Anesthesia for carotid endarterectomy
•Download as PPTX, PDF•
15 likes•2,249 views
This document discusses anesthesia considerations for carotid endarterectomy. It begins with an overview of the anatomy and indications for the procedure. Important preoperative evaluations are outlined, including risk assessment, neurological examination, and imaging studies. Intraoperative management focuses on hemodynamic stability, cerebral perfusion monitoring via EEG, TCD, jugular bulb oximetry, and stump pressure. General anesthesia and regional anesthesia techniques are compared. Postoperative concerns like wound hematoma, embolism, and hypertension are also reviewed.
Recommended
Recommended
More Related Content
What's hot
What's hot (20)
Similar to Anesthesia for carotid endarterectomy
Similar to Anesthesia for carotid endarterectomy (20)
More from Kundan Ghimire
Recently uploaded
Recently uploaded (20)
Anesthesia for carotid endarterectomy
- 1. Anesthesia for carotid Endarterectomy Moderator: Dr. Pawan P. Baral Presenter: Dr Kundan Kishor Ghimire UCMS-TH, Bhairahawa, Nepal
- 2. Objectives: • Basic anatomy • Preoperative evaluation of patients planned for CEA • Intraoperative management and cerebral perfusion monitoring • Post operative management and complications
- 3. Introduction • Stroke • leading causes of death in modern countries • Ischemic → 80% haemorragic →20% • Common cause is carotid artery stenosis by atheroma • mainstay of treatment carotid endarterectomy
- 4. Anatomy • 80- 90% from carotids • 10-20% from vertebrobasilar • Incomplete in 15 %
- 5. Important Anatomic Structures Near Carotid Dissection • Hypoglossal nerve • Vagus Nerve • Recurrent Laryngeal Nerve • Mandibular Branch of Facial Nerve • Important to document preoperative neurologic examination
- 6. Indications • Symptomatic patients: • Carotid artery stenosis >70% Asymptomatic patients: with stenosis > 70% if the preoperative risk is acceptable
- 7. Preoperative risks • age ≥ 75 years • symptomatic lesions • uncontrolled hypertension • angina • carotid thrombus • occlusions near the carotid siphon
- 8. Preoperative evaluation • Asymptomatic bruits • Transient ischemic attack • Amaurosis fugax • Stroke • Dizziness • Weakness • Numbness • Paralysis
- 9. Preoperative evaluation • Co morbidities: • Elderly -- CAD • Hypertension -- Stroke • Diabetes • Assess the neurological status of the patient and document • Optimize the co-morbities • BP & HR within acceptable range
- 10. Preoperative evaluation • Carotid bruits • Laboratory tests: • CBC, blood sugar • Lipid profile • CXR,ECG, echo • Baseline ABG: PaCO2 • Noninvasive testing: • Doppler scanning - preferred method • Magnetic resonance angiography • Computerized tomography • angiography • CT scan or MRI of the brain if there is a history of stroke • Invasive testing: • Carotid angiography
- 11. Preoperative evaluation • Continue all long-term cardiac medications • Aspirin can be continued throughout the perioperative period • Premedication is important: • BZP (Alprazolam/ diazepam) • Prepare general & emergency drugs & equipments: • Esmolol, GTN, Phenylepherine, • cardioversion
- 12. Anesthetic management • Monitoring: • Standard ASA monitoring • Cardiovascular monitoring • lead II and lead V ECG monitoring with ST analysis • Invasive arterial monitoring • Central venous catheter • In uncompensated heart failure or recent MI with ongoing ischemia • Subclavian or femoral insertion sites
- 13. Cerebral perfusion monitoring: • EEG • SSEPs • Transcranial Doppler • Cerebral oximetry • Jugular venous oxygen saturation • Carotid stump pressure distal to the cross-clamp • Brain Tissue PO2
- 14. EEG • Most commonly employed neurophysiologic monitor for carotid surgery. • Records electrical activity and changes in cerebral blood flow in EEG waveforms. • Clinical usefulness limited • may not detect subcortical or small cortical infarcts • false-negative results are not uncommon • Not specific for ischemia • False positive results
- 15. Somatosensory Evoked potential • response of sensory cortex from peripheral sensory nerve stimulation. • Can detect subcortical sensory pathway ischemia. • Decrease in rCBF by characteristic SSEP tracing • Decrease in amplitude • increase in latency, or Both
- 16. Transcranial Doppler • Noninvasive monitoring • Continous measurement of CBF velocity in the major vessels of circle of willis. • Helps in detection • Cerebral ischemia • Malfunctioning of shunt • detection of microemboli • Postoperative hyperperfusion syndrome • Postoperative intimal flap or thrombosis
- 17. Cerebral oximetry: Near-Infrared Spectroscopy • Noninvasive method • Detects the oxygenation in cerebral venous blood • Falling saturation indicate decline perfusion. • Limitation: • Inaccuracy over the areas of previous infarction • No detection of ischemia other than frontal gray matter.
