Abdominal Aorta Aneurysm Flashcards

1
Q

Risk factors

A

initial diameter
- expansion rate
- smoking/COPD
- family hisory
- shape and wall stress
- hypertension
- gender (women)
** 4-6cm expand 10% per year
** expansion > 1cm/year indication for elective repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Risk of rupture

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Management options

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Conservative mx

A

Non-surgical, conservative:
- reduce modifiable risk factors
i) Smoking cessation can slow down aneurysmal growth by 15–
20% and decrease perioperative morbidity relating to wound
healing and cardiorespiratory complications.
- statins (reduce perioperative MI and alter anaeurysm growth)
- low dose aspirin
- high CVS risk = B-blockers, ACE-i

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Surgical management
- open
- endovascular (EVAR)
- laparoscopic
- choice depends on aneurysm morphology

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Open vs EVAR

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
A

COMPLICATIONS
- postoperative pulmonary complications (pneumonia, atelectasis)
- MI
- arrythmias
- stroke
- postoperative cognitive dysfunction, delirium
- AKI
- acute tubular necrosis
- ureteral injury
- bowel ischaemia
- abdominal compartment syndrome
- spinal cord ischaemia
- bleeding
- wound dehiscence
- incisional hernia
- DVT/PE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Endoleak

A

Endoleak is defined as persistent blood flow outside an endovascular graft, but within the aneurysm sac

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
A

POST-IMPLANTATION SYNDROME:
- fever
- raised CRP, white cells in the abscence of infection
- lasts 2-10 days
- Rx: NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Advantage and disadvantages of EVAR

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Define

A

An aortic aneurysm is a permanent dilatation
(.30 mm) anywhere along the path of the
aorta (ascending, arch, thoracic, or abdominal).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Male vs female AAA

A

Women are less likely
to develop AAA than men of similar age.
However, if an AAA has developed, women
have an increased risk of aneurysm rupture and
a higher mortality rate, especially where there
is coexisting cardiovascular morbidit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Ethnicity differences

A

Epidemiological data in-
dicate that there is a decreased prevalence of
AAA in Black and Asian ethnic groups com-
pared with Caucasians.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
A

(i) local elastin resorption caused by increased
elastase activity;
(ii) localized wall inflammatory changes;
(iii) increased protease activity;
(iv) mural thrombus formation in the arterial
wall and plasminogen activation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
A

The annual risk of rupture for large
AAA 5.5 cm in diameter is 18% in women
[95% confidence interval (CI), 8–26%] and
12% in men (95% CI, 5–20%).
Reduced expansion rates are seen in patients with diabetes mellitus.
The risk of aneurysm rupture increases in
a non-linear fashion when aneurysms expand; the risk of rupture becomes clinically significant
when the aneurysm diameter reaches 5 cm, but there is considerable variation between pub-
lished studies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q
A

Abdominal ultrasound is
the first-line imaging tool in the diagnosis andsurveillance of AAA with a detection specificity and sensitivity of
almost 100%.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

The UK Small Aneurysm Trial and the Aneurysm Detection and
Management Study (ADAM–US)

A
19
Q

The UK Small Aneurysm Trial and the Aneurysm Detection and
Management Study (ADAM–US)

A
20
Q
A

Clamp application increases the afterload of the heart and a
sudden increase in arterial pressure proximal to the clamp

21
Q
A

this can
be attenuated with vasodilators [e.g. glyceryl trinitrate (GTN),
sodium nitroprusside], opioids, or deepening of anaesthesia. These
measures may also allow fluid loading in preparation for clamp
release; however, the effect of vasoactive drugs is unpredictable;
they may change haemodynamics without improving cardiac
output and tissue perfusion due to blood redistribution.10

22
Q
A

Increased afterload and left ventricular end-diastolic volume
both increase myocardial contractility and oxygen demand. This
increase in myocardial oxygen demand is usually met by an in-
crease in coronary blood flow and oxygen supply, but can cause
myocardial ischaemia

23
Q
A

Strategies to manage hypotension after aortic cross-clamp
release include gradual release of the clamp, volume loading,
vasoconstrictors, or positive inotropic drugs (e.g. ephedrine,
meteraminol, phenylephrine, epinephrine, and norepinephrine). It is
important to be aware that vasoactive drugs should only be used after
adequate volume repletion.10 Management of aortic cross-clamp
application and release requires excellent communication with the
surgeon in order to anticipate and manage the physiological effects.

