Transcranial Doppler ultrasonography
Transcranial Doppler ultrasonography is an attractive technique for the detection of embolic events and cerebral ischaema during cross-clamping of the carotid artery because it is continuous and non-invasive, and the transducer probes can be used successfully without impinging on the surgical field. It is also an important tool in the pre-operative assessment and post-operative care of patients with carotid disease.
Cerebral ischaemia is considered severe if the mean fl ow velocity in the middle cerebral artery (FV) after clamping is 0-15% of the pre-clamping value, mild if F V is 16-40% and absent if FV >40%. Tis criterion correlates well with subsequent ischaemic EEG changes and hence can be used as an indication for shunt placement (Fig. 13.1). Transcranial Doppler ultrasonography has been used successfully to detect intraoperative cerebral ischaemia, malfunctioning of shunts due to kinking and high-velocity states associated with hyperper-fusion syndromes, as well as intra- and post-operative emboli. It appears to be a useful adjunct to other monitoring modalities such as EEG.
Fig. 13.1. Graphic display of right middle cerebral arteryflow velocity (FV) and cerebral function analysing monitor (CFM) in two patients undergoing carotid endarterectomy. (a) On cross-clamping the carotid artery (ON), FV and CFM decrease, indicating cerebral ischaemia. Insertion of a shunt restores the signals to near pre-clamping value. Hyperaemia is observed upon release of the carotid artery cross-clamp at the end of the procedure (OFF). (b) Cross-clamping of the carotid artery results in no significant change in either FV or CFM and hence no shunt was used. Hyperaemia is also observed upon release of the clamp, but to a lesser degree than in (a).
Emboli, or high-intensity ‘chirps’, are easily detectable using TCD. Tey can occur throughout the operation but are more frequent during dissection of the carotid arteries, upon release of the ICA cross-clamp and during wound closure. Te rate of microembolus generation can indicate incipient carotid artery thrombosis, has been related to intraoperative infarcts and can predict post-operative neuropsychological morbidity. Many units use TCD monitoring routinely.
Following closure of the arteriotomy and release of the carotid clamps, the FV will typically increase immediately to levels above baseline and gradually correct back to the pre-clamping baseline over the course of a few minutes. Tis hyperaemic response is to be expected, as the vascular bed vasoconstricts in an autoregulatory response to increased perfusion pressure. However, approximately 10% of patients are at risk of cerebral oedema or haemorrhage because of gross hyperaemia with velocities of 230% of the baseline value lasting for several hours to days. Tis persistent post-operative hyperaemia or reperfusion, more likely to occur in patients with high-grade stenosis, is probably the result of defective autoregula-tion in the ipsilateral hemisphere. A reduction in blood pressure is effective in normalizing the FV and alleviating the symptoms. Transcranial Doppler ultrasonography provides the means of early detection and effective treatment of this potentially fatal complication.
Finally, a progressive fall in FV post-operatively to below pre-clamping baseline levels can be indicative of post-operative occlusion of the ipsilateral carotid artery and can be an indication for re-exploration of the endarterectomy. Te development of sudden symptoms post-operatively should prompt an immediate TCD examination and early re-exploration.
Near-infrared spectroscopy
Near-infrared spectroscopy, first described by Jobsis in 1977, continues to receive attention as a monitor of cerebral oxygenation. By using near-infrared light, cerebral oximetry can theoretically be used to monitor haemoglobin oxygen saturation (HbO2) in the total tissue bed including capillaries, arterioles and venules. One of the limitations of this technology is its inability to differentiate reliably between intra- and extracranial blood. However, during CEA, as the external carotid artery is clamped, most of the contamination due to extracranial blood flow is removed. Tere is now evidence to suggest that it is possible to obtain useful intraoperative information about cerebral oxy-genation in patients undergoing CEA using NIRS. In patients undergoing CEA under general anaesthesia, changes in jugular venous oxyhaemoglobin saturation and middle cerebral artery blood velocity correlate well with changes in cerebrovascular haemoglobin oxygen saturation (ScO, ). Similarly, Samara and colleagues demonstrated that NIRS can be used to track changes in carotid blood flow in the majority of patients undergoing CEA under regional anaesthesia. Kirkpatrick and co-workers observed that NIRS-based measurements can provide a warning of severe cerebral ischaemia (SCI) with high specificity and sensitivity provided the extracranial vascular contamination is accounted for. Despite numerous publications on the use of NIRS in CEA, its use as a monitoring tool for detecting cerebral ischaemia remains undefined. A recent study has suggested that it may be of use in predicting hyperperfusion syndrome after carotid stent-ing.
