Subarachnoid hemorrhage
| Subarachnoid hemorrhage | |
 | |
|---|---|
| CT scan of the brain showing subarachnoid hemorrhage as a white area in the center | |
| ICD-10 | I60, S06.6 |
| ICD-9 | 430, 852.0-852.1 |
| DiseasesDB | 12602 |
| MedlinePlus | 000701 |
| eMedicine | med/2883 neuro/357 emerg/559 |
| MeSH | D013345 |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
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Overview
Subarachnoid hemorrhage (SAH), or subarachnoid haemorrhage, is bleeding into the subarachnoid space surrounding the brain, i.e., the area between the arachnoid membrane and the pia mater. It may arise due to trauma or spontaneously, and is a medical emergency which can lead to death or severe disability even if recognized and treated in an early stage. Treatment is with close observation, medication and early neurosurgical investigations and treatments. Subarachnoid hemorrhage causes 5% of all strokes. 10-15% die before arriving in hospital, and average survival is 50%.[1]
Signs and symptoms
The classic symptom of subarachnoid hemorrhage is thunderclap headache ("most severe ever" headache developing over seconds to minutes). This headache is often described like being "kicked in the head".[2] 10% of all people with this symptom turn out to have a subarachnoid hemorrhage, and is the only symptom in about a third of all SAH patients. Other presenting features may be vomiting (non-specific), seizures (1 in 14) and meningism. Confusion, decreased level of consciousness or coma may be present. Intraocular hemorrhage (bleeding into the eyeball) may occur. Subhyaloid hemorrhages may be visible on fundoscopy (the hyaloid membrane envelopes the vitreous body).[1]
In a patient with thunderclap headache, none of the signs mentioned are helpful in confirming or ruling out hemorrhage, although a seizure makes bleeding from an aneurysm more likely. Oculomotor nerve abnormalities (affected eye looking downward and outward, pupil widened and less responsive to light) may indicate a bleed at the posterior inferior cerebellar artery.[1]
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, cardiac arrhythmias, electrocardiographic changes (some resembling a heart attack) and cardiac arrest (3%) may occur rapidly after the onset of hemorrhage.[3][1]
Bleeding into the subarachnoid space may occur as a result of injury or trauma. SAH in a trauma patient is often detected when a patient who has been involved in an accident becomes less responsive or develops hemiparesis (one-sided weakness) or changed pupillary reflexes, and Glasgow Coma Score calculations deteriorate. Headache is not necessarily present.
Risk factors for subarachnoid hemorrhage are smoking, hypertension (high blood pressure) and excessive alcohol intake; all are associated with a doubled risk for SAH. Some protection of uncertain significance is conferred by Caucasian ethnicity, hormone replacement therapy, a higher than normal cholesterol and the presence of diabetes mellitus.[4]
Diagnosis
The initial steps in a case of possible subarachnoid hemorrhage are obtaining a medical history and performing a physical examination; these are aimed at assessing the likelihood of the condition, and identifying other potential causes of the symptoms. Neck stiffness and other signs of meningism may be present, as well as a reduced level of consciousness. Only 25% of admitted patients to the emergency department with a thunderclap headache are suffering from a SAH, and as such carefully consideration of differentials should be completed (e.g. evaluation of meningitis, migraine headaches and/or central venous thrombosis).[2]
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/CAT) of the brain. This has a high sensitivity (it will correctly identify >95% of the cases), especially on the first day after the onset of bleeding. Some data suggests that magnetic resonance imaging (MRI) may be more sensitive after several days. In those where the CT/MRI scan is normal, lumbar puncture (removal of cerebrospinal fluid/CSF with a needle from the lumbar sac under local anesthetic) will identify another 3% of the cases by demonstrating xanthochromia (yellow appearance of centrifugated fluid) or bilirubin (a breakdown product of hemoglobin) in the CSF.[1]
Once a subarachnoid hemorrhage is confirmed, the next question is about its origin. CT angiography (using radiocontrast) to identify aneurysms is generally the first step, as invasive angiography (injecting radiocontrast through a catheter advanced to the brain arteries) has a small rate of complications but is useful if there are plans to obliterate the source of bleeding, such as an aneurysm, at the same time.[1]
Causes
Spontaneous SAH is most often due to rupture of cerebral aneurysms (85%), weaknesses in the wall of the arteries of the brain that enlarge. 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. A further 10% of cases is due to non-aneurysmal perimesencephalic hemorrhage, in which the blood is limited to the area of the midbrain. No aneurysms are generally found. The remaining 5% are due to vasculitic damage to arteries, other disorders affecting the vessels, disorders of the spinal cord blood vessels, and bleeding into various tumors.[1]
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.[5]
- Hunt and Hess scale
The first scale of severity, described by Hunt and Hess in 1968:[6]
- Grade 1: Asymptomatic; or minimal headache and slight nuchal rigidity. Approximate survival rate 70%.
