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Related Subjects: |Subarachnoid Haemorrhage |Perimesencephalic Subarachnoid haemorrhage |Haemorrhagic stroke |Cerebellar Haemorrhage |Putaminal Haemorrhage |Thalamic Haemorrhage |ICH Classification and Severity Scores

Any new severe headache with onset to maximum severity within 5 minutes lasting for at least 60 minutes should be treated as a possible SAH. 50% of patients die within 48 hours irrespective of therapy. Early clipping or coiling, within 72 hours, is now the goal for all grades of SAH

About

• Bleeding from blood vessels on the surface of the brain into the subarachnoid space.
• Blood tends to track into Sulci and ventricles and basal cisterns.
• Convexity SAH on the outer surface of the brain and sulci

Incidence

• 1-2% of population have an unruptured aneurysm
• SAH 6 cases per 100 000 patient years
• Most patients are < 60 years of age.

The question is often between traumatic and aneurysmal SAH. Did the fall cause the bleed or the bleed cause the fall. If suspected aneurysm then needs CTA and neurosurgical consult. Traumatic Bleed due to fall will have external evidence of head injury or skull fracture and other trauma and probably convexity blood and contre coup injury and blood will not be in the territory of a typical aneurysm site or distribution and will not have been preceded by headache before they fell rather than after.

Causes

• Aneurysmal SAH due to a berry aneurysm leaking 85%
• Non-Aneurysmal Perimesencephalic (may be diffuse or just see some blood in front of the pons) 10%. Seen mostly in middle age 50+. The headache may be less acute. Loss of consciousness and syncope are exceptional.
• Traumatic: mild to moderate head injury often in elderly
• Dissection: Dissection commoner in carotid but vertebral artery dissections are more likely to cause SAH. May see lower cranial nerve palsies and lateral medullary syndrome.
• Arteriovenous malformations: rare to bleed only into subarachnoid space only and there is usually an intraparenchymal haematoma. Aneurysms can form on the feeding arteries of an AVM and these are more likely to bleed than the AVM.
• Reversible cerebral vasoconstriction syndrome tends to cause convexity SAH
• Dural Arteriovenous malformations: usually affect the tentorium and resembles aSAH.
• Neoplasms, dural AVM, venous angiomas, infectious aneurysm
• Vasculitis: (rare)
• Cerebral amyloid angiopathy tends to cause convexity SAH
• Intracranial arterial dissections (rare)

Berry/Saccular aneurysms causing aSAH

• Berry aneurysms - majority. Most of these aneurysms will never rupture.
• Any aneurysm can rupture, although usually larger (>1cm - 4%) aneurysms are more likely to do so.
• Smaller aneurysms are however more common so most bleeds are from small aneurysms between 5 - 10 mm
• Risk for aSAH
  • Women > Men, Age, deficient media has been refuted as a cause.
  • Aneurysms not seen in neonates and rarely in childhood
  • They appear to develop through life
  • 10-15% of patients presenting with SAH have multiple aneurysms
• Commonest sites of intracranial aneurysms
  • (a) posterior inferior cerebellar artery
  • (b) basilar artery tip 5%
  • (d) internal carotid artery (ICA) and Pcomm 35%
  • (e) anterior communicating artery (ACA) 35%
  • (f) bifurcation of the middle cerebral artery (MCA) 20%
• Risks of aSAH
  • Smoking, Binge drinking, Illicit drugs
  • No real evidence for role for hypertension
  • Adult polycystic kidney disease
  • Marfan's/Ehlers Danlos syndromes
  • Pseudoxanthoma elasticum
  • SLE and Sickle cell

