1 / 63

Anaesthesia for carotid endarterectomy

Anaesthesia for carotid endarterectomy. Dr. S. Parthasarathy MD., DA., DNB, MD ( Acu ), Dip. Diab.DCA , Dip. Software statistics PhD ( physio ) Mahatma Gandhi Medical college and research institute , puducherry - India . Why of it ??. Stroke is the third largest cause of death

lynde
Télécharger la présentation

Anaesthesia for carotid endarterectomy

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Anaesthesia for carotid endarterectomy Dr. S. Parthasarathy MD., DA., DNB, MD (Acu), Dip. Diab.DCA, Dip. Software statistics PhD (physio) Mahatma Gandhi Medical college and research institute ,puducherry- India

  2. Why of it ?? • Stroke is the third largest cause of death • Carotid artery disease occurs in 30 % of stroke patients • TIA is followed by stroke in almost all cases of thrombotic stroke

  3. Circle of Willis 80-90 %

  4. Normal CBF • Normal CBF is approximately 50 mL/100 g/minute for the entire brain. • blood flow is about four times higher in gray matter than it is in white matter, with the flows being 80 and 20mL /100 g/minute • Neuronal destruction occurs with CBF less than 10 mL/100 g/minute.

  5. Regulation of CBF • Cerebral autoregulation is the tendency of the tissue to maintain normal blood flow despite variations in blood pressure. • In normotensive individuals, cerebral blood flow (CBF) is constant between mean arterial pressures of 50 and 150 mm Hg. • this means is that cerebrovascular resistance increases, through vasoconstriction, as mean arterial pressure increases from 50 to 150 mm Hg. • THEN ?? • At pressures less than 50 mm Hg, cerebral vessels are maximally vasodilated, so that as mean arterial pressure falls CBF decreases

  6. In hypertension

  7. PCO2 --- 20 -80 mmHg • Hypercarbia results in cerebral vasodilation and hypocarbia in cerebral vasoconstriction. CBF changes approximately 4% for each mm Hg increase or decrease in arterial PCO2 • pH and PaO2 and neurogenic – also influence

  8. PaCO2 and PaO2

  9. What is that ?? • In carotid artery disease, atherosclerotic plaques develop at the lateral aspect of the bifurcation of the carotid artery. • In addition to traditional CEA, carotid angioplasty and stenting (CAS) is increasingly used.

  10. Why at carotid bifurcation • Impedance mismatch, • altered hemodynamic conditions that accompany division of a vessel into vessels of substantially different sizes, • be implicated in the vessel injury

  11. Luxury perfusion • blood flow that is in excess of metabolic need (increased cerebral blood flow [CBF] relative to cerebral metabolic rate for O2). • It is most frequently observed in tissues surrounding tumors or areas of infarction. • It has also been described in tissues that have been manipulated during surgery.

  12. Steal and inverse steal • Intra cerebral steal is a paradoxical response to carbon dioxide in which hypercapnea decreases the blood flow in an ischemic area. • Inverse steal is the effect of hypo capnea producing increased blood flow to ischemic regions of the brain.

  13. Procedure • occluding the common, external, and internal carotid arteries, isolating the diseased segment, opening the vessel wall, and removing the plaque. • The vessel is then closed. If the remaining intima is too thin, the vessel is closed with a vein graft or a synthetic (Dacron) patch. • Shunt or no

  14. Symptoms • TIA • Asymptomatic bruit • Amaurosisfugax • Posterior • Binocular vision loss • Vertigo • “Drop Attacks”

  15. Diagnosis • duplex scan, which combines B-mode anatomic imaging and pulse Doppler spectral analysis of blood flow velocity. The accuracy of duplex scanning reaches 95% in experienced hands when compared with angiography. • magnetic resonance angiography

  16. Indications • symptomatic, high-grade carotid stenoses (70% to 99%) • 50 – 70 % stenosis but – recents stroke, males hemisphere symptoms • Surgically accessible stenosis • Stable medical and neurologic condition

  17. Inappropriate candidate for CEA •  Asymptomatic 50 - 60% stenosis • Symptomatic or asymptomatic with  Intracranial stenoses more severe than the extracranial stenosis • Uncontrolled diabetes mellitus, hypertension, congestive heart failure, or unstable angina pectoris • A major neurologic deficit or decreased level of consciousness

  18. Preanaesthesia • Basic health • Chart review • Head and neck – • airway • Coexisting disease (CAHD,COPD) • Neuro status

  19. Risks ??

  20. Risks • Medical risk • angina , MI within 6 months ,CCF , Severe HT, COPD, >70 years • Neurological risk • Multiple cerebral infarcts, progressive deficit, newer deficit in 24 hours, frequent daily TIA

  21. Angiographic risk • Other side carotid occlusion • Siphon stenosis • Bifurcation • Soft thrombus • All risks – I to IV ---- 1 – 10 % mortality

  22. Preop stabilization • Hypertension - > 150 greater risk • Diabetes – 150 -180 mg% • CAHD – adequate medical control • Special investion – depend on the original disease and urgency of surgery • COPD, parkinsons, renal, hepatic etc. • Dangers – uncontrolled systemic diseases

  23. Nerves close to dissection of surgery • Hypoglossal nerve • Vagus Nerve • Recurrent Laryngeal Nerve • Mandibular Branch of Facial Nerve • Important to document preoperative neurologic examination

  24. Most feared complications • CVA 4.5% • BP to be maintained • higher side • Myocardial Infarct 2.2% • BP to be maintained • lower side

  25. Anaesthesia • Ablate stimulatory and stress response to surgery • Awake, cooperative patient at end of procedure allowing clear neurologic evaluation

  26. GA Vs LA • A meta-analysis of the randomized studies showed that the use of local anaesthetic was associated with a reduction in the risk of local haemorrhage within 30 days of surgery, but there was no evidence of a reduction in the odds of operative stroke.

