Clinical Trial Details
— Status: Completed
Administrative data
| NCT number |
NCT04662177 |
| Other study ID # |
2018-00220 |
| Secondary ID |
|
| Status |
Completed |
| Phase |
Phase 4
|
| First received |
|
| Last updated |
|
| Start date |
November 21, 2018 |
| Est. completion date |
December 4, 2020 |
Study information
| Verified date |
December 2020 |
| Source |
University Hospital Inselspital, Berne |
| Contact |
n/a |
| Is FDA regulated |
No |
| Health authority |
|
| Study type |
Interventional
|
Clinical Trial Summary
All neurosurgical patients at the Neurosurgery University Hospital Bern who will be operated
for carotid endarterectomy (CEA) are routinely operated in deep anae¬sthesia with suppression
of the electrical activity of the electroencephalogram (EEG). To achieve this suppression of
the EEG activity (burst suppression, BS) high effector concentrations (Cet) of Propofol doses
are needed. However, a protracted infusion of large amounts of Propofol to reach a BS during
the operation can lead to accumulation and a protracted wake-up phase with poorer
neurological assessability. Somatosensory evoked potentials (SSEP), and trans-cranial Doppler
flow velocity in the middle cerebral artery are measured to detect ischemia until the
operation. The SSEPs are used to verify the functional integrity of the nervous system in
combination of the EEG and both together exclude severe global ischemia during the operation.
The central acting α2-agonist Dexmedetomidine could help to reduce the amount of Propofol
without influencing electrophysical studies. However, no data are currently known for
practical use in carotid endarterectomy with Propofol with co-administration of
Dexmedetomidine in conjunction with electrophysiological studies (SSEPs and MEPs).
Description:
In the investigators clinic, as a neuroprotective measure, all neurosurgical patients
operated for carotid endarterectomy (CEA) are routinely operated in deep anaesthesia with
suppression of the electrical activity of the electroence-phalogram (EEG). To achieve this
suppression of the EEG activity (burst suppression, BS) high effector concentrations (Cet) of
Propofol doses are needed. However, a protracted infusion of large amounts of Propofol to
reach a BS during the operation can lead to accumulation and a protracted wake-up phase with
poorer neurological assessability.
Somatosensory evoked potentials (SSEP), and trans-cranial Doppler (TCD) flow velocity in the
middle cerebral artery are measured to detect ischemia. A significant decrease in TCD
velocity and/or SSEPs amplitudes during cross-clamping of the internal carotid artery (ICA)
gets treated with an adapted increase of arterial blood pressure or placement of a shunt.
Intraoperative monitoring and recording of data in every patient undergoing CEA median nerve
SEPs and MCA flow velocity have been constantly monitored by an additional intraoperative
monitoring (IOM) technician who has been trained and certified in the assessment of
intraoperative monitoring. The median nerve SEP amplitudes are recorded at least at these
events: baseline value before skin incision, EEG burst suppression before cross clamping of
the internal carotid artery, at time of ICA cross clamping, 10 minutes after cross clamping
or immediately after placement of shunt (ICA clamping), reperfusion of ICA and haemostasis /
end of surgery. The predefined criterion for temporary shunting was the reduction of more
than 50% of the SEP amplitude.
Median nerve somatosensory evoked potentials (SEPs) were performed by stimulation at the
wrist with a pair of needle electrodes (Inomed Germany®). This is a single pulse stimulation
with 0.5 ms pulse duration and a low repetition rate ranging from 0.7 - 2.3 Hz. Recording is
performed via corkscrew electrodes placed accordingly to the 10-20-EEG system on the patient
scalp. For the right median nerve SEP C3´/Fz and for the left median nerve SEP C4´/Fz is
chosen as standard derivation. Alternatively, Cz' or the contralateral Cp' served as
reference to improve quality of recording. To improve the signal to noise ratio the responses
are averaged 150-200 times.
The investigator use the somatosensive evoked potentials (SSEPs) to verify the functional
integrity of the nervous system. Standardized surgical and anaesthesiological measures at the
CEA with defined EEG endpoints and depending on the anaesthetic effect can - in normal EEG
and SSEPs - effectively exclude severe global ischemia. The effects of burst suppression and
the volatile anaesthetics on SSEPs were also investigated and showed no significant
difference. Since 2016, motor-induced evoked potentials (MEPs) have also been used, which
are, however, suppressed by volatile anaesthetics in a dose-dependent manner. On the other
hand, Dexmedetomidine in combination with Propofol seems to suppress only insignificantly.
The indication spectrum for the centrally acting α2-agonist Dexmedetomidine has been
increasingly extended since its approval in Switzerland. In addition to the use of
Dexmedetomidine in the intensive care units, Dexmedetomidine is also increasingly being used
perioperatively up to premedication in children. In some studies, an anaesthetic reduction of
40-60% could be achieved or the opioid consumption after the addition of a α2-agonist could
be reduced by 50-75%. The blood pressure response to a Dexmedetomidine dose depends on the
rate of infusion). In addition, administration of Dexmedetomidine does not result in
respiratory depression or compromising of the respiratory tract. It has been shown that
Dexmedetomidine can cause a "sleep-like" sedation state and this state can be interrupted by
verbal stimuli), examined the EEG activity in sedations on voluntary subjects compared to a
control group with physiological sleep pattern. In this study, it was shown that the EEG
spindle activity in subjects with Dexmedetomidine infusion was comparable to that of a
physiological non-rapid eye-movement (nonREM) sleep stage II in the control tests. The
authors concluded from their investigations that a "sleep-like state" (stage II non-REM) can
be achieved by the Dexmed-etomidine infusion. However, no data are currently known for
practical use in carotid endarterectomy with Propofol and Dexmedetomidine in conjunction with
electrophysiological studies (somatosensory evoked potentials (SSEP) and motor evoked
potentials (MEP)).
In addition, there is a high risk of postoperative delirium (POD) in many of these patients.
This was examined in a recently published Lancet study by Xian Su and colleagues in 700
patients with non-cardiac interventions in elderly patients). A reduction of the delirium
incidence from 23% to 9% was found after a low-dose Dexmedetomidine dose of 0.1 μg/kg body
weight/h. In addition, Dexmedetomidine is attributed a neuroprotective effect against
ischemic and hypoxic influences). Other animals-experimental studies indicate neuroprotection
in ischemic insult and subsequent reperfusion).
