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. PCO 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 Amaurosis fugax 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 % 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 – 10 % mortality

22. Preop stabilization Hypertension - > 150 greater risk
Diabetes – 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%
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
Pentothal provides 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–remifentanil anaesthesia

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

51. GA Vs RA Reg Anesth Pain Med 2008;33:340-345
Marrocco-Trischitta et al. J Vasc Surg 2004; 39:
McCarthy et al. Eur J Vasc Endovasc Surg 2001; 27:
Watts et al Am. J Surg 2004; 188:

52. Conclusions of RA Vs GA
No clear data to suggest improved outcome in perioperative neurologic problems
GA can be combined with plexus block and can result in greater hemodynamic stability and shorter operating times
We can do whichever technique we are familiar with understanding the disease and drugs

53. Problems are plenty after also

54. Postoperative problems
Hypertension
Hypotension
Myocardial ischemia or infarct
Cranial nerve injury
Recurrent Laryngeal Nerve injury
Stroke
Bleeding

55. Hypertension – 25 – 58 % poorly controlled BP
Carotid sinus local infiltration
esmolol and nitroglycerin
Nicardipine and SNP next

56. Hypotension %
May be related to carotid baroreceptor hypersensitivity after plaque removal
Can result in myocardial or cerebral ischemia
Consider judicious amounts of fluid sympatho mimetics for support

57. Other causes of haemodynamic instability
Pneumothorax
Pain
Bladder distension
Arrhythmias
Hypoxemia

58. Postoperative Respiratory Insufficiency
Massive hematoma formation (active bleeding, coagulopathy)
Bilateral recurrent laryngeal nerve injury
Soft tissue swelling, supraglottic mucosal edema

59. Carotid Body Denervation
Secondary to surgical manipulation
Results in impaired response to hypoxia
Can be clinically significant in presence of agents which depress respiration
May be exaggerated with moderate to severe COPD
Consider using non-narcotic analgesia

60. Hyperperfusion syndrome
1 and 3% of patients develop very dramatic
increases in cerebral blood flow with middle cerebral artery blood flow velocities more than 100% above the preoperative value
Why ??
Treat BP aggresively

61. Myocardial Infarction
A major cause of morbidity 0.5 % - 4%
Symptoms and EKG changes should be investigated promptly
Hemodynamic instability, Arrhythmia to be treated
Maximize the balance between myocardial oxygen supply and demand
40 % of the perioperative mortality

62. Cranial Nerve Dysfunction
Generally secondary to surgical traction not transection
Generally transient- resolution within 6 months
Dysphagia/ Hoarseness- recurrent laryngeal nerve injury
Tongue deviation – hypoglossal nerve injury

63. Carry home message Circle of willis Cerebral blood flow
Carotid endarterectomy
Neurological monitoring
Thank you all