Subarachnoid hemorrhage
Subarachnoid hemorrhage | |
---|---|
Other names | Subarachnoid haemorrhage |
Diagnostic method | CT scan, lumbar puncture[2] |
Differential diagnosis | Meningitis, migraine, cerebral venous sinus thrombosis[3] |
Treatment | Neurosurgery or radiologically guided interventions[1] |
Medication | Labetalol, nimodipine[1] |
Prognosis | 45% risk of death at 30 days (aneurysmal)[1] |
Frequency | 1 per 10,000 per year[1] |
Subarachnoid hemorrhage (SAH) is
SAH may occur as a result of a
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
Signs and symptoms
The classic symptom of subarachnoid hemorrhage is
Neck stiffness usually presents six hours after initial onset of SAH.
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
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]
Causes
Most cases of SAH are due to
In 85 percent of spontaneous cases the cause is a
In 15–20 percent of cases of spontaneous SAH, no aneurysm is detected on the first
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.
Diagnosis
As only 10 percent of people admitted to the emergency department with a thunderclap headache are having an SAH, other possible causes are usually considered simultaneously, such as meningitis, migraine, and cerebral venous sinus thrombosis.[3] Intracerebral hemorrhage, in which bleeding occurs within the brain itself, is twice as common as SAH and is often misdiagnosed as the latter.[28] It is not unusual for SAH to be initially misdiagnosed as a migraine or tension headache, which can lead to a delay in obtaining a CT scan. In a 2004 study, this occurred in 12 percent of all cases and was more likely in people who had smaller hemorrhages and no impairment in their mental status. The delay in diagnosis led to a worse outcome.[29] In some people, the headache resolves by itself, and no other symptoms are present. This type of headache is referred to as "sentinel headache", because it is presumed to result from a small leak (a "warning leak") from an aneurysm. A sentinel headache still warrants investigations with CT scan and lumbar puncture, as further bleeding may occur in the subsequent three weeks.[30]
The initial steps for evaluating a person with a suspected subarachnoid hemorrhage are obtaining a medical history and performing a physical examination. The diagnosis cannot be made on clinical grounds alone and in general medical imaging and possibly a lumbar puncture is required to confirm or exclude bleeding.[2]
Imaging
The modality of choice is
Angiography
After a subarachnoid hemorrhage is confirmed, its origin needs to be determined. If the bleeding is likely to have originated from an aneurysm (as determined by the CT scan appearance), the choice is between
In emergency department patients complaining of acute-onset headache without significant risk factors for SAH, evidence suggests that CT scanning of the head followed by CT angiography can reliably exclude SAH without the need for a lumbar puncture.[33] The risk of missing an aneurysmal bleed as the cause of SAH with this approach is less than 1%.[33]
Lumbar puncture
The CSF sample is also examined for xanthochromia—the yellow appearance of centrifugated fluid. This can be determined by spectrophotometry (measuring the absorption of particular wavelengths of light) or visual examination. It is unclear which method is superior.[35] Xanthochromia remains a reliable ways to detect SAH several days after the onset of headache.[36] An interval of at least 12 hours between the onset of the headache and lumbar puncture is required, as it takes several hours for the hemoglobin from the red blood cells to be metabolized into bilirubin.[4][36]
ECG
Also one of the characteristic
Classification
There are several grading scales available for SAH. The Glasgow Coma Scale (GCS) is ubiquitously used for assessing consciousness. Its three specialized scores are used to evaluate SAH; in each, a higher number is associated with a worse outcome.[41] These scales have been derived by retrospectively matching characteristics of people with their outcomes.