- 18. Jugular Bulb Venous Oximetry • Retrograde insertion of catheter • Tip sits at base of skull in jugular bulb • Advantage: • Continuous pressure monitoring • Measures balance of oxygen supply & demand of a larger portion • Withdrawal of a jugular venous blood sample for gas analysis • Limitation: unable to detect focal ischemia • Confirmation of location →lateral cervical spine film
- 19. Carotid stump pressure • backpressure resulting from collateral flow through the circle of Willis via the contralateral carotid artery & vertebrobasilar system • Advantages: • Inexpensive • Relatively easy to obtain • Continuously available during carotid clamping (dynamic stump pressure) • Pressures< 50 mm Hg are associated with hypoperfusion
- 20. • 29 studies included • Results: The pooled diagnostic odds ratios (DOR) and 95% confidence intervals (CI) were obtained for EEG, TCD, stump pressure, evoked potentials, and cerebral saturation: (DOR 65.3; 95% CI 20.5 to 207.7; I2 [56.8%]); (DOR 58.1; 95% CI 23.0 to 146.3; I2 [24.9%]); (DOR 27.8; 95% CI 13.4 to 57.9; I2 [59.9]); (DOR 17.2; 95% CI 2.4 to 123.9 I2 [69.1]); and (DOR 12.1; 95% CI 3.5 to 41.2; I2 [30.8]), respectively • Conclusion: No monitor can reproduce the detection of brain ischemia achievable with regional anesthesia. A combination of stump pressure and either TCD or EEG appears to give the best results. For EEG, a high number of channels should be used
- 21. Anesthetic management • Methods: • General Anaesthesia • Local Anaesthesia/ Regional Anaesthesia • Combined: • GA+ superficial cervical plexus block + clonidine= hemodynamic stability.
- 22. Anesthetic Management • Goals • Protect brain and heart from ischemic injury • Maintain hemodynamic stability • Ablate stimulatory and stress response to surgery • Awake, cooperative patient at end of procedure allowing clear neurologic evaluation
- 23. General (GA) or Local Anaesthesia (LA)/ Regional Anesthesia (RA) for carotid surgery: pros and cons • Advantages to LA • ‘Awake neurological testing’ during carotid clamping = ↓shunting • Potential benefits of LA • ‘safer’ in high risk elderly ‘vascular’ patients • less ‘stress’ response to surgery • better postoperative pain relief • earlier mobilisation, less traumatic , less expensive v GA
- 24. Local anesthesia • Disadvantages of LA • More traumatic for the patient and the surgeon • alteration of mental status with cerebral ischemia, seizures • Conversions (LA to GA) can be problematic • Patient might prefer GA • Local anesthesia toxicity
- 25. Regional anesthesia • Superficial and deep cervical plexus • C2-C4 dermatomes
- 26. Techniques of RA • Superficial cervical plexus blocks • Complications: • Intravascular injection • Recurrent nerve palsy • Partial brachial plexus block
- 27. Techniques of RA .. • Deep cervical plexus blocks • Complications: • Intravascular injection • Brainstem anesthesia • Phrenic nerve block • Recurrent laryngeal block • Vagus block • Horners syndrome
- 28. Techniques of RA • Cervical epidural: • Provides good operating conditions • But risk of significant anesthetic risk which includes: • Dural puncture • Epidural venipuncture • Respiratory muscle paralysis
- 29. General Anaesthesia: • Advantages: • Immobility • Potential for neuroprotection • Controlled ventilation and CO2 • Attenuated stress response • Disadvantages: • Lack of direct neurological monitoring during surgery • Intraoperative hypotension • Postoperative hypertension • Increased rate of shunt use • Delayed recovery from GA may mask postoperative neurological complications
