1. AAA Flashcards
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
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
Intra-operatively
Cardiovascular instability
- Induction:
Before aortic cross-clamping
When the clamp is removed
- Large blood losses:
Blood, FFP and platelets required - Effects of massive transfusion
- Temperature control
- Metabolic acidosis
Post-operatively
- Respiratory support may be required for
poor gas exchange and metabolic acidosis. - Cardiovascular complications include
haemorrhage, myocardial
and lower limb ischaemia. - 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). - Neurological sequelae such as paraplegia or stroke may occur secondary to
damaged spinal arteries or embolic/ischaemic events.
What is your immediate management on the ward?
ABC approach – highest FiO2 obtainable should be commenced.
Two large-bore intravenous cannulae should be inserted and fluids given
How much fluid would you use?
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
What else would you do?
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.
What monitoring would you use?
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.
How would you proceed with anaesthesia?
PreInduction / Induction
- Big drips
- All vaso-active drugs should be drawn up prior to induction.
- Blood should be immediately available.
- A method of delivering warmed fluids rapidly and continuously is beneficial
such as a ‘Level-1TM infusor’. - Anaesthetise in theatre on the table
- 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).
How would you proceed with anaesthesia?
Maintenance / Other monitors
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.
Renal protection?
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).
How would you control the hypertension associated with cross-clamping?
- 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.
How would you manage the patient at the end of the operation?
- Intensive care is usually required.
- 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. - Predictors of survival to discharge include patient age, total blood loss and
post-operative hypotension.
Application of an Aortic Cross Clamp
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
increase in preload
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.
Aortic clamp level. Infrarenal.
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