Aortic surgical patients in the ICU can be some of the most challenging patients. Further, these are the patients for whom good intensive care management can make a big difference to the outcome. Most of these patients are admitted to the ICU following an operation. Sometimes the patients may need to be admitted to the ICU for preoperative optimisation. Knowledge of the aortic disease pathology, the surgical interventions for it, and the expected ICU support is important for delivering optimal care for these complex patients.
Aortic Pathology and Treatment
Aortic dissection forms part of a group of interrelated pathologies where blood breaches the aortic lumen typically into the aortic media, to produce a so-called acute aortic syndrome. In aortic dissection there is an intimal tear. However, penetrating ulcer or rupture of vasa vasorum (intramural haematoma) causes similar presentation and imaging. The blood in the media may track proximally or distally, producing a dissection plane, which may rupture through the adventitia or back through the intima into the lumen again. The propagating dissection may also rupture into the pericardium, causing cardiac tamponade; it can disrupt the aortic valve, causing aortic regurgitation; or impinge on side branches of the aorta causing malperfusion syndromes (including cardiac ischaemia, stroke, intestinal or renal malperfusion and pulseless limbs).
Penetrating ulcer occurs in relation to atherosclerosis and has similar risk factors. Intramural haematoma and acute aortic dissection are typically associated with medial degeneration in the aorta. A number of conditions are known to predispose to these changes, including Marfan’s syndrome, Loeys–Dietz syndrome, Ehlers–Danlos syndrome, Turner’s syndrome and bicuspid aortic valve. Vasculitides such as giant cell arteritis and Takayasu’s arteritis are also predisposing conditions. In all cases, hypertension is strongly implicated.
Presentation is most commonly with chest pain, described as severe and sharp and initially corresponding with the site of intimal tear then migrating according to the extent of dissection of the aorta. Syncope may occur, as may symptoms of malperfusion. There may be signs of haemodynamic upset or indeed hypertension, as well as aortic regurgitation, cardiac tamponade and reduced pulses. The most common differential diagnoses are myocardial infarction or pulmonary embolism. Diagnosis is urgent.
Figure 42.1 Classification of aortic dissection.
An anatomical classification (Figure 42.1) underpins clinical management. The Stanford classification divides acute aortic dissection according to whether or not the ascending aorta is involved, regardless of the site of intimal tear. In type A dissection, the ascending aorta is involved and emergency open surgery is indicated in a cardiothoracic centre. This is an emergency procedure with high (10–20%) operative mortality. The goal of surgery is to excise the intimal entry tear and direct blood down the true lumen by obliterating the false lumen proximally. Frequently, dissection extends down into the aortic root, causing prolapse of the aortic valve and regurgitation. Often reconstituting these layers with sutures and/or glue can resuspend the aortic valve and so it does not need to be replaced. If the root is already abnormal or irreparable, then a root replacement is required, with or without valve replacement depending on the condition of the aortic leaflets and the surgical expertise. Another principle of the surgery is that the aorta, which is left behind, should not have had a vascular clamp placed across it. This weakens the aorta, which is dissected and likely to be intrinsically abnormal. Therefore the distal repair is performed ‘open’, i.e. without a clamp, necessitating a period of circulatory arrest, which can be partial or total.
In type B dissection, the ascending aorta is not involved and surgery is usually not indicated for uncomplicated cases, which are typically managed by cardiologists in a CCU setting, with blood pressure control and serial imaging until symptoms settle and imaging is stable. Complicated cases involve malperfusion syndromes, ongoing pain or other suggestions of imminent rupture and then endovascular stenting is indicated in a vascular surgery unit.
The thoracic aorta is never normal at 4 cm in diameter and this size serves as a pragmatic cut-off to diagnose TAA. Unlike abdominal aortic aneurysms, which are commonly the result of atherosclerosis, this is much less likely in TAA, although TAA shares a number of risk factors with atherosclerosis, including hypertension, smoking and chronic obstructive pulmonary disease. TAA is also predisposed by connective tissue defects due to a number of genetic syndromes or inflammatory disorders. There is an association with congenital bicuspid aortic valves, which affects 2% of the population. Atherosclerosis is more common in the descending thoracic aorta.