- 30. General Anaesthesia: • Induction: • Titrate as per haemodynamics parameter • No ideal agent • Opioids/ BZDs/ Propofol/ Etomidate • Muscle relaxation: • Intubation: must be in the deep plane, blunting the reflexes, • IV fluid: adequate as NPO/ patient status
- 31. General Anaesthesia.. • Maintenance: • Low dose volatile agent • ISO/SEVO • Combined remifentanil and propofol • Avoid hyperthermia • Avoid hypo/hypercapnia • Avoid hypo/hyperglycemia
- 32. Shunting • During the operation, a shunt may be inserted • Common carotid to the internal carotid artery • Maintains blood flow during the course of surgery • Complications: • Air or plaque embolization • Intimal tears • Carotid dissection • Haematoma, nerve injury, infection, and late carotid restenosis
- 33. Intraoperative hemodynamics • Should be maintained on higher side • Increase collateral flow • Prevent cerebral ischemia • If contralateral ICA occlusion or severe stenosis,10%-20%>baseline during carotid clamping • Increased blood pressure & heart rate increase risk for myocardial ischemia or infarction
- 34. Intraoperative complications: • Bradycardia & hypotension: • d/t Surgical manipulation of the carotid sinus • Treatment: • Cessation of surgical manipulation • IV atropine • Infiltration of the carotid bifurcation with 1% lidocaine
- 35. Intraoperative complications • Cerebral ischemia: • Primary management is shunt insertion • Maintain blood pressure 20% above preoperative level • Supplemental oxygen • Normocarbia
- 36. Extubation • Awake • Goal- extubation of patient on the table • Neurological evaluation • Haemodynamic instability should be managed • Blunting reflexes
- 37. Postoperative considerations: • Wound hematoma • Embolism & sequale • Postoperative cerebral hyperperfusion syndrome • Myocardial Infraction • Nerve damage • Hypertension/Hypotension • Carotid body denervation • Blunting of ventilatory response to hypoxemia
- 38. References • Millers Anesthesia, 8th Edition • Clinical anesthesia, Barash 8th Edition • Morgan and Mikhail’s clinical anaesthesiology 6th edition
- 39. Thankyou
Editor's Notes
- Prophylactic intervention to prevent cerebral infarction and relieve symptoms of carotid atherosclerosis. Involves occluding the common, external and internal carotid arteries isolating the disease segment, opening the vessel wall and removing the plaque. Then the vessel is closed. If the remaining intima is too thin, the vessel is closed with the vein graft.
- Carotid circulation supplies 80-90% of cerebral blood supply and vertebral circulation supplies 10-20% of cerebral blood supply. Continued blood supplly to the brain will depend entirely on adequate collateral blood flow through the cirlce of Willis if no shunt is used during CEA.
- Asymptomatic Carotid Atherosclerosis Study(ACAS) demonstrated asymptomatic carotid stenosis >=60% The european Asymptomatic carotid surgery trial asymptomatic carotid stenosis >70%
- Morgan 6th edition Carotid siphon is a U shaped or S shaped part to the ICA that begins at the posterior bend of the cavernous part of ICA and ends at the cerebral part. At ICA bifurcation.
- Amaurosis fugax: transient attack of monoocular blindness. Small emboli in ophthalmic branches
- Deferred in significant aortic stenosis, significant arrythmias, uncompansated heart failure, or unstable angina. Diabetes, HTN, renal dysfunction should be optimized. Hyperglycemia occurs frequently after stroke and can worsen cerebral ischemic damage.
