Abnormal dilation of the aorta (1.5x or diameter >3cm), giving
rise to the possibility of rupture with cardiovascular collapse and
death, caused by degeneration of the vessel wall.
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3% of the general population aged 50-55 years.
5.4% of the population aged 55-75 years.
Declining in last decade; probably related to reduced
smoking rates and hypertension management.
Over 50s at-risk.
M>F, 11:1 (60-65 years).
The difference declines with advancing age.
Mortality is higher for women with ruptured AAAs.
More common in Maori.
Less common in Asians.
First degree relatives --> 10x increased risk.
PVD, smokers, hypercholesterolaemia, hypertension.
Atheroma risk factors.
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Although 75% seem simply related to arterial sclerosis, 25% have no
evidence of such.
- sclerosis is arterial hardening with hyalinisation.
3 theories for these 25% - genetic, proteolytic enzymes, and
Plus a few other anomalous causes possible.
IEM - congenital defects, eg Marfan's, EDS.
Excess elastase activity.
Haptoglobin activity - localised to chromosome 16.
Infection - unusual organisms causing sepsis may create severe
inflammation in vessel walls and aneurisms.
Eg Syphilis, salmonella.
Proteolytic enzyme theory
Inflammatory cell activity in the vessel wall.
Also effects of smoking - increased protease activity, in tandem
with genetic factors.
Trace metal theory
Copper deficiency and calcium overload can impair maturation of
muscle & elastic and collagen fibres, weakening the aortic wall.
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Degeneration of the collagen and elastin components of the artery.
Note that above the renal artery, the aorta is more elastic, below
it, progressively more rigid.
Note also that the aorta relies on simple diffusion for nutrition
(has no vasa vasorum).
The dilations typically contain thrombus.
They are unlike to cause symptoms until 2-3 times the size of the
Fusiform - full circumferential (most are this).
Saccular - bulging out from one side.
False aneurism - damaged artery wall leaks, self-limiting haematoma
forms outside arterial wall.
Important to note site relevant to renal arteries.
- >80% are isolated to infra-renal arteries.
Ie Supra-renal, infra-renal, or in-between the renal arteries.
Juxtarenal = within 1cm of renal arteries.
May lead to compromise of renal blood flow.
Also may extend to the common iliacs, though generally terminates at
Hence may compromise blood supply to the legs.
Risk factors for developing aneurism different than those for
1. Size of aneurysm is major risk factor for this.
- see management
2. Type of aneurysm - fusiform are more likely to rupture than
Note that patients may live up to days or even months after contained (retroperitoneal)
rupture of an aneurysm.
- free rupture into the peritoneal cavity occurs sooner or later,
leading to rapid death.
Erosion into neighbouring structures.
Rupture into vein, with resulting AV fistula.
Compression of neighbouring structures.
Thrombosis with occlusion or formation of an embolism with distal
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Go undetected until they develop a complication.
A pulsatile swelling may be observed by the patient
- eg the 'bouncing book sign'.
Or detected by an astute clinician.
Pain portends rupture and any pt with an aneurysm and recent abdo
pain should be regarded as at imminent risk.
- this may be for four or five days before rupture.
- tends to be throbbing before rupture, then steady once ruptured.
Pain is often located directly over the aneurysm.
- however almost always pain also in back or loin
- commonly radiates to testicles, rectum or groin.
Sudden rupture may be preceded by back ache possibly radiating to
the buttock or legs.
(As the aneurysm stretches, erodes or leaks).
Or persistent vague aching epigastric or central abdominal pain.
Sudden rupture results in sudden onset constant severe abdominal
pain which localises to the back (due to retroperitoneal
Those that survive to hospital may be stabilized by a plug of
Syncope, shock (not necessarily catastrophic due to containment).
Nausea and vomiting not common, but may occur.
Sometimes they rupture into duodenum with haematemesis and melaena.
- surprisingly this may start and stop over many weeks (Cope)
- any pt with a known aneurysm and such bleeding needs
May rupture into adjacent IVC
- severe heart failure, not responding with a continuous murmur.
May be found incidentally.
If large, pulsatility may be visible.
Check popliteal artery for aneurysms - associated.
A steady methodical hand is needed.
Not a rash darting hand.
Expansile, pulsatile swelling in the abdomen.
May be movable from side to side, but not up and down as the aorta
is tethered by the renal and iliac arteries.
The pulsatility remains palpable when the patient kneels on all
(Useful in distinguishing from patients with transmitted pulsatility
through an abdominal mass).
