CICM SAQ 2013.1 Q5

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.

Haemodynamic strategies

• Avoid hypotension.
• 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

Other agents

• E.g. NO donors, EPO, enoxaparin, rho-kinase inhibitor either shown not to be beneficial or still being studied

Endovascular procedures

• 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