Abstract
The incidence of ruptured abdominal aortic aneurysm (rAAA) has been reduced by a national screening programme targeting early identification and treatment of aneurysms. Despite these efforts, rAAA remains a common anaesthetic and surgical emergency responsible for over 5000 deaths per year in the UK. rAAA leads to complex multiorgan critical illness which requires immediate multidisciplinary collaboration and intervention. Anaesthetists play a key role in resuscitation, coordination of care and managing major haemorrhage and multi-organ sequelae of a ruptured aorta. In this article, we describe an overview of the risk factors, current guidelines, service organization, and treatment for rAAA; with focus on the perioperative anaesthetic considerations for open aneurysm repair and endovascular aneurysm repair.
After reading this article you should be able to:
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outline the risk factors for abdominal aortic aneurysm (AAA) and their rupture
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discuss the guidance on transfer of patients with ruptured AAA (rAAA), and the different treatments offered
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explain the preoperative, intraoperative and postoperative anaesthetic considerations for rAAA repair
Introduction
Ruptured abdominal aortic aneurysm (rAAA) is a life-threatening emergency which carries a mortality rate approaching 100% in the absence of appropriate treatment. rAAAs are responsible for between 5000 and 6000 deaths in the UK every year. Approximately 50% of patients die before reaching hospital, and the patients that survive to reach hospital face mortality rates of around 40%. An urgent multidisciplinary approach by an experienced team is required to provide life-saving interventions that meet the complex needs of these patients.
Pathophysiology, epidemiology and risk
An abdominal aortic aneurysm (AAA) is a dilatation of greater than 50% of the expected diameter of the aorta; thus a normal aortic diameter of 2 cm becomes diagnostic for aneurysm at ≥3 cm. AAAs are usually classified according to their antero-posterior diameter and their location relative to the renal arteries; this can be infra-renal, juxta-renal or supra-renal, with 80% occurring in the infra-renal position, between the renal arteries and the aortic bifurcation.
The prevalence of AAA ranges from 3% to 8% according to various national screening programmes, with higher incidence in males and those aged over 60 years.
Recognized risk factors for the development of AAA are listed in Table 1 .
| Main risk factors | Additional risk factors: related to pathophysiology of atherosclerosis |
|---|---|
| Male gender Increasing age (>60 years) | Current or previous smoking history (and chronic obstructive pulmonary disease) Hypertension Hyperlipidaemia Existing vascular disease (coronary, cerebrovascular or peripheral vascular disease Genetic factors – AAA in a first-degree relative, connective tissue disorders (Ehlers–Danlos syndrome and Marfan’s syndrome) |
According to these risk factors, in the setting of an ageing population, the prevalence of AAA is expected to rise, however this may be offset by declining rates of cigarette smoking.
AAAs continue to increase in size over time, however the rate at which this occurs is highly variable. The risk of rupture increases as the diameter of the aneurysm increases (see Table 2 ). Rupture of an AAA occurs when the mechanical stress and pressure acting on the aneurysmal aortic wall exceeds the tensile strength of the aortic wall tissues. While the diameter of the aneurysm is the predominant risk factor used to guide clinical management, it is further complicated by factors such as the geometry of the aneurysm, the presence of intraluminal thrombus, the thickness of the aortic wall and the extent of calcification and inflammation.
| Diameter of AAA | Annual rupture risk | Additional risk factors for rupture |
|---|---|---|
| <4 cm | 0% | Rate of expansion (>0.5 cm in 6 months) |
| 4–4.9 cm | 0.5–5% | Continued smoking |
| 5–5.9 cm | 3–15% | Uncontrolled hypertension |
| 6–6.9 cm | 10–20% | Female sex associated with higher risk of rupture for a given diameter AAA |
| 7–7.9 cm | 20–40% | |
| ≥8 cm | 30–50% |
Screening and centralization of care
Due to the high mortality rate associated with rAAA, efforts to improve mortality have focused on prevention of rupture (via a national screening programme to identify and treat aneurysms earlier) and centralization of care to high-volume centres of excellence.
The NHS AAA Screening Programme has been fully implemented since 2013 and consists of an ultrasound scan being offered to all men during the year they turn 65. Ultrasound imaging of the abdominal aorta is quick, cheap, non-invasive, does not involve ionizing radiation and is highly sensitive and specific. For people with an aneurysm of 3–4.4 cm an annual follow up scan is offered. For people with an aneurysm between 4.5 cm and 5.4 cm, a scan every 3 months is offered. Patients with an aneurysm over 5.5 cm are referred to a regional vascular service for review within 2 weeks.
