Perioperative management of thoracic and thoracoabdominal aneurysms

Key points.

• •Aneurysm and dissection can both occur in the thoracic aorta.
• •Thoracoabdominal aortic surgery is associated with high morbidity and mortality.
• •Surgery involving the aortic arch is performed with full cardiopulmonary bypass and deep hypothermic circulatory arrest.
• •Surgery involving the descending aorta with no arch involvement is performed using left heart bypass.
• •Paraplegia is a devastating complication of thoracic aortic surgery; the risks of paraplegia can be reduced by using neurophysiological monitoring and augmenting spinal CSF pressure.

Learning objectives.

By reading this article, you should be able to:

• •Distinguish the differences between true aneurysm, false aneurysm, and dissection.
• •Explain the perioperative management of patients undergoing surgery involving the aortic arch and the descending aorta.
• •Illustrate the physiological changes that occur during left heart bypass for descending thoracic aortic surgery.
• •Describe the postoperative care of patients undergoing major aortic surgery and, in particular, the measures used to ensure maintenance of spinal cord perfusion.

Thoracoabdominal aortic surgery is associated with high morbidity and mortality. An experienced team must work together to provide preoperative assessment, perioperative management, and postoperative care of the patient.

Pathology

Disease of the thoracic aorta can take the form of aneurysm and dissection, occurring separately or together, and may be congenital or acquired. An acquired disease is usually a result of hypertension and atherosclerosis. Congenital causes include the connective tissue diseases (Marfan syndrome, Ehlers–Danlos syndromes, Turner's syndrome, and Loeys–Dietz syndrome) and polycystic kidney disease.

A true aneurysm of the aorta is a permanent dilatation at least 50% greater than its original size involving all wall layers. A pseudoaneurysm is a rupture through the layers of the aorta held together by blood and surrounding tissues. A dissection is a disruption of the intimal layer of the aorta, with bleeding within the wall.

Aneurysms

Untreated aneurysms of the descending and thoracoabdominal aorta exceeding 6 cm in diameter have a 14.1% annual rate of rupture, dissection, or death.¹ The 5 yr survival of patients managed conservatively is 10–20%.² Indications for surgery are based on individual assessment of the patient, whereby the predicted operative risks are lower than the risks of medical management.2, 3 Indications include the following:

• (i)rupture or acute dissection
• (ii)symptomatic enlargement: pain or compression of adjacent structures
• (iii)aneurysm enlargement >1 cm yr⁻¹ or rapid increase in size
• (iv)absolute size >6.5 cm or >6.0 cm in patients with connective tissue disease

Classification of aneurysms

Thoracoabdominal aortic aneurysms (TAAAs) are described using the Crawford classification (Fig. 1) according to the location of aneurysmal sections:

• (i)Extent I: from the left subclavian artery to below the diaphragm
• (ii)Extent II: from the left subclavian artery to the aortic bifurcation
• (iii)Extent III: from the lower half of the descending thoracic aorta extending to the aortic bifurcation
• (iv)Extent IV: disease confined to the abdominal aorta

Fig 1.

Classification of aortic dissection and aneurysm.⁴ Reproduced with permission.

Dissection

Dissection of the aorta is often associated with an increase in physical activity or stress, leading to acute hypertension. An intimal tear occurs, usually in the presence of a weakened aortic wall and at a location experiencing significant mechanical shear forces, particularly the relatively fixed ascending and isthmic segments.

The survival rate of untreated patients with Type A aortic dissection is poor, with a 2-day mortality up to 50% and a 6-month mortality approaching 90%.⁵ The usual cause of death is rupture of the false lumen and fatal haemorrhage. The overall surgical mortality is approximately 30%,⁵ but surgical therapy is often the only viable option for most patients.

Classification of dissection

Aortic dissection can be described using the DeBakey and Stanford classifications (Fig. 1).

