Discussion
Despite its benefits in abbreviating side effects of deep hypothermia
and longer cardiopulmonary bypass periods, ASCP with moderate
hypothermia bears risks of warm ischemia for the abdominal viscera and
especially spinal cord during lower body circulatory arrest if prolonged
operations times are required or technical challenges occur
unexpectedly. Spinal cord injury and ensuing paraplegia after aortic
arch surgery is a rare but devastating complication for the patients.
Spinal cord perfusion is maintained by segmental arteries from the
thoracic and abdominal aorta and increased with the contribution of left
subclavian, intercostal, lumbar, hypogastric arteries and the local
paraspinous arterial tree embedded in the paraspinous muscles according
to the current collateral network concept 6,11,12. As
ASCP eliminates the segmental and hypogastric artery contribution to the
spinal cord blood supply it is suggested that nearly two thirds of total
flow is lost leaving the vertebral and intercostal arteries only to
perfuse the cord 6,11-13. Routine addition of distal
aortic perfusion to overcome this problem may complicate the surgical
field and lengthen the procedure with its inherent problems related to
retrograde femoral artery perfusion 6. On the other
hand, additional subclavian perfusion may cause significant back
bleeding from the intercostal arteries to the descending aorta causing a
steal phenomenon and insufficient perfusion of the lumbar segments
although blood to the cervical and mid-thoracic segments can be provided14. Therefore, when additional distal perfusion is not
used, duration of ischemic period and the degree of hypothermia become
the critical issues for spinal cord protection during arch surgery.
There is no consensus as to the safe duration of ASCP to rule out spinal
cord ischemic injury during arch surgery with lower body circulatory
arrest. As most reports are based on experimental studies concerns about
safe period remain 1,15-17. Spinal cord injury was
inevitable after 120 minutes and probable after 90 minutes in an
experimental study at 28°C. In the clinical setting, when temperatures
between 25-28°C are considered, Kamiya et al reported that LBCA duration
up to 60 minutes was safe but beyond that limit paraplegia rate
increases 18. The rate was 0% with deep hypothermia
(20°C to 24.9°C) with bilateral ASCP but when patients with lower-body
circulatory arrest greater than 60 minutes were further evaluated,
overall paraplegia rate rose to 2.1% (8/377). They concluded that
moderately hypothermic LBCA can be safely applied up to 60 minutes.
Beyond that limit they question the safety. Paraplegia rates are usually
5 to 8% in contemporary series but rates as high as 18.2% have been
reported with moderate hypothermia (25-28°C) 5,18.
Zierer et al reported 0.3% paraplegia rate in 1002 patients operated at
26-34°C and mostly unilateral ASCP (67.2%). All patients with
paraplegia had aortic dissection with a wide range of ASCP period (24,
41 and 127 minutes) 19. In another large series of
patients operated with moderate hypothermia (20-24°C) occurrence of
paraplegia was (0.5%) attributed to the creation of elephant trunk20. Elephant trunk formation causes a delay for
delayed reperfusion injury or inadequate perfusion. Mean ASCP duration
was relatively short (25.13 ± 19.02 minutes) in the present study (range
10-90 min) with 3 patients’ duration exceeding 60 minutes (63, 64 and 90
minutes). The only patient in the present study with postoperative
paraparesis (%3.3) had previous chronic aortic dissection, 90 minutes
of ASCP and elephant trunk formation consistent with the above mentioned
studies.
NIRS is effectively used for monitoring cerebral oxygen saturation
during ASCP in aortic arch surgery and has also been shown to be
feasible for spinal cord ischemia detection in procedures involving
thoracoabdominal aorta 4. As it reflects mixed tissue
oxygenation -both arterial and venous blood hemoglobin oxygenation-
rather than absolute values, usually a decrease of 20–30% from the
reference level suggests a possible risk of ischemia. For cerebral NIRS
monitoring during aortic surgery, a relative rSO2decrease to 64–80% of baseline (corresponding to 36-20% decrease of
baseline) is suggested to be closely associated with neurologic events
by the Japanese Society of Cardiovascular Anesthesiologists21. As there is no such predetermined critical NIRS
value in the literature for spinal cord injury to occur we evaluated
both 20 and 36% reductions in rSO2 values in our study
group. More than half of the patients experienced more than %20 drop in
T5 and T10 levels and only one of them had postoperative paraparesis.
Less patients had more than %36 drop in their baseline NIRS values
during ASCP as can be expected but none of them suffered from
paraplegia. The only patient with paraparesis had NIRS reductions in T5
level by 31.5% and T10 level by 34.7% in T10 which returned to 22.2%
drop in baseline after bilateral ASCP was instituted at the
33rd minute. However, his ASCP period was long enough
to cause paraparesis (90 minutes). On the other hand, the only patient
with more than 36% reduction in both T5 T10 values had only 17 minutes
of ASCP with no postoperative complication. It is clear that the time
period during which NIRS values remains low is very important. But we
could not record instantaneous time related changes in NIRS values
during the operation which is one of the limitations of the present
study.