Gauge the size of it with your hands, then radiologically.
And do a full work up to assess safety of surgery.
Dull if large enough to displace the bowel laterally and reach the
anterior abdominal wall.
A bruit may be present.
Pale, sweaty, obtunded.
Syncope / collapse is strongly indicative.
Abdomen may be tender and guarded if intra-peritoneal blood (rare to
survive this to hospital)
The aneurysm may or may not be palpable (BP may be too low,
haematoma formation may make it less clearly defined).
- a non-pusatile mass or fullness may be felt instead.
- the mass may occupy any part of the abdomen being haematoma, but L
flank is most common.
Femoral pulses are usually present.
- most often excellent pulses will be found and relying on this sign
is misleading (Cope)
There is usually no bruit audible and relying on this sign is
Other complications include:
- mural thrombus formation and embolism of debris; trash foot.
- compression of adjacent organs
- associated aortic dissection (rare)
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Abdominal ultrasound is usually sufficient.
Or CT to verify presence of complications and detailed extent.
Angiography / CT angiogram pre-op.
May see calcified wall on plain X-ray.
Blood group and cross match +++.
Get FBC, electrolytes, ECG, creatinine &c.
CT usually rarely required to make diagnosis.
- pulsatile mass and symptoms warrant immediate exploration.
- USS in the ED can be helpful.
Features indicating urgent surgery include:
- frank rupture
- heterogenous mural thrombus with intraplaque haemorrhage
- loss of fat planes around aorta
- peri-aortic inflammation
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Indications for repair
Associated symptoms warrants early repair independent of aneurysm
Role of EVAR
EVAR has dramatically altered management in recent decade.
- used in over 70% of repairs
Dacron tube ganfts are fixed into aorta using balloon-expandable
Contraindications to EVAR
Technical failure; unfavorable access or anatomy
- 30% of people may have accessory renal arteries, which are a
- angulation of AAA 60o or more leads to problems with implantation
- need clear common ilac artery graft site 1-2cm of good distal
- need a decent femoral artery of 7mm to get the graft through.
When unavailable in rupture
Complex aortic neck anatomy, e.g. pararenal and suprarenal aneurysms
- most common problem; need 15mm below renals, or then consider
special suprarenal fixation grafts.
- if neck >32mm then problematic
- need precise diameter and length measurements along aorta and
iliac for reconstruction plan.
- need to oversize graft by 10-20% to diameter of neck; undersizing
may lead to an inadequate seal and failure to exclude the aneurysm.
Consider the SMA/IMA patency; don't want to occlude the IMA in a
patient with a compromised SMA
Screening and Prophylactic Repair
Majority are asymptomatic; balance rupture risk with surgical
morbidity and mortality.
Two recent RCTs have evaluated role of early repair of smaller
UK small aneurysms trial
- Rupture rates: 0.3% if <4cm; 1.5% if <4-4.9cm; 6.5%
- Surveillance warranted until reaches 5.5cm
Aneurysm detection and management (ADAM) trial
- operative mortality about 3%,
- annual rupture rate in surveillance group <5.5cm was 0.6%
Decision to operate also based on life expectancy, quality of
Large aneurysm study
Rupture rate (annual): 5-5.9cm = 10%; 20% 6-6.9; 30% 7cm+
- if 8cm+ 25% rupture within 6m
5.5cm is typical threshold for repair in males based on level 1
- but consider risk factors for rupture; smoking, female, family
history of AAA, concomitant COPD
So, typically operate on 5cm aneurysms in women.
- If <4cm, watch ever 6-12mo, USS every 12 mo.
- If 4-5cm then USS 6 monthly.
- If rapidly expanding, ie >0.5cm within a 6 month interval,
consider surgical treatment.
- (6 cm for thoracic aneurysms).
-General rate of increase 2-8 mm / yr.
- Risk factors for rupture may provoke earlier threshold.
- If >6cm, chance of rupture is 50% in two years, so high
- Elective repair mortality (open) generally less than 5%, benchmark
Justified at population level:
Men screened in their 65th year --> reduces death from premature
rupture by 50%
USS males at that age = evidence based.
Consider possible need for visceral / renal artery reconstruction
using thin-slice CT images
- some may need arteriography if complex neck.
Consider also pre-op:
- extent of resection, location of cross-clamp, quality of lumen and
risk of embolism, visceral vessel topography, iliac disease.