• (i)
  DeBakey classification: comprises three different types, depending on where the intimal tear is located and which section of the aorta is involved

  • (a)
    Type I: intimal tear in the ascending portion; involves all portions of the thoracic aorta
  • (b)
    Type II: intimal tear in the ascending aorta; involves the ascending aorta only, stopping before the innominate artery
  • (c)
    Type III: intimal tear located in the descending segment; almost always involves the descending thoracic aorta only, starting distal to the left subclavian artery; can propagate proximally into the arch
• (ii)
  Stanford classification: comprises two types, depending on which section of the aorta is involved

  • (a)
    Type A: with any involvement of the ascending aorta, regardless of intimal tear location or extent of dissection; runs a more virulent course
  • (b)
    Type B: involves the aorta distal to the origin of the left subclavian artery; generally medically managed unless there is evidence of a life-threatening complication, such as impaired organ perfusion, aortic rupture, severe pain, or uncontrollable hypertension

Preoperative assessment

Patients presenting with aortic disease often have multiple significant comorbidities. A thorough preoperative assessment, as time allows, should include the following:

• (i)assessment of functional capacity and reserve of each organ system for risk stratification and prediction of postoperative complications. Any history of previous cardiac, respiratory, renal, hepatic or neurological disease should be elucidated;
• (ii)examination for evidence of compression of adjacent structures. Stridor or dyspnoea indicates encroachment onto the trachea or left main bronchus; dysphagia indicates oesophageal compression; hoarseness is caused by stretching of the recurrent laryngeal nerve;
• (iii)baseline neurological examination and recording of any existing neurological deficit.

Preoperative investigations are performed according to the urgency of surgery and the stability of the patient. Pulmonary function testing with calculation of transfer factor is useful where one-lung ventilation is anticipated. Assessment for coronary artery disease that may need to be dealt with simultaneously should be performed via coronary catheterisation or CT angiography. Cardiopulmonary exercise testing is used in some centres. CT imaging can reveal compression of the trachea or left main bronchus that may make the insertion of a double-lumen tracheal tube (DLT) for one-lung ventilation challenging.

Transoesophageal echocardiography

Where surgery is emergent or urgent, opportunities for imaging the aorta may be limited, and transoesophageal echocardiography (TOE) gives essential information both to guide the surgical approach and to anticipate potential problems weaning from cardiopulmonary bypass (CPB). Transthoracic echocardiography (TTE) allows the assessment of ventricular and valvular function, but a negative TTE does not rule out dissection. The use of TOE is limited to the perioperative period after the induction of anaesthesia, as the haemodynamic impact of examination, even under sedation, could precipitate aortic rupture.⁶

Aneurysms of the aortic root and proximal ascending aorta are often associated with bicuspid aortic valve, a cause of aortic stenosis. Where aortic dilatation is significant and involves the aortic valve annulus, there may be central aortic regurgitation. TOE allows measurement of aortic root dimensions; in some circumstances, replacement of the valve may be avoided. Type A dissection may be associated with pericardial collection that can cause cardiac tamponade. TOE can also assist the surgical team in the placement of the coronary sinus cannula for delivery of cardioplegia and to confirm adequate positioning of the venous line of a bypass circuit where it is sited via the femoral vein. On conclusion of surgery, TOE supports adequate de-airing, and allows the assessment of ventricular function and for residual aortic regurgitation where the native valve remains in situ.

Surgery involving the aortic root and ascending aorta

The management of anaesthesia for replacements of the aortic root and the ascending aorta, where a clamp can be applied proximal to the innominate artery, is similar to aortic valve surgery involving a median sternotomy and routine cardiac anaesthesia.7, 8

Surgery involving the aortic arch

Full CPB with deep hypothermic circulatory arrest

Repair of the aortic arch involves interruption to the cerebral blood supply necessitating the use of CPB with deep hypothermic circulatory arrest (DHCA). Cerebral perfusion may be maintained antegrade via cannulation of arteries as they branch from the aortic arch or via the arterial line into the right axillary, subclavian, or innominate artery, or retrograde via cannulation of the internal jugular vein.

