The anaesthetic management of patients undergoing endovascular repair of abdominal aortic aneurysms is well described in the literature [1,2] but there is little which describes the detailed anaesthetic management of patients requiring endovascular repair of thoracic aneurysms. We describe our anaesthetic management of a patient undergoing stenting of a thoracic aortic aneurysm at the site of an aortic coarctation.
A 29-year-old man was referred for a cardiology opinion after a systolic murmur and mild hypertension were found at a routine employee medical examination. Subsequent investigation revealed an aortic coarctation distal to the left subclavian artery with a pressure of 40 mmHg across the stenosis. A spiral computerized tomography (CT) image showed a small sacular thoracic aneurysm protruding posterolaterally from the coarctation site. After discussion with the patient, vascular radiologists and thoracic surgeons it was decided that this would be best treated by the placement of a covered stent.
The patient had an unremarkable past history and played sport regularly. He was taking atenolol 50 mg once a day to control his blood pressure. Examination revealed a blood pressure of 150/70 mmHg (equal in both arms) and a systolic murmur at the left sternal edge which radiated upwards to the carotid arteries. Electrocardiography (ECG) showed a sinus bradycardia of 50 beats min–1 and the chest radiograph was unremarkable. The patient had normal standard blood indices.
The patient received lorazepam 2 mg premedication 2 h preoperatively and was brought to the vascular radiology theatre. A cardiac theatre with cardiopulmonary bypass was available if necessary. Vascular access was gained at the right hand via a 16-gauge cannula, and a right radial artery catheter was placed prior to induction of anaesthesia. The patient was kept supine. Standard oxygen saturation and ECG monitoring were instituted. After preoxygenation the patient received midazolam 2 mg, fentanyl 200 μg, propofol 150 mg and vecuronium 8 mg. The trachea was intubated with a single lumen armoured tube placed just above the carina, over the right main bronchus, and was confirmed radiographically (Figure 1). An 8-gauge Swan Ganz introducer was sited in the right internal jugular vein for large central venous access. A triple lumen catheter was placed through the introducer for infusion of drugs. If major problems should occur this would also allow the placement of a pulmonary catheter. The patient’s lungs were ventilated to end-tidal carbon dioxide 4.8 kPa with 33% oxygen, 66% nitrous oxide and isoflurane (end-tidal concentration 0.8–1.4%). An infusion of 0.01% sodium nitropruside was prepared and attached to the central venous catheter for acute control of arterial pressure.
The radiologists introduced two arterial sheaths. A brachial puncture allowed placement of a catheter along the left subclavian artery to help with placement of the stent and to permit inflation of an occlusive balloon proximal to the aneurysm if necessary. A left femoral ‘cutdown’ allowed placement of the sheath for positioning of the self-dilating stent. Just prior to introducing the stent, 5000 IU heparin was given intravenously (i.v.). The stent was then advanced under radiological guidance to the arch of the aorta.
During placement and dilation of the covered stent the radiologists requested a short period of hypotension. We used nitropruside 0.8–1.6 μg kg–1 min–1 to reduce the systolic arterial pressure to 55–60 mmHg for 10 min and for a second period of 3 minutes to 60 mmHg. This produced no changes in the ECG or oxygen saturation. During these periods, when a radiologist inflated the balloon to dilate the stent, the total occlusion increased the systolic arterial pressure to 70–110 mmHg. After placement and return of systolic arterial pressure to 120 mmHg, the radiologists injected contrast material i.v. to confirm the position of the stent and the occlusion of the aneurysm (Figure 2). This caused the systolic arterial pressure to fall by 20 mmHg to 100 mmHg. During the rest of the procedure the systolic arterial pressure was maintained at 110–130 mmHg. During imaging the patient was momentarily rendered apnoeic to permit acquisition of clear images.
At the end of the procedure the gradient across the coarctation had been reduced to 10 mmHg. The femoral artery was then repaired and anaesthesia discontinued. The patient received 2000 mL Hartmann’s solution i.v. during the 3-h procedure.
The patient made an uneventful recovery. The next day he was eating a normal diet and was fully mobile. His total analgesic requirement was simply three doses of two cocodamol tablets (codeine 8 mg, paracetamol 500 mg per tablet).