Since wall tension increases with greater diameter, TAA is an exponentially progressive condition with the result that the aorta is increasingly at risk of rupture or dissection. Patients occasionally present with symptoms such as change in voice (indicating recurrent laryngeal nerve palsy), chest pain or shortness of breath, and even dysphagia (mostly down to compression of surrounding structures). More typically, TAA is found incidentally on imaging for some other indication. Symptoms may be a reason for intervention, but more commonly size is the main factor driving intervention. In these cases, the predicted risk of rupture or dissection (per annum) must be balanced against the procedural risks (essentially one time) in the individual patient. Limited natural history studies have shown that the risk of an event increases significantly at 6 cm for the ascending and 7 cm for the descending aorta. In the absence of other factors therefore, a TAA of 5.5 cm in the ascending aorta and of 6.5 cm in the descending aorta would indicate intervention.
TAA is not a homogenous condition. The natural history varies according to the predisposing condition, and according to which segment of the thoracic aorta is affected. TAA is commonly associated with aortic valve disease, coronary artery disease and abdominal aortic aneurysm. Thoracoabdominal aortic aneurysms are a particular form, which include thoracic and abdominal components, typically in continuity. The management of TAA is influenced by anatomical factors, patient factors, pathological factors and institutional experience and is mostly decided by multidisciplinary teams.
The options for management include the following:
This involves resection of the aneurysm and replacement of that segment with a polyester graft. Therefore that segment must be excluded from the circulation by vascular clamps or by arrest of circulation. For TAA of the ascending aorta, it is carried out through a median sternotomy with the patient on cardiopulmonary bypass. Adjunctive procedures on the heart are possible. It is also possible to deal with involvement of the arch and/or proximal descending aorta, but this requires advanced perfusion techniques such as deep hypothermic circulatory arrest or selective antegrade cerebral perfusion, and carries an additional risk of mortality, stroke, paraplegia and recurrent laryngeal nerve palsy. For TAA of the descending aorta, open surgery is carried out via lateral thoracotomy. There are a number of surgical techniques to augment the distal aortic perfusion to reduce the risk of paraplegia during clamping of the aorta, described below. Even with intercostal artery reimplantation, spinal cord ischaemia can occur, and adjuncts such as spinal cord drainage and motor evoked potentials may be used to mitigate this risk. Patients need to have a degree of physiological reserve to withstand this level of invasiveness and achieve suitable recovery times.
This involves exclusion of the TAA. A guidewire is passed within the TAA, over which the ESG is passed from a peripheral artery, usually retrogradely. The ESG is positioned under X-ray guidance and deployed, resulting in exclusion of the aneurysm. A number of different devices are used, which are generally constructed of a polyester graft supported by nitinol or stainless steel Z, which self-expand when deployed. There are some anatomical requirements. First, the proximal and distal landing zones should be at least 2 cm in length to ensure an adequate fixation and seal. In addition, the access vessels should be sufficiently large to permit passage of the delivery system. There are ways of getting around both problems, such as performing extra-anatomical bypass or using branched or fenestrated stents to increase the potential landing zone, and using temporary surgical grafts to improve access to the aorta, but all these procedures add to the complexity of the intervention.
Anatomical factors refer to the exact site with respect to branches of the aorta and the extent of aorta involved. The site of the aneurysm determines the feasibility of both stent placement and/or clamp placement in open surgery without compromising important aortic branches. Patient factors include age and comorbidities, particularly respiratory and renal function. Pathological factors include whether there is a connective tissue defect, the presence of infection and whether the aneurysm is true or a chronic dissection.
Blunt aortic injury is common in trauma from major decelerating forces, typically road traffic accidents, falls, or aeroplane crashes. The majority of patients die at the scene, but a significant proportion may reach hospital and may survive with timely diagnosis and treatment. Associated injuries are common and may complicate diagnosis and management.
