Keywords
midbrain cavernoma - sitting position - SSEP - MEP - venous air embolism
Introduction
Midbrain tumors account for approximately 14.2 to 25% of cerebral cavernous malformations.[1] Between 80 and 100% present symptomatically due to hemorrhagic conversion.[2] Surgical resection is the definitive treatment, and goal is complete resection with
sophisticated strategy. Complex neuroanatomy of midbrain can be challenging to both
neuroanesthesiologist and neurosurgeon. Sitting position is one among the many positions
utilized for posterior fossa surgeries, due to the advantages offered in terms of
better surgical exposure airway accessibility, better ventilation, and less bleeding
due to venous drainage. Risks involved are venous air embolism (VAE), pneumocephalus,
and ischemic injury.[3] Intraoperative neuromonitoring, namely somatosensory-evoked potential (SSEP) and
motor-evoked potentials (MEP), are indicated for midbrain surgeries for dynamic functional
assessment of neural structures.[4] We hereby present a case report of woman posted for midbrain cavernoma excision
in sitting position with SSEP, MEP, and bispectral index (BIS) monitoring.
Case Report
A 56-year-old homemaker, known hypertensive and hypothyroid, weighing 75 kg presented
with diplopia since 2 months. She was diagnosed with left midbrain cavernoma 3 years
ago.
There was no history of nausea vomiting, blurring of vision, facial numbness, altered
hearing, weakness or altered sensorium. There were no preoperative neurologic deficits.
Perioperative magnetic resonance imaging brain (T2 and fluid-attenuated inversion
recovery) showed 9.6 × 9.4 × 14.3 mm3 hyperdense lesion with popcorn appearance showing hemosiderin rim in left hemi midbrain.
Extensive blooming on gradient echo images was suggestive of chronic hemorrhage. Diffusion
tensor imaging (DTI) showed left-sided corticospinal tracts were anterolateral to
the lesion and intact. Craniotomy and excision of midbrain cavernoma in sitting position
was planned with MEP, SSEP, and BIS monitoring. Written informed consent was taken.
In the operating room, preinduction monitors, electrocardiography, pulse-oximetry,
noninvasive blood pressure, were attached. General anesthesia and endotracheal intubation
were facilitated by intravenous fentanyl—2 mcg/kg, propofol—2mg/kg, and vecuronium—0.1 mg/kg.
Postinduction temperature, invasive blood pressure, central venous pressure, transesophageal
echo, MEP, SSEP, and BIS monitoring were done. Sitting position was gradually given
over a span of 3 minutes, keeping a watch on hemodynamics ([Fig. 1]). The patient tolerated the position well and did not require any vasopressors to
maintain hemodynamics. Anesthesia was maintained by propofol infusion—100 to 150 mcg/kg/min,
fentanyl infusion—0.5 mcg/kg/h, along with sevoflurane minimum alveolar concentration
of 0.3 to 0.4, titrated to maintain a BIS of 40 to 60. Baseline MEP, SSEP in supine
position as well as in sitting position were normal ([Fig. 2A]). Surgical access to the cavernoma was achieved by midline suboccipital craniotomy.
During the procedure, two episodes of VAE were detected by transesophageal echo. Sudden
drop in end-tidal CO2 from 27 to 23 mm Hg was noted. The surgeon was notified, surgical site was flooded
with saline and packed with gauze, 10 mL of air was aspirated through central venous
catheter, and bilateral jugular compression was given. There were no hemodynamic changes
during the VAE. Throughout the procedure mean arterial pressure (MAP) was maintained
above 90 mm Hg via pulse pressure variation-guided fluid therapy. During the resection
of cavernoma, MEP signal of right brachioradialis was lost completely. Anesthetic
and technical causes were ruled out. The stimulus intensity was increased in aliquots
of 50 V from 300 to 450 V, but still no MEP was obtained from the right brachioradialis.
