Viva 1

A 55 - year - old female is admitted to the ICU with a diagnosis of subarachnoid haemorrhage. She had 24 hours of severe headache, her CT and CTA showed subarachnoid haemorrhage, significant intraventricular blood and early hydrocephalus and a left middle cerebral artery aneurysm. The aneurysm has been confirmed with a formal angiogram and is not amenable to endovascular treatment, and she is admitted to the ICU pending surgical intervention.

On admission, she is alert and oriented with no focal neurological deficits. Her BP is 170/80 mmHg.

In detail, outline your initial assessment and management.
  • History, including risk factors
  • Examination, looking for:
    • Subtle neurodeficit
    • Neurogenic cardiomyopathy
    • Pulmonary oedema
    • Partial seizures
    • Evidence of coagulopathy
    • Any 
  • Investigations and monitoring
    • Arterial line
    • EVD 
How would you grade the severity of this SAH? Describe the grading systems you could use, and their utility.
WFNS Grading Scale for Subarachnoid Haemorrhage


Motor deficit
Grade 1 15 absent
Grade 2 14-13 absent
Grade 3 14-13 present
Grade 4 12-7  
Grade 5 3-6

Another method of scoring SAH severity (with implications for vasospasm) is the Fisher scale:

  • Grade 1 - no haemorrhage
  • Grade 2 - SAH less than 1mm thick, diffuse
  • Grade 3 - SAH more than 1mm thick, with localised clots
  • Grade 4 - intraventricular or parenchymal extension, with clots

Essentially, this scale relates the amount of blood to the risk of vasospasm.

Grades 3 and 4 almost always develop it, and the other grades seem to be spared.

Which is the best? Hard to say. It may well be that admission GCS is the single best predictor of neurological outcome. In the 2005 piece by Rozen and Macdonald from Neurocritical care,  the authors  conclude that "because of the limitations of the current grading scale data, it is unreasonable to strongly advocate universal adoption of any of the available SAH grading scales"

What are the risk factors you might look for on history?

Uncontrollable risk factors:

  • Family history
  • being African-American
  • Polycicstic kidney disease

Modifiable risk factors

  • Heavy drinking
  • Heavy smoking
  • Hypertension
  • The use of recreational sympathomimetics, eg. cocaine.
What initial management would you propose?
  • Control BP: 
  • EVD to control hydrocephalus
  • Management of hypertension:
    • Neurocritical care society guidelines (2011) recommend to keep SBP under 140
    • AHA guidelines recommend keeping the SBP under 160 mmHg, or the MAP under 110 mmHg.
  • Control any coagulopathy
  • Consider tranexamic acid
What are the advantages of endovascular  vs. surgical approaches in SAH?
Coiling vs clipping in ruptured aneurysms

Advantages of coiling:

  • minimally invasive
  • improved survival at 1 year
  • Better effects in posterior fossa aneurysms
  • Less risk of cognitive decline or epilepsy

Advantages of clipping:

  • More certain: 81% of aneurysms are completely obliterated
  • Less risk of rebleeding (0.9%)
  • MCA aneurysms are more amenable to clipping

Disadvantages of coiling

  • Greater risk of rebleeding (2.9%)
  • Fewer aneurysms get completely obliterated (58%)
  • Small aneurysms (<3mm) are impossible to coil

Disadvantages of clipping:

  • More invasive
  • Greater risk of cognitive decline or epilepsy
  • Survival rates equivalent at 5 years
  • Posterior fossa aneurysms are inaccesible to clipping

The AHA recommend that "For patients with ruptured aneurysms judged to be technically amenable to both endovascular coiling and neurosurgical clipping, endovascular coiling should be considered".

The ISAT trial of 2009 did not find any difference in terms of death or severe disability. They recommended " for everyday clinical practice and decision making, coiling and clipping are to be considered equivalent in the long term".

The patient undegoes craniotomy and clipping. The neurosurgical team recommend vigilant monitoring for cerebral vasospasm and delayed cerebral ischaemia.
What is the definition of vasospasm?

"Vasospasm is a term applied to arterial narrowing after SAH demonstrated by radiographic images or sonography"

- Vergouwen et al, 2010, via Diringer et al, 2011

What is "delayed cerebral ischaemia"?

"Symptomatic vasospasm or the appearance of new infarction on CT or MR when the cause was felt to be attributable to vasospasm"

- Frontera et al, 2009

Clinical deterioration caused by DCI

"The occurrence of focal neurological impairment... or a decrease of at least 2 points on the Glasgow Coma Scale.... This should last for at least 1 hour, is not apparent immediately after aneurysm occlusion, and cannot be attributed to other causes by means of clinical assessment, CT or MRI scanning of the brain, and appropriate laboratory studies."

- Vergouwen et al, 2010

In brief, you know it's vasospasm when...

