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SAH

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Cerebral vasospasm

Subarachnoid haemorrhage

Charles Gomersall & Ross Calcroft

Epidemiology

  • overall M=F. In patients <40 yrs M>F, >50 yrs M<F
  • peak incidence 55-60 yrs

Aetiology

  • intracranial aneurysm (18-76%)
  • AVM (6%)
  • trauma
  • neoplasm
  • coagulopathy
  • collagen vascular disease
  • sickle cell anaemia
  • cerebral infarction
  • drug abuse

Pathogenesis

  • vast majority of intracranial aneurysms are saccular (berry) aneurysms
  • less common types are atherosclerotic, mycotic and traumatic
  • saccular aneurysms occur at bifurcation of arteries forming circle of Willis, and at bifurcation of those arteries that arise from circle of Willis. 90-95% occur in anterior part of circle of Willis. 5-10% in vertebrobasilar system. Originally thought to be congenital and due to a defect in tunica media. Now thought that they are acquired. Due to degeneration of internal elastic membrane at apex of bifurcation due to haemodynamic stress, producing initial sac. Enlargement due to hypertension and turbulent flow in sac which produces further degeneration of aneurysm wall. Picture
  • risk of rupture increases with increasing size. Usually occurs when aneurysm reaches 5-10 mm diameter.
  • rupture commonly occurs in association with activities that increase BP
  • of the various environmental factors that may confer a predisposition to SAH, cigarette smoking is the only factor that has consistently been identified in all the populations studied. Hypertension is the most frequently studied risk factor for SAH; several studies have shown an increased risk with hypertension. ? role of hormonal factors-different incidence between men and women at different ages. Moderate to high alcohol consumption: is an independent risk factor for SAH. Data for hypercholesterolaemia are inconsistent
  • considerable evidence supports the role of genetic factors in the pathogenesis of aneurysms.

Clinical features

  • premonitory features in many patients. May be headache, orbital pain, diplopia, ptosis, visual loss, fits, motor or sensory deficit, dysphasia, bruit or dizziness. Due to sentinel haemorrhage preceding major bleed
  • headache (85-95%). Sudden and intense
  • followed by pain radiating into the occipital or cervical region
  • nuchal rigidity and other signs of meningism
  • photophobia, nausea, vomiting, lethargy or altered mentation
  • variable conscious level. Depends on size of haematoma, development of hydrocephalus, ICP, vasospasm and cerebral blood flow
  • may be motor or sensory deficits, hyper-reflexia, visual field deficits, abnormal BS reflexes, abnormal motor posturing
  • mild pyrexia
  • hypertension
  • intraocular haemorrhages. Subhyaloid or pre-retinal haemorrhages in particular are associated with SAH. Subhyaloid haemorrhages appear as bright red, sharply demarcated regions adjacent to optic disc
  • III nerve palsy associated with PCA aneurysms, less frequently may be seen in association with other aneurysms

Investigations

CT

(image)

  • will demonstrate subarachnoid blood in 85% of patients scanned within 48 h of bleed.
  • distribution of blood may give an indication of location of aneurysm eg blood within supratentorial ventricular system often due to ruptured ACA aneurysm, focal blood in 4th ventricle associated with vertebral artery aneurysm in vicinity of PICA

LP

  • may confirm diagnosis if CT is negative but procedure not without risk in patients with SAH
  • significant neurological deterioration following LP in 10-15%.
  • xanthochromia develops only after RBCs lyse. Detectable after 4 h, maximal at 1 week, usually undetectable at 3 weeks
  • if CSF is bloody due to SAH blood usually will not clot if left to stand

4 vessel angiography

  • as soon as patient is fit enough.
  • complications include transient hemiparesis, permanent neurological deficits, death, worsening of ischaemic deficit, aneurysmal re-bleeding.
  • overall complication rate should be <1% with an experienced neuroradiologist
  • 3D angiography useful in assessing neck of aneurysm and determining best angle of approach when using endovascular coiling

