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Subarachnoid hemorrhage

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Subarachnoid hemorrhage
SpecialtyEmergency medicine, neurology, neurosurgery Edit this on Wikidata

Subarachnoid hemorrhage (SAH), or subarachnoid haemorrhage, is bleeding into the subarachnoid space surrounding the brain, the area between the arachnoid membrane and the pia mater. The bleeding may occur spontaneously, usually from a cerebral aneurysm, or may result from trauma. Subarachnoid hemorrhage causes between 1 and 7% of all strokes.[1] Symptoms include an intense headache with a rapid onset ("thunderclap headache"), vomiting, and an altered level of consciousness.[2]

SAH is a serious medical emergency which can lead to death or severe disability — even if recognized and treated at an early stage. Diagnosis is generally made with computed tomography (CT scanning), or occasionally by lumbar puncture. Treatment is with close observation, medication and early neurosurgical investigations and treatments to prevent recurrence and complications. Of all people with SAH, 50% die, and 10–15% die before arriving at a hospital.[2]

Signs and symptoms

The classic symptom of subarachnoid hemorrhage is thunderclap headache (a headache described as the "worst ever" developing over seconds to minutes). This headache is often described like being "kicked in the head".[3] Thunderclap headache is a symptom in only about a third of all SAH patients, and one in ten people who attend for medical care with this symptom turn out to have a subarachnoid hemorrhage. Patients may also present with vomiting, and 1 in 14 have seizures. Neck stiffness and other signs of meningism may be present. Confusion, decreased level of consciousness or coma may be present. Intraocular hemorrhage (bleeding into the eyeball) may occur in response to the raised pressure around the brain.[2] Subhyaloid (the hyaloid membrane envelopes the vitreous body of the eye) and vitreous hemorrhage may be visible on fundoscopy. This is known as Terson syndrome (occurring in 3–13% of cases), and is more common in more severe SAH.[4]

In a patient with thunderclap headache, none of the signs mentioned are helpful in confirming or ruling out hemorrhage, although seizures are more common if the bleeding is the result of a ruptured aneurysm as opposed to other causes. Oculomotor nerve abnormalities (affected eye looking downward and outward, pupil dilated and less responsive to light) may indicate bleeding from the posterior cerebral artery. Isolated dilation of a pupil may also reflect brain herniation as a result of rising intracranial pressure (pressure inside the skull).[2]

As a result of the bleeding, blood pressure often rises rapidly, together with a release of adrenaline and similar hormones. As a result, substantial strain is put on the heart, and neurogenic pulmonary edema (accumulation of fluid in the lungs), cardiac arrhythmias (irregularities in the heart rate and rhythm), electrocardiographic changes (with occasional giant inverted 'cerebral' T waves) and cardiac arrest (3%) may occur rapidly after the onset of hemorrhage.[2][5]

Subarachnoid hemorrhage may also occur in people who have suffered a head injury. Symptoms may include headache (but not necessarily), decreased level of consciousness or hemiparesis (paralysis of one side of the body). It is regarded as a severe complication of head injury, especially if it is asssociated with lower Glasgow Coma Scale levels.[6]

Diagnosis

File:Subarachnoid hemorrhage aneurysm numbered.JPG
A brain CT angiography, showing a large aneurysm (1) at the basilar artery (2). The basilar artery arises from the vertebral artery (3), into which radiocontrast was injected. Further along its course, the basilar artery splits into the two posterior cerebral arteries (4) that are part of the circle of Willis.

The initial steps for evaluating a person who may have a subarachnoid hemorrhage are obtaining a medical history and performing a physical examination; these are aimed at assessing the likelihood that the symptoms are caused by SAH and identifying their other potential causes. Only 10–25% of patients admitted to the emergency department with a thunderclap headache are suffering from a SAH; therefore other possible causes are usually considered simultaneously, such as meningitis, migraine, and cerebral venous sinus thrombosis.[3] Intracerebral hemorrhage, which is twice as common as SAH, is often misdiagnosed as the latter.[7]

The diagnosis of subarachnoid hemorrhage cannot be made on clinical grounds alone. Medical imaging is usually required to confirm or exclude bleeding. The modality of choice is computed tomography (CT scan) of the brain. This has a high sensitivity (it will correctly identify over 95% of the cases), especially on the first day after the onset of bleeding. Some studies suggest that magnetic resonance imaging (MRI scan) may be more sensitive after several days, compared to CT. In people with normal CT or MRI scans, lumbar puncture, in which cerebrospinal fluid (CSF) is removed with a needle from the lumbar sac, shows evidence of haemorrhage in 3% of the group in whom the CT was found to be normal. The CSF sample is examined for xanthochromia, the yellow appearance of centrifugated fluid, or using spectrophotometry (measuring the absorption of particular wavelengths of light) for bilirubin, a breakdown product of hemoglobin in the CSF.[2][8]

