Keywords
aneurysm - intraoperative neuromonitoring - somatosensory-evoked potential - extradural
hemorrhage
Introduction
Intraoperative neuromonitoring (IONM) is the standard of care to prevent the risk
of perioperative stroke following aneurysm clipping. New ischemic insults, which can
occur due to various surgical, physiological, and anesthetic factors, can be promptly
detected and reversed with the help of IONM. This report describes an unusual cause
of IONM signal loss and its management during microvascular aneurysm clipping.
Case Description
A 50-year-old woman patient was scheduled for a craniotomy and clipping of the right
middle cerebral artery (MCA) bifurcation aneurysm under general anesthesia, with IONM.
Her neurological examination was unremarkable, with a Glasgow coma scale (GCS) score
of 15/15, and she exhibited no sensorimotor or cranial nerve deficits. Diagnostic
cerebral angiography revealed two aneurysms located at the bifurcations of the right
and left MCAs, respectively. Anesthesia was induced and maintained with target-controlled
infusion of propofol, 1 µg/kg/h fentanyl, and 0.05 mg/kg/h vecuronium to maintain
a bispectral index of 40 to 50. The patient was positioned supine in a Mayfield 3-pin
fixator, and bilateral baseline median nerve somatosensory-evoked potential (SSEP)
measurements were obtained.
Intraoperatively, the aneurysm dome was embedded within the brain parenchyma, necessitating
the placement of a temporary clip on the M1 segment of the right MCA to facilitate
the dissection of the aneurysm neck. The initial two temporary clip applications (7
and 8 minutes, with a 5-minute interval) did not produce any signal changes in SSEPs.
Upon the third application, there was a reduction in left median SSEP amplitude within
2 minutes of clip application ([Fig. 1]).
Fig. 1 Stack of all the SSEP recordings during the entire procedure in (A) left median stimulation, (B) left tibial stimulation, and (C) right median stimulation (reference); SSEP, somatosensory-evoked potential.
The team was alerted, and an IONM checklist was carried out immediately, which did
not show any technical or physiological abnormalities; consequently, the clip was
removed. Following the clip removal, the amplitude increased gradually but did not
return to the baseline level. Given the stability of the recovered signals, the dissection
was continued, and the temporary clip was applied again, which immediately led to
a marked reduction in the left median and tibial SSEPs ([Fig. 1]). Hence, the clip was removed, resulting in SSEP recovery with time, albeit with
reduced amplitudes compared with baseline.
Considering a possible vasospasm resulting from vessel manipulation, blood pressure
was augmented by 20% above baseline, resulting in a partial recovery of the SSEP amplitude.
Further elevation of blood pressure was deemed inadvisable due to the potential risk
of rupture of an unsecured aneurysm on the contralateral MCA. A permanent clip was
applied, which did not induce any new changes in the SSEPs, and the indocyanine green
angiography confirmed obliteration of the aneurysm and distal flow in the right MCA.
Following hemostasis, the cranium was closed, anesthetic agents were discontinued,
and neuromuscular blockade was reversed. Upon neurological evaluation, the patient's
GCS was E1VTM5, with dense hemiplegia on the left side necessitating neuroimaging,
which revealed a right parieto-occipital extradural hemorrhage (EDH) with a 9-mm midline
shift.[Fig. 2] The patient underwent recraniotomy and evacuation of the EDH, after which she returned
to her baseline neurological status (E4V5M6 without focal deficits) ([Fig. 2]).
Fig. 2 Hyperacute MRI stroke protocol T2 FLAIR sequence shows a biconvex hyperintense lesion
in the right parieto-occipital region with midline shift to the left; FLAIR, fluid-attenuated
inversion recovery; MRI, magnetic resonance imaging.
Discussion
For anterior circulation aneurysms, SSEPs, motor-evoked potentials (MEPs), and electroencephalography,
either individually or in combination, are employed for intraoperative ischemia detection,
whereas MEP and brain stem auditory-evoked responses are utilized in posterior circulation
aneurysms.[1] In our case, given the aneurysm's location in the MCA, we monitored median nerve
SSEPs.
A 10% increase in latency and/or a 50% decrease in the peak-to-peak amplitude of cortical
SSEP is regarded as a warning criterion.[2]
[3] Changes in SSEP signals can be multifactorial. Technical factors include alterations
in electrode impedance, electrode dislodgement, disconnections, and electrical interference.
Physiological parameters such as hypotension, anemia, hypothermia, hypoxia, hypocarbia,
acidosis, and dyselectrolytemia significantly impact evoked potentials.[4] All anesthetic agents (inhalational > >intravenous) induce dose-dependent suppression
of SSEPs, which is more pronounced with boluses than infusions.[5] During aneurysm surgery, brain retraction, prolonged temporary clipping, inadvertent
clipping of the parent vessel or perforators, and vasospasm resulting from vessel
handling can cause cortical ischemia and signal change.[6]
[7] Therefore, troubleshooting changes in IONM signals should be conducted systematically
using a checklist.
The troubleshooting ruled out technical, anesthetic, and physiological causes in this
case, indicating a probable surgical insult. Due to the temporal correlation between
the signal change and the placement of a temporary clip, we initially hypothesized
that the repeated temporary occlusion might have induced ischemia. However, the clip
removal did not restore the baseline SSEP amplitude. Also, the brain was relaxed following
durotomy, thereby ruling out retractor-induced ischemia. Given the extensive sylvian
dissection, vasospasm was considered a potential factor, and blood pressure augmentation
(20% from baseline) and papaverine-soaked gel foam application to the MCA trunk were
attempted. However, all these efforts did not aid in further recovery of the SSEP
by the conclusion of the surgery, thereby excluding vasospasm as a cause.
The partial recovery of SSEP correlated with the new-onset left hemiplegia observed
during neurological assessment, suggesting an intraoperative ischemic event. The imaging
revealed a substantial right parieto-occipital EDH, which, on evacuation, resulted
in complete neurological recovery. We propose that the intraoperative expansion of
the EDH likely led to compression of the brain parenchyma and ischemia, thereby causing
the persistent depression of SSEP. The source of this EDH could be theoretically attributed
to the skull pin of the Mayfield fixation system. But hemodynamic stability was maintained
during and after skull pin fixation, and there were no apparent intraoperative signs
of EDH, such as a brain bulge. This could be due to the previously resolved subarachnoid
hemorrhage, cerebrospinal fluid release from the cisterns, ipsilateral origin of the
hematoma, and venous rather than arterial source of EDH, which is consistent with
the delayed presentation.
Conclusion
Any intraoperative change in evoked potentials during aneurysm clipping should be
addressed immediately. A root cause analysis using the IONM checklist can identify
reversible causes of signal loss, which can be promptly rectified to avoid potential
morbidity. Sometimes, the signal change can be due to a rare cause such as the one
we encountered; hence, any change in IONM should not be overlooked.
