Delayed Cerebral Ischaemia

DCI was historically referred to as vasospasm due to the narrowed cerebral vasculature seen on angiogram. The nomenclature has changed due to recognition that:

  • The pathophysiology is more complex than just vasoconstriction
  • Not all patients with radiological vasospasm are symptomatic
  • Not all symptomatic patients have radiological vasospasm

Acute neurological deterioration in the setting of SAH that:

Epidemiology and Risk Factors

Risk factors:

  • SAH
    • Directly related to volume of interventricular blood.
    • Risk between 4-21 days
      • Greatest risk between 4-10 days
      • Develops in one-third of SAH patients between 4 and 14 days
  • Hyponatraemia

Pathophysiology

Mechanisms include:

  • Vasospasm
    Of large and medium-sized intracranial arteries.
  • Microcirculatory dysfunction
  • Microthrombosis
  • Cortical spreading depolarisation
  • Neuro-inflammation

Aetiology

Clinical Manifestations

Diagnostic Approach and DDx

Investigations

Imaging:

  • CT Brain & Circle of Willis angiogram

Management

Aggressive management of vasospasm is critical to prevent neurological injury and should progress in a stepwise fashion:

  • Euvolaemia
  • Induced hypertension
  • Formal angiography with:
    • Cerebral angioplasty
    • Direct cerebral vasodilators

Specific Therapy:

  • Pharmacological
    • Volume resuscitation
      To euvolaemia.
    • Induced hypertension
      Process of ↑ SBP and monitoring for neurological improvement or complications of hypertension.
      • Depending on preference for MAP or SBP targets, initially aim:
        • MAP 20mmHg above baseline
        • SBP 20-40mmHg above baseline
      • Use noradrenaline
        Avoid vasopressin, may ↑ water retention and ↓ Na+.
      • Continue to augment SBP until:
        • Neurology resolves
        • SBP 200mmHg
        • Complications of hypertension
        • Noradrenaline 20μg/min
          Consider echocardiography to evaluate pump function.
    • Nimodipine
      • 60mg Q4H PO
        Can adjust to 30mg Q2H PO if symptomatic hypotension.
      • Administered to all SAH patients for 21 days
      • Improves outcome but does not appear to reduce radiological vasospasm
        Neuroprotection probably by another mechanism.
  • Procedural
    • Consider interventional radiology for vasospasm-related DCI for provision of:
      • Intraarterial vasodilators
      • Angioplasty

Anaesthetic Considerations

Marginal and Ineffective Therapies

Complications

  • C
    • APO
    • Stress induced cardiomyopathy
      Via ↑ catecholamines.
      • Milrinone 1st-line if inotropes required
  • D
    • Seizures
    • Infection
    • Cerebral oedema
  • I
    • Infection
    • Fever
      Intracranial blood is pyrogenic.

Prognosis

Key Studies

References

  1. Okazaki T, Kuroda Y. Aneurysmal subarachnoid hemorrhage: intensive care for improving neurological outcome. Journal of Intensive Care. 2018 May 8;6(1):28.
  2. Muehlschlegel S. Subarachnoid Hemorrhage. Continuum (Minneap Minn). 2018 Dec;24(6):1623–57.
  3. Bersten, A. D., & Handy, J. M. (2018). Oh’s Intensive Care Manual. Elsevier Gezondheidszorg.