Patients receiving treatment for AAA in a high-volume centre have been shown to have better outcomes in terms of mortality and length of stay. This applies to both elective AAA repair and rAAA repair and has led to centralization of services, with a ‘hub’ and ‘spoke’ model, with central ‘hubs’ being larger centres undertaking a high case load with outreach to peripheral ‘spoke’ hospitals. A suspected rAAA patient should ideally be brought directly to a specialist hospital, similar to patients experiencing stroke or myocardial infarction, however if they are initially taken to a different hospital first, before transfer to the specialist centre, the mortality benefits of centralization should outweigh the negative effects of a small delay of up to an hour.
Clinical presentation
Symptoms of rAAA include abdominal pain, back pack pain, sweating, agitation and collapse. Clinical signs of rAAA include pallor, hypotension, tachycardia, a pulsatile abdominal mass and signs of acute lower limb ischaemia. Patients that survive to reach hospital are more likely to have a retroperitoneal haemorrhage with some tamponade effect; while intra-peritoneal rupture is more likely to cause cardiovascular collapse and death.
Diagnosis, initial management and emergency medicine guidance
As per the Royal College of Emergency Medicine (RCEM) best practice guidelines, clinical diagnosis of rAAA should be considered in:
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Patients >50 years with acute onset of abdominal/back pain AND hypotension
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Patients with a known AAA, with symptoms of either abdominal/back pain OR hypotension/collapse
Additional investigation with CT scan to confirm or exclude the diagnosis of rAAA is required for patients with alternate presentations. In haemodynamically stable patients a CT angiogram confirms the diagnosis and aids with treatment planning, ideally this is performed at the specialist centre or the images are transferred there electronically.
If specialist vascular services are not available at the location of presentation, the patient requires transfer to an appropriate centre. The most senior doctor available should lead this process in order to expedite transfer and reduce delay.
Pre-existing systemic disease and current clinical status (conscious level and blood pressure) should be used to guide decisions on suitability of transfer. Table 3 outlines RCEM guidelines on criteria for transfer.
| Age <85 years without severe systemic disease | Refer immediately to the regional on-call vascular service |
| Age >85 years or with severe systemic disease | Consultant to consultant discussion prior to transfer |
| Cardiac arrest in the current admission Requirement for intubation due to deterioration Requirement for inotropic support | Contraindications to transfer due to poor outcome This cohort of patients are considered unlikely to survive transfer and surgery |
Initial resuscitation during this period should achieve an alert patient & the overall aim is to:
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avoid hypotension (associated with increased mortality)
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avoid hypertension (could disrupt clot formation, targeting a systolic blood pressure 90–120 mmHg).
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transfer should occur <30 minutes of diagnosis and is normally to the receiving hospital’s emergency department resuscitation area.
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Transfer should not require blood products unless already commenced.
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Patients should not be anaesthetized for transfer or imaging as the associated loss of tone and sympathetic drive can result in irreversible cardiovascular collapse.
Management options
- 1.
Open surgical repair
- 2.
Endovascular repair
- 3.
Conservative management
Open aneurysm repair (OAR) versus endovascular aneurysm repair (EVAR)
In the context of rAAA, open aneurysm repair (OAR) and endovascular aneurysm repair (EVAR) were compared in the IMPROVE randomized control trial. The 30-day and 90-day mortality was similar in patients undergoing either EVAR or OAR. At 3 years, EVAR offered a survival advantage (42% vs 54% mortality for OAR) and a gain in quality adjusted life years over OAR. However, by 7 years, there was no clear difference between EVAR and OAR.
Secondary outcome benefits that were identified in favour of EVAR included cost effectiveness and a shorter hospital stay with greater chance of discharge directly home. This may be related to the avoidance of laparotomy incision, reduced tissue damage and handling, reduced blood loss and the potential for shorter procedure time and avoidance of general anaesthesia. The National Vascular Registry Annual Report 2022 identified in-hospital mortality rates of 20.7% for EVAR and 44.2% for OAR for the 2019–2021 period. However, the report cautions against comparing these findings, because the OAR group may represent a more complex patient cohort not suitable for EVAR.
Limitations of EVAR may include availability of services, aneurysm characteristics (length, neck angulations, proximal and distal landing zones, presence of thrombus) and vascular access.
UK National Institute for Health and Care Excellence guidelines recommend EVAR or OAR for rAAA with the following considerations:
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EVAR provides more benefit than OAR for most people, especially women and men >70
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OAR is likely to provide better risk-benefit profile in men <70
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Do not offer complex EVAR for rAAA when OAR is suitable, except as part of a trial.