Intraoperative cerebral protection
Ischaemia from hypoperfusion is most likely to occur during carotid cross-clamping. herefore, cerebral protection is ‘most’ effective when a carotid shunt is never used, at which time it is reasonable to administer a bolus of either thiopentone 5 mg kg-1 or propofol 2 mg kg-1 prior to cross-clamping of the carotid artery. With selective shunting based on monitoring cerebral ischaemia EEG, evoked potentials or a reduction in CBF detected by TCD, thiopentone should not be given as it will interfere with monitoring, and a shunt is inserted.
The anaesthetic itself m ay provide neuroprotection. Isoflurane may pre-condition the brain so that it is better able to tolerate an ischaemic insult, and can be used to provide anaesthesia or in low doses to supplement an intravenous technique. Propofol (and benzodi-azepines) produces a dose-related decrease in cerebral metabolic rate and CBF, and can be used in combination with a short-acting opioid to provide balanced intravenous anaesthesia. In addition to anaesthetic drugs, several other drugs have been evaluated, with varying degrees of success, to provide neuroprotec-tion. Sadly, drugs that have shown promise in animal studies have failed to translate into effective drugs in humans. To date, there is no ‘silver bullet’, which probably reflects the complex timing of events and series of pro- and anti-inflammatory cascades initiated by an ischaemic insult to the brain.
Non-pharmacological methods of cerebral protection include mild hypothermia (temperature of about 35°C), which may easily be achieved and may decrease cerebral metabolism sufficiently with no obvious disadvantages. Should stroke occur on the table, hypothermia should be continued, the patient transferred to intensive care and gradually rewarmed after 24 h of continuous cooling .
Carotid stenting
During work-up of patients with carotid disease, some are considered too high risk for surgical intervention or general anaesthesia. hese patients are increasingly being offered carotid stenting. Carotid stenting is not without risk, and despite its initial popularity as an alternative to surgery (and the thought that it may even supersede surgical intervention), comparisons of patient groups have shown poorer outcome in the stenting group. he worst outcome in this group of patients may be due to their worse pre-morbid state preventing general anaesthesia and surgery. Patients undergoing carotid stenting have a greater risk of stroke (even when filters are used to catch emboli) and adverse cardiovascular events. Nonetheless, there are patients in whom endovascular therapy remains their only treatment option.
Deployment of the stent can cause parasympathetic stimulation with subsequent bradycardia and nausea. It is our practice to site a peripheral intravenous can-nula prior to intervention and to administer an anti-cholinergic. In our institute, we choose to use 200 ^g of glycopyrrolate, as it is less likely to cause sedation than atropine. An intra-arterial catheter is also placed to monitor blood pressure and facilitate blood sampling. Standard m onitoring is used including a five-lead ECG. Supplemental oxygen is provided throughout the procedure by a face mask or nasal cannulae, as tolerated by the patient. No sedation is given unless the patient is especially anxious.
For those considered at high risk of hyperperfusion syndrome, tight blood pressure control is maintained after the stent has been deployed. An intravenous infusion of ^-blocker, either labetalol or esmolol, may be necessary. At times, a second agent may be required; hydralazine, nitrate and sodium nitroprusside have been used with success. Blood pressure control is titrated against the patient’s symptoms, predominantly headache relief. Oral antihypertensives are commenced and the patient transferred to a high-dependency environment to continue blood pressure control and wean the antihypertensive infusion .
Combined or staged carotid endartarectomy and coronary artery bypass grafts
More than 50% of patients undergoing CEA have overt coronary artery disease: previous infarct, angina or ischaemic ECG abnormalities. Similarly, up to one-fifth of patients undergoing coronary artery bypass grafting have duplex ultrasound-detected moderate (>50%) carotid stenosis, with 5.9-12% of those having severe (>80%) stenosis. herefore, it is not surprising that stroke complicates up to 4% of all coronary artery bypass operations. here are many potential causes for coronary bypass-related stroke, namely embolization from the carotid arch, endocardium or pump oxygen-ator, hypoperfusion related to occlusive arterial lesion or ICH. Coronary angiography has been used to select high-risk patients for staged CEA or combined with coronary artery bypass grafting.
