Internal carotid artery stenosis = 1 source of cerebral emboli which cause TIAs and strokes.
Aim of surgery is to prevent future embolic phenomena by removal of atheromatous plaque to leave smooth
arterial wall with blood-tight closure.
Myocardial infarction = most frequent cause of perioperative mortality.
Risk/benefit analysis: European Carotid Surgery Trial (ECST) and North American Symptomatic Carotid
Endarterectomy Trial (NASCET)  later benefits of surgery outweigh immediate risks of operation only in
severe (70-99%) stenosis; with moderate (30-69%) stenosis benefits unclear and for mild (<30%) stenosis
risks outweigh benefits.

SURGERY: skin incision anterior to sternocleidomastoid; carotid artery dissection; systemic
heparinisation; vessel occlusion above and below lesion (oxygen delivery to compromised hemisphere
maintained by collateral flow via Circle of Willis or vertebral arteries; in primates unilateral carotid
occlusion s perfusion pressure in ipsilateral middle cerebral artery by 14%; collateral flow less certain in
elderly atherosclerotic pt); longitudinal arteriotomy; plaque dissection; shunt controversial (maintains
cerebral blood flow, but  complexity and operating time with risk of embolisation and intimal damage).

PREOPERATIVE ASSESSMENT: patients elderly with generalised vascular disease (particularly
ischaemic heart disease), hypertension (up to 70%), smoking history, COAD, diabetes. Control of
hypertension s post-op hypertension and neurological deficit. Check BP in both arms. MI = major
complication and most frequent cause of perioperative mortality. Extensive cardiac evaluation with ECG,
CXR and exercise ECG.
Aim = BP control and optimal general medical status.
Mayo Clinic study:
 outcome adversely affected by angina, MI within 6 months, congestive heart failure, BP>180/110mmHg,
   COLD, age>70yrs and obesity.
 although 30 day outcome unaffected by presence or absence of coronary artery disease (CAD), 8yrs after
   CE 49% of all deaths cardiac and only 7% related to stroke: CAD, rather than cerebrovascular disease,
   most frequent cause of morbidity and mortality in long-term follow-up of CE pts.
PREMEDICATION: good rapport; light benzodiazepine premed; continue most routine medications
especially -blockers, Ca antagonists and centrally acting antihypertensives to avoid rebound hypertension.

INTRAOPERATIVE MANAGEMENT: aim is to prevent both myocardial and cerebral ischaemia.
Myocardial ischaemia is reduced by attempting to maintain a balance between myocardial oxygen delivery
and demand.
Myocardial oxygen delivery = arterial oxygen content x coronary blood flow.
Coronary blood flow is related to :
         coronary perfusion pressure for LV = aortic diastolic pressure - LVEDP; of total LV blood flow
           80-90% occurs during early diastole.
         duration of diastole (systolic duration fairly constant):  by HR especially at lower HRs
           (non-linear relationship)
         transmural distribution: due to compression subendocardial myocardium more vulnerable to
           ischaemia than subepicardial.
Myocardial oxygen demand has 2 major determinants:
         LV wall tension: T = (intraventricular pressure x volume)/(wall thickness) - LaPlace’s law
           indicating that  pressure and volume both  MVO2; pressure work costs more myocardial
           oxygen than volume work; wall tension highest subendocardially.
         contractility.
Optimal myocardial supply-demand balance is achieved when the heart is slow (maximum diastolic time),
small (minimising wall tension) and well-perfused (adequate coronary perfusion pressure). Hypertension
and tachycardia ( myocardial O2 consumption) and hypotension ( myocardial O2 delivery) are avoided.
Cerebral ischaemia: while most cerebral morbidity results from thromboembolic phenomena resulting
from combination of atheroma and surgery, hypotension can lead to cerebral hypoperfusion.
Thus blood pressure control requires avoidance of extremes with hypertension causing cardiac and
hypotension cerebral morbidity: a reasonable goal is > (lowest pre-op systolic - 40mmHg). Treatment of

                                            Dr WGM Bremner 20/7/96

intraoperative hypotension involves intrasvascular volume optimisation and use of vasopressors; however
the use of phenylephrine was associated with a 3-fold  in myocardial ischaemia.

 stump pressure (pressure distal to surgically occluded carotid artery reflecting collateral perfusion
  pressure via Circle of Willis which in turn reflects systemic BP and adequacy of collateral circulation by
  other 3 collateral extracranial arteries): maintain above critical value of 50-60mmHg; correlates poorly
  with cerebral blood flow, clincal cerebral ischaemia and EEG changes.
 EEG: delayed changes requiring skilled interpretation; correlates well with cerebral blood flow changes,
  but lacks specificity as similar changes are seen with GA, hypothermia and hypotension; only 10% with
  serious EEG changes intraoperatively develop permanent postop neurological dysfunction.
 somatosensory evoked potentials (SSEP): summated sensory cortical responses to repeated peripheral
  nerve stimuli; ?  amplitude better than  latency at indicating ischaemia; as sensitive and specific as
  EEG; significant false positive rate.
 jugular venous saturations: reflection of global ischaemia; based on  oxygen extraction with
  hypoperfusion; jugular bulb blood contaminated with contralateral venous blood; correlates poorly with
  cerebral blood flow and stump pressures.
 awake arterial line: prior to induction (BP) and intubation (BP).
 ECG: CM5 detects ST segment changes more frequently than many other 3 lead configurations: right
  arm electrode over manubrium sterni, left arm electrode over V 5 (LAAL in 5th ICS) with ground
  electrode on L shoulder; simultaneous lead 2 monitoring in addition to V 5 increased detection of
  ECG-detectable ischaemic changes from 89 to 95%.

