Ruptured abdominal aortic aneurysm
Background
Around two-thirds of patients with a ruptured abdominal aortic aneurysm (AAA) do not reach hospital alive. In-hospital mortality for those patients that do reach hospital is >50%. This is therefore a vascular emergency, and the patient may decompensate dramatically at any time. A number of scoring systems (e.g. Glasgow aneurysm score or the Hardmann index) have been developed to help predict the outcome of surgery following a ruptured AAA.
Learning outcomes
1 Describe the preoperative preparation and immediate anaesthetic management of a patient with a ruptured abdominal aortic aneurysm
2 Interpret point-of-care coagulation testing, and manage clotting dysfunction appropriately
3 Anticipate and manage perioperative myocardial ischaemia in the high-risk vascular patient.
CPD matrix matches
2A05; 2A07
Case history
A 70-year-old retired engineer presents to accident and emergency (A&E) with abdominal pain and a pulsatile mass in his epigastrium. Initial examination confirms that he is alert and orientated, maintaining a patent airway, and has a palpable radial pulse. His HR is 100 bpm, BP 84/60 mmHg, and SpO2 94% on air. His previous medical history includes well-controlled hypertension and type II diabetes mellitus. He lives alone, is self-caring, and enjoys a reasonably active lifestyle, being able to walk up to 2 miles without stopping.
An urgent contrast CT scan is performed and reveals a 6.9 cm infrarenal aortic aneurysm with a large periaortic retroperitoneal haematoma. The AAA is not suitable for endovascular repair. However, given this man’s relatively good health and functional status, it is very likely that he will be offered emergency open aneurysm repair.
You are the on-call anaesthetist who is called to the A&E department to help with his management. What is your initial approach?
Senior anaesthetic help is required and should be summoned immediately. A rapid ABC approach to patient assessment is taken at this stage. Whilst simultaneously stabilizing the patient, the vascular surgical and theatre teams are mobilized. Ideally, two experienced anaesthetists should be available. One anaesthetist should prepare the theatre environment and draw up the appropriate drugs, whilst the other transfers the patient to theatre.
Prior to transfer, at least two large-bore IV cannulae should be inserted; blood should be sent for basic biochemistry, FBC, and coagulation studies, and a 12-lead ECG should be performed. It is imperative that a sample of blood is also sent to the transfusion laboratory for urgent cross-matching. Depending on local hospital protocols, it may be desirable to initiate the ‘major haemorrhage’ protocol at this point. It is best to have red blood cells available in the operating theatre prior to the start of surgery; therefore, if there is any delay in the cross-matching process, O-negative blood should be made available. Almost invariably, FFP and platelet concentrates will be required during surgery, and this should be requested at this early stage. Ten units of red cells, 4 U of FFP, and two pools of platelets are commonly requested quantities.
Having made the diagnosis of a ruptured AAA, it is important that aggressive fluid resuscitation is avoided prior to the start of surgery and the application of an aortic cross-clamp. Unless consciousness is lost or there is evidence of myocardial ischaemia, no IV fluids should be given. This is because large volumes of IV fluids may worsen the haemorrhage by increasing the BP and causing clot disruption. In addition, they may contribute to a dilutional and hypothermic coagulopathy. This practice is referred to as hypotensive resuscitation.
Once the decision for treatment has been made, the patient should be transferred to the operating theatre, fully monitored and with resuscitation equipment available, without delay.
Describe a suitable anaesthetic induction plan for this patient
Prior to the induction of anaesthesia, invasive arterial BP monitoring is desirable. However, this should not delay the start of surgery in very unstable patients. Rapid and significant haemodynamic decompensation can occur, following the induction of anaesthesia. This is caused by a number of mechanisms, including the cardiodepressant and vasodilatory effects of anaesthetic agents, the reduction in tamponade following relaxation of the abdominal musculature, and a reduction in the sympathetic tone. Induction should therefore take place with the patient fully prepared and draped and the surgeons scrubbed and ready for incision. Large-bore IV access should be connected to a primed rapid fluid infusion/warming device. The blood and blood products should be available for immediate use.
