1. AAA

Question 1

You are called to the ward to see a 74-year-old man with a ruptured
aortic aneurysm. His blood pressure is 70/40.

What are the major problems in managing a ruptured AAA?

Preoperatively

Answer 1

Pre-operatively

Severe hypovolaemia

Initial fluid resuscitation must be cautious

Assessment of concomitant medical problems

Patients are usually ‘arteriopaths’ with significant coronary disease

No time for lengthy investigations

Access to vascular surgery – may need to transfer out

Question 2

Intra-operatively

Answer 2

Cardiovascular instability

1. Induction:
   Before aortic cross-clamping

When the clamp is removed

2. Large blood losses:
   Blood, FFP and platelets required
3. Effects of massive transfusion
4. Temperature control
5. Metabolic acidosis

Question 3

Post-operatively

Answer 3

1. Respiratory support may be required for
   poor gas exchange and metabolic acidosis.
2. Cardiovascular complications include
   haemorrhage, myocardial
   and lower limb ischaemia.
3. Renal failure is common due to
   peri-operative hypotension,
   aortic cross-clamping
   (infra-renal clamp still significantly reduces renal blood flow by about 40%),
   atheromatous emboli,
   surgical insult,
   intra-abdominal hypertension (>12mmHg) or compartment syndrome (>20 mmHg).
4. Neurological sequelae such as paraplegia or stroke may occur secondary to
   damaged spinal arteries or embolic/ischaemic events.

Question 4

What is your immediate management on the ward?

Answer 4

ABC approach – highest FiO2 obtainable should be commenced.

Two large-bore intravenous cannulae should be inserted and fluids given

Question 5

How much fluid would you use?

Answer 5

This would depend on the blood pressure and
the clinical state of the patient.

A patient who has an unrecordable blood pressure
and is about to arrest should be given fluids quickly,

but in this man fluids should be given cautiously.

Repeated 250 ml fluid boluses titrated to physiological endpoints
(consciousness, base deficit, lactate) should be used.

One should not necessarily aim to restore blood pressure to ‘normal’ as this may reverse
vasoconstriction and disrupt fibrin clots that were contributing to haemostasis

Question 6

What else would you do?

Answer 6

Take blood for
full blood count,
urea and electrolytes,
clotting screen,
blood gas.

Cross-match for 10 units,
consider type O-negative or group-specific blood.

Second anaesthetist (preferably consultant) is required.

Haematology should be alerted to the need for
large volumes of blood, FFP and platelets.

An assessment of co-existing medical problems and the likelihood of
difficult intubation should be made.

Do not delay surgery whilst awaiting lengthy investigations.

Transfer the patient to the operating theatre as soon as possible.

Only haemodynamically stable patients can be taken for CT scanning to
diagnose rupture and assess suitability for open or endovascular repair.

Question 7

What monitoring would you use?

Answer 7

ECG, non-invasive BP, SpO2 and capnography initially.

Surgery should not be delayed by
prolonged attempts to insert arterial and central lines at this stage.

Question 8

How would you proceed with anaesthesia?

PreInduction / Induction

Answer 8

1. Big drips
2. All vaso-active drugs should be drawn up prior to induction.
3. Blood should be immediately available.
4. A method of delivering warmed fluids rapidly and continuously is beneficial
   such as a ‘Level-1TM infusor’.
5. Anaesthetise in theatre on the table
6. A rapid sequence induction is performed with the surgeon scrubbed and
   the patient already cleaned and draped
   (muscle relaxation may release the tamponade on the aorta
   worsening bleeding and the combined effects of
   induction agents and IPPV can cause profound hypotension).

Question 9

How would you proceed with anaesthesia?

Maintenance / Other monitors

Answer 9

Anaesthesia is maintained with an appropriate agent in oxygen/air.

Avoid nitrous oxide because bowel distension may increase intra-abdominal
pressure post-operatively.

When the cross-clamp is on and there is ‘relative’ stability, invasive lines may
be inserted if not already in place.

Temperature probe

Nasogastric tube

Urinary catheter

Active warming such as with a warm air blower over the chest helps to
maintain temperature, but should be avoided on the legs during
clamping.

Question 10

Renal protection?

Answer 10

Loop diuretics (e.g. furosemide), dopamine, mannitol, fenoldapam and
N-acetylcysteine have been proposed as renoprotective agents.

There is no Level 1 evidence to support their use.

The mainstay of renal preservation is maintenance of
renal oxygen delivery and the avoidance of nephrotoxins

(e.g. non-steroidal anti-inflammatory drugs,
angiotensin-converting enzyme inhibitors,
contrast and aminoglycosides).

Question 11

How would you control the hypertension associated with cross-clamping?

Answer 11

1. SVR may rise by up to 40% resulting in myocardial ischaemia.

2 .If increasing the inspired volatile concentration and giving opioid and/or propofol are not
effective,
then GTN can be used, especially if myocardial ischaemia is present.