- Grade 2: Moderate to severe headache; nuchal rigidity; no neurologic deficit except cranial nerve palsy. 60%.
- Grade 3: Drowsy; minimal neurologic deficit. 50%.
- Grade 4: Stuporous; moderate to severe hemiparesis; possibly early decerebrate rigidity and vegetative disturbances. 20%.
- Grade 5: Deep coma; decerebrate rigidity; moribund. 10%.
- Fisher grade
The Fisher Grade classifies the appearance of subarachnoid hemorrhage on CT scan:[7]
- Grade 1= No hemorrhage evident
- Grade 2= Subarachnoid hemorrhage less than 1 mm thick
- Grade 3= Subarachnoid hemorrhage more than 1 mm thick
- Grade 4= Subarachnoid hemorrhage of any thickness with intra-ventricular hemorrhage (IVH) or parenchymal extension
- World Federation of Neurosurgeons
The World Federation of Neurosurgeons classification:[8]
- Class 1 - GCS (Glasgow Coma Scale)15
- Class 2 - GCS 13-14 without focal neurological deficit
- Class 3 - GCS 13-14 with focal neurological deficit
- Class 4 - GCS 7-12 with or without focal neurological deficit
- Class 5 - GCS <7 with or without focal neurological deficit
Treatment
General measures
The first priority is stabilization of the patient. In those with a depressed level of consciousness, intubation and mechanical ventilation may be required. Blood pressure, pulse, respiratory rate and Glasgow Coma Scale are monitored frequently. Once the diagnosis is confirmed, admission to an intensive care unit (ICU) 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, as sedation would interfere with the monitoring of the level of consciousness. There is emphasis on the prevention of complications; for instance, deep vein thrombosis is prevented with compression stockings and/or intermittent pneumatic compression.[1]
Prevention of rebleeding
Those patients with a large hematoma, depressed level of consciousness or focal neurology may be candidates for urgent surgical removal of the blood or occlusion of the bleeding site. The remainder are admitted and stabilized more extensively, and undergo an transfemoral angiogram or CT angiogram at a later stage. In those where the bleeding is from an aneurysm (as opposed to non-aneurysmal perimesencephalic hemorrhage), most neurosurgical centers use either coiling or clipping of the aneurysm to prevent rebleeding. After the first 24 hours, rebleeding risk is about 40% over four weeks, suggesting that interventions should be aimed at reducing this risk.[1]
Currently there are two treatment options for brain aneurysms: surgical clipping or endovascular coiling. Surgical clipping was introduced by Walter Dandy of the Johns Hopkins Hospital in 1937. It consists of performing a craniotomy, exposing the aneurysm, and closing the base of the aneurysm with a clip.[9] The surgical technique has been modified and improved over the years. Surgical clipping remains the best method to permanently eliminate aneurysms. Endovascular coiling was introduced by Guido Guglielmi at UCLA in 1991.[10] It consists of passing a catheter into the femoral artery in the groin, through the aorta, into the brain arteries, and finally into the aneurysm itself. Once the catheter is in the aneurysm, platinum coils are pushed into the aneurysm and released. These coils initiate a clotting or thrombotic reaction within the aneurysm that, if successful, will eliminate the aneurysm. In the case of broad-based aneurysms, a stent is passed first into the parent artery to serve as a scaffold for the coils ("stent-assisted coiling").