Image

CT angiography

  • some evidence to suggest that this has a similar sensitivity to conventional angiography
  • advantages are short time for data acquisition and ability to reconstruct multiple views from the raw data
  • disadvantages: exposure to IV contrast

Image

MRI

  • not useful in the acute diagnosis of SAH but helpful in identifying most probable source of haemorrhage when multiple aneurysms found on angiography and in assessment of giant intracerebral aneurysms
  • MR angiography sensitivity only 90% when compared to DSA. Also, has limited resolution in the setting of vasospasm

ICP monitoring

  • useful in comatose patients and those with cerebral oedema and hydrocephalus

Transcranial Doppler

  • increases in mean arterial velocity may be associated with vasospasm but TCD is not a reliable method of diagnosing vasospasm

Somatosensory evoked potentials

  • may be indicative of clinical grades and neurological deficits, particularly intra-operatively

Grading

Hunt & Hess '74

  • Grade 0: Unruptured aneurysm without symptoms
  • Grade 1: Asymptomatic or minimal headache and slight nuchal rigidity
  • Grade 1a: No acute meningeal or brain reaction, but with fixed neurological deficit
  • Grade 2: Moderate-to-severe headache, nuchal rigidity, no neurological deficit other than cranial nerve palsy
  • Grade 3 Drowsy, confused, or mild focal deficit
  • Grade 4 Stupor, moderate-to-severe hemiparesis, possible early decerebrate rigidity and vegetative disturbances
  • Grade 5 Deep coma, decerebrate rigidity, moribund appearance

Presence of serious systemic disease or vasospasm puts patient into next worse grade

NB Important to specify name and date of classification system to allow comparability of patients. Original Hunt & Hess classification published in 1968.

World Federation of Neurological Surgeons

Grade

GCS

Motor deficit

I

15

Absent

II

13-14

Absent

III

13-14

Present

IV

7-12

Absent/present

V

3-6

Absent/present

Fischer scale

Grade    Description
1    No clot seen on CT scan
2    Diffuse thin layer of SA clot (<1mm thickness)
3    Localised clot or thicker layer of SA clot (>1mm thickness)
4    Intracerebral or intraventricular clot with diffuse or no SA clot.

Management

  • control blood pressure except in patients with cerebral vasospasm. Use sedation, analgesics and antihypertensives. b blockers, methyldopa and hydralazine have been used. Maintain circulating volume and avoid hypotension
  • calcium antagonists
    • Nimodipine drug of choice
    • Nicardipine as effective but more likely to cause hypotension
    • Do not alter incidence of vasospasm but do improve mortality. It appears that the beneficial activity of this drug is in the decrease of neuronal calcium, which is elevated following injury.
    • Neurologic outcome and mortality rates of SAH victims prophylactically treated with 4mg/kg/day nimodipine are improved 25-50% over controls. (Has been shown to decrease the incidence of overall cerebral infarction after SAH by 34% and the incidence of poor outcome by 45%). Fewer infarcts are noted, although the incidence of vasospasm is not altered.
    • Side effects of nimodipine are mild and include mild hypotension.
    • Current recommendations are to administer 60 mg of nimodipine orally/IV every 4 hours for a 21 day course beginning at the onset of the SAH.
  • free radical scavengers: free iron can catalyse free radical reactions, including lipid peroxidation.
    • Nizofone has shown some promising results. Also trilazad which inhibits; lipid peroxidation and protects cell membranes by scavenging free radicals, similar to Vit E.
  • serial CT to detect hydrocephalus and rebleeding
  • use of antifibrinolytics (eg epsilon aminocaproic acid) to prevent clot lysis and rebleeding controversial. Associated with increase in ischaemic neurological deficits, increased incidence of hydrocephalus, and diarrhoea. Probably have little role in patients who are to undergo early surgery and do not alter mortality
  • maintenance of fluid and electrolyte balance

Surgical/radiological intervention

  • Early surgery for aneurysmal SAH associated with lower incidence of rebleeding but increased incidence of vasospasm and mortality is the same. Possible exception are those patients who are alert and have a low grade on admission who have most favourable results with early surgery

