Etiology and predisposing factors
Spontaneous (non-traumatic) subarachnoid hemorrhage is traditionally divided into two main forms: aneurysmal and non-aneurysmal.
In the vast majority of cases (70 to 85% of clinical observations), the source of the extravasated blood is a ruptured saccular aneurysm. These vascular defects have a predilection for certain locations — they most commonly form within the basin of the arteries of the Circle of Willis at the base of the brain.
The probability of vascular wall rupture increases significantly in the presence of triggering factors. The main risk factors contributing to the disruption of aneurysm integrity include arterial hypertension, cigarette smoking, and regular alcohol abuse. The bleeding episode itself is frequently triggered by sudden physical or emotional overexertion during active wakefulness.
Clinical presentation
The disease manifests in an extremely acute manner. Unlike some other forms of stroke, there are no prodromal symptoms.
The symptom complex consists of a combination of focal and pronounced general cerebral disturbances:
- Pain syndrome. A sudden, sharp, and unusually intense headache is the earliest and most frequent sign of the vascular catastrophe.
- General cerebral symptoms. Pronounced nausea, photophobia, and vomiting (often recurrent) join almost immediately.
- Impaired consciousness. Observed in more than half of patients (50–60%). The severity of the condition can range from obtundation to deep coma.
- Seizures. Generalized epileptic seizures develop in approximately 10% of cases, predominantly within the first 24 hours after rupture.
- Meningeal syndrome. Classic signs of meningeal irritation (e.g., nuchal rigidity) do not appear in the first minute, but develop 3–12 hours after disease onset.
Specific complications of SAH
The pathomorphological evolution of the extravasated blood and the reaction of brain structures determine the high risk of life-threatening conditions in the post-stroke period. Main complications include:
- Rebleeding. Recurrent hemorrhage is the most formidable early complication. It occurs in 20–25% of patients during the first three weeks (especially frequently in the first days) if the aneurysm has not been surgically excluded from the bloodstream.
- Cerebral vasospasm. Recorded in 30% of saccular aneurysm rupture cases. Spasm begins to develop from day 3, reaches maximum severity on days 5–8, and can persist until days 15–20. This condition causes profound ischemia of brain tissue, leading to secondary cerebral infarction in almost 50% of patients with this complication.
- Communicating (resorptive) hydrocephalus. Detected in 15% of surviving patients. The pathogenesis is associated with blood elements impairing normal cerebrospinal fluid resorption. Hydrocephalus most commonly manifests within the first three months after the episode.
Diagnostic principles and management
Clinical diagnosis is based on the hyperacute onset of combined neurological disturbances and the appearance of meningeal signs. Instrumental methods are required to confirm and precise the nature of the lesion.
Imaging methods:
- Computed tomography (CT) — the leading method for determining blood localization, detecting hydrocephalus, structural displacement, and intraventricular extension of blood.
- Cerebral angiography — used, in particular, in young patients without overt risk factors to rule out saccular aneurysms, arteriovenous malformations, tumors, or vasculitis.
Surgical treatment: If an arterial aneurysm or vascular malformation is diagnosed, early surgical intervention (within the first 3 days from onset) is the standard. The primary goal of the surgeon is to remove the accumulated hematoma and clip the aneurysm to prevent a fatal re-rupture. Contraindications to early surgery include coma and severe decompensated somatic disorders.
In case of impaired consciousness, general intensive care measures are performed, including endotracheal intubation and mechanical hyperventilation to reduce brain edema and prevent structural herniation.
Briefly: answers to topical questions
What are the causes of non-aneurysmal subarachnoid hemorrhage?
Causes of non-aneurysmal subarachnoid hemorrhage may include:
- non-aneurysmal perimesencephalic hemorrhage — about 10% of cases;
- trauma;
- arteriovenous malformations;
- dural venous sinus or cortical vein thrombosis;
- intracranial dissection;
- drug abuse, including cocaine;
- pseudoaneurysms;
- mycotic aneurysms;
- reversible cerebral vasoconstriction syndrome.
What instrumental methods are used to diagnose subarachnoid hemorrhage?
Neuroimaging methods and cerebrospinal fluid analysis are used for the instrumental diagnosis of subarachnoid hemorrhage.
- Computed tomography — native CT (without contrast) is the leading primary diagnostic method with high sensitivity in the first 12 hours.
- Magnetic resonance imaging — used alongside CT to visualize brain structures.
- Lumbar puncture — performed when CT and MRI are unavailable or insufficiently informative, to detect blood in the CSF.
- Contrast cerebral angiography — indicated in all cases when planning surgical treatment to identify a potential aneurysm.
What clinical scales are used to assess the severity of subarachnoid hemorrhage?
To assess the severity and classify subarachnoid hemorrhage, the following are used:
- World Federation of Neurosurgical Societies (WFNS) scale — to assess the severity of patients with SAH;
- Glasgow Coma Scale — used as part of the WFNS score to assess the level of consciousness;
- Fisher scale and modified Fisher scale — to classify SAH taking into account the thickness of the subarachnoid blood layer and the presence of intraventricular hemorrhage based on neuroimaging data.
Which drug is used for the medical prophylaxis of cerebral vasospasm in SAH?
Nimodipine is used for the medical prophylaxis of cerebral vasospasm and brain ischemia in subarachnoid hemorrhage.
- Nimodipine — a drug from the calcium channel blocker group.
Used in tablet form at a dose of 60 mg 6 times a day (every 4 hours). The maximum daily dose is 360 mg. The drug is administered per os or via a nasogastric tube. The duration of the prophylactic course is 21 days.
What CSF changes are detected during lumbar puncture in patients with SAH?
Lumbar puncture in patients with subarachnoid hemorrhage reveals characteristic visual and cytological changes in the cerebrospinal fluid.
- Bloody CSF — in the first days of the disease, the cerebrospinal fluid is colored red to varying degrees due to the presence of erythrocytes.
- Xanthochromia — subsequently, the CSF acquires a yellow, yellow-gray, yellow-brown, or green color. This phenomenon occurs as a consequence of hemoglobin degradation from lysed erythrocytes.
Class and exam questions
Why is severe nuchal rigidity not the first sign to look for when suspecting SAH?
Meningeal symptoms, including nuchal rigidity, do not develop instantaneously. They are usually detected in the majority of patients only 3–12 hours after disease onset.
On which day does a patient with SAH face the highest risk of cerebral vasospasm?
Vasospasm begins to form from day 3 post-hemorrhage, and its maximum clinical severity (with the risk of cerebral infarction) occurs on days 5–8.
What are the absolute contraindications for early clipping of a ruptured aneurysm?
Early surgical intervention (in the first 3 days) is contraindicated if the patient is in a coma or has severe somatic disorders.
What else to study on this topic
- Mechanisms of formation and localization of saccular aneurysms of the circle of Willis
- Pathophysiology of communicating hydrocephalus development following hemorrhage
- Methodology and objectives of targeted cerebral angiography
- Medical management of patients with severe cerebral vasospasm
- Prevention of recurrent hemorrhage in patients with concomitant arterial hypertension
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