Presently it appears that the risks associated with surgical clipping and endovascular coiling, in terms of stroke or death from the procedure, are the same. The major problem associated with endovascular coiling, however, is the high recurrence rate and subsequent bleeding of the aneurysms. For instance, a major French study reported in 2007 indicates that 28.6% of aneurysms recurred within one year of coiling, and that the recurrence rate increased with time.[11] These results are similar to those previously reported by other endovascular groups; a series from Canada reported in 2003 found that 33.6% of aneurysms recurred within one year of coiling.[12] The long-term coiling results of one of the two prospective randomized studies comparing surgical clipping versus endovascular coiling (the International Subarachnoid Aneurysm Trial or ISAT), too, suggest that the need for late retreatment of aneurysms is 6.9 times more likely for endovascular coiling as compared to surgical clipping.[13]
Therefore it appears that although endovascular coiling is associated with a shorter recovery period as compared to surgical clipping, it is also associated with a significantly higher recurrence and bleeding rate after treatment. Patients who undergo endovascular coiling need to have annual studies (such as MRI/MRA, CTA, or angiography) indefinitely to detect early recurrences. If a recurrence is identified, the aneurysm needs to be retreated with either surgery or further coiling. The risks associated with surgical clipping of previously-coiled aneurysms are very high.Ultimately, the decision to treat with surgical clipping versus endovascular coiling should be made by a cerebrovascular team with extensive experience in both modalities. At present it appears that only older patients with aneurysms that are difficult to reach surgically are more likely to benefit from endovascular coiling. These generalizations, however, are difficult to apply to every case, which is reflected in the wide variabilty internationally in the use of surgical clipping versus endovascular coiling.
Medical treatment is available to both reduce the risk of repeat bleeding, and to treat a serious complication of SAH called vasospasm. In the case of spontaneous SAH from an aneurysm, there is a significant risk of repeat bleeding until definitive surgical intervention can be performed. During this waiting period medical treatments to control blood pressure, bed rest, and a quiet environment reduce the risk of rebleed.
Prevention of vasospasm
Vasospasm is a serious complication of SAH. It may be seen in 50% of SAH patients studied with angiography, and is symptomatic roughly 30% of the time. This condition can be verified by transcranial doppler or cerebral angiography, and can cause ischemic brain injury that can cause permanent brain damage, and if severe can be fatal. Nimodipine, an oral calcium channel blocker, has been shown to reduce the chance of a bad outcome, even if it does not significantly reduce the amount of angiographic vasospasm.[14][15]
Follow-up
A patient who recovers without immediate intervention may receive follow-up angiography to identify aneurysms which may be amenable to either surgical clipping or endovascular coiling to prevent recurrent episodes of SAH.
Complications
Complications of SAH can be acute, subacute, or chronic.
- Acute:
- Coma and brainstem herniation due to increased intracranial pressure (ICP)
- Pulmonary edema ("neurogenic pulmonary edema") as a result of the suddenly increased ICP
- Cardiac arrhythmias and myocardial damage
- Hydrocephalus, which may also happen in the subacute time frame
- Subacute:
- Vasospasm, leading to ischemia of the brain
- Hyponatremia (low sodium levels) - due to SIADH or cerebral salt wasting syndrome
- Chronic:
- Long-term immobility
- Pneumonia and pulmonary embolism (due to immobility)
- SAH recurrence (20% within two weeks if the aneurysm is not secured by clipping or coiling)
- Persistent neurologic deficits
Prognosis
Nearly half the cases of SAH are either dead or moribund before they reach a hospital. Of the remainder, a further 10-20% die in the early weeks in hospital from rebleeding. Delay in diagnosis of minor SAH without coma (or mistaking the sudden headache for migraine) contributes to this mortality. Patients who remain comatose or with persistent severe deficits have a poor prognosis.
After the SAH is treated the patients can experience prolonged, even permanently reoccurring headaches.
