place: tension is determined by the radius of the aneurysm and the pressure gradient across the wall of the aneurysm The rate of rupture is directly related to the size of the aneurysm < 5 mm: 2% risk of rupture 6-10 mm: 40% have already ruptured upon diagnosis

Aneurysmal Rupture Blood extravasates under arterial pressure into the subarachnoid space and quickly spreads through the CSF around the brain and spinal cord Direct damage to local tissues Increased ICP Meningeal irritation

Hunt and Hess Classification of SAH Grading SAH Hunt and Hess Classification of SAH Grade Description 1 Asymptomatic or mild H/A and slight nuchal rigidity 2 CN palsy (III, VI), moderate to severe H/A, nuchal rigidity 3 Mild focal deficit, lethargy, confusion 4 Stupor, moderate to severe hemiparesis, early decerebrate rigidity 5 Deep coma, decerebrate rigidity, moribund appearance Add one grade for serious systemic disease (HPN, DM, severe atherosclerosis, COPD), or severe vasospasm on arteriography.

Grading SAH Grades 1 & 2: operated ASAP as soon as an aneurysm is diagnosed Grade > 3 managed until condition improved to grade 2 or 1 Exception: life threatening hematoma or multiple bleeds (operated on regardless of grade)

Grading SAH MORTALITY Admission Grade 1 or 2: 20% OR Grade 1 or 2: 14% Rebleed: major cause of death for Grade 1 or 2 Signs of meningeal irritation increases surgical risk

Grading SAH WFNS SAH Grade WFNS Grade GCS Score Major Focal Deficit 0** 1 15 - 2 13-14 3 + 4 7-12 + or - 5 3-6 *aphasia, hemiparesis or hemiplegia ** intact anseurysm

Grading SAH Fischer Scale (CT scan appearance) Grade Description 1 No blood detected 2 Diffuse deposition of subarachnoid blood, no clots, and no layers of blood greater than 1 mm 3 Localized clots and/or vertical layers of blood 1 mm or greater in thickness 4 Diffuse or no subarachnoid blood, but intracerebral or intraventricular clots are present

SAH Grading The Hunt and Hess and the WFNS grading systems correlate well with patient outcome The Fischer classification predicts the likelihood of symptomatic cerebral vasospasm, one of the most feared complications of SAH All 3 grading systems are useful in determining the indications for and timing of surgical management

Outcome of Aneurysmal SAH 10-15% die before reaching medical care 45% overall mortality rate NO SURGERY: Rebleeding is the major cause of M&M in 15% SURGERY: Vasospasm kills 7% 66% who underwent clipping never return to the same QoL