- Doppler ultrasound of carotid arteries,
- Continue aspirin, beta- blockers, clopidogril, statins also on the day of surgery Avoid premedication with sedatives to facilitate rapid emergence and immediate assessment of a neurological examination. If needed smallest effective dose of midazolam titrated to effect..
- A line-for hemodinamic lability as a result of surgical and anesthetic manipulation.. Maintain autoregulation.
- Most common manifestation of cerebral ischemia are ipsilateral slowing and/or attenuation. False negative result( neurologic deficit with no ischemic EEG intraoperatively). Not specific for ischemia and may be affected by changes in temperature, BP and anesthetic depth. False positive( no perioperative neurologic deficit with significant ischemic EEG changes intraoperatively) EEG changes occur within seconds and can be reversed withj hemodynamic augmentation and/or temporary shunt placement.
- Anesthetics, hypothermia, and blood pressure may affect SSEPs significantly, and false negative results have been reported
- Detection of cerebral ischemia during cross clamping of the carotid artery. Hyperfusion syndrome: sustained elevation of flow velocities after removal of carotid occlusion and often develop headache. Prompt reduction of BP is effective in normalizing ipsilateral flow velocity and alleviating symptoms. Occlusion of carotid artery from clot formation or the presence of an intimal flap.
- Relative absorption of specific wavelength of light by oxyhemoglobin and deoxyhemoglobin to estimate frontal lobe cerebral perfusion and estmiate cerebral oxygen balance. Relative decrease of 20% or more in regional cerebral O2 saturation suggested cerebral ischemia.
- Direct monitoring of cerebral oxygenation. Catheter inserted into the jugular bulb ipsilateral to the surgical site.
- Estimates the ipsilateral hemispheric blood flow by directly measuring the pressure in the carotid stump distal to the carotid clamp. Distal stump pressure of less than 50 mm Hg has been traditionally used as indication
- Choice depends upon the preference of the surgeon and the experience and expertise of the anesthesiologist.
- Greater stability of BP, decreased vasopressor requirement, reduced operative site bleeding, and reduced hospital cost. Level of consciousness, speech, and contralateral handgrip are assessed throughout the procedure. Disadv: inability to use pharmacologic cerebral protection with anesthetics, patient panic and loss of cooperation, seizure or LOC with carotid clamping and inadequate access to airway should conversion to GA. 2-3 min test clamp in awake patients allows prompt identification of those who would benefit from shunt placement.
- Do not excessivly palpate the neck, because part of the plaque in the carotid artery may dislodge and embolize.
- Performed by infiltrating along with middle third of the posterior border of sternocleidomastoid muscle with local anesthetic.
- Performed with 3 inj. Along a line drawn from Chassaignac’s tubercle to the mastoid process. Alt, a single inj on the line betn mastoid process and chassaignac tuberlce at c4 with niddle directed midially. Accidental subarachnoid injection causing brainstem anesthesia , intravascular injection may cause potential seizure,. Accidental blockade of phrenic, vagus or recurrent laryngeal nerve with respiratory complication
- Phenyephrine alpha agoinst, has no direct effect on the cerebral vasculature, cerebral perfusion is increased by an elevation in CPP. Limited total perioperative fluid due to small intraoperative losses, short surgical time with limited exposure, and frequent diastolic dysfunction
- Hypocapnia causes cerebral vasoconstriction and decrease cerebral blood flow during critical period of carotid cross clamping. Hypercapnia causes cerebral vasodilation leading to steal phenomena with diversion of blood flow from hypoperfused area to normal area. Hyperglycemia may worsen ischemic brain injury Hypothermia can depress cerebral activity and decrease cellular oxygen requirements below the critical level required to maintain cerebral viability.
- Bradycardia and hypotension may be caused by baroreceptor reflexes with surgical irritation of carotid sinus.
- Other causes of hypertension: hypoxemia, hypercapnia, bladder distension, and pain. Postoperative cerebral hyperfusion syndrome: abrupt increase in blood flow with loss of autoregulation in the surgically reperfused brain: manifestation: headache, seizure, focal neurological signs, brain edema, and intracerebral hemorrhange. Nerve damage: most are transient, recurrent laryngeal, superior laryngeal, hypoglossal and marginal mandibular nerves.