The placement of the stent had to be precise because of the combination of a thoracic coarctation and aneurysm in this patient. This was assisted by induced hypotension, which reduces the ‘windsock effect’ . It also reduces the possible risks of the hypertension produced with complete aortic occlusion close to the major arteries originating from the aortic arch. This could theoretically cause problems with dissection or rupture of the aorta. Sudden increased myocardial afterload may cause acute cardiac dilatation, increased left ventricular pressure, depressed left ventricular function and pulmonary oedema . Cerebral haemorrhage secondary to sudden hypertension would also be exacerbated by the heparin required for the procedure. An alternative method for reducing the risk of displacement has been to produce a period of asystole with adenosine , or a period of induced ventricular fibrillation .
The degree of hypotension required varies according to different authors. A mean arterial pressure of 60 or 70 mmHg seems adequate for abdominal stents [2,7]. For thoracic stents lower pressures have been induced with mean arterial pressures of 50 mmHg being quoted . We decided to use sodium nitroprusside in this case because we are familiar with the technique. This produced rapid hypotension with rapid recovery for our patient. He was adequately β-blocked prior to the procedure, which stopped any compensatory tachycardia. Because our patient was young and otherwise fit we felt that he could tolerate short periods of marked hypotension. This allowed us to produce quite low systolic arterial pressures. In less healthy patients the risk of this degree of hypotension may outweigh the benefits.
The risk of thoracic aortic rupture requires forethought. We believe that general anaesthesia was essential in this case. The single lumen endotracheal tube was placed above the right main bronchus to allow rapid endobronchial placement if this was required. Large bore i.v. access is mandatory as there is the possibility of major haemorrhage from arterial access as well as its requirement if aortic rupture occurred. Although one series had no conversions required with 108 patients with thoracic aortic aneurysms treated with stents , conversion to an open procedure for rupture or unintentional complete occlusion is still a possibility.
The radiological suite can be a cramped and unfamiliar environment. Extra preoperative planning and checking of all possible equipment is thus mandatory. In our hospital this area is fully equipped for general anaesthesia including excellent monitoring. Unfortunately it is separate from the main theatre suite. Ideally this type of procedure should be performed adjacent to, or within, the cardiac theatre complex with cardiac bypass facilities available.
The potential advantages of stent repair were shown by the remarkable recovery of our patient. A femoral incision rather than a thoracotomy, and the minimal changes in perioperative physiology led us to meeting our patient on a routine postanaesthetic visit the next day as he was walking along the corridor. Surgical treatment involves considerable mortality (5–28%) and significant morbidity. These include paraplegia or paraparesis (5–40%), renal failure (0.9–19%), neurogenic bladder dysfunction (0.5%), postoperative stroke (0.5–3%), pulmonary complications (6–33%), pulmonary embolism (1–9%), cardiac complications (10–44%), postoperative sepsis (8–19%), gastrointestinal complications (7%) and postoperative coagulopathy (4%) [2,4–7]. Stent repair is a new technique and requires careful evaluation. However, early results are very encouraging. Mortality rates of 10 in a series of 108  seem quite large but many of these patients were deemed unfit for surgical repair. The incidence of paraplegia and paraparesis is low. In the above series only four patients were rendered paraplegic, two during combined procedures with open suprarenal abdominal aortic repairs . Only two patients suffered strokes and postoperative thromboembolic phenomena have not been reported as being a problem. Other potential advantages include reduced bed occupancy, especially of intensive care or high-dependency beds.
The major disadvantages of this technique are the limited number of patients suitable for the procedure, and the lack of data regarding long-term surgical outcome. There needs to be suitable anatomical configuration. The origin needs to be a suitable distance from the subclavian artery and there also needs to be a sufficient length of normal aorta prior to the coeliac axis. It is also preferable for the aneurysm to be part of a relatively straight portion of the descending aorta.
This technique clearly has implications for anaesthesia, but appears to offer huge potential advantages over conventional surgical repair. In the near future self-expanding stents will remove the risks of balloon dilatation and may make possible placement of these stents under local anaesthetic alone. To see our patient walking around the ward looking so well the day after a repair of his coarctation and thoracic aneurysm certainly engenders enthusiasm for this technique.
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