Hypothermia is an effective technique for the protection of the central nervous system and other viscera in the presence of reduced or absent blood flow. The lower temperature reduces tissue metabolic activity and attenuates the inflammatory response to reperfusion.⁹ The core temperature is allowed to decrease spontaneously with additional cooling from the heater/cooler on the CPB circuit. Application of topical cooling to the head is performed in some centres to minimise passive warming, although the benefits of this have been extrapolated from studies in animals.¹⁰ Where used, particular care should be taken to protect the patient's eyes. Opinions vary on the degree of hypothermia required. Deep hypothermia (14.1–20°C) allows 20–30 min of safe circulatory arrest time compareed with 10–20 min where moderate hypothermia (20.1–28°C) is used.¹¹ There is some evidence of a reduction in the incidences of acute renal and liver failure, stroke, paraplegia, and death when deep hypothermia is used.¹³ Profound cooling contributes to morbidity through the development of coagulopathy and an increased inflammatory response.

Considerations for anaesthesia

Invasive arterial blood pressure monitoring via the right radial artery ensures continued assessment should the aortic cross-clamp be applied proximal to the left subclavian artery. If the right axillary artery is used for antegrade cerebral perfusion, a left radial arterial catheter may be required. Haemodynamic instability should be anticipated at induction of anaesthesia, and appropriate vasopressor infusions should be available. Cooling and rewarming are lengthy processes. Temperatures measured within the nasopharynx have been shown to most accurately reflect cerebral temperature, and monitoring is usually via probes positioned in the nasopharynx and either rectum or bladder. In some centres, jugular bulb venous oxygen saturation and EEG are monitored as surrogate markers of cerebral metabolism.

Pharmacological protection of the brain and spinal cord is used variably as an adjunct to hypothermia, as there is little consistent evidence. Drugs occasionally administered include thiopental, methylprednisolone, magnesium, and lidocaine.

Cerebral oxygenation monitoring

Near-infrared spectroscopy is increasingly used during surgery involving the aortic arch to provide continuous, real-time non-invasive monitoring of anterior cerebral oxygenation. The proportion of light absorbed attributable to oxygenated and deoxygenated haemoglobin within the cerebral cortex is calculated using adhesive diodes on the forehead. Intracerebral oxygen saturation (rSO₂) is calculated and should be maintained within 25% of baseline. Inadequate cerebral perfusion should prompt assessment of cannulation sites; increased flow rate within the CPB circuit; optimised haemoglobin concentration; and, if necessary, increased hypothermia and Pco₂ to promote vasodilatation.

Surgery involving the descending aorta

Surgical approach

The surgical approach will vary according to the extent of the aneurysm, and a clear communication between the surgical and anaesthetic teams is essential. Where a clamp can be placed distal to the left subclavian artery and there is to be no interruption to the cerebral blood supply, the use of partial left heart bypass (PLHB) is preferable. The prolonged duration of CPB and hypothermia required in the presence of an extensive, adherent aneurysm, is associated with a significant inflammatory response and marked coagulopathy; whilst this can also develop after PLHB, it is of a lesser severity. Other techniques that have been used include the use of the Gott shunt between the proximal and distal aorta or partial femoral–femoral CPB (Fig. 2). Where there is an Extent I or II TAAA with involvement of the distal aortic arch, full CPB with DHCA must be used. This may be performed as a two-stage operation, replacing the diseased aortic arch with an elephant trunk graft first, and then returning to replace the diseased descending aorta using PLHB at a later date.

Fig 2.

Surgical approaches to TAAA repair.¹² Redrawn with permission. (A) A clamp-and-sew technique, where the distal aorta is not perfused, generally avoided, as proximal hypertension can cause myocardial ischaemia, and there is a significant degree of mesenteric ischaemia, as the distal aorta is not perfused. (B) Distal aortic perfusion via a Gott shunt. (C) PLHB, where a cannula is placed in the left atrium via the left inferior pulmonary venotomy, and connected to the drainage line of the left heart bypass circuit. Oxygenated blood then returns via a cannula in the distal descending thoracic aorta. (D) Partial femoral–femoral CPB. Blood flows from a femoral vein to a femoral artery with or without an oxygenator in the circuit, allowing some distal perfusion, but without the control achieved with LHB.

Physiology of left heart bypass

Replacement of the abdominal aorta can be performed with the use of an aortic cross-clamp. Cross-clamping of the descending thoracic aorta causes a sudden increase in left ventricular afterload and proximal arterial blood pressure. The increase in myocardial contractility and oxygen demand may outstrip supply, precipitating acute myocardial ischaemia. All organs distal to the clamp will suffer from a lack of perfusion, which may last for hours.