If the procedures are combined, the risk of stroke and mortality is increased. When staged procedures are planned, it is preferable to operate on the presenting lesion first. One centre has reported success when performing combined coronary artery bypass and carotid stenting for those patients with severe disease.
Extracranial-intracranial bypass grafting
Anastomosing the extracranial to the intracranial arterial circulation (an EC/IC bypass) should in theory increase CBF to ischaemic areas, thus reducing the risk of stroke. he only large prospective randomized trial on EC/IC failed to demonstrate a benefit when compared with medical therapy alone. Hence, the popularity of this procedure for preventing strokes in patients with carotid stenosis has declined markedly.
Prophylactic EC/IC bypass procedures are increasingly performed for patients in whom therapeutic occlusions are required for controlling aneurysmal or vascular lesions not amenable to surgical clipping, such as giant internal carotid artery aneurysms with wide necks. he procedures carry a significantly higher mortality than CEA, which may in part be due to patient selection. he perioperative management of patients presenting for EC/IC bypass surgery is similar to those presenting for CEA, and particular attention is focused on preventing coughing and control of blood pressure to ensure patency of the graft.
Post-operative care and complications
In order to continue the benefits of a carefully conducted anaesthetic, recovery should be smooth and prompt to allow immediate post-operative neurological assessment. We find that careful reduction in anaesthetic concentration with discontinuation upon wound closure results in satisfactory haemodynamics. Lidocaine 1-1.5mgkg-1 may be given intravenously to minimize cough during emergence. When the patient is responsive and awake, the trachea is extubated. It is advisable to leave the intra-arterial cannula in the immediate post-operative period to permit continuous blood pressure monitoring and blood gas analyses. All our patients receive supplemental oxygen and are monitored in recovery for a prolonged period (2 h or more if necessary). his allows rapid intervention should wound haematoma or intimal flap thrombosis develops .
Although the need for intensive care depends on the pre-morbid state and the intraoperative course, a neurovascular unit staffed with nurses familiar with the post-operative course and potential complications allows the majority of patients to be monitored closely for cardiac, respiratory and neurological complications without the need for intensive care.
Carotid chemoreceptor and baroreceptor dysfunction
Post-operative haemodynamic instability is common (incidence >40%) after CEA and is thought to be due to carotid baroreceptor dysfunction. It is postulated that the atheromatous plaques dampen the pressure wave reaching the carotid sinus baroreceptors and with the removal of these plaques increased stimulation of baroreceptors may result in bradycardia and hypotension. he hypotension can be prevented or treated by blocking the carotid sinus nerve with a local anaesthetic, intravenous fluid administration or, if necessary, the administration of vasopressor drugs such as phenylephrine .
Hypertension after CEA is less well understood and has been reported to be more common in patients with pre-operative hypertension, particularly if poorly controlled, and in patients undergoing CEA if the carotid sinus is denervated. Hypertension after CEA in which the sinus nerve is preserved has been postulated to be due to temporary dysfunction of the baroreceptors or nerve, caused by intraoperative trauma. Mild increases in blood pressure are acceptable (up to about 20% above pre-operative levels), but marked increases are treated with an infusion of antihypertnsive drugs such as nitroglycerine or ^-blockers, depending on the patient’s condition in the immediate post-operative period.
Other causes of haemodynamic instability after CEA include myocardial ischaemia/infarction, dys-rhythmias, hypoxia, hypercarbia, pneumothorax, pain, confusion and bladder distension, which should be treated appropriately.
Hypotension may lead to hypoperfusion and ischaemic infarction of the brain. Hypertension may increase the incidence of wound haematoma formation with possible airway obstruction. Similarly, myo-cardial ischaemia/infarction may occur as a result of either complication. Terefore, the blood pressure must be closely monitored and controlled in the immediate post-operative period. Regional anaesthesia appears to be associated with a higher incidence of post-operative hypotension while general anaesthesia is more often associated with post-operative hypertension.