Endovascular therapy

  • most amenable aneurysms are those with narrow necks
  • early experience is that procedural risks are fairly low (periprocedural haemorrhage rate is 2%, with the permanent morbidity and mortality rates at 0% and 0.5% respectively) but long term effectiveness is not yet proven
  • First line therapy for:
    • ruptured posterior circulation aneurysm
    • ruptured small (<10 mm) anterior circulation aneurysm in good grade patients (World Federation of Neurological Surgeons grade I-III)
    • aneurysm causing nerve compression
    • unruptured aneurysm where risk:benefit ratio favours any treatment at all
  • International Subarachnoid Aneurysm Trial (SAT):
    • prospective randomized comparative trial
    • 2143 patients with ruptured aneurysm that in opinion of clinician that was equally amenable to surgery or coiling
    • mainly small, anterior circulation aneurysms
    • mainly good grade SAH
    • ~24% of coiled patients dead or dependent at 1 year compared to ~31% of patients undergoing surgery. Improvement predominantly due to decreased incidence of dependency (mortality at 1 year was ~8% and ~10%)

Post-operative complications

  • brain swelling
  • bleeding at operative site
  • complications of SAH
  • vasospasm
  • EDH, SDH, ICH, hydrocephalus
  • metabolic abnormalities.

Complications

Re-bleeding

  • Incidence depends on site of aneurysm, presence of clot, degree of vasospasm, age and sex.
  • 16-25% incidence in first 2 weeks with associated mortality of 40%.
  • Frequency highest in first 48 h.
  • Incidence only 4% in first 6 months for the 20% of patients in whom no source of SAH discovered. Re-bleeding less common after SAH due to AVM than following aneurysmal SAH

Vasospasm

Details

Hydrocephalus.

  • Communicating hydrocephalus may develop in up to 1/3 of patients, especially patients with ruptured anterior communicating artery aneurysms.
  • Due to fibrosis in subarachnoid space.
  • May cause a decreased level of consciousness a few days/weeks after SAH.
  • Occasionally disturbance of CSF flow may not be present until some years after SAH and clinical picture is then one of "normal" pressure hydrocephalus

Cerebral oedema

Image

Electrolyte disturbance

  • DI
  • SIADH
  • cerebral salt wasting

Others

  • fits
  • ECG changes: T inversion, ST changes, U waves, QT prolongation
  • arrhythmias
  • sympathetic hyperactivity
  • reduction in total blood volume and in red cell mass

Seizures

  • seizures or seizure-like episodes are reported in approximately 13%-26%
  • routine use of prophylactic anticonvulsants is not recommended, unless in the presence of risk factors such as MCA aneurysm, intraparenchymal haemorrhage, infarcts and history of hypertension or seizures.

Prognosis

Grade (Hunt & Hess)

Mortality (%)

I

1

II

5

III

19

IV

42

V

77

Total

18

There is limited evidence that patients with poor grade (Hunt & Hess IV or V) may do moderately well with aggressive management with 57% of grade IV and 53% of grade V being independent in daily activities at 3 months

Further reading

Commichau C, Mayer SA. Critical care of subarachnoid and intracerebral hemorrhage. Current Opinion in Critical Care, 1998; 4:94-100

International Subarachnoid Aneurysm Trial (ISAT) Collaborative Group. International Subarachnoid Aneurysm Trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised trial

Oropello JM, Weiner L, Benjamin E. Hypertensive, hypervolaemic, hemodilutional therapy for aneurysmal subarachnoid haemorrhage. Is it efficacious ? No. Critical Care Clinics, 1996; 12: 709

Johnstone SC Stroke 2000 31:111-117

Ullman JS, Bederson JB. Hypertensive, hypervolaemic, hemodilutional therapy for aneurysmal subarachnoid hemorrhage. Is it efficacious? Yes. Critical Care Clinics, 1996; 12: 697-708

 


 

©Charles Gomersall, February, 2015 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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