PLHB allows the passage of oxygenated blood from the left side of the heart to the head and neck vessels via the native circulation, and to the distal aorta via the bypass machine. This ensures continued perfusion of organs distal to the clamp and relief of left ventricular afterload. PLHB involves proximal cannulation of the left atrium or pulmonary vein with a return cannula in the common femoral artery or the aorta distal to the clamp. The limited extracorporeal circulation without the need for an oxygenator requires only partial heparinisation (activated clotting time: 200–300 s). Maintenance of cerebral perfusion negates the need for anything more than passive cooling to around 34°C.

Partial left heart bypass is instituted before the application of the cross-clamp, and vigilant monitoring of proximal and distal arterial pressures is required. Proximal MAP is maintained at 80–90 mm Hg and the distal aortic pressure at 60–70 mm Hg by augmenting flow from the bypass circuit. Proximal hypertension may be alleviated by increasing flow through the bypass circuit or by pharmacological means. Titrating administration of anaesthetic agents or use of short-acting drugs, such as glyceryl trinitrate, can be useful. Proximal arterial pressure should not be overly reduced, however, to ensure maintenance of adequate coronary blood flow.

After the application of the cross-clamp, the aorta is opened leading to significant blood loss and haemodynamic compromise. Cell salvage, together with rapid infusion devices, allows the return of circulating volume to the patient. The perfusionist and anaesthetist work in harmony to ensure maintenance of cerebral perfusion, which may involve reduction or even cessation of distal flow via the PLHB circuit. To reduce the duration of visceral ischaemia, the aortic cross-clamp can be advanced sequentially to allow segmental aortic reconstruction, or vessels, including the coeliac axis, superior mesenteric artery, and renal arteries, can be cannulated directly.

Unclamping of the aorta in the latter stages of surgery is also associated with haemodynamic compromise. The resumption of flow through the descending aorta precipitates a sudden decrease in left ventricular afterload and a decrease in MAP. Where there has been hypoperfusion of tissue, the release of vasoactive mediators leads to myocardial depression and a further decrease in systemic vascular resistance. It is essential to prepare for this with the use of vasoactive drugs and optimisation of intravascular volume. The gradual controlled release of the cross-clamp can avoid a precipitous decrease in blood pressure.

Positioning

Surgical access is achieved via a thoracolaparotomy. The patient is positioned with support from a vacuum bean bag in the left helical or semi-lateral position, with the torso and shoulders rotated approximately 60° and the hips 30°.

Anaesthetic considerations

A standard anaesthetic induction is performed using a short-acting non-depolarising neuromuscular blocking agent to facilitate neurophysiological monitoring. One-lung ventilation allows exposure of the thoracic aorta via deflation of the left lung. A left-sided DLT is used for ease of positioning, although external compression of the left main bronchus by the enlarged aorta may preclude this, and a right-sided DLT or single-lumen tube with bronchial blocker may be required. Where a DLT is used, it is usually exchanged for a single-lumen tube at the end of surgery. In our centre, anaesthesia is maintained with infusions of propofol and an opioid to allow neurophysiological monitoring; infusions of a benzodiazepine, and volatile anaesthetic agents can also be used, as described later.

An arterial catheter is sited in a femoral artery, in addition to the right radial artery, to allow monitoring of distal perfusion pressure. Large-bore i.v. access is instituted using a haemofiltration catheter into a femoral vein allowing rapid infusion. A central venous catheter and percutaneous introducer sheath are inserted into the left internal jugular vein; insertion into the right may lead to problems with kinking once the patient is positioned. Hypothermia of varying degrees is used, and temperature probes should be positioned in both the nasopharynx and either rectum or bladder.