 bypass shunts: divert blood and continuously perfuse ipsilateral cortex; previously implicated in
  thrombosis, embolisation, intimal dissection and obstruction of surgical field.
 hypothermia: s CMRO2; protective in animals.
 thiopentone: s CMRO2, s ICP, inhibition of oxygen free radical formation, s cerebral oedema;
  titrated to EEG burst suppression or isoelectricity during carotid clamping; not helpful when ischaemia
  already present.
 isoflurane: ? protective agent for cerebral ischaemia.
 normoglycaemia: hyperglycaemia aggravates tissue acidosis which correlates with cerebral infarct size;
   avoid dextrose and lactate solutions.
 the rest: nimodipine, etomidate (s CMRO2), midazolam (s CMRO2), methylprednisolone.

 combined deep and superficial cervical block (high failure rate) or
 cervical extradural (C6-7 or C7-T1 midline approach; 18G Tuohy; 15mls 0.375% bupiv + 50-100g
  fentanyl; majority needed supplementary sedation; complications = hypotension, bradycardia, extradural
 advantages: awake pt best CNS monitor; low incidence of neuological complications.
 disadvantages: anxiety; stress response with hypertension and tachycardia;
 role: ? in severe lung disease, severe LVF or high risk for neurological complications.

Allows effective control of oxygenation, airway (intubation essential), BP (avoiding hypotension and
excessive hypertension) and PaCO2 (normocapnia avoiding hypo and hypercapnia).

                                            Dr WGM Bremner 20/7/96

Induction (large bore IV cannula and intra-arterial BP monitoring awake): pre-O2 then haemodynamically
stable induction sequence (eg fent 1-5g/kg or alf 10-50g/kg, STP 3-7mg/kg or etom 0.2-0.3mg/kg, vec
0.1mg/kg) with vasopressor to hand (ephedrine or methoxamine); intubation with COETT.
Maintenance: IPPV to normocapnia; isoflurane (no EEG ischaemia or new neurological deficits occur with
CBF 10ml/kg/100g; <1MAC no  CBF); ? avoid N2O as s CBF (metabolic activation), ? s effect of air
embolis; ? negates STP cerebroprotection.
Extubation: time of severe CVS stress with hypertension and tachycardia: ? prophylactic antihypertensive
Postoperatively: to ITU for observation of neurological status and BP, and the development of
complications such as unilateral headache and wound haematoma.

Baroreceptor mechanism:
 hypotension and bradycardia may result from strong blood flow and distension of newly
    endartrectomised artery ing afferent stimulation through sinus carotid nerve (branch of 9 th) thereby
    ing sympathetic tone.
 hypertension explained by baroreceptor denervation causing ed sympathetic stimulation.
Intraoperative bupivicaine to carotid bifurcation ed postop hypotension, but ed postop hypertension.

 hypertension (systolic>180mmHg or 40mmHg  on preop): may be first sign of impending neurological
  deterioration or cause of hyperperfusion syndrome; contributes to myocardial oxygen imbalance;
  however one study found no correlation between periop hypertension and pt outcome.
 hypotension: due to relative hypovolaemia, oversedation or response of carotid sinus to  blood flow
  causing  baroreceptor stretching; management is correction of cause and restoration of cerbral perfusion
 neurological deficit (1-7%): angiography or immediate return to theatre.
 hyperperfusion syndrome (9.6%): cerebral blood flow excessive to metabolic needs in
  non-autoregulating area previously distal to stenosis; unilateral migrainous type headache, seizures,
  intracranial haemorrhage; CT and angiography may be normal; management = BP control.
 cranial nerve injury (13.4%): unilateral vocal cord paralysis, hypoglossal, facial and spinal accessory
  nerve injury; most caused by retraction and oedema.
 haematoma (up to 6.5%): jeopardises airway through external compression and obstruction to venous
  and lymphatic drainage causing laryngeal oedema; immediate management = release clips; RSI
  potentially hazardous; ? LA otherwise cautious inhalational induction or awake intubation.

 Coronary artery disease, rather than cerebrovascular disease, is the most frequent cause of perioperative
  and longterm mortality in patients undergoing carotid endartrectomy.
 The most common cause of perioperative stroke is emoblisation.
 Use of vasopressors to treat hypotension, while improving cerbral perfusion pressure, may cause
  myocardial ischaemia.

1. BJA. 1993; 71: 569-579.

                                           Dr WGM Bremner 20/7/96

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