Carotid endarterectomy may result in loss of carotid body function with reduced ventilatory response to hypoxaemia and hypercarbia. Tis effect is further exaggerated in patients with coexisting pulmonary disease, especially in the presence of respiratory depressant drugs. Provision of supplemental oxygen and close monitoring of ventilatory status is particularly important in these patients and, if necessary, they should be admitted to the high-dependency unit/ICU for observation.
Hyperperfusion syndrome
Patients who become hypertensive in the postoperative period (defined as systolic blood pressure >200 mmHg) are at much greater risk of developing neurological deficit (10.2%) than patients who remain normotensive (3.4%). Hypertension may cause excessive cerebral perfusion in a circulation unable to autoregulate, resulting in hyperperfusion syndrome and ICH. Patients at greater risk include those with reduced pre-operative hemispheric CBF caused by bilateral high-grade stenosis, unilateral high-grade carotid stenosis with poor collateral cross-flow or unilateral carotid occlusion with contralateral high-grade stenosis. Te syndrome is thought to develop after restoration of per-fusion to an area of the brain that has lost its ability to autoregulate because of chronic maximal vasodilation.
Restoration of blood flow after CEA thus leads to a state of hyperperfusion until autoregulation is re-established, which occurs over a period of days. Clinical features of this syndrome include headache (usually unilateral), face and eye pain, cerebral oedema, seizures and ICH. Patients at risk for this syndrome should be closely monitored in the perioperative period, and their blood pressure should be meticulously controlled.
Rapid management of haemodynamic instability in the post-operative period can alter patient outcome. A guideline in each unit to direct therapy and offer targets may help.
Myocardial ischaemia and infarction
Perioperative MI is the most frequent cause of mortality following CEA. In general, the reported incidence of fatal post-operative MI is 0.5-4% and the proportion of total perioperative mortality (within 30 days of operation) attributed to cardiac causes is high. All causes of increased cardiac work must be minimized in order to avoid myocardial ischaemia. Te patient should be warm, pain free, well oxygenated and norm o-tensive with no tachycardia. Any signs of myocardial ischaemia should be treated immediately. ^-Blockade should not be started in the perioperative period, but should be continued if the patient is already taking this medication .
Haemorrhage and airway obstruction
Persistent oozing from deep tissues, insecure ligation of vessels and the disruption of suture lines may all lead to bleeding from the wound site. Tis can be further aggravated by compromised coagulation due to the use of anticoagulants or antiplatelet agents. An expanding haematoma in the neck may cause airway obstruction and may necessitate re-exploration of the wound site. Difficult intubation may result from this complication and the unwary may mismanage these patients with catastrophic results. Clinical assessment of the airway can underestimate the potential hazard of a rapid sequence induction technique. Opening the sutures and letting the haematoma out or surgical evacuation of the haematoma under local anaesthesia are possible options. If general anaesthesia is necessary, an inha-lational induction with halothane or sevoflurane, or a fibre-optic awake intubation, are the methods of choice.
Neurological complications
Post-operative neurological deficit occurs in 1-7% of patients after CEA, regardless of the anaesthetic technique. Neurological deficits following CEA are multifactorial in origin: they may result from embol-ization at the site of surgery, cerebral ischaemia due to hypoperfusion or thrombosis at the endarterectomy site and intimal flap, or ICH. Te manifestations include transient deficits and ischaemic strokes. All potentially treatable causes including thrombosis must be sought and re-exploration may be necessary. Re-exploration for evacuation of a haematoma requires meticulous airway management as discussed above. Cranial nerve injuries have also been reported, the most commonly injured nerves being the hypoglossal and recurrent laryngeal nerves, leading to possible problems with upper-airway control. Damage to the recurrent laryngeal nerves may reduce the upper-airway protective reflexes and place the patient at risk of aspiration, as well as cause airway obstruction (if the abductor fibres are not the only ones affected).
Conclusions
The maintenance of adequate cerebral perfusion, the avoidance of hypotension and the prevention and treatment of raised ICP are essential for good recovery in patients with intracranial haemorrhage, cerebral trauma or encephalopathies. Terefore, clinicians caring for these patients must have a thorough understanding of cerebral physiology and the factors that affect cerebral haemodynamics. Te principles of anaesthetic management of patients with SAH described above are applicable to any patient with an intracranial vascular lesion .
