Carotid Flashcards
What are 2 interventions for carotid revascularisation?
carotid stenting & CEA
What Ix are recommended as part of pre-anaes Ax for carotid revascularisation?
12-lead ecg
Should aspirin/clopidogrel be taken prior to CEA or CAS?
yes
How is the anaesthetic usually given for CAS?
LA at the puncture site
What are the 3 primary anaesthetic goals for carotid revascularisation procedures?
- Running an anaesthetic that allows the pt to be promptly woken post-procedure for neuro Ax
- avoid wide BP or HR variations throughout procedure
- minimise PONV (retching risk neck haematoma)
Benefits & cons of LA vs GA
-continual monitoring neurologic function by talking to pt/asking them to perform basic tasks vs relying on EEG or other continuous neuromonitoring
-relative haemodynamic stability: lower incidence hypoT during & post-procedure
-more likely to allow for selective vs routine placement of a carotid shunt (however selective shunting based on continuous neuromonitoring under GA still possible)
-does not subject the patient to risks ass’d with GA agents (eg. muscle relaxants), for some patients GA may be high-risk (eg. pulmonary comorbidity)
-possibly lower los/cost/ponv/pocd
-overall the data swayed slightly to suggest LA/RA is better but overall LA vs GA has no sig impact on clinically important outcomes (large meta-analysis with observational and randomised trials suggested that LA/RA had lower stroke/tia/mi/mortality risk vs GA but when looked @ just the randomised trials, no difference (eg. a 2021 Cochrane meta-analysis of >4000 pts showed neither stroke nor mortality incidence were significantly different between LA/regional vs GA))
GALA trial no diff GAvsLA (MI, stroke, death) provided centre familiar w technique
-cons: LA risk pt discomfort, some pts may prefer (eg. anxiety), not possible if pt has neurocognitive dysfunction/uncooperative, not possible if unable to lie supine awake (eg. CCF), if requires sedation this may impede accurate Ax of neuro status, RISK OF NEEDING URGENT CONVERSION which is a big issue if open CEA (limited access to the airway & limited ability to pre-oxygenate during conversion) but not such an issue for CAS.
How long do CEA or CAS usually last?
<90 mins
What are some considerations when choosing GA technique for carotid revascularisation?
A: ETT if GA for CEA (limited access to airway), LMA if CAS
*care with emergence esp if ETT- risk coughing & neck haematoma for CEA, risk groin haematoma after CAS
limit haemodynamic lability w deep extubation & gentle mask vent until awake if safe
B: maintain normocapnia (carotid dilation w hypercapnia may incr risk of embolisation, risk intracerebral vascular “steal” if incr blood flow to normally perfused brain tissue, reduced CBF with hypocapnia)
Drugs: Want rapid emergence & the procedure may require neuromonitoring: Short acting agents (lignocaine, remi, prop) for induction, prop or volatile/remi maintenance (if using neuromonitoring team may want a ceiling of volatile (<= 0.5 to 1 MAC) to avoid signal suppression that may interfere w detection of brain ischemia) or TIVA (pref as less PONV risk, useful to also avoid N2O)
What are techniques for LA/regional/sedation for CEA?
either just LA at art puncture site (for CAS)
for CEA, may use LA +/- nerve block
for both, run sedation for pt comfort but minimal to allow frequent intra-op neuro exams
What nerve blocks are done for CEA?
Pros & cons of each?
superficial or deep cervical plexus blocks
Superficial recommended as provides adequate anaesthesia (may need to be supplemented with LA by the surgeons) while avoiding potentially serious complications of deep block (vertebral artery or subarachnoid injection, Horner syndrome, unwanted blockade of phrenic (ant to ant scalene), RL (post to L) lobe thyroid) & vagus (carotid sheath) nerves), it’s easier to perform & only requires 1 vs 3 injections (advance needle ant to post direction to C2 TP, after -ve aspiration inject 5mL LA which should be visualised spreading adj to the TP. repeat for C3 & C4 TPs).
also risks LAST, haematoma, infection
other nerve injuries (from block or OT)
-marginal mandibular branch facial nerve (drooping corner mouth)
-accessory
-hypoglossal (tongue deviation to side of injury)
RLN (unilat VC)
ext branch SLN (voice quality)
accessory (traps, SCM)
Systematic review of 69 studies showed there was less risk of converting to GA or developing serious complications with superficial vs deep plexus block
rick of conversion to GA 2.5% (not just from block failure; also from pt anx/agitation, resp compromise)
What dose of dexmed could be used for CEA sedation? problems w dexmed for this indication?
1mcg/kg loading over 20 mins, then (separate syringe) 0.3mcg/kg/hr
slightly decrease CBF (vasoconstriction), hypotension (which could be counteracted w vasopressor), relatively prolonged sedation due to prolonged DOA
What’s the risk of conversion to GA for CEA under LA/RA? cf clot retrieval?