24
Q
A

Monitoring
Minimum standard monitoring should be placed before induction
of anaesthesia. A five-lead ECG is more sensitive in detecting
myocardial ischaemia. Invasive arterial pressure monitoring should
be established before but central venous access is usually secured
after induction of anaesthesia. Urinary catheterization and tempera-
ture monitoring should be initiated. Different cardiac output moni-
toring strategies have their limitations and may respond slowly to
haemodynamic changes with aortic cross-clamp application and
release. Oesophageal Doppler uses flow velocity in the aorta to
calculate cardiac output and is unreliable when the aorta is
clamped. Pulse wave contour analysis cardiac output and other
monitors are gaining popularity, but their use has not yet been
fully evaluated in aortic surgery.

25
Q
A

Anaesthetic management focuses on the acute haemodynamic
changes with aortic cross-clamping and unclamping, maintaining
organ perfusion and oxygenation, attenuating ischaemic reperfu-
sion injury, and providing intra- and postoperative analgesia.
Anaesthesia is usually maintained by a balanced volatile/opioid
technique (fentanyl, remifentanil, morphine).

26
Q
A

A thoracic epidural catheter is usually placed before induction
of anaesthesia at a level corresponding to the upper dermatomal
level of the incision (usually T8–T10) for postoperative analgesia.
Stability during induction of anaesthesia must be maintained,
avoiding massive swings in arterial pressure and heart rate.
Tracheal intubation and artificial ventilation is routine practice, a
ventilator capable of administering PEEP is preferable. Antibiotic
prophylaxis should be administered within 30 min of skin incision.

27
Q
A

Intraoperative analgesia can be provided using opioids or by
using epidural analgesia; however, high doses of epidural local
anaesthetics can cause profound hypotension after aortic cross-
clamp release due to sympathetic blockade. It is common practice
to limit epidural local anaesthetic administration until after cross-
clamp release and haemostastis has been achieved.

28
Q
A

Heparin 75–150 units kg21 is given i.v. before aortic cross-
clamp application. Activated clotting time can be used to guide
heparin therapy (2–3 times more than baseline). Cell salvage
equipment should be used when available. Serial arterial blood gas
samples are usually analysed to monitor respiratory and metabolic
status. Facilities for the rapid infusion of warm fluids and blood
should be available for immediate use. All efforts should be made
to maintain normothermia; however, lower body warming during
aortic cross-clamp application is discouraged.

29
Q
A

The hypertensive response seen with aortic cross-clamp appli-
cation can be managed by an infusion of short-acting vasodilators
(e.g. GTN), increasing the administered dose of inhalation anaes-
thetic agents or by administering i.v. opioids. The mean arterial
pressure should be maintained within the autoregulation limits of
vital organs. In preparation for aortic unclamping, vasodilators can
be weaned down with adequate fluid loading. Vasoconstrictors and
positive inotropic drugs should be available for immediate use.

30
Q
A

Haemoglobin should be maintained .9–10 g dl21 as IHD is
common in these patients. Blood products (FFP, platelets, and
cryoprecipitate) are usually given according to the clinical need
when haemostasis is secured and aortic cross-clamp is removed.
Thromboelastography testing can be used to monitor and help to
manage coagulopathy. Fluid loading while the aortic cross-clamp
is applied is usually achieved using crystalloids and colloids.
While the limitations of central venous pressure (CVP) as a
measure of intravascular volume are increasingly recognized, it is
common practice to titrate fluids to maintain a CVP of 12–15
cm H2O before cross-clamp release. Other monitors or measures of
cardiac output or fluid responsiveness may also be used, although
few specific data are available in aortic surgery.

