Subarachnoid Haemorrhage

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Learning objectives

  • Causes of SAH and their management
  • Understand Risks and complications of SAH
  • Management of aneurysmal and non aneurysmal SAH

Introduction

Subarachnoid haemorrhage is spontaneous (excludes trauma causing SAH) 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. 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. The main cause is a ruptured aneurysm.

Epidemiology

However 1-2% of population have an unruptured aneurysm. There are 6 cases per 100 000 patient years and most patients are < 60 years of age.

Causes

CausesDetails
Berry/Saccular Aneurysmal 85% Commonest cause. Needs urgent referral for diagnostic angiography and clipping or coiling as high risk of rebleed and death. These cause majority. Most intracranial aneurysms will never rupture. Any aneurysm can rupture, although statistically larger (>1cm - 4%) aneurysms are more likely to do so. However smaller aneurysms are commoner so most bleeds are from small aneurysms between 5 - 10 mm, when they rupture. Seen more so in women, and increasing age. The old theory that it was due to deficient media has been refuted. They are never seen in neonates and rarely in childhood and are so developmental through life. 10-15% of patients presenting with SAH have multiple aneurysms
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 May bleed only into subarachnoid space only and there is usually a intraparenchymal haematoma. Aneurysms can form on the feeding arteries of an AVM and these are more likely to bleed than the AVM.
Dural Arteriovenous malformations Usually affect the tentorium and resembles aSAH.
Neoplasms, dural AVM, venous angiomas, infectious aneurysm Can cause SAH bleeding related to anatomical position
Vasculitis (rare) SAH can be anywhere related to underlying focus of vasculitis. May be infarction or associated intraparencymal haemorrhage.
Cerebral amyloid Convexity SAH
Reversible cerebral vasoconstriction syndrome Usual or Convexity SAH often associated as thunderclap headache

Pre and post SAH

CT in patient with painful Left IIIrd nerve palsySame patient several hours later who bleed when on way to neurosurgeons
<img src="pcomm2.jpg" width=250><img src="pcomm1.jpg" width=250 >

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

  • 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

  • Worst ever headache comes on over seconds to maximal within 2-5 minutes and usually persists
  • Severe "hit round back of head with a shovel"
  • Comes on at rest, sleep, coitus and straining
  • May be associated with episode of collapse and then recovery
  • Headache may be back of head and cervical in some cases
  • Photophobia and meningism
  • Coma and coning and sudden death
  • Some claim warning headaches over preceding weeks "herald bleeds"
  • Fundoscopy - subhyaloid haemorrhage
  • Headache + 3rd nerve palsy due to compression of the IIIrd nerve by the PCommA. The pupil is dilated which is different from diabetes which typically spares the pupil
  • Monocular blindness may result from an anterior communicating artery aneurysms if it is exceptionally large

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 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 pressure and haematoma and obstructive hydrocephalus due to mass effect
  • Epilepsy may be seen acutely and late
  • 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

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

Images of SAH

<img src="sah.jpg" width=250></a><img src="sah1.jpg" width=250></a>
<img src="sah4.jpg" width=250></a><img src="sah3.jpg" width=250></a>

Investigations

  • Bloods FBC And U&E may detect hyponatraemia
  • ECG 20% have ECG evidence of myocardial ischaemia and ST segment elevation, T wave changes due to high levels of circulating catecholamine. Measure troponin if concerned which may be elevated
  • CT head If 3rd generation CT negative < 6 hrs then SAH excluded. If done after 6 hrs must still do LP to look for xanthochromia. CT scan is 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

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-sev deficit, decerebrate rigidity
  • 5:Deep coma, decerebrate, moribund

Management

  • Absolute bed rest, codeine and laxative/stool softener
  • Hydration and slight hypervolaemia is suggested. Give 3 L of N-saline over 24 hours (unless poor cardiac function). Do not water restrict if hyponatraemia as more likely due to renal salt loss.
  • In those with suspected aneurysmal SAH Start Nimodipine 60 mg 4 hrly to reduce vasospasm for 21 days. Nimodipine has been shown to reduce neurological deficit, cerebral infarction and mortality.
  • May need ITU if comatose and needs airway protection
  • If an aneurysm is identified then transfer to neurosurgeons for coiling or clipping
  • Pain: codeine, sedation, opiates as last resort

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, which has proved to be a safe alternative to traditional surgical clipping of the aneurysm, and may be associated with a better outcome in selected patients.
  • The technique consists of packing the aneurysm with detachable coils, and is performed under general anaesthesia. 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
  • 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
  • 30.6% clipping at 1y (ARR 7% NNT 14)

Management of Vasospasm

  • The triple H refers to hypertension, hypervolaemia, and haemodilution.
  • Increase blood pressure to offset loss of autoregulation and 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
  • Early clipping or coiling, within 72 hours, is now the goal for all grades of SAH
  • 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