4%
up to 15%
What are the options for neuromonitoring during CEA?
gold standard= neuro exam in awake pt
Brain activity monitoring:
1.
a) EEG (most commonly used method of neuromonitoring in pts having CEA under GA- get a baseline EEG prior to induction, second baseline after induction before carotid manipulation, then continuous EEG waveform evaluation. need continual communication w neuromonitoring team. Severe EEG changes (>50% decr waveform amplitude in generalised or lateralised distribution) indicates need for augmentation of BP by me or shunt insertion by surgeon; ensure adequate MAP & 100% O2, cerebral protection (CO2, glucose, temp)).
measures only cortical not deeper structure. requires expert team (cost,time0 for interpretation, GA may alter signal, can’t identify emboli.
b) SSEPs: rarely used- poor predictor of intraop neuro deficits, can’t identify emboli, GA may alter the signal, no more S&S vs EEG.
- Cerebral perfusion monitoring:
a) internal carotid artery stump pressure (during CEA)- only a single pressure obtained vs continuous but it combined w EEG (or TCD)= best predictive technique for cerebral ischemia monitoring. by itself, stump pressure is a specific but non-sensitive measure of cerebral ischaemia, can’t identify emboli.
b) transcranial doppler (during either CEA or CAS)- uses pulsed wave doppler to measure blood velocities in middle cerebral artery. Lacks S&S for detection of cerebral ischemia (changes in blood flow velocity can reflect changes in arterial diameter vs flow changes), but useful for detecting & quantifying emboli & the instant audio feedback helps guide surgical manipulation of carotid artery. TCD probe position problematic for surgeons access to neck & anaes access to airway (petrous temporal bone). operator dependent. acoustic window not found in 10-20% of pts.
- Brain O2 sat monitoring:
a) jugular venous bulb monitoring (sats (SjVO2) & lactate)- catheter inserted into ipsilat IJV. limitation= it’s a global vs regional marker of ischemia. Also the range of normal SjVO2 is wide (55-75%). Lack of evidence for benefit.
b) cerebral oximetry- uses near-infrared spectroscopy (NIRS) to detect regional cerebral O2 saturation (rSO2) via adhesive pad on forehead. Reduction of rSO2 of >=20% below baseline during carotid clamp predicts periop stroke (sens 86%, spec 57%). baseline rSO2 <=50% before induction predicts stroke (sens 91%, spec 67%). more research required to determine if a 15 or 20% decr from baseline after clamping= best trigger for shunt placement.
limitations= sensitivity for detecting ischemia limited by the small window of frontal cortex captured. also, wide variety of baseline readings within & btwn pts, lack of agreement re: threshold for shunt/other interventions, multiple factors that cause decr rSO2. interference from non-cerebral blood flow & light, can’t identify emboli.
What are potential causes of cerebral ischemia during CEA? Rx for it? how about CAS?
hypoperfusion after carotid clamping (minimising clamp time senior surgeon limits risk)
embolism after carotid clamping or unclamping (heparin should have been given prior to shunt).
notify team if change in cognition/motor or cerebral perfusion
first step is AUGMENT MAP with vasopressor (for prevention, MAP should be 110% of normal to enhance collateral flow via CoW), reassess, FiO2 100%, surgical placement of a carotid shunt (risks incl arterial dissection, embolic phenomena)
If no improvement in status of awake pt & reduced GCS/airway compromise, secure airway to control oxygenation/ventilation. ongoing haemodynamic, glucose optimisation.
during CS, ischemia may be due to carotid vasospasm, emboli or dissection- interventionalist would do a cerebral angiogram to identify a potential treatable condition
How is the neuro exam done in awake pt?
baseline pre-procedure, every 10-15 mins during exposure of carotids, immediately b4 carotid clamping & continuously during carotid clamping
Noting answers to simple questions, asking pt to squeeze hand or a noise-making toy to ensure contralateral grip strength is normal
If agitation/slurred speech, disorientation or extremity weakness, possible ischemia & need for shunt placement
What are limitations of EEG?
unable to monitor subcortical structures
complex interpretation (need specialised neuromonitoring staff), limited sensitivity
Unprocessed EEG definitely preferred (BIS only frontal)
Why are both CEA & CAS associated with extreme lability of BP & HR?
What are the times of the operation w higher risk for haemodynamic instability & myocardial ischemia?
altered baseline carotid baroreceptor function & intraop manipulation of these baroreceptors
-induction
surg manipulation of carotid sinus & carotid artery (may cause either SNS or PSNS activity, insufficient evidence that LA injection peri-adventitially blunts this
-Carotid X-clamp, must maintain pts SBP from baseline to 20% above it (some target a MAP above the pts baseline eg. 80mmHg), to optimise collateral perfusion
-Unclamping may–> hypoT
-During CAS, balloon expansion may –> Brady & hypoT.. may Rx w 0.2-0.4mg atropine or may give 0.2mg glycol prior to balloon dilatation & re-administered as necessary
-emergence (tracheal irritation; cough, HTN)
How may induction induce hypoT?
reduce SVR
myocardial depression
inducing bradycardia
depress SNS
lack of venous return
What are some strategies for management of intra-op myocardial ischemia?
reducing myocardial demand (incr HR eg. w metoprolol 1mg over 1 minute) or increasing supply (eg. metaraminol to incr DBP)
What continuous monitoring is required for CEA or CAS?
SpO2
ECG
art line (pre-induction, given pt w vascular disease; use the UL w the highest BP, if CAS confirm w surgeon that not using radial art for sheath)
What’s the BP goal during carotid X-clamp?
Maintain SBP baseline to 20% above, to optimise collateral cerebral perfusion (even if a shunt is used)