It is not unusual for SAH to be initially misdiagnosed as migraine or tension headache, leading to a delay in obtaining a CT scan. In a 2004 study, this occurred in 12% 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.[9]

Once a subarachnoid hemorrhage is confirmed, the next question is about its origin. CT angiography (visualizing blood vessels with radiocontrast on a CT scan) to identify aneurysms is generally the first step, as invasive angiography (injecting radiocontrast through a catheter advanced to the brain arteries) has a higher risk of complications. The latter is useful if there are plans to obliterate the source of bleeding, such as an aneurysm, at the same time.[2]

Causes

Aneurysm (indicated by white arrow) of the posterior cerebral artery, findings during open brain surgery.

Spontaneous SAH is most often due to rupture of cerebral aneurysms (85%), weaknesses in the walls of arteries of the brain that become enlarged. They tend to be located in the circle of Willis and its branches. While most cases of SAH are due to bleeding from small aneurysms, there is evidence from research that larger aneurysms (which are rarer) are still more likely to rupture.[2]

In 15–20% of cases of spontaneous SAH, no aneurysm is detected from the first angiogram.[10] Non-aneurysmal perimesencephalic hemorrhage, in which the blood is limited to the area of the midbrain, causes another 10% of SAH cases. In these, no aneurysms are generally found. The remaining 5% of cases are due to vasculitic damage to arteries, other disorders affecting the vessels, disorders of the spinal cord blood vessels, and bleeding into various tumors.[2] Cocaine abuse and sickle cell anemia (usually children) and, rarely, anticoagulant therapy and problems with blood clotting can also result in SAH.[10] In cases that result from physical trauma, most SAHs occur near a skull fracture or intracerebral contusion.[10]

Classification

There are several grading scales available for subarachnoid hemorrhage. These have been derived by retrospectively matching characteristics of patients with their outcomes. In addition to the ubiquitously used Glasgow Coma Scale, three other specialized scores are in use. In all scores, a higher number is associated with a worse outcome.[11]

The first scale of severity was described by Hunt and Hess in 1968:[12]

Grade Signs and symptoms Survival
1 Asymptomatic; or minimal headache and slight neck stiffness 70%
2 Moderate to severe headache; neck stiffness; no neurologic deficit except 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:[13]

Grade appearance of hemorrhage
1 None evident
2 Less than 1 mm thick
3 More than 1 mm thick
4 Any thickness with intra-ventricular hemorrhage or parenchymal extension

The World Federation of Neurosurgeons classification uses Glasgow coma score (GCS) and focal neurological deficit to gauge severity of symptoms.[14]

Grade GCS Focal neurological deficit
1 15
2 13–14 None
3 13–14 Present
4 7–12 Present or absent
5 <7 Present or absent

Treatment

The management of subarachnoid hemorrhage consists of general measures to stabilize the patient, specific measures to prevent rebleeding by obliterating the bleeding source, prevention of a phenomenon known as vasospasm, and prevention and treatment of complications.[2]

General measures

The first priority is stabilization of the patient. Those with a depressed level of consciousness may need to be intubated and mechanically ventilated. Blood pressure, pulse, respiratory rate and Glasgow Coma Scale are monitored frequently. Once the diagnosis is confirmed, admission to an intensive care unit may be considered preferable, especially given that 15% have a further episode (rebleeding) in the first hours after admission. Nutrition is an early priority, with oral or nasogastric tube feeding being preferable over parenteral routes. Analgesia (pain control) is generally restricted to non-sedating agents, because sedation might change the mental status and thus interfere with the ability to monitor the level of consciousness.[2]

Prevention of rebleeding

Patients with a large hematoma, depressed level of consciousness or focal neurological symptoms may be candidates for urgent surgical removal of the blood or occlusion of the bleeding site. The remainder are admitted to the hospital and stabilized more extensively, and undergo an transfemoral angiogram or CT angiogram later. After the first 24 hours, rebleeding risk is about 40% over four weeks, suggesting that interventions should be aimed at reducing this risk.[2]

