One of the serious complications of aneurysmal sub-arachnoid haemorrhage (SAH) is Delayed Cerebral Ischaemia (DCI).
Briefly discuss DCI, including in your answer its assessment and management with reference to accepted and postulated strategies.
DCI is a common (occurring in about 30%) and serious complication following SAH. Defined as any neurological deterioration presumed related to ischaemia that persists for more than an hour and cannot be explained by any other physiological abnormalities. It is mostly caused by vasospasm.
May be reversible but may develop into cerebral infarction. Its highest risk of occurrence is from day 3 to 14 after presentation.
Aetiology still poorly understood
Assessment of DCI
Whilst up to 20% of patients can have a cerebral infarct despite being entirely asymptomatic, the mainstay of clinical monitoring is repeated clinical neurological examination.
DSA is the gold standard for vasospasm but as a screening test, multimodal CT imaging with CT perfusion is accurate and less invasive.
Transcranial Doppler has a high specificity but only moderate sensitivity. The other physiological modalities including EEG, brain tissue oxygen monitoring, cerebral microdialysis are less well established as monitoring modalities
Management of DCI
Aim is to prevent or minimise secondary injuries by haemodynamic management, drugs and endovascular procedures.
Triple H therapy:
- Induced hypertension improves CBF independent of blood volume. The most common agents used being Norad and phenylepherine. Secure aneurysm first.
- Hypervolaemia does not offer any benefit over euvolaemia, however it is important to avoid hypovolaemia.
- There is no place for haemodilution except for people with polycythaemia. Milrinone infusion has been used as alternative to Triple H.
Pharmacological management · Calcium-channel blockers
The main intervention shown to be beneficial is the use of Nimodipine.
Other CCBs have been shown to reduce vasospasm with beneficial effects on DCI but RCTs still needed.
· Intra-cisternal thrombolytics
Used in some centres on selected patients · Statins
Evidence is conflicting. Awaiting results of STASH · Magnesium sulphate
MASH-II did not show a benefit compared with placebo · Endothelin-1 antagonists
Recent published studies evaluating clazosentan have shown no clinical benefit
E.g. NO donors, EPO, enoxaparin, rho-kinase inhibitor either shown not to be beneficial or still being studied
Angioplasty and/or Intra-arterial vasodilators may be used in addition to nimodipine and haemodynamic management if indicated and expertise available.
Overall optimal triggers for escalating and de-escalating therapy not well defined
The discussion of DCI in the college answer is a complete and satisfying summary of the topic.
To make it easier to remember, one can trim some fat.
- Any new neurological deficit
- Occurs on days 3-14
- Can progress to stroke
- Repeat examination is a screening tool with poor sensitivity but little cost.
- DSA is gold standard
- CTA is next best option
- Transcranial Doppler is another option with poor sensitivity
- Nimodipine infusion
- Triple H therapy - remains debated;
- hypertension may not be helpful; at least maintain normotension
- hypervolemia may not be helpful; at least maintain normovolemia
- hemodilution is not helpful. Fullstop.
- Intra-arterial vasodilators such as papaverine and verapamil are a good option.
A LITFL review of vasospasm and DCI is a treatment with satisfying levels of detail.
Apocryphal notes on the diagnosis and management of SAH are also available:
Chapter 51 (pp. 568) Acute cerebrovascular complications by Bernard Riley and Thearina de Beer