Clinical of all SAH

• Worst ever headache before any fall or head injury
• Headache comes on over seconds
• Maximal headache within 1 minutes
• Severe "hit round back of the head with a shovel"
• Comes on at rest, sleep, coitus and straining
• Headache may be followed by collapse and then recovery
• Headache may be back of head and cervical in some cases
• Associated Photophobia and meningism
• Coma and coning and sudden death
• Some claim warning headaches over preceding weeks "herald bleeds"
• Fundoscopy if done subhyaloid haemorrhage
• Headache + full 3rd nerve palsy: suspect PCommA aneurysm.
• Monocular blindness: large anterior communicating artery aneurysm

Complications of SAH

• Vasospasm can cause later cerebral infarction usually at 3-12 days. A large amount of subarachnoid blood on CT is a predictor of the development of vasospasm. Prevent with Nimodipine for 21 days, positive fluid balance, and prevention of hyponatraemia
• Re bleeding: seen in 20% of patients in the first 2 weeks. Peak incidence of rebleeding occurs the day after SAH. This may be from lysis of the aneurysmal clot
• Hydrocephalus: may develop on the first day due to obstruction of CSF outflow in the ventricular system by clotted blood. Can occur early (EVD) or late (VP shunt). Careful with drainage as a sudden reduction in ICP can increase the risk of rebleeding. CT shows that temporal horns are dilated and there is diffuse SAH and blood in the 4th ventricle with diffuse cerebral oedema
• Coning due to mass effect
• Seizures seen in 6% of cases
• Hypothalamic dysfunction: excess sympathetic stimulation, which may lead to myocardial ischaemia or labile BP
• Hyponatraemia may be due to renal salt wasting or due to SIADH
• Nosocomial pneumonia seen in ITU

Differential

• Venous sinus thrombosis
• Benign orgasmic cephalgia
• Migraine
• Primary Intra Parenchymal haemorrhage
• Brain tumour with bleed
• Carotid/vertebral dissection

Investigations

• New NICE guidance confirms if CT negative < 6 hrs after headache then SAH excluded. If done after 6 hrs must still consider need for LP to look for xanthochromia. The LP should be delayed until 12 hrs after headache to allow xanthochromia to form.
• FBC, U&E may detect hyponatraemia often due to salt wasting. Give fluids.
• ECG: 20% have ECG changes of myocardial ischaemia. ST segment elevation, T wave changes due to high levels of circulating catecholamine. Do not start ACS management.
• CXR: may show pulmonary oedema or aspiration pneumonia
• Troponin: if ECG changes measure troponin if concerned. Do not start ACS management if ACS is suspected and SAH has not been ruled out.
• CT head: CT scan is 100% sensitive in 6 hrs and 90% sensitive within the first 24 hours, 80% sensitive at 3 days, and 50% sensitive at 1 week. There is high signal attenuation in the basal cisterns, Sylvian fissure, or intra hemispheric fissure. CT higher concentrations of blood over the convexities or within the superficial parenchyma of the brain are more consistent with the rupture of an AVM or a mycotic aneurysm. Can detect hydrocephalus.
• Lumbar Puncture: If CT is negative but the history convincing then LP is done at 6-12 hours after onset. Blood in itself is not diagnostic as even the smoothest puncture can hit a vein. What is needed is evidence of blood breakdown products suggesting a bleed over 6-12 hours ago. A RBC < 2000 x 10⁶ and negative and negative xanthochromia excludes SAH. Xanthochromia (which measures bilirubin by photo spectrometry) is still present up to 2 weeks. False-negative with severe anaemia or small-volume SAH. Xanthochromia is a classic sign, but not present early - look for equal or increasing blood in the sample tubes or D-dimer
• Catheter angiography for detecting aneurysms is being replaced by CTA. If bleeding is identified then Cerebral angiography is the definitive study to identify the source of subarachnoid haemorrhage but CTA generally being used. If multiple aneurysms are found treatment targeted towards aneurysm adjacent to largest blood collection. Sometimes there may be significant difficulty identifying the source performed.
• Transcranial doppler can detect vasospasm

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Assessments of Severity for Neurosurgeons

