Subarachnoid hemorrhage
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Transcript of Subarachnoid hemorrhage
Anatomy of Subarachnoid space In the central nervous system, the
subarachnoid cavity (subarachnoid space) is the interval between the arachnoid membrane and pia mater.
It is occupied by spongy tissue consisting of trabeculae (delicate connective tissue filaments that extend from the arachnoid mater and blend into the pia mater) and intercommunicating channels in which the cerebrospinal fluid is contained.
This cavity is small on the surface of the hemispheres of the brain. On the summit of each gyrus the pia mater and the arachnoid are in close contact, but in the sulci between the gyri, triangular spaces are left, in which the subarachnoid trabecular tissue is found.
Whilst the pia mater closely follows the surface of the brain and dips into the sulci, the arachnoid bridges across them from gyrus to gyrus.
At certain parts of the base of the brain, the arachnoid is separated from the pia mater by wide intervals, which communicate freely with each other and are named subarachnoid cisternae; in these the subarachnoid tissue is less abundant.
The subarachnoid space is the location of the interface between the vascular tissue and the cerebrospinal fluid and is active in the blood brain barrier.
Subarachnoid Hemorrhage
Bleeding into the subarachnoid space, between the pia mater and the arachnoid
Most commonly occurs between ages of 25 to 65, increasing in frequency with age
Causes
Intracranial aneurysms Cause of approximately 80% of non
traumatic subarachnoid hemorrhage Most occur around the circle of Willis
(berry aneurysm) at Middle cerebral artery bifurcation Anterior communicating artery Posterior communicating artery Also
Ophthalmic arteries Vertebral and basilar arteries
Head trauma
Benign perimesencephalic hemorrhage Blood limited to midbrain
Less frequent causes of SAH Arteriovenous malformation (AVM) Extension from intracerebral
hemorrhage Arteriovenous fistulae Meningitis Neoplasm
Risk Factors
Vasculitis Fibromuscular dysplasia (FMD) Hypertension History of polycystic kidney
disease Smoking
Clinical Findings
Headache is most common symptom
Frequently reported as severe (“worst headache of life"), of abrupt onset, reaches maximum intensity within seconds (“thunderclap headache”)
Nausea Vomiting Change in mental status -- confusion Decreased level of consciousness
including coma Spinal fluid may be bloody
CT Scan
Unenhanced CT of the brain is the study of choice for establishing presence of SAH
Acute hemorrhage is most evident 2-3 days after the acute bleed
Acute hemorrhage appears as high-attenuation material that fills the normally black subarachnoid spaces, which include The basilar cisterns
Especially the suprasellar cistern The sulci
Especially the Sylvian fissures Over the convexities of the brain, SAH
produces white, branching densities representing the normally black sulci filled with blood
Cortical vein sign = visualization of cortical veins passing through extra axial fluid collection
False positives may occur by mistaking normal visualization of the falx cerebri and tentorium cerebelli for SAH
A, Axial brain CT scan shows an isolated slight right frontal subarachnoid hyperattenuation. B, Because of clinical aggravation the next day, another brain CT was performed and demonstrated a larger right Sylvian SAH.
There is high-attenuation blood in the Sylvian fissures (blue arrows) and the inter hemispheric fissure (red arrow) seen on this non-contrast enhanced CT of the brain. Do not confuse normal, physiologic calcifications (white and black arrows) for blood.
Non-enhanced CT scan demonstrates increased density at the convexity consistent with a small amount of subarachnoid hemorrhage in the right frontal lobe.
CT scan reveals subarachnoid hemorrhage in the right sylvian fissure; no evidence of hydrocephalus is apparent.
Axial NECT section shows hyperattenuating acute SAH in the Sylvian fissures (yellow ovals) and interhemispheric fissures (yellow arrows). Third ventricle and atria of the lateral ventricles are mildly dilated. Small amount of intraventricular hemorrhage is seen in the dependent occipital horn of left lateral ventricle (red arrow).
(A)Noncontrast CT demonstrates subarachnoid hemorrhage (arrows). (B)3-D reconstruction image from a CT angiogram demonstrates an aneurysm (arrow) from the anterior communicating artery as the cause of the bleed.
Non-contrast CT scan brain demonstrating a subarachnoid hemorrhage in the right Sylvian fissure and a hypodense filling defect due to the cysticercal cyst within the fissure B. Craniocaudal view of the reconstructed CT angiogram showing an aneurysm (arrow) at a branch of the middle cerebral artery.
MRI
MR is relatively insensitive within first 48 hours Hyperintense sulci and cisterns on FLAIR
(more sensitive than CT for small amounts of blood)
‘’Dirty’’ CSF isointense to brain on T1WI �+ T2WI
Low-signal intensity on brain surfaces in recurrent subarachnoid hemorrhages (hemosiderin deposition)
41-year-old man 3 days after traumatic subarachnoid hemorrhage. Axial FLAIR MR image shows posttraumatic subarachnoid hemorrhage (arrows) overlying temporal lobes.
MR imaging shows subarachnoid hemorrhage (SAH). SAH appears hyperintense on the T2-weighted and fluid-attenuated inversion recovery (FLAIR) images
MRI images show an extensive subarachnoid hemorrhage along the right cerebral convexity, most prominently in the frontal region. Also depicted are edema in the underlying cerebral parenchyma, mass effect, and compression of the right lateral ventricle. The hemorrhage appears hyperintense on T1-weighted images, with low signal on T2-weighted images
CT angiography and MRA have replaced conventional angiography in most institutions for the identification and location of the aneurysm itself
Cerebral angiography is used for the detection of intracranial aneurysms Such features as aneurysm size and
shape can help determine which aneurysm has bled
Still considered the “gold” standard for diagnosis of intracranial aneurysm
Management
Relief of associated vasospasm (occurs in as many as 50% of patients with SAH) may be accomplished medically with calcium channel blockers
Urgent surgical removal of blood may be indicated
Early surgical clipping is used to prevent rebleeding
Endovascular management is also now widely used Coiling
Complications
Acute obstructive hydrocephalus (in <1 week) secondary to intraventricular hemorrhage / ependymitis obstructing aqueduct of Sylvius or outlet of 4th ventricle
Delayed communicating hydrocephalus (after 1 week) secondary to fibroblastic proliferation in subarachnoid space and arachnoid villi interfering with CSF resorption
Cerebral vasospasm + infarction (develops after 72 hours, at maximum between 5-17 days, amount of blood is prognostic parameter)
Transtentorial herniation (cerebral hematoma, hydrocephalus, infarction, brain edema)
Prognosis
About 10 to 30% die before reaching medical help with first bleed
Nontraumatic subarachnoid hemorrhage in patients who reach the hospital still has a mortality rate of 30 to 60%
SAH from an arteriovenous malformation has a better prognosis than SAH from a ruptured aneurysm