- Trauma: is the most common cause of SAH
- Spontaneous SAH: most cases of SAH are caused by a rupture of an intracranial saccular aneurysm but in the 15-20% of the cases the etiology is different (NASAH, non-aneurysmal SAH)
The rupture of a saccular aneurysm is a devasting event with a 50% mortality rate and higher rate of morbidity of the survivals.
Risk factors of aneurysm formation overlaps with risk factors of SAH:
- Cigarette smoking
- Hypertension (diurnal variation in blood pressure)
- Genetic risk: the risk is higher in post-menopausal women than in men with the same age. Younger women are protected thanks to estrogens
- Anti-thrombotic therapy
- Low Cholesterol and Statin use: these factors interact
- Oral contraceptive
- Pregnancy and partitition
After the rupture of the saccular aneurysm, the blood is reversed in the CSF.
The first consequence is the raising of the intracranial pressure (ICP). Depending on the location of the aneurysm, the blood can spread both in the brain parenchyma and in the ventricular space.
Note that the bleeding lasts for few second but there are several complications.
- Headache: sudden and severe, also known as “sentinel headache” (rated 9 or 10 in a scale ranging 1 to 10), lateralized (30%) to the side of the aneurysm. It begins abruptly because of the rupture of the aneurysm.
- Vegetative symptoms
- Loss of consciousness
- Meningite: it develops only after several hours because the product of the blood breakdown blood has to generate themselves in the CSF
- Sudden death
- Terson's syndrome
Complications and Clinical course
The risk of rebleeding is higher in the 24 hours after a SAH with a peak in the six hours later.
The mortality rate associated to the rebleeding is 70%
Some factors are useful to predict the risk of rebleeding:
- Hunt-Hess grade on admission
- Maximal aneurysm diameter
- Higher blood pressure
- Sentinel headache
- Early ventriculostomy
- Longer interval from ictus to admission
Note that the rebleeding is diagnosed upon a clinical and radiological findings. There is a deterioration of the neurological status and the presence of a new SAH on CT.
Vasospasm and Delayed Cerebral Ischemia (DCI)
Vasospasm cause symptomatic ischemia and infartcion.
A 20-30% of cases with SAH develop vasospasm.
Generally, the vasospasm starts at day three from the admission, reaching a peak at day seven but it can occur earlier.
- Severity of bleeding
- Proximity to the major intracerebral vessels
- Age < 50 years old
It is caused by the rupture of the blood clots in the subarachnoid space that lead to an endothelium damage and interfere with the smooth muscle contraction. The damage of the endothelial cells decrease the production of NO (nitric oxide) so that there is a vasoconstriction and impaired response to vasodilators.
Note that the release of endothelin is another factors involved in vasospasm.
The vasospasm cause a cerebral hypoperfusion and delayed cerebral ischemia (DCI).
There are two types of DCI:
- Single cortical infarcts located near the site of the ruptured aneurysm
- Multiple widespread infarcts in bilateral and subcortical regions, distal to the site of the ruptured aneurysm (40-50% of cases)
The younger patients and the smokers are at high risk of DCI.
Clinically, DCI is characterized by deterioration of the level of consciousness and new focal deficits. Anyway, in some patients DCI could be silent.
It is a condition characterized by an abnormal accumulation of CSF in the brain.
It is a common complication of SAH and occurs in 15% of patients (40% of symptomatics).
Clinically it is characterized by deterioration of the level of consciousness, miosis, downward eye deviation and evidence of the ventricles enlargement on CT.
As far as the pathogenic point of view, the hydrocephalus is caused in two different manners:
- Obstruction of the CSF flow: in this case hydrocephalus is an acute complication caused by the obstruction of the CSF flow by the blood clots.
- Reduction of the absorption of the CSF by the arachnoidal granulations: this complication develops few week later.
Increased ICP (intracranial pressure)
Due to hemorrhage volume, acute hydrocephalus, reactive hyperemia, distal arteriolar cerebral vasodilation
If aneurysm of MCA, thick blood clot, intracerebral hemorrhage, DCI
Due to the release of catecholamine after the hypoperfusion of the hypothalamus:
- ST depression
- QT prolongation
- Deep T wave inversion
- Prominent U waves
- Left ventricular dysfunction
- Troponin release
- Elevated BNP (brain natriuretic peptide)
It is based on non-contrast head CT scan and lumbar puncture.
Hyperdensity in the subarachnoid space, most common in the region of the circle of Willis and around the Sylvian fissure.
If blood is located in the interpeduncular fossa, it appears as a hyperdense triangle.
Blood can be detected in temporal horns of the lateral ventricles, too.
The lumbar puncture is mandatory if there is the suspicious of SAH with a normal CT scan.
Several characteristics are evaluated:
- Clearing of blood (declining of RBC count in CSF): a 63% reduction of the RBC count indicate a SAH
- Xantochromia: yellow appearance of the CSF. It means that the blood has been in the CSF for at least two hours. So if a lumbar puncture is performed prior to two hours after a SAH, CSF can be normal in colour. Xantochromia can last for two week or more.
- Spectrofotometry: detects products of blood clots degradation (from oxyhemoglobin to methemoglobin and bilirubin). Normally it isn’t used for the diagnosis.
NASAH (Non-Aneurysmal SAH)
- Perimesencephalic non-aneurysmal SAH: represent two third of NASAH cases. It is characterized by typical localization of blood clots on CT scan, normal cerebral angiography and a benign course.
- Occult aneurysm: it is an aneurysm not detected in the first angiography (24% of cases)
- Vascular malformations: spinal or intracranial
- Others: cerebral venous thrombosis, sickle cell disease, bleeding disorders, pituitary apoplexy, traumatic SAH, cocaine abuse, cerebral amyloid angiopathy
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Giorgio Saraceno, MS
University of Brescia (Italy)
Federico Nicolosi, MD
University of Milan