  • A focal neurological deficit develops (and persists for longer than an hour)
  • The GCS drops by 2 points (and stays that low for longer than an hour)
  • A new stroke occurs (on CT/MR)
  • No better explanation for any of the above.
What are the risk factors for cerebral vasospasm?
  • Fisher Grade 3 or 4 (see LITFL's article on SAH grading systems)
    • The thicker the blood in the basal cisterns, the greater the risk
  • Smoking
  • Cocaine use
  • Age under 50
  • SSRI and statin use
  • Rebleeding
  • Hypertension
  • Daily alcohol intake
  • Leukocytosis, WCC > 10.0
  • Hyperglycaemia
  • QTc > 450msec
  • LVH on ECG
  • ST depression on ECG

No difference in risk between clipping and coiling.

What forms of monitoring can be used to detect vasospasm?
Techniques used to monitor for vasospasm
Technique Advantages Disadvantages
Clinical examination
  • Cheap
  • Available at the bedside
  • Easily sequentialised
  • Inaccurate
  • Operator-dependent
  • Many episodes of vasospasm are not associated with physical signs
  • Gold standard
  • Offers a means of treating the vasospasm
  • May overtreat by picking up narrowing which is not associated with a decreased flow
  • Radiation exposure
  • Contrast exposure
  • Need for transport
  • Need for skilled personnel
  • invasive
  • 1% risk of stroke or dissection
  • Reasonable sensitivity and specificity
  • Non-invasive
  • Radiation exposure
  • Contrast exposure
  • Need for transport
  • Need for skilled personnel
  • Frustrated by the presence of coils and clips (artifact is generated)

Transcranial Doppler

  • High (100%) specificity;
  • non invasive
  • Easily sequentialised
  • Operator-dependent
  • Mediocre sensitivity
  • Highly sensitive and specific
  • Can pick up features of ischaemia and vasospasm earlier than the development of obvious signs or radiological features
  • Non invasive
  • Requires skilled operator and interpreter; may not be available
  • Ideally, EEG monitoring should be continuous.
  • potentially very useful in detecting ischaemia and cerebral hypoperfusion
  • Not validated, and mainly a tool of research
What techniques might be useful to prevent vasospasm?
  • Nimodipine
    • The objective is to prevent symptomatic vasospasn, i.e. features of ischaemia and radiologically obvious strokes
    • The BRANT trial: patients receiving nimpodipine were 34% less likely to develop stroke. One ought to continue nimodipine for 21 days to get the optimal effect.
    • Owing to the difficulty in identifying patients who will go on to develop vasospasm, nimodipine is given to all SAH patients.
  • Nicardipine
    • Analogous to nimodipine, but with less RCT support behind its use
  • "Triple H therapy"
    • Largely discredited practice of forced hypervolemia, hypertension and haemodilution.
    • A Cochrane review of this "circulatory volume expansion therapy" (2004) did not find any benefit. However, there was only one RCT and one "quzi-randomised" trial. The numbers were simply too small to make a recommendation.
    • On purely theoretical physiological grounds, as well as from the standpoint of lacking evidence, this therapy was savagely shredded by Myburgh in an excellent review article (2005)
    • Hypertension is the only component broadly supported by a consensus of neurosurgeons.
What management strategies are available to manage established vasospasm?

Conventional 4 vessel DSA (Digital Subtraction Angiography):

  • This is the gold standard for both diagnosis and management of vasospasm. One can confirm that vasospasm is occurring by a CT angiogram- or, if one were to go straight to DSA one could progress to some sort of definitive treatment. Verapimil and papaverine are the two most commonly used intra-arterial vasodilators.
  • However, this requires a skilled interventional radiologist. It exposes the patient to contrast and it it in vasive, with a (not insignificant - around 1%) risk of atheroma embolism or vessel dissection..
  • There is a small chance that this technique will lead to over-treatment: vessel narrowing may be detected, but this decrease in diameter may not reflect a decrease in flow, and may not warrant an injection of vasodilator.


  • Ultimately, this component of Triple H therapy ended up being the only one broadly supported by a recent multidisciplinary consensus conference. Among a group of neurocritical care specialists and neurosurgeons, hypertension "was considered reasonable by most participants", even though there was a great variety in opinion regarding how hight he blood pressure should be, which blood pressure variable to aim for (MAP vs SBP?) and which agents we should use to achieve it.
  • If pushed, most would agree that the "correct" blood pressure is the pressure at which your neurological deficits disappear.

Additional comments:
Overall, well  answered.  Some  candidates  were  formulaic  in  their  approach  to  the  initial
assessment and management, stating “Resuscitation and ABC” and proposing intubation, rather than  considering  aspects  of  the  history,  examination,  investigations  and  specific  treatment strategies in a stable patient with GCS 15.

Disclaimer: the viva stem above may be an original CICM stem, acquired from their publicly available past papers. Or, perhaps it is a slightly altered version of the original CICM stem. Or, it is a completely original viva stem, concocted by the monstrously amoral author of Deranged Physiology for nothing more than his own personal amusement. In either case, because the college do not make the main viva text or marking criteria available, almost everything here has been confabulated. It might sound like a plausible viva and it could be used for the purpose of practice, but all should be aware that it does not represent the "true" canonical CICM viva station.