carotid artery disease carotid disease

Would you operate on a mild (<50%) symptomatic carotid stenosis?

10/01/2016

Source: EJVES Sep 2016

According to the trials, NO …. but what would you do when the plaque is ‘vulnerable’? Well … this study from Sweden for three years showed that the recurrent rate for stroke is about 7% in 3 yrs in Symptomatic mild stenosis. This is too high.

The commentary on the article put very nice rules:

A combinations of mild (20–49%) and moderate (50–69%) percent stenosis with stable or unstable plaque morphology is given in the following 2 × 2 matrix.

The four combinations for recurrent stroke risk are:

  • (a) low % stenosis and stable plaque,
  • (b) low % stenosis and unstable plaque,
  • (c) moderate % stenosis and stable plaque, and
  • (d) moderate stenosis and unstable plaque.

One might predict that

  • (a) be strongly considered for current best medical therapy and that
  • (d) be recommended for CEA.
  • The optimal management outcomes for (b) and (c) are unknown and clearly deserve a trial.
  • If I had a TIA or minor stroke and (b), mild stenosis and an unstable plaque, I would strongly consider CEA.
  • In contrast, if I had (c), moderate stenosis, and stable plaque, I might choose current best medical management, unless I was already on it.

This is really interesting argument …

 

AAA aortic surgery complex AAA; FEVAR; BEVAR complex EVARs EVAR Spinal cord ischaemia

Protecting patients with complex aneurysm repair from paraplegia. Possible?

10/01/2016

Source: EJVES Sep 2016

The first large TEVAR series reported comparable neurological adverse events to open surgery, at ~ 30% of cases!

Bidirectional and reversible flow patterns in the longitudinal arteries suggest the existence of watershed zones. These are vulnerable whenever the arterial inflow becomes diminished, or if the collateral circulation becomes inadequate. Grey and white matter blood supply depends primarily on systemic and local blood pressure. Local spinal cord haemodynamics are also significantly influenced by venous drainage.

Delayed paraplegia is a complex phenomenon and probably follows aggravation of intraoperative subclinical spinal cord damage because of postoperative reductions in blood pressure, insufficient local haemodynamics, and reactive, inflammatory processes.

SCI is a multifactorial phenomenon where contributory factors vary within individuals, as well as interacting differently between individuals. Accordingly, the pragmatic approach (while accepting that many pathophysiological mechanisms remain unknown) is to revascularise as many inflow arteries as possible while also optimising haemodynamic management, cerebrospinal fluid (CSF) drainage, and strategies that aid the development of collateral arteries.

Approaches –

  • Monitoring motor evoked potential (MEP) – highly sensitive for assessing spinal cord function. If critical spinal cord perfusion is identified, then protective measures can be taken:

    • increasing mean arterial pressures

    • draining more CSF

    • restoring flow early to the internal iliac arteries

    • staging the procedure

    • MEP monitoring is a relatively complex technique, requiring dedicated and experienced neurophysiological support, and requires the procedure to be performed using no muscle relaxants. Spinal near-infrared spectroscopy might, however, become an alternative and easier technique for the future.14

  • Temporary aneurysm sac perfusion – during both open and endovascular repair of extensive TAAAs, staged repair has resulted in significant reductions in SCI.8

  • CSF drainage remains controversial.

    • A Cochrane review concluded that only limited data supported the role of CSF drainage.9

    • A recent meta-analysis demonstrated that CSF drainage decreased SCI by nearly half. However, this significant difference did not extend to patients who developed delayed paraplegia.10

    • Another systematic review reported an overall SCI rate less than 4%, with no difference between prophylactic CSF drainage and no drainage following TEVAR.11

    • Another recent study on endovascular TAAA repair reported a 16% rate of SCI, with no reduction using prophylactic CSF drainage, and CSF drainage was associated with a 6% rate of cranial hypotension syndrome.12

    • Despite these conflicting data, however, CSF drainage continues to be used by almost all aortic teams during TAAA repair.

  • Other methods –

    • Assessment of CSF biomarkers for neuronal injury. Recently, two biomarkers for axonal injury (T-tau and NFL) were shown to rise significantly in patients with postoperative SCI. Unfortunately, however, these biomarkers did not increase until after clinical signs of paraplegia had appeared.15

    • Regenerative medicine for spinal cord injury, mainly after trauma.16 Scientists expect to be able to regenerate injured spinal cord within a decade.

    • High-resolution computed tomography and magnetic resonance imaging allow anatomic assessment of crucial collateral pathways and can guide surgical and endovascular strategies. However, functional and dynamic information is lacking.