The first widely used scale for neurological condition following SAH was published by Botterell and Cannell in 1956 and referred to as the Botterell Grading Scale. This was modified by Hunt and Hess[42][43][44] in 1968:[45]
Grade | Signs and symptoms | Survival |
---|---|---|
1 | Asymptomatic or minimal headache and slight neck stiffness | 70% |
2 | Moderate to severe headache; neck stiffness; no cranial nerve palsy |
60% |
3 | Drowsy ; minimal neurologic deficit |
50% |
4 | Stuporous; moderate to severe hemiparesis; possibly early decerebrate rigidity and vegetative disturbances |
20% |
5 | Deep coma; decerebrate rigidity; moribund | 10% |
The Fisher Grade classifies the appearance of subarachnoid hemorrhage on CT scan.[46]
Grade | Appearance of hemorrhage |
---|---|
1 | None evident |
2 | Less than 1 mm thick |
3 | More than 1 mm thick |
4 | Diffuse or none with intraventricular hemorrhage or parenchymal extension
|
This scale has been modified by Claassen and coworkers, reflecting the additive risk from SAH size and accompanying intraventricular hemorrhage (0 – none; 1 – minimal SAH w/o IVH; 2 – minimal SAH with IVH; 3 – thick SAH w/o IVH; 4 – thick SAH with IVH);.[47]
The World Federation of Neurosurgeons (WFNS) classification uses Glasgow coma score and
Grade | GCS | Focal neurological deficit |
---|---|---|
1 | 15 | Absent |
2 | 13–14 | Absent |
3 | 13–14 | Present |
4 | 7–12 | Present or absent |
5 | <7 | Present or absent |
A comprehensive
Screening and prevention
Screening for aneurysms is not performed on a population level; because they are relatively rare, it would not be cost-effective. However, if someone has two or more first-degree relatives who have had an aneurysmal subarachnoid hemorrhage, screening may be worthwhile.[4][50]
Autosomal dominant polycystic kidney disease (ADPKD), a hereditary kidney condition, is known to be associated with cerebral aneurysms in 8 percent of cases, but most such aneurysms are small and therefore unlikely to rupture. As a result, screening is only recommended in families with ADPKD where one family member has had a ruptured aneurysm.[51]
An aneurysm may be detected incidentally on brain imaging; this presents a conundrum, as all treatments for cerebral aneurysms are associated with potential complications. The International Study of Unruptured Intracranial Aneurysms (ISUIA) provided prognostic data both in people having previously had a subarachnoid hemorrhage and people who had aneurysms detected by other means. Those having previously had a SAH were more likely to bleed from other aneurysms. In contrast, those having never bled and had small aneurysms (smaller than 10 mm) were very unlikely to have a SAH and were likely to sustain harm from attempts to repair these aneurysms.[52] On the basis of the ISUIA and other studies, it is now recommended that people are considered for preventive treatment only if they have a reasonable life expectancy and have aneurysms that are highly likely to rupture.[50] Moreover, there is only limited evidence that endovascular treatment of unruptured aneurysms is actually beneficial.[53]
Treatment
Management involves general measures to stabilize the person while also using specific investigations and treatments. These include the prevention of rebleeding by obliterating the bleeding source, prevention of a phenomenon known as vasospasm, and prevention and treatment of complications.[4]
Stabilizing the person is the first priority. Those with a depressed level of consciousness may need to be
People with poor clinical grade on admission, acute neurologic deterioration, or progressive enlargement of ventricles on CT scan are, in general, indications for the placement of an
Preventing rebleeding
Efforts to keep a person's
People whose CT scan shows a large hematoma, depressed level of consciousness, or focal neurologic signs may benefit from urgent surgical removal of the blood or occlusion of the bleeding site. The remainder are stabilized more extensively and undergo a transfemoral angiogram or CT angiogram later. It is hard to predict who will have a rebleed, yet it may happen at any time and carries a dismal prognosis. After the first 24 hours have passed, rebleeding risk remains around 40 percent over the subsequent four weeks, suggesting that interventions should be aimed at reducing this risk as soon as possible.[4] Some predictors of early rebleeding are high systolic blood pressure, the presence of a hematoma in the brain or ventricles, poor Hunt-Hess grade (III-IV), aneurysms in the posterior circulation, and an aneurysm >10 mm in size.[55]
If a
In general, the decision between clipping and coiling is made on the basis of the location of the aneurysm, its size and the condition of the person. Aneurysms of the
Vasospasm
