An 81 -year-old female with critical aortic stenosis has a valve replacement procedure. Post-operatively
she is diagnosed with an anterior spinal artery syndrome at the T6-T7 level on an MRI.
a) Describe the signs you would expect on sensory examination of her lower limbs. (20% marks)
b) What are the deep tendon reflexes likely to show? (20% marks)
c) What perioperative factors may contribute to this syndrome? (30% marks)
d) What therapies have been advocated to optimise spinal cord perfusion? (30% marks)
- Sensory neurological examination of the lower limbs would reveal loss of pain and temperature sensation with a sensory level of T6-T7 with relative sparing of proprioception and vibratory sense below this level.
- The acute stages are characterised by flaccidity and loss of deep tendon reflexes (with spasticity and hyperreflexia developing over ensuing days and weeks).
- Prolonged aortic cross clamp ,low perfusion pressure to the spinal cord as well as IABP, or ECMO are associated with spinal infarction
- Mean arterial pressure is increased in increments of 10mm Hg every five minutes (with volume and vasopressor agents) until symptoms resolve, bleeding complications ensue, or additional blood pressure augmentation would cause an unacceptably high risk of bleeding at the surgical bed.
If a lumbar drain is in place, it should be opened and set to drain at 8 to 12mm Hg. If not in place, a lumbar drain should be placed if there is no response to blood pressure augmentation within 10 to 20 minutes.
The sensory signs of an anterior spinal artery syndrome are:
- Preserved bilateral proproception and vibration
- Lost bilateral pain, temperature
- Usually, preserved light touch sensation (Triggs & Beric, 1992)
There would also be bilaterally absent motor control, and probably incontinence. The affected tracts are:
- Anterior spinothalamic tract (pain)
- Vestibulospinal tract (postural motor control)
- Tectospinal tract (reflexive postural head neck and eye movements)
- Anterior reticulospinal tract (postural motor control)
- Anterior corticospinal tract (gross motor control)
Tendon reflex examination would reveal a flaccid loss of reflexes. "Flaccid motor paralysis and absent deep tendon reflexes may later progress to spasticity and hyperactive tendon reflexes", say Santamato et al (2013), but they do not say how long it will take. Spinal reflex arcs below the level of the injury will be intact, but they are facilitated by input from upper motor neurons and when this is interrupted the deep tendon reflexes are transiently lost.
Perioperative factors in cardiothoracic or abdominal aortic surgery which promotes anterior spinal artery syndrome are
- Perioperative hypotension
- Prolonged aortic crossclamp time
- Other instrumentation of the atheromatous aorta (eg. angiography, IABP, VA ECMO)
- Inadequate heparinisation of the bypass circuit
- Air emboli
- Vascular malformations (aortic aneurysms, haemangioma etc.)
- Infection (tuberculosis)
- Haematological disorders (polycythaemia, hypercoagulability)
- Trauma of the spine (fracture. haematoma, foreign body etc.)
- Chronic respiratory disease with polycythaemia
- Anatomical changes of the spine (kyphoscoliosis, spondyloarthrosis, disc herniation etc.)
Management of an infarcted anterior cord involves maximising the perfusion of the cord via collaterals. The best information about this about this seems to come from Hnath et al (2007), who published a fairly successful protocol. This consisted of:
- Increasing perfusion pressure
- Hnath et al maintained the MAP at ≥90 mm Hg. In their answer, the college examiners recommend cranking the vasopressors until symptoms resolve or complications develop. This comes from the "Spinal Cord Infarction" UpToDate article by Mullen et al (2016).
- Decreasing spinal CSF pressure
- Hnath et al actively drained the CSF to maintain pressures <15 mm Hg. The college recommend simply draining to a positive pressure of no more than 8-12 mmHg, which is again from the same UpToDate source. The systematic review by Cina et al (2004) suggests that if you're going to do this, you should aim to decrease the CSF pressure to at least below 10 mmHg, for at least 48-60 hours. The rationale for this is that the lower CSF pressure minimise the resistance to afferent spinal cord blood flow, thereby increasing perfusion of at-risk regions (Strohm et al, 2017)
Hnath et al reported a 60% improvement, but their series had only 5 patients in the treatment arm, which somewhat dampens the enthusiasm of anybody following their footsteps. Chiesa et al (2005) list several other possible strategies:
- Distal aortic perfusion by bypass of the left heart (i.e. piping oxygenated blood into the distal aorta), which doesn't seem to work according to Coselli et al (2004)
- Deep hypothermic circulatory arrest which should theoretically protect the cord perioperatively (Safi et al, 1998)
- Regional cooling of the cord by infusing normal saline at 4° C into a thoracic epidural (Cambria et al, 1997)
- Protective pharmacological agents, used perioperatively (steroids, naloxone, barbiturates, papaverine, magnesium sulfate)
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