Predicting outcomes for rAAA
There is insufficient evidence to recommend the use of a single sign, symptom, risk factor or scoring system to decide if aneurysm repair is suitable or to predict outcome of an intervention for a person with rAAA. Thus, decisions regarding suitability of intervention versus palliation is made by the vascular surgeon, often with input from the radiologist and anaesthetist.
Clinical management
Preoperative considerations
Once rAAA with intention to treat is confirmed, initial anaesthetic priorities are patient assessment alongside resuscitation and good communication to prepare theatre and achieve timely multi-disciplinary input.
Initial assessment takes place in the emergency department or en-route to theatre depending on urgency of the situation as it can rapidly deteriorate to cardiovascular collapse. Prompt transfer to theatre with required personnel and resources is of utmost importance.
A focused history and assessment should identify:
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Allergies and medications – elucidate presence of anticoagulant and antiplatelet agents which will exacerbate haemorrhage and may require advice from a haematologist to reverse their coagulopathic effects
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Past medical history – identify comorbidities associated with atherosclerotic disease; ischaemic heart disease, heart failure, renal impairment, smoking history, respiratory disease, and cerebrovascular disease).
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Functional status – estimated with the use of metabolic equivalents of task (METs) and clinical frailty scale.
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Clinical assessment – assess airway for any anticipated difficulty, current cardiorespiratory status and signs of end organ dysfunction. Check for IV access, blood samples sent and if blood transfusion already started. Ensure blood products are available to administer during transfer to theatre if signs of haemodynamic compromise; this may require activation of major haemorrhage protocol
Initial treatment of cardiovascular disruption requires a balanced approach. The heart rate, respiratory rate, blood pressure (check in both arms, and use the higher of the two readings), capillary refill time, level of consciousness, acidosis and lactate can be used to approximate the extent of blood loss and volume status.
Where volume replacement is indicated by evidence of shock with end organ dysfunction, early balanced use of blood products, with packed red cells, fresh frozen plasma (FFP) and platelets used in a 1:1:1 ratio is advised. Fluid resuscitation with crystalloid will dilute clotting factors, increase blood pressure and destabilize clot formation. Significant hypertension can be treated with titrated short-acting analgesics (such as fentanyl 12.5–25 micrograms, where pain is the causative factor) or short-acting β-blockade or vasodilators.
Conversely, periods of hypotension (systolic pressure <70 mmHg) are associated with increased mortality. Current guidance targets a systolic blood pressure of 90–120 mmHg or an alert patient.
Table 4 outlines the steps required to prepare for induction of anaesthesia.
| Two large bore IV access (14G or best possible) should be obtained and connected to rapid infuser Blood samples sent for:
| Ensure availability of:
|
Drugs for induction:
|
Induction
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Initial monitoring before induction of anaesthesia should consist of ECG, pulse oximeter, non-invasive blood pressure, alongside anaesthetic machine monitoring; consisting of gas analysis and pressure monitoring.
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Arterial cannulation for continuous invasive blood pressure monitoring is desirable but should not delay surgery.
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Central venous access can usually be deferred initially, unless there is no alternative intravenous access. A urinary catheter can be sited before induction.
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During induction of anaesthesia, fluid and/or blood should be administered, a rapid infusion device prepared and ready to give additional boluses as needed, alongside vasoactive drugs (metaraminol, ephedrine, adrenaline, noradrenaline) in anticipation of cardiovascular collapse.
Considerations for OAR
The induction of anaesthesia risks cardiovascular collapse due to the loss of sympathetic drive, loss of muscle tone, cardiodepressant effects of anaesthetic agents and reduction in venous return with positive pressure ventilation. For this reason, induction occurs on the operating table, with the patient prepared and draped and surgeon scrubbed ready to start and place a proximal aortic clamp as soon as possible once the patient is intubated.
A rapid sequence induction is usually indicated for induction of anaesthesia, with a focus on choosing drugs that offer cardiovascular stability along with fluid boluses. An opiate, such as fentanyl or alfentanil, is often used to reduce the dose of induction agent. The drug(s) used for induction vary, with no agent superior, a titrated dose of ketamine, propofol or thiopentone can be used if blood pressure is stable. Muscle relaxation is achieved with either rocuronium or suxamethonium.
Intraoperative considerations are outlined in Table 5 .
| Establish invasive monitoring |
|
| Temperature |
|
| Maintenance of anaesthesia and depth of anaesthesia monitoring |
|
| Cardiac output monitoring |
|
| Haemodynamic goals |
|
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