The pathogenesis of cerebral vasospasm following subarachnoid hemorrhage is attributed to the higher levels of
The use of calcium channel blockers, thought to be able to prevent the spasm of blood vessels by preventing calcium from entering smooth muscle cells, has been proposed for prevention.[23] The calcium channel blocker nimodipine when taken by mouth improves outcome if given between the fourth and twenty-first day after the bleeding, even if it does not reduce the amount of vasospasm detected on angiography.[69] It is the only Food and Drug Administration (FDA)-approved drug for treating cerebral vasospasm.[26] In traumatic subarachnoid hemorrhage, nimodipine does not affect long-term outcome, and is not recommended.[70] Other calcium channel blockers and magnesium sulfate have been studied, but are not presently recommended; neither is there any evidence that shows benefit if nimodipine is given intravenously.[63]
Nimodipine is readily authorized in the form of tablets and solution for infusion for the prevention and treatment of complications due to vasospasm following subarachnoid hemorrhage. Another sustained formulation of nimodipine administered via an external ventricular drain (EVD), called EG-1962, is also available. In contrast to the tablets and solution formulations of Nimodipine which require an administration every 4hrs for a total of 21 days, the sustained formulation, EG-1962, needs to be administered once directly into the ventricles. The CSF concentrations from EG-1962, however, were at least 2 orders of magnitude higher than those with oral nimodipine. These results supported a phase 3 study that demonstrated a favorable safety profile for EG-1962 but yielded inconclusive efficacy results due to notable differences in clinical outcome based on baseline disease severity.[71][72][73]
Some older studies have suggested that statin therapy might reduce vasospasm, but a subsequent meta-analysis including further trials did not demonstrate benefit on either vasospasm or outcomes.[74] While corticosteroids with mineralocorticoid activity may help prevent vasospasm their use does not appear to change outcomes.[75]
A protocol referred to as "triple H" is often used as a measure to treat vasospasm when it causes symptoms; this is the use of
If the symptoms of delayed ischemia do not improve with medical treatment, angiography may be attempted to identify the sites of vasospasms and administer
Other complications
People have often been treated with
Prognosis
Short-term outcomes
SAH is often associated with a poor outcome.
So-called "angiogram-negative subarachnoid hemorrhage", SAH that does not show an aneurysm with four-vessel angiography, carries a better prognosis than SAH with aneurysm, but it is still associated with a risk of ischemia, rebleeding, and
The prognosis of head trauma is thought to be influenced in part by the location and amount of subarachnoid bleeding.
There is also modest evidence that genetic factors influence the prognosis in SAH. For example, having two copies of ApoE4 (a variant of the gene encoding apolipoprotein E that also plays a role in Alzheimer's disease) seems to increase risk for delayed ischemia and a worse outcome.[86] The occurrence of hyperglycemia (high blood sugars) after an episode of SAH confers a higher risk of poor outcome.[87]
Long-term outcomes
Neurocognitive symptoms, such as
Epidemiology
According to a review of 51 studies from 21 countries, the average incidence of subarachnoid hemorrhage is 9.1 per 100,000 annually. Studies from Japan and Finland show higher rates in those countries (22.7 and 19.7, respectively), for reasons that are not entirely understood. South and Central America, in contrast, have a rate of 4.2 per 100,000 on average.[90]
Although the group of people at risk for SAH is younger than the population usually affected by stroke,[84] the risk still increases with age. Young people are much less likely than middle-age people (risk ratio 0.1, or 10 percent) to have a subarachnoid hemorrhage.[90] The risk continues to rise with age and is 60 percent higher in the very elderly (over 85) than in those between 45 and 55.[90] Risk of SAH is about 25 percent higher in women over 55 compared to men the same age, probably reflecting the hormonal changes that result from the menopause, such as a decrease in estrogen levels.[90]
Genetics may play a role in a person's disposition to SAH; risk is increased three- to fivefold in first-degree relatives of people having had a subarachnoid hemorrhage.
Overall, about 1 percent of all people have one or more cerebral aneurysms. Most of these are small and unlikely to rupture.[52]
History
While the clinical picture of subarachnoid hemorrhage may have been recognized by
The first surgical intervention was performed by Norman Dott, who was a pupil of
References
- ^ PMID 27741994.