If a cerebral aneurysm is identified on angiography, two measures are available to reduce the risk of further bleeding from the same aneurysm: clipping[15] and coiling.[16] Clipping requires a craniotomy (opening of the skull) to locate the aneurysm, followed by the placement of clips around the neck of the aneurysm. Coiling is performed through the large blood vessels: a catheter is inserted into the femoral artery in the groin, and advanced through the aorta to the arteries (both carotid arteries and both vertebral arteries) that supply the brain. When the aneurysm has been located, platinum coils are deployed that lead to formation of a blood clot in the aneurysm and obliteration. The decision as to which modality is to be preferred is typically made by a multidisciplinary team consisting of a neurosurgeon, a neuroradiologist and often other experts.[2] Rebleeding is hard to predict but may happen at any time and carries a dismal prognosis. Interventions to prevent rebleeding are therefore performed as early as possible.[2]

There is little direct scientific evidence available to guide this decision other than technical experience. On the whole, aneurysms of the middle cerebral artery and its related vessels are hard to reach with angiography and tend to be amenable to clipping, while those of the basilar artery and posterior cerebral artery are hard to reach surgically and are more accessible for endovascular management.[17] The only situation where a randomized controlled trial has been conducted is in relatively well patients with small (less than 10 mm) aneurysms of the anterior cerebral artery and anterior communicating artery (together the "anterior circulation"), who constitute about 20% of all patients with aneurysmal SAH.[17][18] This trial, the International Subarachnoid Aneurysm Trial (ISAT), showed in this group of patients that the likelihood of death or dependency was reduced (23.5% in relative terms and 7.4% in absolute terms) if endovascular coiling was used as opposed to surgery.[17] The main drawback of coiling is the possibility that the aneurysm will recur; this risk is extremely small in the surgical approach. In ISAT, 8.3% needed further treatments in the longer term. Hence, patients who have undergone coiling are typically followed up for many years with angiography or other measures to ensure recurrence of aneurysms is identified early.[19] Other trials, too, have found a higher rate of recurrence necessitating further treatments.[20][21]

Vasospasm

Vasospasm, in which the blood vessels constrict, restricting blood flow, is a serious complication of SAH. It can cause ischemic brain injury that can cause permanent brain damage, and if severe can be fatal. This condition, which can be verified by transcranial doppler or cerebral angiography, is detected in about a third of all people admitted with subarachnoid hemorrhage, and causes permanent damage in half those people.[22]

Nimodipine, an oral calcium channel blocker, has been shown in clinical trials to reduce the chance of a bad outcome, even if it does not significantly reduce the amount of angiographic vasospasm.[23] 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.[22] In traumatic subarachnoid hemorrhage, nimodipine does not affect long-term outcome, and is not recommended.[24]

A treatment protocol referred to as "triple H" is often used as a measure to prevent vasospasm; this is the use of intravenous fluids to achieve a state of hypertension (high blood pressure), hypervolemia (excess fluid in the circulation) and hemodilution (mild dilution of the blood).[25] Evidence for this approach is inconclusive, and no sufficiently large randomized controlled trials have ever been undertaken to demonstrate its benefts.[26][27]

Other complications

In SAH treatment, there is emphasis on the prevention of complications; for instance, deep vein thrombosis is prevented with compression stockings, intermittent pneumatic compression, or both.[2]

Hydrocephalus (obstruction of the flow of cerebrospinal fluid) may complicate SAH both acutely and chronically. It is detected on CT scanning, on which there is enlargement of the lateral ventricles. If the level of consciousness is decreased, surgical drainage of the excess fluid is occasionally necessary.[2]

Fluctuations in blood pressure and electrolyte disturbances, as well as pneumonia and cardiac decompensation occur in about half the hospitalized patients with SAH, and may worsen prognosis. They are managed symptomatically.[2]

Prognosis

SAH is often associated with a poor outcome.[1] The mortality rate for SAH is between 40 and 50%,[7] although trends for survival are improving.[2] Delay in diagnosis of minor SAH without coma (or mistaking the sudden headache for migraine) contributes to this mortality.[9] Numerous other factors are associated with poorer outcome, such as higher age, poorer neurological grade on admission, occurrence of delayed ischemia resulting from vasospasm, location of an aneurysm in the posterior circulation, occurrence of heart damage, and presence of fever on the eighth day of admission.[28] Of those who survive initial hospitalization, treatment and complications, more than a quarter have significant restrictions in their lifestyle, and less than a fifth have no residual symptoms whatsoever.[17]

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; however it is still associated with a risk of ischemia, rebleeding and hydrocephalus.[10] Perimesencephalic SAH, however, has a very low rate of rebleeding and the prognosis of this subtype is excellent.[29]