External links
- behindthegray.net Subarachnoid Haemorrhage support group with forums, articles, chat and general advice.
- Addressing the Challenges Faced as a Result of Brain Haemorrhage or Brain Injury for Sufferers Families and Carers.
- Neuroland SAH page
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 Van Gijn J, Kerr RS, Rinkel GJ. Subarachnoid haemorrhage. Lancet 2007;369:306-18. PMID 17258671.
- ↑ 2.0 2.1 Longmore, Murray (2007). Oxford Handbook of Clinicial Medicine. Oxford. p. 841. ISBN 0-19-856837-1. Unknown parameter
|coauthors=ignored (help) - ↑ Banki NM, Kopelnik A, Dae MW; et al. (2005). "Acute neurocardiogenic injury after subarachnoid hemorrhage". Circulation. 112 (21): 3314–9. doi:10.1161/CIRCULATIONAHA.105.558239. PMID 16286583.
- ↑ Feigin VL, Rinkel GJ, Lawes CM; et al. (2005). "Risk factors for subarachnoid hemorrhage: an updated systematic review of epidemiological studies". Stroke. 36 (12): 2773–80. doi:10.1161/01.STR.0000190838.02954.e8. PMID 16282541.
- ↑ Rosen D, Macdonald R (2005). "Subarachnoid hemorrhage grading scales: a systematic review". Neurocrit Care. 2 (2): 110–8. PMID 16159052.
- ↑ Hunt W, Hess R (1968). "Surgical risk as related to time of intervention in the repair of intracranial aneurysms". J Neurosurg. 28 (1): 14–20. PMID 5635959.
- ↑ Fisher C, Kistler J, Davis J (1980). "Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning". Neurosurgery. 6 (1): 1–9. PMID 7354892.
- ↑ Teasdale G, Drake C, Hunt W, Kassell N, Sano K, Pertuiset B, De Villiers J (1988). "A universal subarachnoid hemorrhage scale: report of a committee of the World Federation of Neurosurgical Societies". J Neurol Neurosurg Psychiatry. 51 (11): 1457. PMID 3236024.
- ↑ Dandy WE (1938). "Intracranial aneurysm of the internal carotid artery: cured by operation". Ann. Surg. 107 (5): 654–9. PMID 17857170. PMC 1386933
- ↑ Guglielmi G, Viñuela F, Dion J, Duckwiler G (1991). "Electrothrombosis of saccular aneurysms via endovascular approach. Part 2: Preliminary clinical experience". J. Neurosurg. 75 (1): 8–14. PMID 2045924.
- ↑ Piotin M, Spelle L, Mounayer C; et al. (2007). "Intracranial aneurysms: treatment with bare platinum coils--aneurysm packing, complex coils, and angiographic recurrence". Radiology. 243 (2): 500–8. doi:10.1148/radiol.2431060006. PMID 17293572.
- ↑ Raymond J, Guilbert F, Weill A; et al. (2003). "Long-term angiographic recurrences after selective endovascular treatment of aneurysms with detachable coils". Stroke. 34 (6): 1398–403. doi:10.1161/01.STR.0000073841.88563.E9. PMID 12775880.
- ↑ Campi A, Ramzi N, Molyneux AJ; et al. (2007). "Retreatment of ruptured cerebral aneurysms in patients randomized by coiling or clipping in the International Subarachnoid Aneurysm Trial (ISAT)". Stroke. 38 (5): 1538–44. doi:10.1161/STROKEAHA.106.466987. PMID 17395870.
- ↑ Allen GS, Ahn HS, Preziosi TJ; et al. (1983). "Cerebral arterial spasm--a controlled trial of nimodipine in patients with subarachnoid hemorrhage". N. Engl. J. Med. 308 (11): 619–24. PMID 6338383.
- ↑ Dorhout Mees S, Rinkel G, Feigin V; et al. (2007). "Calcium antagonists for aneurysmal subarachnoid haemorrhage". Cochrane database of systematic reviews (Online) (3): CD000277. doi:10.1002/14651858.CD000277.pub3. PMID 17636626.
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