Maintaining spinal cord perfusion

Paraplegia after thoracic aortic surgery is a devastating and life-limiting complication, reported to occur in 4–16% of cases overall and in up to 50% of Extent II aneurysms.9, 14 Aortic cross-clamping reduces arterial blood flow and increases central venous pressure, compromising spinal cord perfusion. Replacement of diseased sections of aorta requires temporary or permanent interruption of arterial collaterals, leading to spinal cord ischaemia and subsequent reperfusion injury.9, 15, 16 Ischaemia causes spinal oedema, hyperaemia, and inflammation, thus increasing the CSF pressure (CSFP) and compromising spinal cord perfusion pressure (SCPP). Risk factors for spinal cord ischaemia include the extent of the aneurysm; longer duration of aortic cross-clamping; requirement for emergency surgery; previous surgery to the distal aorta; severe peripheral vascular and atherosclerotic disease; perioperative hypotension; advanced age; and diabetes mellitus.¹⁵

A number of interventions can be used to reduce the risk of spinal cord ischaemia, including sequential clamping of the aorta with reimplantation of intercostal and lumbar segmental vessels, drainage of CSF to maintain SCPP, and the use of neurophysiological monitoring.

CSF drainage

Spinal cord perfusion pressure is represented as

SCPP=MAP–CSFP

Insertion of a CSF drainage catheter to augment CSFP aids in the maintenance of an adequate SCPP, an intervention found to reduce the incidence of postoperative neurological deficits by 80%.¹⁷ CSFP is maintained at 10–15 mm Hg, and CSF is drained to maintain this at rates up to 20 ml h⁻¹. Monitoring of CSFP and drainage continue for up to 72 h after surgery.

An SCPP target of 70 mm Hg is used in most centres, requiring a CSFP of less than 15 mm Hg and a minimum MAP of 80 mm Hg; this target may require infusion of a vasopressor, such as noradrenaline (norepinephrine). Where it is not possible to maintain the CSFP below 15 mm Hg through CSF drainage, the MAP must be augmented further. Where there is evidence of spinal cord ischaemia, the SCPP and MAP target can be increased in 5 mm Hg increments.⁹

The spinal drain consists of a transduced intrathecal catheter inserted at the level of L3–4 or L4–5 to reduce the risk of direct spinal cord damage, although there are risks associated with their placement.¹⁸ Complications include spinal headache, neuraxial haemorrhage or haematoma, meningitis, intracranial hypotension, and catheter fracture.

Neurophysiological monitoring

With normal metabolism in the context of no perfusion, cell death occurs within 3–5 min. Neurophysiological monitoring with sequential clamping of the aorta identifies key vessels for spinal cord perfusion that must be reimplanted, and helps to ascertain the minimum acceptable MAP for adequate spinal cord perfusion. Monitoring of neurological function can be achieved with the use of motor-evoked potentials (MEPs) or somatosensory-evoked potentials (SSEPs).

Motor-evoked potentials monitor the activity in the anterior spinal cord where the descending motor pathways travel. Stimulation of the motor cortex is via subdermal electrodes, and recordings of muscle contractions are collected peripherally. Paraplegia caused by spinal cord ischaemia significantly dampens the lower-limb potentials when compared to those of the upper limb. MEPs disappear in the presence of neuromuscular blocking agents, and volatile anaesthetics also cause dose-dependent depression of the MEP at doses within the range used in clinical practice.¹⁹ Total i.v. anaesthesia is preferred if MEPs are to be used. SSEPs, although less frequently used, allow monitoring of the posterior ascending sensory columns, and are not affected by neuromuscular blocking agents or volatile anaesthetic agents.

A decrease in MEP amplitude greater than 50% should prompt reinsertion of intercostal arteries into the graft along with measures to improve spinal cord perfusion.²⁰ A MAP exceeding 80 mm Hg and distal aortic pressure exceeding 60 mm Hg are targeted. Haemoglobin concentration should be maintained at or above 100 g L⁻¹. CSF may be drained at 20 ml h⁻¹.²¹ The decision for surgical intervention is usually made within 3–5 min of the change in the neurophysiological variables.

Haemostasis

Peri- and postoperative bleeding occurs commonly. Antifibrinolytics, such as tranexamic acid, aminocaproic acid, or aprotinin, are administered. Cell salvage should be used routinely. On separation from CPB, protamine is used to reverse the residual effects of heparin, and blood products are given as indicated by point-of-care coagulation tests. Blood products may be fresh frozen plasma, cryoprecipitate, and platelets, or, more recently, prothrombin complex and fibrinogen concentrates. Further transfusions are guided by the results of repeated tests. In cases of ongoing bleeding, the use of recombinant factor VIIa has been advocated.