31
Q

Organ protection general measures

A

GENERAL PRINCIPLES
- maintain good oxygen saturation
- haemoglobin concentration
- blood flow

32
Q
A

MYOCARDIAL PROTECTION
- maintain myocardial O2 supply, minimise demand
- avoid tachycardia and hypotension
- vasodilators: reduce LV end diastolic volume —> decrease wall tension, contractility —> improve
endocardial perfusion

33
Q
A

RENAL
- decreased renal blood flow
- decreased renal perfusion pressure
- increased renal vascular resistance
- myoglobin release from ischaemic tissues
- ischaemic-reperfusion injury
- decreased renal cortical blood flow
- prostaglandin imbalance
- increaed renin-angiotensin activity
- contrast
Strategies:
- maintain euvolemia
- maintain renal blood flow and perfusion with adequate MAP
- avoid nephrotoxins
- glycemic control
- N-acetylcysteine (CIN)
- limit duration of AOXC

34
Q
A

there must be minimal atherosclerotic plaque inside the neck so that a good seal between the stent graft and the wall of the aorta can be obtained.

35
Q
A

Distally, there must be disease-free zones in the iliac arteries to ensure good leg perfusion and at least one of the femoral arteries should be >8 mm in internal diameter.This is to enable insertion of the stent through the arteriotomy. (Acollapsedstent grafthasan external diameter up to 7.5 mm.)

36
Q

Classification

A
37
Q
A

Anumberofinterventionscanbeusedtoreducetheriskof spinal cord ischaemia, including sequential clamping of the aorta with reimplantation of intercostal and lumbar segmental vessels, drainage of CSF to maintain SCPP, and the use of neurophysiological monitoring

38
Q

CSF drainage

A

Spinal cord perfusion pressure is represented as SCPP¼MAPeCSFP Insertion of a CSF drainage catheter to augment CSFP aids in the maintenance of an adequate SCPP, an intervention found to reduce the incidence of postoperative neurological deficits by80%.17CSFPismaintainedat10e15mmHg,andCSF is drained to maintainthis at rates up to20mlh1.Monitoring of CSFP and drainage continue for up to 72 h after surgery. An SCPP target of 70 mm Hg is used in most centres, requiring a CSFP of less than 15 mm Hg and a minimum MAP of 80 mm Hg; this target may require infusion of a vasopressor, such as noradrenaline (norepinephrine). Where it is not possible to maintain the CSFP below 15 mm Hg through CSF drainage, the MAP must be augmented further. Where there is evidence of spinal cord ischaemia, the SCPP and MAP target can be increased in 5 mm Hg increments.9 The spinal drain consists of a transduced intrathecal catheter inserted at the level ofL3e4orL4e5toreducetherisk of direct spinal cord damage, although there are risks associated with their placement.18 Complications include spinal headache,neuraxialhaemorrhageorhaematoma,meningitis, intracranial hypotension, and catheter fracture

39
Q

Neurophysiological monitoring

A

With normal metabolism in the context of no perfusion, cell death occurs within 3e5 min. Neurophysiological monitoring withsequential clampingoftheaortaidentifieskeyvesselsfor spinal cord perfusion that must be reimplanted, and helps to ascertain the minimum acceptable MAP for adequate spinal cord perfusion. Monitoring of neurological function can be achieved with the use of motor-evoked potentials (MEPs) or somatosensory-evoked potentials (SSEPs). Motor-evoked potentials monitor the activity in the anterior spinal cord where the descending motor pathways travel. Stimulation of the motor cortex is via subdermal electrodes, and recordings of muscle contractions are collected peripherally. Paraplegia caused by spinal cord ischaemia significantly dampens the lower-limb potentials when compared to those of the upper limb. MEPs disappear in the presence of neuromuscularblockingagents,andvolatileanaestheticsalso cause dose-dependent depression of the MEP at doses within the range used in clinical practice.19 Total i.v. anaesthesia is preferred if MEPs are to be used. SSEPs, although less frequently used, allow monitoring of the posterior ascendingsensory columns, and are not affected by neuromuscular blocking agents or volatile anaesthetic agents. A decrease in MEP amplitude greater than 50% should prompt reinsertion of intercostal arteries into the graft along with measures to improve spinal cord perfusion.20 A MAP exceeding 80 mm Hg and distal aortic pressure exceeding 60 mm Hg are targeted. Haemoglobin concentration should be maintained at or above 100 g L1.CSF maybedrainedat20ml h1.21 The decision for surgical intervention is usually made within 3e5 min of the change in the neurophysiological variables.