As to the optimal NIRS optode placement location for spinal cord, which
is surrounded by vertebral bodies, supporters of positioning over the
bilateral paraspinal muscles argue that these muscles supplied by the
longitudinal collateral network indirectly reflects spinal cord
perfusion 22. On the other hand, it is claimed that
placing optodes on both sides of the vertebral column over the
paraspinal muscles interfere with each other if the light from the
contralateral side is received 23. Thinking that
poorly vascularized adipose tissue overlying the muscles especially in
obese patients may obscure light transmission if it is thick enough to
exceed the penetration depth of NIRS light (12 to 20 mm). Therefore, we
chose to place the optodes over the vertebral bodies distal to the
spinal processes.
The level to which the NIRS optodes should be placed is another issue.
When proximal aorta is clamped 3 cm below the subclavian artery leaving
both subclavian arteries intact, high thoracic region (T4-6) levels do
not show major fluctuations in NIRS value owing to extensive
collateralization in this area 5. Mid thoracic (T7-9)
and low thoracic (T10-12) values on the other hand drop significantly
with high lumbar (T13-L2) and low lumbar (L2-5) values being the most
prominent. As there is not such extensive collateralization below T8-9
thoracic level, mid-thoracic to lumbar region monitoring is usually
preferred in thoracoabdominal interventions and regarded as a baseline
reference to the more caudally placed optodes 1,5. In
aortic arch surgery however, where associated coronary artery bypass
grafting and harvesting of the left internal thoracic artery is a common
procedure, inclusion of high thoracic levels for spinal cord NIRS
monitoring should be undertaken as one major collateral is sacrificed
(LIMA use in 23.3% of the cases in the present series). A fairly good
positive correlation was observed between T5 and T10 levels in the
present study when thoracic NIRS values fell significantly during lower
body ischemic period (ASCP). In a pioneering study conducted by
Kinoshita et al in patients undergoing arch replacement optodes of NIRS
were placed at the level of 3rd and
10th thoracic vertebra over the paraspinous muscles
and they have observed that regional oxygen saturations fell
significantly with the start of ASCP 8. While T10
values continued to decrease to about 20% of baseline T3 NIRS levels
remained relatively stable unlike the present series. They a had similar
rate of CABG (17% and 23.3%) and most probably a similar rate of
internal thoracic artery harvesting with our series but we think that
additional perfusion of the left carotid and left subclavian artery
might have accounted for the higher T3 NIRS values in their practice.
They reported that with the advent of lower body circulation via a side
branch from the graft the difference between 4 NIRS optodes (right and
left forehead, T3 and T10) disappeared. They recovered 30 minutes after
resumption of CPB similar to the present study. They did not observe any
paraplegia in their 18 patients and concluded that cooling was the most
important means of protecting the spinal cord from injury (core
temperature about 25°). They had a higher mean lower body circulatory
arrest compared to our study (49±14 vs 25.13 ± 19.02 minutes) but when
LBCA times are compared in both studies they did not have any patient
with more than 90 minutes of LBCA duration (ranges between 24 and 72
minutes). The only patient with postoperative paraparesis in our study
had 90 minutes of LBCA. Therefore, we can conclude that when LBCA
durations are expected to approach 90 minutes, additional lower body
perfusion should be implemented as was also shown in animal studies1.
One important result of the present study is moderately negative
correlation between the lactate levels in blood obtained from descending
thoracic aorta and T10 NIRS values during the ASCP period. Lactate
levels from the radial artery and descending aorta were moderately
correlated (r=0.655) but they were significantly higher in descending
aorta probably due to the retrograde blood flow to descending aorta from
the visceral, thoracic and lumbar arteries rich in lactate. We think
that lactate level measurement during open distal anastomoses
accompanied with T10 NIRS monitoring can be a useful adjunct during arch
operations with long ASCP periods. However, studies with larger volumes
may help to determine a threshold limit to be used as an alarming sign
for spinal cord ischemia.
Regarding s100β levels, in patients with spinal cord injury after
thoracoabdominal operations Kunihara et al. observed that serum levels
reached peak levels just after the operation and patients with spinal
cord injury had a second peak at 24 hours postoperatively (1.3 ± 1.4
μg/L) 24. We do not have a baseline s100β value
preoperatively, but the values in 6th postoperative
hour fell significantly compared to values at the end of ASCP. Our
values are somewhat higher but serious neurological complication
occurred in one patient whose s100β levels were 0.33 ng/ml and 1.929
ng/ml respectively and one patient is not enough to make a reliable
statistical evaluation.
One of the most important drawbacks of the present study is failure to
monitor lumbar spine NIRS values. We could have observed significant
fall in lumbar NIRS values before any reduction occurred in the thoracic
level. Another shortcoming is absence of basal s100β level determination
before any procedure took place. Patients with acute aortic dissection
was excluded but there were 2 patients with chronic aortic dissection
with previous intervention to the ascending aorta and aortic valve.
Instantaneous display of NIRS during the operation was available however
we could not record them. This study was conducted in a small patient
group. Large scale studies are needed to arrive at a better conclusion
regarding alarming signs for spinal cord injury during aortic arch
surgery.