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Etiology

  • 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)

Mortality rate

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

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

 

Pathophysiology

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.

 

Clinical Presentation

  • 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
  • Seizures
  • Sudden death
  • Terson's syndrome

 

Complications and Clinical course

Rebleeding

The risk of rebleeding is higher in the 24 hours after a SAH with a peak in the six hours later.

Mortality rate

The mortality rate associated to the rebleeding is 70%

Risk factors

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.

Incidence

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.

Risk factors

  • Severity of bleeding
  • Proximity to the major intracerebral vessels
  • Age < 50 years old
  • Hyperglycemia

Pathophysiology

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.

Consequences

The vasospasm cause a cerebral hypoperfusion and delayed cerebral ischemia (DCI).

There are two types of DCI:

  1. Single cortical infarcts located near the site of the ruptured aneurysm
  2. 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.

Clinical manifestations

Clinically, DCI is characterized by deterioration of the level of consciousness and new focal deficits. Anyway, in some patients DCI could be silent.

 

Hydrocephalus

It is a condition characterized by an abnormal accumulation of CSF in the brain.

Incidence

It is a common complication of SAH and occurs in 15% of patients (40% of symptomatics).

Clinical manifestations

Clinically it is characterized by deterioration of the level of consciousness, miosis, downward eye deviation and evidence of the ventricles enlargement on CT.

Pathophysiology

As far as the pathogenic point of view, the hydrocephalus is caused in two different manners:

  1. 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.
  2. 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

 

Seizures

If aneurysm of MCA, thick blood clot, intracerebral hemorrhage, DCI

 

Cardiac Abnormalities

Due to the release of catecholamine after the hypoperfusion of the hypothalamus:

ECG abnormalities

  • ST depression
  • QT prolongation
  • Deep T wave inversion
  • Prominent U waves
  • Left ventricular dysfunction
  • Troponin release
  • Elevated BNP (brain natriuretic peptide)

 

Diagnosis

It is based on non-contrast head CT scan and lumbar puncture.

Head CT

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.

Lumbar puncture

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

 

References

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Suarez JI, et.al. Aneurysmal subarachnoid hemorrhage. N Engl J Med 2006; 354:387.

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Inagawa T, et.al. Rebleeding of ruptured intracranial aneurysms in the acute stage. Surg Neurol 1987; 28:93.

Larsen CC, et.al. Rebleeding after aneurysmal subarachnoid hemorrhage: a literature review. World Neurosurg 2013; 79:307.

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de Rooij NK, et.al Delayed cerebral ischemia after subarachnoid hemorrhage: a systematic review of clinical, laboratory, and radiological predictors. Stroke 2013; 44:43.

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UK National External Quality Assessment Scheme for Immunochemistry Working Group. National guidelines for analysis of cerebrospinal fluid for bilirubin in suspected subarachnoid haemorrhage. Ann Clin Biochem 2003; 40:481.

Beetham R, UK NEQAS for Immunochermistry Working group. Recommendations for CSF analysis in subarachnoid haemorrhage. J Neurol Neurosurg Psychiatry 2004; 75:528.

Rinkel GJ, et.al. Prevalence and risk of rupture of intracranial aneurysms: a systematic review. Stroke 1998; 29:251.

Knekt P, et al. Risk factors for subarachnoid hemorrhage in a longitudinal population study. J Clin Epidemiol 1991; 44:933.

Sobey CG, Faraci FM. Subarachnoid haemorrhage: what happens to the cerebral arteries?. Clin Exp Pharmacol Physiol 1998; 25:867.

Abraham MK, Chang WW. Subarachnoid Hemorrhage. Emerg Med Clin North Am. 2016 Nov;34(4)

Findlay JM, et.al. Cerebral Vasospasm: A Review. Can J Neurol Sci. 2016 Jan;43(1)

 

Authors

 

 

Federico Nicolosi, MD

Neurosurgeon
University of Milan
"Spedali Civili" Hospital Brescia (Italy)
Scientific Team - UpSurgeOn

Giorgio Saraceno, MS

Medical Student
University of Brescia (Italy) 
Scientific Team UpSurgeOn