40
Q

Haemostasis

A

Peri- and postoperative bleeding occurs commonly. Antifibrinolytics, such as tranexamic acid, aminocaproic acid, or aprotinin, are administered. Cell salvage should be used routinely. On separation from CPB, protamine is used to reverse the residual effects of heparin, and blood products are given as indicated by point-of-care coagulation tests. Blood products may be fresh frozen plasma, cryoprecipitate, and platelets, or, more recently, prothrombin complex and f ibrinogen concentrates. Further transfusions are guided by the results of repeated tests. In cases of ongoing bleeding, the use of recombinant factor VIIa has been advocated.

41
Q

Postoperative management

A

Sedation and analgesia Sedation is maintained in the postoperative period.
Agents utilised vary between units, but ultimately, minimal sedation with intermittent sedation holds should be used to allow assessment of neurological function.
Where there has been disruption to cerebral blood flow, there is an increased incidence of neurocognitive dysfunction, potentially influencing the timing of emergence from the effects of sedative drugs. The extensive surgical incision leads to significant pain that can impair weaning from sedation and artificial ventilation.
A multimodal analgesic regimen is essential. Epidural analgesia has been advocated, but it can be challenging to decide the timing of insertion of the catheter, and also to maintain a sensory but not a motor block, thus allowing neurological assessment. The presence of the spinal catheter provides a route for administration of intrathecal diamorphine.

42
Q

What Postoperative Spinal cord ischemia management strategies

A

Maintaining spinal cord perfusion in the ICU Neurophysiological monitoring, ICP monitoring and CSF drainage continue for up to 72 h after surgery. Monitoring of MEPs and SSEPs is continued whilst patients are sedated.
The postoperative period is a critical time in which significant ischaemia can still develop.
○ Delayed paraplegia has a better prognosis than immediate, and can be reversed if recognised and treated promptly.
○ Regular reassessment of lower limb power is essential. Neurological impairment initiates the use of the COPS protocol to optimise spinal cord perfusion.
○ COPS is an acronym of CSF drain status; optimise Oxygen delivery; and Patient Status assessment in terms of MAP, SCPP, and cognitive status.
○ Where the spinal catheter is patent, the patient should be positioned flat and the CSFP maintained at <5mm Hg.
○ Oxygen delivery should be optimised through the administration of supplementaloxygenortracheal intubationand artificial ventilation to ensure SpO2 greater than 95%. Haemoglobin concentrations should be greater than 120 g L1 and cardiac index greater than 2.5 L min1 m2. SCPP is maintained at >80 mm Hg and MAP at >90 mm Hg. Where a drain was not sited during surgery,for example, in emergency surgery, the development of delayed neurological symptoms has been successfully treated with postoperative drain insertion.

43
Q

Complications

A

Complications of major aortic surgery Whilst surgery for aortic aneurysm is potentially life-saving, there is a significant morbidity and mortality. Early complications include hypothermia, coagulopathy, delirium, cardiovascular instability, respiratory failure, metabolic disturbance, renal failure, and stroke. Preoperative hydration, intraoperative administration of mannitol and cold renal perfusion have been used for their potential nephroprotective effects. Because of the size of the surgical incision for TAAA repair, the division of the diaphragm, and the potential for injury to the phrenic andrecurrentlaryngeal nerves, there is a significant risk of wound dehiscence and respiratory failure. The reported incidence of an adverse outcome after TAAA surgery, including renal failure requiring dialysis at hospital discharge, stroke, permanent paraplegia, or paraparesis, is 16% with an overall operative mortality of 8e10%.24

44
Q

What are the anatomic and surgical considerations for EVAR

A

○ The neck of the aneurysm must be straight (as opposed to the usual fusiform shape) and longer than 15 mm.
○ Additionally, there must be minimal atherosclerotic plaque inside the neck so that a good seal between the stent graft and the wall of the aorta can be obtained.
○ Distally, there must be disease-free zones in the iliac arteries to ensure good leg perfusion and at least one of the femoral arteries should be >8 mm in internal diameter. This is to enable insertion of the stent through the arteriotomy. (A collapsed stent graft has an external diameter up to 7.5 mm.)