The patient is not fasted, and so a modified RSI will be required, with the placement of a cuffed ETT. The exact choice of induction drugs is not of crucial importance. However, drugs that minimize haemodynamic disturbance may be beneficial (etomidate or ketamine). These are often supplemented by opioids (fentanyl, alfentanil, or remifentanil). A dose of suxamethonium will be required to facilitate tracheal intubation. It may be necessary to use vasopressor or inotropic drugs at this point, and a selection of drugs should be prepared in advance (e.g. ephedrine, phenylephrine, adrenaline, calcium gluconate). Anaesthesia is then maintained with either a volatile agent or propofol infusion, ideally guided by a depth of anaesthesia monitor (e.g. BIS) to reduce the likelihood of patient awareness and excessive anaesthetic depth. After the induction of anaesthesia, a CVC should be inserted.
Remember that senior experienced help is required and that good communication between the anaesthetists, surgeons, and other team members is imperative for the smooth running of the case.
The operation begins, and the surgeon manages to clamp the infrarenal aorta. However, there is still ongoing haemorrhage, and the estimated blood loss by this point is 3500 mL. Describe the management of haemorrhage in this case
In emergency aortic surgery, significant blood loss can occur very rapidly. Circulating volume must be maintained with appropriately warmed fluids (crystalloids, colloids, and blood products) administered via large-bore central or peripheral cannulae using a rapid infusion system. Fluid therapy should be guided by the clinical haemodynamic status, CVP, and, if available, cardiac output monitoring. Monitors using pulse pressure or stroke volume variation from arterial waveform analysis can provide a valuable indication of fluid responsiveness and volume status. Where skills exist, transoesophageal echocardiography (TOE) can provide extremely useful information regarding the volume status, in addition to myocardial contractility. It is imperative that the anaesthetists keeps up to date with the volumes of blood lost and fluid infused throughout the procedure.
In a major haemorrhage, a combination of colloids, crystalloids, and blood products will be required. Where available, red cell salvage should be employed, in order to reduce the requirement for allogeneic blood. The patient’s Hb concentration should be monitored regularly using point-of-care monitors (e.g. HemoCue® or an ABG analyser with an inbuilt co-oximeter). This will allow anaemia to be detected rapidly and transfusion to be targeted at an appropriate Hb concentration, typically aiming to maintain above 8 g/L. Tolerance of dilutional anaemia may be associated with an increased risk of myocardial ischaemia or stroke.
It is likely that a coagulopathy will develop due to a combination of consumption (of coagulation factors and platelets) and dilution. Efforts should be made to prevent and treat hypothermia, acidaemia, and hypocalcaemia (that will worsen coagulopathy). Near-patient coagulation monitoring is now frequently used in major vascular surgery. Rotational thromboelastography (TEG®), or thromboelastometry (ROTEM®) allows the rapid diagnosis and targeted treatment of coagulopathy within minutes of a blood sample being taken.
Comment on the following ROTEM® results, and describe an appropriate management
ROTEM® is one of the commonly available forms of rotational thromboelastometry (see Figure 9.1). A citrated blood sample is added, along with reagents which activate the extrinsic (EXTEM) and intrinsic (INTEM) coagulation pathways, to a cuvette in which a pin rotates. The rotational movement of the pin is measured precisely. As clotting begins, increasing resistance to the rotational movement of the pin occurs. This is plotted against time to produce the characteristic ROTEM® trace (see Figure 9.1). A number of parameters can then be measured. In simple terms, clotting time (CT) is the time taken from the start of measurement until the first clot is detected. It represents the speed of fibrin formation and is influenced by the number of clotting factors available. It is prolonged by clotting factor deficiencies. Maximum clot firmness (MCF) is measured at the widest point of the trace. It represents stabilization of the clot by fibrin polymerization and platelet function. It is reduced by fibrinogen and platelet deficiencies.
Fig. 9.1 ROTEM® results obtained after an estimated blood loss of 3500 mL.
The FIBTEM trace is produced by adding a platelet inhibitor to an EXTEM sample; thus, the contribution of platelets to the clot stabilization process is removed, and, by examining the FIBTEM MCF, it can be deduced whether the patient is deficient in platelets (a normal MCF) or fibrinogen (a low MCF) when the EXTEM or INTEM MCF is abnormal.