- ^ PMID 27306497.
- ^ ISBN 978-0-19-856837-7.
- ^ S2CID 29126514.
- ^ PMID 2199609.
- ^ from the original on 14 November 2005.
- ^ Dixon A. "Pseudosubarachnoid hemorrhage | Radiology Reference Article | Radiopaedia.org". Radiopaedia.
- PMID 12591643.
- PMID 24370126.
- PMID 30039044.
- ^ ISBN 978-0-19-852072-6.
- ^ ISBN 978-0-19-857013-4.
- PMID 14966173.
- ISBN 978-0-19-856609-0.
- PMID 16286583.
- S2CID 18066655.
- S2CID 20268064.
- S2CID 29858980.
- S2CID 38900336.
- S2CID 5511658.
- ISBN 9780323089296. Archivedfrom the original on 10 September 2017.
- ^ PMID 8362440.
- ^ S2CID 23726077.
- S2CID 227321.
- S2CID 8755665.
- ^ .
- S2CID 23626380.
- ^ PMID 8610327.
- ^ PMID 14970066.
- ^ S2CID 45645505.
- S2CID 7268382.
- ^ PMID 31543134.
- ^ PMID 20370785.
- ^ Thomas L, et al. (July 2009). "Evidence-Based Approach to Diagnosis and Management of Aneurysmal Subarachnoid Hemorrhage in the Emergency Department". Emergency Medicine Practice. 11 (7). Archived from the original on 14 March 2012.
- PMID 24635988.
- ^ S2CID 24393459.
- S2CID 9169045.
- PMID 5033416.
- PMID 7897337.)
{{cite journal}}
: CS1 maint: multiple names: authors list (link - S2CID 8830952.
- S2CID 13925503.
- PMID 26381258.
- .
- S2CID 13925503.
- S2CID 2871628.
- PMID 7354892.
- PMID 11546890.
- PMID 3236024.
- ^ PMID 9588539.
- ^ from the original on 20 December 2010.
- PMID 15086900.
- ^ PMID 9867550.
- PMID 20634431.
- ^ "Care of the Patient with Anuerysmal Subarachnoid Hemorrhage". AANN Clinical Practice Guidelines. American Association of Neuroscience Nurses. Archived from the original on 29 December 2013. Retrieved 14 June 2013.
- PMID 24911172.
- ^ PMID 17857170.
- ^ PMID 2045924.
- ^ S2CID 18777412.
- PMID 30110521.
- PMID 17395870.
- PMID 17293572.
- PMID 12775880.
- ^ S2CID 1767194.
- S2CID 23626380.)
{{cite journal}}
: CS1 maint: multiple names: authors list (link - S2CID 23446475.
- PMID 15626454.
- )
- S2CID 6830602.)
{{cite journal}}
: CS1 maint: multiple names: authors list (link - ^ PMID 6338383.
- S2CID 43488740.
- S2CID 208870207.)
{{cite journal}}
: CS1 maint: multiple names: authors list (link - S2CID 212569228.)
{{cite journal}}
: CS1 maint: multiple names: authors list (link - PMID 28873993.)
{{cite journal}}
: CS1 maint: multiple names: authors list (link - PMID 19875741.
- PMID 27173669.
- ^ PMID 7133349.
- S2CID 38149776.
- S2CID 37400347.
- S2CID 24028808.
- S2CID 18547651.
- ^ PMID 17569871.
- PMID 15662039.
- ISBN 978-0-443-04345-1.
- ^ PMID 16282541.
- PMID 17332451.
- S2CID 8596810.
- S2CID 7684816.
- PMID 12023423.
- PMID 17895459.
- ^ PMID 17470467.
- PMID 23704101.
- ^ PMID 3890278.
- ^ Bramwell B (1886). "Spontaneous meningeal haemorrhage". Edinburgh Medical Journal. 32: 101.
- .
- PMID 19983808.
- PMID 4654697.
- PMID 2496789.
- PMID 6228084.
- S2CID 1628687.
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