Between 40-50% operative mortality.
- if low volume centre (<30 per year), mortality is doubled
electively; also improvement for acute repairs though not as much.
Do not resuscitate
vigorously, managed hypotension prevents loss of containment and
- limit resuscitation goal to 80-90mmHg
CT generally performed despite urgency
- e.g. very important to know if it may be a thoracoabdominal
aneurysm, which changes incision and strategy.
Acute EVAR becoming common; through CT and straight to angio lab
- careful evaluation by vascular surgeon for accurate determination
of graft type needed.
Occasionally patients are too unstable and must go to OR
See repair notes
EVAR vs open in rupture?
Open = main benefit is known to last well for many many years.
But much greater physiologically strain on a critically ill patient
- GA also contributes to physiological demand with vasodilation and
- retroperitoneal dissection leads to third spacing, hypothermia,
Higher rates of abdominal compartment syndrome; laparostomy may be
Stents require local anaesthesia alone and sedation in >70% of
EVAR has many of the same complicatoins as open (below) but:
- abdomen closed, no cross clamp
- and one worse aspect in renal fx is contrast burden
- EVAR specific risks identifiable by CTA prior to discharge
Complications of surgery
Death, rate varies by co-morbidities.
Bleeding in 2-5%.
Abdominal compartment syndrome
- extensive blood loss and transfusion, volume shifts during repair.
Ischaemia of bowel due to ligation of inferior mesenteric.
Embolisation and lower limb ischaemia.
Most common cause of death is MI
Renal failure is relatively common, risks morbidity and mortality.
- malperfusion as well as systemic hypotension
Imaging to assess device migration and endoleak.
Aneurysm sac will eventually thrombose and decrease in size by 12m
- CT at 1m, 6m and 12m
- then if stable or shrinking sacs, and no migration, yearly CT is
- alternatively, duplux USSS, but limited by operator dependence and
CT more reliable.
Persistent flow of blood into a sac after endograft placement;
failure to completely exclude sac.
Most common cause of morbidity after EVAR; four types described:
Type I. Inadequate seal at proximal or distal attachment site
- repaired if discovered
Type II. Flow into sac from an aortic branch vessel eg. lumbar
- most common type; in up to 25% of EVAR.
- spontaneously resolve in 30%; may need percutaneous coil
Type III. Endograft fabric tear
Type IV. Endograft porosity
- these 2 much less common; treat with additional stent to cover
Elevated sac pressure leading to expansion in absence of
- may be a low-flow leak
Fenestration of sac described; some need conversion to open repair
Leads to leak, expansion of aneurysm and rupture or even stent
Risk factors: short neck, dilated aortic neck over time, severe
angulation, oversizing >30%, thrombus at proximal neck.
Rate varies by device and technique; perhaps 4-5% risk
Outcomes of EVAR vs Open; Elective
Multiple trials demonstrate substantial early survival benefit with
And much reduced serious post-operative morbidity.
Large RCT evdience that it is preferable short term
However, long-term data not yet well established, though no current
reason for concern.
Survival benefit probably evens out by 1-4years after therapy; lower
aneurysm death but these patients die of other problems at rates
that wash-out statistical differences b/n approaches
---> No diff in all-cause mortality at 4y
Current focus is on whether best to repair smaller aneurysms
earlier with EVAR given lower complication rate.
Trials underway, probably will change practice.
AAA and Unexpected Intra-Abdo Pathology
EVAR has revolutionised this issue
- due to low morbidity, incidentally discovered concomittant AAA can
usually be managed prior to treating a Ca without undue delay to
1. Unrecognised other pathology during elective AAA repair
Judgement required; depends.
- incidental gallstones? leave them alone.
- incidental appendix / meckels? defintely leave them alone or risk
of graft infx
- GI malignancy? Concomitant sugery inadvisable due to graft infx
risk; staged approach prefered based on whatever is higher; can
always stent the malignancy after AAA repair
- GU malignancy / solid organ lesions: more appropriate for
simultaneous fixing unless complex aneurysm with high risk features
e.g. blood loss
Note after EVAR there is significant fibrotic reaction around the
aorta, which can make bowel dissections more difficult.
2. Emergency Repair and Concomitant disease
As per clinical judgement, however repair of the aneurysm is
obviously usually the greater priority
3. Laparotomy and incidental AAA
As per clinical judgement, however repair of the other abdominal
problem is obviously usually the greater priority
SMA compromise should warrant urgent vascular consultation.
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