In the ROTEM® traces from the patient, both the CT is prolonged, and the MCF is reduced in both the EXTEM and INTEM channels, suggesting clotting factor and fibrinogen deficiencies. This diagnosis is supported by the reduced MCF in the FIBTEM. Initial treatment should be with FFP (10 mL/kg). The ROTEM® should then be repeated immediately to assess the effect of this intervention.
What are the adverse effects associated with a massive transfusion?
Transfusion of large amounts of allogeneic blood products can be lifesaving, but they may also be associated with a number of adverse effects:
◆ Biochemical abnormalities: hyperkalaemia, hypocalcaemia
◆ Acidosis
◆ Hypothermia
◆ Coagulopathy
◆ Allergic reactions
◆ Transfusion-associated cardiac overload (TACO)
◆ Transfusion-associated acute lung injury (TRALI)
◆ Transfusion-associated immunomodulation (TRIM).
What are the physiological consequences of aortic cross-clamping and subsequent unclamping?
Cross-clamping of the aorta above the area of rupture is obviously a crucial step in the surgical procedure. Whilst it will dramatically reduce the rate of haemorrhage, it also increases the BP as a result of raising afterload. This abrupt increase in afterload increases the work of the LV, and this is a typical time where myocardial ischaemia can occur. There may also be a short-lived rise in preload, as the effective circulating volume is effectively reduced at this time. Tissues distal to the clamp inevitably become ischaemic during the time that the clamp is in place. Anaerobic metabolism continues in these poorly perfused tissues, with the accumulation of ischaemic metabolites and lactic acid. On release of the clamps, there is a sudden fall in afterload, as the circulation is restored to the pelvis and lower limbs. This commonly produces hypotension, resulting from a number of mechanisms—the volume of the circulation is suddenly restored, and, in addition, lactic acid and ischaemic metabolites are washed into the circulation, causing systemic vasodilatation, pulmonary vasoconstriction, and myocardial suppression. It is important to ensure an adequate preload before unclamping. However, despite this, the BP may require support with fluids and vasoconstrictors/inotropes if there is a marked hypotensive response.
How is intraoperative myocardial ischaemia detected? Suggest appropriate treatments
Myocardial ischaemia is detected by performing ST segment analysis of the ECG. Any significant depression or elevation of the ST segment can signify ischaemia. Ideally, a 5-electrode ECG should be used, with two limb leads plus one chest lead being monitored to increase the sensitivity of the test. If TOE is available, new ventricular wall motion abnormalities can indicate ischaemia.
If ischaemia is detected, efforts should be made to optimize oxygen delivery (e.g. by ensuring adequate oxyhaemoglobin saturation and correcting anaemia and hypotension). Attempting to reduce myocardial oxygen consumption may also be appropriate in some circumstances—with a β-blocker if the HR is high, or using vasodilator therapy if there is marked hypertension. Short-acting drugs, such as esmolol and GTN, are ideal in this situation.
How should this patient be cared for in the immediate post-operative period? What are the main issues following surgery for a ruptured abdominal aortic aneurysm?
All patients will require intensive care post-operatively. Careful monitoring of all organ systems is mandatory, as multiple organ dysfunction is possible. In the immediate post-operative period, efforts should be made to re-warm the patient, treat any residual coagulopathy that exists, and correct any acid–base disturbance. Ventilatory support will be required for a variable period of time (a few hours to days), whilst cardiovascular support and renal replacement therapy will be required for some patients. Intra-abdominal hypertension is common after surgery for a ruptured AAA. Ideally, the intra-abdominal pressure should be monitored to identify those patients who are developing abdominal compartment syndrome.
Summary
A ruptured AAA is a vascular surgical emergency that is associated with significant morbidity and mortality. Optimal care requires excellent communication between the different professional groups involved at each stage of the treatment process.
The anaesthetist caring for the patient with a ruptured AAA needs to be aware of the potential for profound haemodynamic instability, myocardial ischaemia, coagulopathy, and marked acid–base disturbance. It is crucial that appropriate treatments are instituted in a timely fashion to minimize the impact of these factors.