  27. Monitoring • ECG- Leads II, V4-5 for rhythm and S-T segments • Continuous arterial pressure monitoring, arterial line • Pulse oximetry • Central lines generally not necessary but should not be placed in jugular area

  28. Advantages of GA • Allows for still, motionless patient • Early control of airway and ventilation • Ability to protect brain if ischemia develops

  29. Blood Pressure Management • Best range is individualized to each patient • Risk of either myocardial or cerebral ischemia is minimized if perfusion pressures are maintained in the patient’s high normal range

  30. Choice of Induction Agent • All available agents reduce cerebral metabolic rate in excess of reduction of cerebral blood flow • Pentothalprovides best protection against focal ischemia • Most rapid awakening with Propofol • Etomidate has most favorable hemodynamic profile may worsen ischemic neurologic injury (animal data)

  31. Hemodynamic Response to Intubation/ Hypertension • Short acting narcotic • Short acting beta-blocker • Nitroglycerin or Nitroprusside Armoured

  32. Maintenance with a Volatile Agent • All presently clinical available agents reduce cerebral metabolic rate • Isoflurane has the most pronounced effect with a minimum of myocardial depression • Newer agents allow for more rapid emergence • Maintain at a lighter plane to allow rapid emergence and an easily interpretable EEG

  33. Plus and minus • The response of the cerebral circulation to carbon dioxide is maintained with sevoflurane • Nitrous oxide should be avoided if possible. It increases the cerebral metabolic rate and produces a concomitant increase in middle cerebral artery blood flow velocity • While cerebral autoregulation is impaired with sevoflurane, it is preserved under propofol–remifentanilanaesthesia

  34. Hypotensive Response to Induction • Hypertensive patients often present in a mildly hypovolemic state • Small fluid boluses • Phenylephrine

  35. Maintenance Events • Cervical incision not especially stimulating • Rapid changes in pulse rate and blood pressure/ hemodynamic instability can be frequent • Role of short acting agents/ vasoactive drugs

  36. Blood Pressure Management • Phenylephrine-√ • α-agonist with no direct effect on cerebral vasculature; cerebral perfusion increased by elevating perfusion pressure • Ephedrine- • Mixed α and β activity

  37. Stimulation of Carotid Baroreceptor • Manipulation can result in sustained bradycardia • Infiltration with local agent in carotid sinus area • atropine

  38. Tachycardia • Not well tolerated in the beta-blocked patient • Short acting beta-blocker – e.g. esmolol

  39. Intra op events and monitors • Maintain normocarbia • SPO2 • Urine • IBP

  40. EEGs • Measures electrical activity of cortical neurons • Cortical ischemia is manifested as ipsilateral cortical slowing, attenuation, or both • EEG signal is usually diminished when cerebral blow flow < 10 ml/ 100 gm of brain tissue

  41. Antiplatelets – Slowing and ischemia • Aspirin to continue • Heparin 100 units / kg • No protamine

  42. Limitations of EEG • deep brain structures are not monitored by EEG. • patients with pre-existing or fluctuating neurologic deficits the EEG may be false-negative; • In these patients, there may be cell populations that are electrically silent

  43. Somatosensory evoked potentials • Stimulation to see response • deeper structures of the brain • Suppressed brain • Infarcted brain • BIS monitor is not suitable for cerebral monitoring in this setting as it primarily detects frontal lobe activity and cannot be relied upon to detect localized changes elsewhere in the brain

  44. stump pressure • Once the common and external carotid arteries are clamped, the pressure measured in the internal carotid artery reflects the perfusion pressure transmitted around the Circle of Willis. • This is the stump pressure. • A number of thresholds for the stump pressure, ranging between 25 and 70 mm Hg , have been proposed below which shunting would be appropriate.

  45. Near infrared spectroscopy • Near infrared spectroscopy (NIRS) gives a value for regional cerebral oxygenation (rSO2) which is a composite measure of arterial venous and capillary oxygenation • Cross clamping decrease rSo2 but ? Predictable

  46. Transcranial Doppler • Petrous part of temporal bone - thin acoustic window - doppler of MCA • Decrease to 15 % - post op stroke • But difficult acoustic window in 10 – 20 % patients

  47. Emergence Issues • Coughing • Hyperdynamic circulation • Stress on suture lines • Deep extubation? • Airway topicalization? • Deal for the needs of the situation

  48. Regional • Awake patient- allowing for repeated neurologic evaluations • Can avoid complicated neurologic monitors • Greater hemodynamic stability • Improved cross clamp tolerance • Reduced hospital stay and costs • Lower (?) incidence of stroke and cardiac morbidity

  49. Regional • Deep and Superficial Cervical Plexus Block • Epidural anesthesia • Local infiltration

  50. Problems with RA • Inability to use pharmacologic cerebral protection • Requires a cooperative, non-claustrophobic patient • Possibility of seizures • Poor access to the airway if GA becomes necessary • Phrenic and superior laryngeal nerve block is common

More Related