Neurocognitive symptoms, such as fatigue, mood disturbances, and other related symptoms are common in people who have suffered a subarachnoid hemorrhage. Even in those who have made good neurological recovery, anxiety, depression, posttraumatic stress disorder and cognitive impairment are common. Over 60% report frequent headaches.[30]

Aneurysmal subarachnoid hemorrhage may lead to damage of the hypothalamus and the pituitary gland, two areas of the brain that play a central role in hormonal regulation and production. A 2007 study showed that more than a quarter of people with a previous SAH may develop deficiencies in one or more of the hypothalamic-pituitary hormones (a state known as hypopituitarism) such as growth hormone, prolactin or thyroid-stimulating hormone.[31]

Epidemiology

Average number of people with SAH per 100,000 person-years, broken down by age.

According to a review of 51 studies from 21 countries, the incidence of subarachnoid hemorrhage is on average 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.[32]

The group of people at risk for SAH is younger than the population usually affected by stroke,[1] but the risk still increases with age. Young people are much less likely (risk ratio 0.1, or 10%) than middle-aged people to suffer a subarachnoid hemorrhage.[32] The risk continues to rise with age and is 60% higher in the very elderly (over 85) than in those between 45 and 55.[32] Risk of SAH is about 25% higher in women above 55, probably reflecting the hormonal changes that result from the menopause.[32]

Genetics may play a role in a person's disposition to SAH, but lifestyle factors are more important.[1] Risk factors for subarachnoid hemorrhage are smoking, hypertension (high blood pressure) and excessive alcohol intake.[7] The risk of SAH for someone who has never smoked is slightly over half that for someone who has been a smoker in the past.[1] Some protection of uncertain significance is conferred by Caucasian ethnicity, hormone replacement therapy, higher than normal levels of cholesterol and diabetes mellitus.[1]

Screening and prevention

Prevention of subarachnoid hemorrhage depends on the detection of cerebral aneurysms, and safety and expected benefit from treatment for aneurysms detected in this way. Due to the relative rarity of cerebral aneurysms, screening is not performed for reasons of cost-effectiveness. An exception may be people who have two or more first-degree relatives who have suffered an aneurysmal subarachnoid hemorrhage.[2][33]

Autosomal dominant polycystic kidney disease (ADPKD), a hereditary kidney condition, is known to be associated with cerebral aneurysms in 8%, but most of these are small (and therefore unlikely to rupture). As a result, screening is only recommended in families with ADPKD where one family member has suffered a ruptured aneurysm.[34]

The incidental detection of an aneurysm (e.g. when someone undergoes an MRI scan of the brain for a different reason) presents a conundrum, as all treatments cerebral aneurysms are associated with potential complications. The International Study of Unruptured Intracranial Aneurysms (ISUIA) provided prognistic data both in people who had previously suffered a subarachnoid hemorrhage and people who had aneurysms detected by other means. Those who had previously suffered SAH were more likely to bleed from other aneurysms. In contrast, those who had never bled and had small aneurysms (<10 mm) were very unlikely to suffer SAH and were likely to sustain harm from attempts to repair these aneurysms.[35] On the basis of the ISUIA and other studies, it is now recommended that people are only considered for preventative treatment if they have a reasonable life expectancy and have aneurysms that have a higher likelihood of rupturing.[33]

History

The recognition of subarachnoid hemorrhage dates back to 1886, when Dr Byrom Bramwell reported some of its features, Dr Charles Symonds completed the picture in 1924. The first surgical intervention was performed by Norman Dodd, a pupil of Dr Harvey Cushing then working in Edinburgh. He pioneered the wrapping of aneurysms, and was an early pioneer in the use of angiograms.[36] American neurosurgeon Walter Dandy was the first to introduce clips.[15] The 1980s saw the introduction of 3H therapy[25] and trials with nimodipine[23] in the quest of trying to prevent delayed ischemia due to vasospasm. The Italian neurosurgeon Guiglielmi introduced his coil treatment in 1991.[16][37]

See also

References

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  35. ^ International Study of Unruptured Intracranial Aneurysms Investigators (1998). "Unruptured intracranial aneurysms--risk of rupture and risks of surgical intervention". N. Engl. J. Med. 339 (24): 1725–33. PMID 9867550. {{cite journal}}: Unknown parameter |month= ignored (help)
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  37. ^ Strother CM (2001). "Historical perspective. Electrothrombosis of saccular aneurysms via endovascular approach: part 1 and part 2". AJNR Am J Neuroradiol. 22 (5): 1010–2. PMID 11337350. {{cite journal}}: Unknown parameter |month= ignored (help)

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