The signal was not restored at the end of the procedure ([Fig. 2B]). The total blood loss was 300 mL. Vasopressors were not used at any point of time
during the surgery. Trachea was extubated at the end of surgery. The patient had power
of ⅗ for flexion of right upper limb that was correlating with the MEP findings. The
patient was shifted to intensive care unit for further postoperative monitoring. Postoperatively
intravenous methylprednisolone (500 mg) was administered twice daily for 3 days. The
power for flexion of right upper limb improved on postoperative day 5.
Fig. 1 Patient in the sitting position.
Fig. 2 (A) Baseline motor-evoked potential (MEP). (B) Complete loss of MEP signals in right
brachioradialis at the end of procedure.
Discussion
The median suboccipital supracerebellar approach to dorsal midbrain lesions requires
patient to be in prone or sitting position. Sitting position gives potential advantages
of good surgical field, access to airway and better ventilation. However, anatomical
and physiological challenges, increased risk of VAE, hypotension, and tension pneumocephalus
can be challenging and devastating. Functional integrity of descending motor pathways
and their selective and specific assessment during critical surgical maneuvers is
accomplished by MEP during brainstem surgeries especially those involving the midbrain.[4] MEP altered signals can result due to surgical insult, hypotension, anesthetic agents,
hypothermia, technical glitch, and brain shift.[5]
[6] Surgeries in semisitting position can alter the MEP and SSEP signals indirectly
by drastically reducing the cardiac output during VAE. It is uncertain whether VAE
impacts SSEPs and MEPs. It has been put forward, therefore, that VAE may result in
MEP and SSEP alterations unrelated to neurological dysfunction.[6]
[7] In our case, VAE did not cause any change in the evoked potentials. MEP signals
were lost for the right brachioradialis while dissecting the tumor. This could be
due to handling of the left sided corticospinal tracts, which were anterolateral to
the lesion as per the DTI scan.
Total intravenous anesthesia (TIVA) offers an advantage of early onset induction in
addition to continuous monitoring of neuronal structures.[8] Further studies have shown that the neuroprotection offered by TIVA and inhalational
agents had no significant differences. We therefore used a combination of TIVA (propofol
and fentanyl) and inhalational agents (sevoflurane) to reduce the dose of one another
and prevent untoward hemodynamic complications. Target-controlled infusion (TCI) is
the TIVA technique that maintains a constant plasma concentration of the desired drug.
However, literature shows both manual and TCI are reasonable methods to achieve BIS-guided
TIVA.[9] We do not have a TCI pump in our institute, and hence we used the manual technique.
Sitting position requires absolute immobility aided through nondepolarizing muscle
relaxants; however, their use in neuromonitoring, especially MEPs, is contraindicated
and poses a challenge for the anesthesiologist. Thus, maintaining adequate depth of
anesthesia is absolutely essential.[10]
[11]
Effective monitoring of depth of anesthesia is crucial during TIVA to prevent intraoperative
awareness, which can have negative implications on patient. BIS values between 40
and 60 ensure adequate depth of anesthesia. Lee et al in their research concluded
that sitting positions reduce BIS values in tandem with MAP when compared with supine
position.[12] We ensured MAP of more than 90 mm Hg and BIS values between 40 and 60 at all times.
A thorough knowledge of the anatomy, physiology, anesthetic technique, methodical
surgical dissection will assist in accurate interpretation of the altered sequence
of MEP intraoperatively.
Standard-of-care anesthesia technique combining TIVA and inhalational anesthesia,
offer a safe anesthesia and optimal surgical conditions in the absence of muscle relaxation.
Conclusion
Midbrain cavernoma excision in sitting position with SSEP and MEP monitoring requires
expertise, individualized anesthesia technique, and vigilance for complications. A
multidisciplinary discussion with anesthesiologist, surgeon, and neurologist is the
key step in diagnosing intraoperative altered SSEP and MEP signals and, thus, the
early detection of new neurological deficits during the procedures at midbrain.
