Subarachnoid hemorrhage

SAH may occur as a result of a head injury or spontaneously, usually from a ruptured cerebral aneurysm.^[1] Risk factors for spontaneous cases include high blood pressure, smoking, family history, alcoholism, and cocaine use.^[1] Generally, the diagnosis can be determined by a CT scan of the head if done within six hours of symptom onset.^[2] Occasionally, a lumbar puncture is also required.^[2] After confirmation further tests are usually performed to determine the underlying cause.^[2]


Treatment is by prompt neurosurgery or endovascular coiling.^[1] Medications such as labetalol may be required to lower the blood pressure until repair can occur.^[1] Efforts to treat fevers are also recommended.^[1] Nimodipine, a calcium channel blocker, is frequently used to prevent vasospasm.^[1] The routine use of medications to prevent further seizures is of unclear benefit.^[1] Nearly half of people with a SAH due to an underlying aneurysm die within 30 days and about a third who survive have ongoing problems.^[1] Between ten and fifteen percent die before reaching a hospital.^[4]


Spontaneous SAH occurs in about one per 10,000 people per year.^[1] Females are more commonly affected than males.^[1] While it becomes more common with age, about 50% of people present under 55 years old.^[4] It is a form of stroke and comprises about 5 percent of all strokes.^[4] Surgery for aneurysms was introduced in the 1930s.^[5] Since the 1990s many aneurysms are treated by a less invasive procedure called endovascular coiling, which is carried out through a large blood vessel.^[6]


A true subarachnoid hemorrhage may be confused with a pseudosubarachnoid hemorrhage, an apparent increased attenuation on CT scans within the basal cisterns that mimics a true subarachnoid hemorrhage.^[7] This occurs in cases of severe cerebral edema, such as by cerebral hypoxia. It may also occur due to intrathecally administered contrast material,^[8] leakage of high-dose intravenous contrast material into the subarachnoid spaces, or in patients with cerebral venous sinus thrombosis, severe meningitis, leptomeningeal carcinomatosis,^[9] intracranial hypotension, cerebellar infarctions, or bilateral subdural hematomas.^[10]

Signs and symptoms

The classic symptom of subarachnoid hemorrhage is thunderclap headache (a headache described as "like being kicked in the head",^[3] or the "worst ever", developing over seconds to minutes). This headache often pulsates towards the occiput (the back of the head).^[11] About one-third of people have no symptoms apart from the characteristic headache, and about one in ten people who seek medical care with this symptom are later diagnosed with a subarachnoid hemorrhage.^[4] Vomiting may be present, and 1 in 14 have seizures.^[4] Confusion, decreased level of consciousness or coma may be present, as may neck stiffness and other signs of meningism.^[4]


Neck stiffness usually presents six hours after initial onset of SAH.^[12] Isolated dilation of a pupil and loss of the pupillary light reflex may reflect brain herniation as a result of rising intracranial pressure (pressure inside the skull).^[4] Intraocular hemorrhage (bleeding into the eyeball) may occur in response to the raised pressure: subhyaloid hemorrhage (bleeding under the hyaloid membrane, which envelops the vitreous body of the eye) and vitreous hemorrhage may be visible on fundoscopy. This is known as Terson syndrome (occurring in 3–13 percent of cases) and is more common in more severe SAH.^[13]


Oculomotor nerve abnormalities (affected eye looking downward and outward and inability to lift the eyelid on the same side) or palsy (loss of movement) may indicate bleeding from the posterior communicating artery.^[4][11] Seizures are more common if the hemorrhage is from an aneurysm; it is otherwise difficult to predict the site and origin of the hemorrhage from the symptoms.^[4] SAH in a person known to have seizures is often diagnostic of a cerebral arteriovenous malformation.^[11]


The combination of intracerebral hemorrhage and raised intracranial pressure (if present) leads to a "sympathetic surge", i.e. over-activation of the sympathetic system. This is thought to occur through two mechanisms, a direct effect on the medulla that leads to activation of the descending sympathetic nervous system and a local release of inflammatory mediators that circulate to the peripheral circulation where they activate the sympathetic system. As a consequence of the sympathetic surge there is a sudden increase in blood pressure; mediated by increased contractility of the ventricle and increased vasoconstriction leading to increased systemic vascular resistance. The consequences of this sympathetic surge can be sudden, severe, and are frequently life-threatening. The high plasma concentrations of adrenaline also may cause cardiac arrhythmias (irregularities in the heart rate and rhythm), electrocardiographic changes (in 27 percent of cases)^[14] and cardiac arrest (in 3 percent of cases) may occur rapidly after the onset of hemorrhage.^[4][15] A further consequence of this process is neurogenic pulmonary edema,^[16] where a process of increased pressure within the pulmonary circulation causes leaking of fluid from the pulmonary capillaries into the air spaces, the alveoli, of the lung.^[17][18]


Subarachnoid hemorrhage may also occur in people who have had a head injury. Symptoms may include headache, decreased level of consciousness and hemiparesis (weakness of one side of the body). SAH is a frequent occurrence in traumatic brain injury and carries a poor prognosis if it is associated with deterioration in the level of consciousness.^[19]


While thunderclap headache is the characteristic symptom of subarachnoid hemorrhage, less than 10% of those with concerning symptoms have SAH on investigations.^[2] A number of other causes may need to be considered.^[20]

Pathophysiology

Cerebral vasospasm is one of the complications caused by subarachnoid hemorrhage. It usually happens from the third day after the aneurysm event, and reaches its peak on 5th to 7th day.^[26] There are several mechanisms proposed for this complication. Blood products released from subarachnoid hemorrhage stimulates the tyrosine kinase pathway causing the release of calcium ions from intracellular storage, resulting in smooth muscle contraction of cerebral arteries. Oxyhaemoglobin in cerebrospinal fluid (CSF) causes vasoconstriction by increasing free radicals, endothelin-1, prostaglandin and reducing the level of nitric oxide and prostacyclin. Besides, the disturbances of autonomic nervous system innervating cerebral arteries is also thought to cause vasospasm.^[27]