Postoperative management

Sedation and analgesia

Sedation is maintained in the postoperative period. Agents utilised vary between units, but ultimately, minimal sedation with intermittent sedation holds should be used to allow assessment of neurological function. Where there has been disruption to cerebral blood flow, there is an increased incidence of neurocognitive dysfunction, potentially influencing the timing of emergence from the effects of sedative drugs.

The extensive surgical incision leads to significant pain that can impair weaning from sedation and artificial ventilation. A multimodal analgesic regimen is essential. Epidural analgesia has been advocated, but it can be challenging to decide the timing of insertion of the catheter, and also to maintain a sensory but not a motor block, thus allowing neurological assessment. The presence of the spinal catheter provides a route for administration of intrathecal diamorphine.

Maintaining spinal cord perfusion in the ICU

Neurophysiological monitoring, ICP monitoring and CSF drainage continue for up to 72 h after surgery. Monitoring of MEPs and SSEPs is continued whilst patients are sedated. The postoperative period is a critical time in which significant ischaemia can still develop.²² Delayed paraplegia has a better prognosis than immediate, and can be reversed if recognised and treated promptly.²³ Regular reassessment of lower limb power is essential.

Neurological impairment initiates the use of the COPS protocol to optimise spinal cord perfusion.¹⁴ COPS is an acronym of CSF drain status; optimise Oxygen delivery; and Patient Status assessment in terms of MAP, SCPP, and cognitive status. Where the spinal catheter is patent, the patient should be positioned flat and the CSFP maintained at <5 mm Hg. Oxygen delivery should be optimised through the administration of supplemental oxygen or tracheal intubation and artificial ventilation to ensure SpO₂ greater than 95%. Haemoglobin concentrations should be greater than 120 g L⁻¹ and cardiac index greater than 2.5 L min⁻¹ m⁻². SCPP is maintained at >80 mm Hg and MAP at >90 mm Hg. Where a drain was not sited during surgery, for example, in emergency surgery, the development of delayed neurological symptoms has been successfully treated with postoperative drain insertion.

Complications of major aortic surgery

Whilst surgery for aortic aneurysm is potentially life-saving, there is a significant morbidity and mortality. Early complications include hypothermia, coagulopathy, delirium, cardiovascular instability, respiratory failure, metabolic disturbance, renal failure, and stroke. Preoperative hydration, intraoperative administration of mannitol and cold renal perfusion have been used for their potential nephroprotective effects. Because of the size of the surgical incision for TAAA repair, the division of the diaphragm, and the potential for injury to the phrenic and recurrent laryngeal nerves, there is a significant risk of wound dehiscence and respiratory failure. The reported incidence of an adverse outcome after TAAA surgery, including renal failure requiring dialysis at hospital discharge, stroke, permanent paraplegia, or paraparesis, is 16% with an overall operative mortality of 8–10%.²⁴

Declaration of interest

SA and CQ no conflicts. JK declared cerebral oximetry - paid advisory work for INVOS (Covidien) and meetings expenses (Masimo).

MCQs

The associated MCQs (to support CME/CPD activity) will be accessible at www.bjaed.org/cme/home by subscribers to BJA Education.

Biographies

Seema Agarwal MA FRCA is a consultant anaesthetist at Manchester University Hospitals NHS Foundation Trust, who has an interest in anaesthesia for major thoracic aortic surgery and haematology related to cardiac surgery. She is an active member of the EACTA haemostasis committee.

John Kendall FRCA is a consultant in cardiothoracic anaesthesia at Liverpool Heart and Chest Hospital NHS Foundation Trust. He is clinical lead for anaesthesia and has a particular interest in anaesthesia for thoracic aortic surgery. He has recently served on the committee of the Association for Cardiothoracic Anaesthetists and Critical Care.

Clare Quarterman BSc FRCA FFICM is a consultant in cardiothoracic anaesthesia and intensive care. In addition to anaesthesia for major aortic surgery, she has interests in perioperative medicine and medical education.

Matrix codes: 1D02, 2A04, 3G00