Monday, 21 April 2014

Subarachnoid Haemorrhage

SAH - the most feared cause of headache. Syncope + headache = think SAH.

Most SAHs occur in the circle of Willis - as this is where the brain gets its blood supply from.

There are two types of aneurysm with slightly different pathophysiology behind them. 
Saccular Aneurysms: Approximately 90%, with high morbidity and mortality. The internal elastic membrane weakens, at the site of vessel bifurcation where blood flow is most turbulent.

Fusiform Aneurysms: These develop from ectatic, tortuous cerebral arteries, most often in the vertebrobasilar system. Patients with fusiform aneurysms characteristically present with symptoms of cranial-nerve or brainstem compression, but the symptoms are not commonly associated with subarachnoid hemorrhage.

Screening is not beneficial, even in those with first degree relative history. If screening is appropriate, cranial MRA is used. 
    NOT Congenital - increased risk if first degree relative has SAH
        With 2 relatives, 10 year risk of 7.1% versus 0.8%
    Occur in about 1 in 40 people (1-5%).
    Most never rupture.
    Multiple aneurysms in 30%.  
    Berry aneuryms have increased rate of formation in:
       Autosomal dominant polycystic kidney disease
       Pseudoxanthoma elasticum
       Ehler-Danlos syndrome type IV.

     1-7% of all strokes.
     More common in young men than young women
     Overall, more common in women. 
     Aspirin increases the mortality if it bleeds
     Oestrogen deficiency (post - menopausal) raises the risk. 
     Sympathomimetic drugs (phenylephrine and cocaine)

Missed in 1/4 of patients as characteristic headache not present. 
50% of patients rebleed within six months of the presentation
After that, 3% per year thereafter

Even in these patients, the possibility of having an intracranial aneurysm is low and screening all patients is not required in the absence of a positive family history. Cranial MRA is the imaging method of choice for screening.

Clinical Presentation - the Headache
Classically Instantaneous:
    Instantaneous – 50%
    2-60 seconds – 24%
    1-5 minutes – 19%
    No idea/unable to remember – 9%
1 hour has been suggested. The typical duration is of the order of 1-2 weeks.

Lateralised in one third of patients

Sentinel Bleed:
No medical attention sout, or one missed. 
  Present in 30 - 50%

The classic headache, caused by aneurysmal rupture, release of blood, and raised ICP, happens in 97% of patients. Only around 25% of patients who visit A&E with this sudden severe headache (so called, “the worst headache of my life”) have acute subarachnoid haemorrhage. In only 12% of them, headache is the only complaint.

Clinical Features - other
Vomiting is not predictive but present in 75% 
Seizure at onset (74%)
Reduced level of consciousness in 2/3 of people
Transient loss of consciousness in 26%
Delirium (1%)
Focal neurology (15%)
3rd nerve palsy due to an aneurysm in the posterior communicating artery.
1 in 7 will have intraocular haemorrhages.
Ischaemic changes (of any type) on ECGare common
Neck stiffness may develop – but usually only after several hours and is due to an inflammatory reaction to the blood in the subarachnoid space, and it may not develop at all if there’s only a small amount of blood.

    CXR: neurogenic pulmonary oedema
    CTH: 90% sensitive within 24 hrs, 50% @ 72 hrs, detects hydrocephalus
    CTA: assesses vascular anatomy
    DSA: gold standard for diagnosis, allows intervention
    MRI: mostly used for detection of AVM

    98% sensitivity if scanned within 12 hours of onset.
    93% within 24 hours.
    50% at 5 days – based on study from 1984.
Sensitivities unlikely to improve because small bleeds will be flushed away by normal CSF flow.   There may not be enough blood present to appear as hyperdense to CSF on scanning.

Cerebral angiography within 48-72 hours of the initial event.

Lumbar Puncture
1 in 10 of patients presenting with thunderclap headaches will have had a subarachnoid haemorrhage.
A non-contrast CT within 12 hours of onset of pain is 98% sensitive for detecting SAH.
Therefore the risk of missing a SAH may be as low as 2 in 1000 if the patient has had a negative CT in this timeframe.
Xanthochromia A fancy way of saying ‘Yellow colour’! - Bilirubin
    96% sensitive if done 12 hours post headache
    Positive for at least 2 weeks (possibly up to 4 weeks)  

Other Investigations
ECG: tall peaked T waves, ST depression, prolonged QT, arrhythmia
Echo: neurogenic cardiomyopathy
Hyponatraemia + hypovolaemia from SAIDH or cerebral salt wasting -> worsens vasopasm
Troponin rise due to cardiomyopathy
Magnesium - may be low, poor prognosis.
Supportive care as appropriate
Neurosurgery - surgical clipping or coil
Treat seizures (occur in 18% of patients) with benzodizepines and load with phenytoin 18 mg/kg IV
Prevent vasospasm - Nimodipine
   (calcium channel antagonist with some selectivity for cerebral circulation)
Lower the SBP to below 140 mm Hg to help reduce the risk of rebleeding using intravenous labetalol. Avoid
   vasodilators, such as nitroglycerin and sodium nitroprusside, because they increase the intracranial blood    volume and intracranial pressure
If your patient is unconscious, you should not try to lower their blood pressure, at least temporarily

Anti-fibrinolytics, e.g. tranexamic acid
— controversial
— may reduce risk of re-bleed but increase risk of VTE
— some centers give until aneurysm is secured if no VTE risk factors, monitor for DVT

Treat fever - occurs in 70% of SAH and requires aggressive control. Look for and treat infection. Antipyretics.

3% will have a cardiac arrest. Aggressive resuscitation is essential as they appear to have a high rate of ROSC and half of the survivors will regain independent living.

Rebleeding - 24 to six hours
Vasospasm - 3 days to 2 weeks 
Death - within three weeks after subarachnoid haemorrhage. 40 - 50% of patients die.
Dependent - in a third of survivors
Hunt and Hess grading
    Grade 0: Unruptured aneurysm without symptoms.
    Grade 1: Asymptomatic or minimal headache and slight nuchal rigidity (1% mortality).
    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 (5% mortality).
    Grade 3: Drowsy, confused or mild focal deficit (19% mortality).
    Grade 4: Stupor, moderate-to-severe hemiparesis, possible early decerebrate rigidity and vegetative disturbances (42% mortality).
    Grade 5: Deep coma, decerebrate rigidity, moribund appearance (77% mortality).
    If there is a co-existing serious illness, this adds a grade.
The Ottawa Sub-Arachoid Rule
For alert patients older than 15 y with new severe nontraumatic headache reaching maximum intensity
within 1 h. Not for patients with new neurologic deficits, previous aneurysms, SAH, brain tumors, or history of recurrent headaches (=3 episodes over the course of =6 mo)
    Investigate if 1 or more high-risk variables present:
-   Age =40 y
-    Neck pain or stiffness
-    Witnessed loss of consciousness
-    Onset during exertion
-    Thunderclap headache (instantly peaking pain)
-    Limited neck flexion on examination


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