Most injuries (80%) occur at the aortic isthmus just beyond the left subclavian artery. This is probably because this area is the transition between the mobile ascending arch and the immobile descending aorta. Other locations include the transverse arch, proximal ascending aorta and descending aorta just proximal to the diaphragm. Rupture of the intima and media occurs at the time of injury and exsanguination is prevented by the adventitia and surrounding tissues, but this remains at high risk without appropriate management.
There are no specific symptoms or signs. A chest radiograph may be suggestive, for example showing a widened mediastinum, but a normal physical examination does not exclude the condition. Chest CT is the investigation of choice.
The initial management is that of any trauma patient, applying ATLS guidelines, whilst making the diagnosis. If thoracic aortic injury is suspected then patients should be managed with a goal systolic blood pressure of approximately 100 mmHg and a pulse of <100. Repair of blunt thoracic aortic injury can be performed using open or endovascular techniques, with a growing preference for ESG.
Acute type A aortic dissection is a surgical emergency. There is a 1% per hour mortality in the first 48 hours, with 50% of untreated patients dead by 1 week. Transthoracic echo may show aortic regurgitation, pericardial effusion or even proximal dissection. However, CT imaging provides the most definitive and reliable information and is indicated immediately where there is clinical suspicion. Transoesophageal echo is best reserved for the anaesthetised patient to prevent hypertensive surges, which could lead to decompensation.
Acute rupture of TAA and aortic transection are also unstable conditions mandating emergency intervention, and anaesthetic management is similar.
Once the diagnosis is made, immediate transfer to a cardiothoracic centre is indicated. In the meantime, blood pressure control is paramount. Admission to an intensive care unit should be considered for close monitoring with insertion of an arterial line, wide-bore venous cannulae and urethral catheter. However, insertion of these lines should not delay transfer to theatre or an accepting hospital.
Medical therapy has the goal of reduction of systemic arterial pressure while at the same time blunting the force of contraction of the heart (dP/dt), and hence the shear forces in the aorta. Intravenous Labetalol is the agent of choice, having both alpha-blocking (blood pressure lowering) and beta-blocking (dP/dt lowering) effects. Infusions of 0.5–2 mg/minute should be administered, aiming for systolic BP 100–120 mmHg and heart rate of 60–70 beats/minute. Pain should be addressed with opiates as required. The patient should be monitored for evidence of malperfusion through ECG monitoring, recording neurological observations, attention to oliguria and abdominal pain, acid–base changes and limb pulses.
The transition period from preoperative to intraoperative is hazardous for these patients. The priority for the anaesthetist must be careful control of blood pressure and avoidance of worsening haemorrhage, which can result in either cardiac tamponade or exsanguination. The priority for the surgeon will be institution of cardiopulmonary bypass. The anaesthetist and surgeon must work together. If there is tamponade, then great care should be taken at the time of pericardial opening, since an acute rise in blood pressure may follow, producing exsanguination if bypass is not immediately available.
Numerous arterial cannulation strategies are feasible (Figure 42.2). The most common are right axillary artery or femoral artery or even carotid artery cannulation before sternotomy or direct aortic cannulation after sternotomy. Left ventricular apex and aortic cannulation after transection are also feasible. Almost invariably, the right atrium is cannulated for venous return, although in rare instances peripheral femoral venous cannulation may be preferred in order to commence bypass prior to chest opening.
Cardiopulmonary bypass is instituted and monitoring is observed to exclude induced malperfusion. The patient is systemically cooled, to 18–20 °C for total circulatory arrest, or 22–28 °C for partial arrest. For the latter, selective antegrade perfusion is continued, providing 10 ml/kg blood flow to the upper body via the right axillary artery (innominate artery clamped), or via separate catheters in the innominate artery itself and/or the left carotid artery. The aortic root can be operated on whilst the patient is cooling, or after the distal repair, whilst the patient is rewarming.