• World federation of Neurological Surgery Grades
  • I. GCS 15 No focal deficits
  • II. GCS 13-14 No focal deficits
  • III. GCS 13-14 focal deficits present
  • IV. GCS 7-12 irrespective of deficits
  • V. GCS 3-6 irrespective of deficits
• Hunt and Hess Grade
  • 0: Unruptured aneurysm
  • 1:Asymptomatic or min headache & without neck rigidity
  • 2:Mod-sev headache, neck rigidity, CN palsy
  • 3:Drowsy, confused, mild focal deficit
  • 4:Stupor, mild-severe deficit, decerebrate rigidity
  • 5:Deep coma, decerebrate, moribund

Management

• Acute
  • ABC, Airways management if GCS reduced. A patient with GCS < 8 usually needs intubation and support. Needs anaesthetic assessment. Discuss with neurosurgeons.
  • Consider ITU/HDU admission to manage BP, Fluid balance and prevent vasospasm. Absolute bed rest, codeine and laxative/stool softener and ensure pain is controlled
  • Patients need urgent imaging to determine if there is an aneurysm or other vascular anomaly that needs urgent treatment. If an aneurysm is identified then transfer to neurosurgeons for coiling or clipping
  • ITU management and lowering pCO₂ can help reduce CSF pressure. Also, manage and lower arterial pressure.
  • Hydration and slight hypervolaemia are suggested. Give 3 L of N-saline over 24 hours (unless poor cardiac function). Do not water restrict if hyponatraemia is more likely due to renal salt loss.
  • Suspected aSAH Start Nimodipine 60 mg 4 hourly to reduce vasospasm for 21 days. It reduces neurological deficit, cerebral infarction and mortality.
• Clipping
  • Neurosurgical aneurysm clipping requires a craniotomy, performed under general anaesthesia.
  • It takes 4-8 hours and has a procedural mortality rate of 1-3%
  • Early clipping - less rebleeding but higher incidence of vasospasm
  • Worst time is day 7 to 10 (highest time for vasospasm) So < 3 days or > 10 days
• Coiling
  • Endovascular obliteration by means of platinum spirals (coiling) is the preferred mode of treatment
  • It is a minimally invasive percutaneous endovascular treatment
  • It has proved to be a safe alternative to traditional surgical clipping of the aneurysm
  • It may be associated with a better outcome in selected patients.
  • The technique consists of packing the aneurysm with detachable coils under GA
  • It avoids craniotomy, and recovery after the procedure is more rapid.
  • It is not indicated in 5-15% of cases, due to morphological or positional aneurysm characteristics
  • It is performed by neurosurgeon or interventional neuroradiologist
• Clipping vs Coiling
  • International Subarachnoid Aneurysm Trial (ISAT) Lancet 2002
  • 2143 patients randomized to NS clipping (n=1070) or endovascular coiling (n=1073)
  • Outcomes at 2 months and 1 year
  • 23.7% coiling dependent or dead at 1 y VS 30.6% clipping at 1y (ARR 7% NNT 14)
• Management/Prevention of Vasospasm
  • Start Nimodipine as mentioned above.
  • The triple H refers to hypertension, hypervolaemia, and haemodilution.
  • Increase BP to offset the loss of autoregulation
  • Hydrate to reduce blood viscosity which may reverse vasospasm.
  • Target SBP 120-150mmHg in untreated aneurysms and up to 200mmHg in aneurysms that have been clipped or coiled
  • It is an accepted technique, despite being unproven.
  • Risks are volume overload and cardiac failure with myocardial ischaemia, and concerns it may provoke rebleed especially in those with unclipped aneurysms.
  • Target Haemodilution Hct 30-35%

References

• J. van Gijn and G. J. E. Rinkel. Subarachnoid haemorrhage: diagnosis, causes and management. Brain (2001), 124, 249-278
• Subarachnoid haemorrhage. Lancet 2007; 369: 306