Subarachnoid hemorrhage

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Subarachnoid hemorrhage
Classification & external resources

CT scan of the brain showing subarachnoid hemorrhage as a white area in the center
ICD-10	I60
ICD-9	430
DiseasesDB	12602
MedlinePlus	000701
eMedicine	med/2883  neuro/357 emerg/559

Subarachnoid hemorrhage (SAH) 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]

Contents 1 Signs and symptoms 2 Diagnosis 3 Causes 4 Classification 5 Treatment 5.1 General measures 5.2 Prevention of rebleeding 6 Complications 7 Prognosis 8 External links 9 Reference

[edit] Signs and symptoms

The classic symptom of subarachnoid hemorrhage is thunderclap headache ("most severe ever" headache developing over seconds to minutes). 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 conciousness or coma may be present. Intraocular hemorrhage (bleeding into the eyeball) may occur.^[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.^[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 hemiplegia (one-sided weakness) or changed pupillary reflexes, and Glasgow Coma Score calculations deteriorate. Headache is not necessarily present.^{[citation needed]}

[edit] Diagnosis

While the initial steps are obtaining a medical history and performing a physical examination, 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]

[edit] 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, it is likely that larger aneurysms are 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]

[edit] 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.^[2]

The Hunt and Hess scale (1968) of subarachnoid hemorrhage severity is:^[3]

• 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%.

The Fischer Grade classifies the appearance of subarachnoid hemorhttp://en.wikipedia.org/w/index.php?title=Subarachnoid_hemorrhage&action=edit Editing Subarachnoid hemorrhage - Wikipedia, the free encyclopediarhage on CT scan:^[4]

• 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 Fedaration of Neurosurgeons classification:^[5]

• 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

[edit] Treatment

[edit] 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]

[edit] 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 is admitted and stabilized more extensively, and undergoes 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]

Two measures are employed at repairing aneurysms. Generally, the first-line approach is endovascular coiling. This mode relies on angiography of the cerebral arteries and inserting platinum coils into the aneurysm to cause them to regress. Alternatively, craniotomy and surgical clipping of the aneurysm may be performed. Recent trials suggest a general advantage of coiling over clipping.^[1] 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.

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 which can cause permanent brain damage, and if severe can be fatal. Nimodipine is an oral calcium channel blocker, that has been shown to reduce the chance of a bad outcome, even if it does not significantly reduce the amount of angiographic vasospasm.^[6]

A patient who recovers without immediate intervention may receive follow-up angiography to identify aneurysms which may be amenable to coiling to prevent recurrent episodes of SAH.

[edit] 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 (can be prevented partially with the calcium channel antagonist nimodipine)
  • 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

[edit] Prognosis

After the SAH is treated the patients can experience prolonged, even permanently reoccurring headaches.

Nearly half the cases of SAH are either dead or moribund before they reach 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.

[edit] 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

[edit] Reference

1. ^ ^{a b c d e f g h i j} Van Gijn J, Kerr RS, Rinkel GJ. Subarachnoid haemorrhage. Lancet 2007;369:306-18. PMID 17258671.
2. ^ Rosen D, Macdonald R (2005). "Subarachnoid hemorrhage grading scales: a systematic review". Neurocrit Care 2 (2): 110-8. PMID 16159052. 
3. ^ 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. 
4. ^ 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. 
5. ^ 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. 
6. ^ Allen GS, Ahn HS, Preziosi TJ, Battye R, Boone SC, Boone SC, Chou SN, Kelly DL, Weir BK, Crabbe RA, Lavik PJ, Rosenbloom SB, Dorsey FC, Ingram CR, Mellits DE, Bertsch LA, Boisvert DP, Hundley MB, Johnson RK, Strom JA, Transou CR. Cerebral arterial spasm--a controlled trial of nimodipine in patients with subarachnoid hemorrhage. N Engl J Med 1983;308:619-24. PMID 6338383.