Question 12

How would you manage the patient at the end of the operation?

Answer 12

1. Intensive care is usually required.
2. Sedation and ventilation may need to be continued until the temperature is
   corrected, cardiovascular stability is established and acid/base status and gas
   exchange are acceptable.
3. Predictors of survival to discharge include patient age, total blood loss and
   post-operative hypotension.

Question 13

Application of an Aortic Cross Clamp

Answer 13

Cardiovascular effects: increased afterload

an immediate increase in afterload,
with a sudden increase in proximal arterial blood pressure,

a reflex increase in myocardial contractility (the Anrep effect)

concomitant increase in myocardial oxygen demand

This may partially be offset by increased
coronary blood flow (depending on the patency of the coronary circulation) and a
decrease in heart rate mediated by baroreceptors.

increase in preload

Question 14

increase in preload

Answer 14

There is also an increase in preload,

which is attributed both to the passive elastic recoil of arterial vessels distal to the
clamp that effectively autotransfuses blood into the venous circulation and to

sympathetic vasoconstriction in the splanchnic bed which occurs in response to
the effective hypovolaemia and which can redistribute as much as 800 ml of blood
centrally.

This manifests as an increase in left ventricular end diastolic volume and pressure. If renal afferent arteriolar perfusion pressure falls, there is activation of the
renin-angiotensin system with increased renin production. This appears to occur
even if the clamp is infrarenal.

Question 15

Aortic clamp level. Infrarenal.

Answer 15

with the least haemodynamic instability.

Afterload increases only by around 5–7%,
and a heart with reasonable left
ventricular function is relatively unaffected

patient does have ischaemic heart disease, then they may develop
significant ventricular wall motion abnormalities

ventricle dilates, an increase in wall tension may initiate a vicious cycle
of increased myocardial oxygen demand
and the potential for further ischaemia

Question 16

Suprarenal/infracoeliac.

Answer 16

the clamp is
applied more proximally at a suprarenal but infracoeliac level, the increase in afterload
is more marked, with a rise in mean arterial pressure (MAP) of up to 10%.

Question 17

Supracoeliac.

Answer 17

If the clamp is supracoeliac, however, MAP can increase by more than
50% with a 35–40% decrease in left ventricular ejection fraction

Question 18

Descending thoracic aorta

Answer 18

. At even higher levels of cross clamping, such as in the descending thoracic
aorta, MAP can rise by 80% and central venous pressure by 35%. These changes may
partly be attenuated in those patients who have occlusive aortic disease and who may
have developed a collateral circulation.

Question 19

Associated complications

Answer 19

1. myocardial ischaemia as described previously,
2. distal arterial occlusion secondary to embolic plaques of atheroma which can
   be dislodged as the clamp is applied
3. ischaemia of the spinal cord
4. 0.2% for elective procedures involving an
   infrarenal clamp, from 5–8% for elective and as high as 40% after emergency thoracic
   aneurysm repair
5. Suprarenal clamps are associated with acute kidney injury. All of these problems
   increase with the duration of cross-clamp time.

Question 20

Release of an Aortic Cross Clamp

Answer 20

qualitatively the same as those that follow any situation in which a previously ischaemic area is reperfused

depending on the duration of
ischaemia, which in a difficult aneurysm repair may be prolonged.

Question 21

Haemodynamic changes

Answer 21

anaerobic metabolism in the ischaemic areas generates
significant vasoactive metabolites,

including hydrogen ions,
lactate
potassium.

Once these enter the general circulation,
they mediate a significant fall in peripheral vascular resistance.

fall by as much as 70–80% with a concomitant
drop in blood pressure of 40–60%.

Question 22

BP drop

Answer 22

effective hypovolaemia
(distal blood flow can increase fourfold with the sequestration of blood in reperfused
tissues) as well as to the direct myocardial depressant effects of cytokines and other
molecules

Coronary blood flow and left ventricular end diastolic volume can drop by
50% unless measures are taken to preempt the problem. Arrhythmias may accompany
the transient hyperkalaemia.

Question 23

Attenuation of Haemodynamic Insults

Answer 23

Application of clamp.

Attenuation of the increase in afterload can be achieved using
a venodilator such as glyceryl trinitrate (GTN at a starting rate of 0.5 μg kg1 min1),

by increasing the inspired concentration of volatile anaesthetic or both.

Some anaesthetists use opioids,
but these are more difficult to titrate against response
and depending on the agent used may still be exerting an effect when the clamp is
released.

The increased capacitance proximal to the clamp also allows a degree of
fluid loading to prime the system.

Question 24

Release of clamp.

Answer 24

Any vasodilator infusion should be stopped in advance.

Depending on the height of the clamp and its duration,

rapid fluid administration will usually be needed to mitigate the problem of functional hypovolaemia.

Vasopressors can be effective, but only in the presence of adequate fluid resuscitation.

In theory, an increase in alveolar ventilation may partially offset the induced metabolic
acidosis, although this is not routine.