Aneur Abd Aorte

7/27/2019 Aneur Abd Aorte

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Abdominal aortic aneurysmHighlights

Summary

Overview

Basics

Definition

Epidemiology Aetiology

Pathophysiology

Classification

Prevention

Screening

Diagnosis

History & examination

Tests

Differential

Step-by-step

Guidelines

Case historyTreatment

Details

Step-by-step

Emerging

Guidelines

Evidence

Follow Up

Recommendations

Complications

Prognosis

Resources

References

Images

Patient leaflets

Credits

OverviewHistory & exam

Key factors

• presence of risk factors

• palpable pulsatile abdominal mass

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• perioperative antibiotic therapy

endovascular repair leak requiring treatment

• corrective procedure

• preoperative cardiovascular risk reduction

• perioperative antibiotic therapyTreatment details

Summary

• Typically asymptomatic and discovered incidentally, but abdominal pain and back pain are the most

common symptomatic complaints.

• Diagnosis relies on imaging. Ultrasound remains the definitive test for initial diagnosis and screening. CT

scan is typically required for preoperative planning.

• Repair is deferred until the theoretical risk of rupture exceeds the estimated risk of operative mortality.

Repair is indicated in patients with symptomatic AAA or asymptomatic AAA with a diameter exceeding 5.5 cm in

men or 5.0 cm in women.

• Complications of treatment include cardiac and pulmonary events, mesenteric ischaemia, renal failure,

bleeding, wound and graft infection, spinal cord ischaemia/paraplegia, embolisation/limb ischaemia, and late

graft complications (i.e., aorto-enteric fistula and aortic pseudoaneurysm). Endovascular repair offers the

additional potential complications of endoleak, graft occlusion, and graft migration with aortic neck expansion.

Other related conditions

• Essential hypertension

• Obesity in adults

• Peripheral vascular disease

Definition Abdominal aorta aneurysm (AAA) is a permanent pathological dilation of theaorta with a diameter >1.5 times the expected anteroposterior (AP) diameter

of that segment, given the patient's gender and body size. [1] [2] Viewimage This is approximately 3 cm in most people. More than 90% of aneurysms originate below the renal arteries. [3]

EpidemiologyIn the UK, Denmark, and Australia, using randomised controlled trials,screening for AAA was carried out. In total, there were 128,891 men and9342 women. A Cochrane review of the data (2007) found that, between the


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age of 65 and 79 years, 5% to 10% of men have AAA. [8] Epidemiology variesby region and with a number of other demographic factors. The generalprevalence of 2.9 cm to 4.9 cm AAAs range from 1.3% for men aged 45 to 54years, to 12.5% for men 75 to 84 years of age (0% and 5.2% for women,respectively). [3] The prevalence of aneurysms among men increases by

about 6% per decade. [7] In 2004 AAA was the 14th leading cause of deathfor the 60- to 85-year-old age group in the US, and there were 13,753 deathsfrom aortic aneurysm and dissection combined in 2004. [9] [10] Prevalenceamong men is 4 to 6 times higher than in women. [1] [11]

AetiologyThe aetiology is multi-factorial. Traditionally, arterial aneurysms were thoughtto arise from atherosclerotic disease, and certainly intimal atherosclerosisreliably accompanies AAA. [12] More recent data suggest that altered tissuemetalloproteinases may diminish the integrity of the arterial wall. [4] Theunderlying pathophysiology remains constant with aortic elastic medialdegeneration and mild cystic medial necrosis resulting in aortic dilation andaneurysm formation.

PathophysiologyThe pathogenesis is complex and multi-factorial. Histologically there isobliteration of collagen and elastin in the media and adventitia, smoothmuscle cell loss with resulting tapering of the medial wall, infiltration of lymphocytes and macrophages, and neovascularisation. [12] There are 4

mechanisms applicable and relevant to development: [13] • Proteolytic degradation of aortic wall connective tissue: matrix metalloproteinases (MMPs) and other

proteases are derived from macrophages and aortic smooth muscle cells and secreted into the extracellular

matrix. Disproportionate proteolytic enzyme activity in the aortic wall may promote deterioration of structural

matrix proteins (e.g., elastin and collagen). [3] Increased expression of collagenases MMP-1 and -13 and

elastases MMP-2, -9, and -12 have been demonstrated in human AAAs. [14] [15] [16] [17]

• Inflammation and immune responses: an extensive transmural infiltration by macrophages and

lymphocytes is present on aneurysm histology and these cells may release a cascade of cytokines that

subsequently activate many proteases. [12] Additionally, deposition of IgG into the aortic wall supports the

hypothesis that AAA formation may be an autoimmune response. There is currently interest in the role of

reactive oxygen species and antioxidants in AAA formation. [14] [18] [19] [20] [21]

• Biomechanical wall stress: elastin levels and the elastin-collagen ratio decrease progressively distal

down the aorta. Diminished elastin is associated with aortic dilation and collagen degradation predisposes to

rupture. [11] Additionally, data support increased MMP-9 expression and activity, disordered flow and an

increase in wall tension, and relative tissue hypoxia in the distal aorta (i.e., infra-renal). [14] [22] [23]
































































































• Molecular genetics: while there is no single genetic defect or polymorphism responsible, there is familial

clustering, a common HLA subtype, and several altered gene expressions and polymorphisms linked,

suggesting a genetic role in pathogenesis. [14] [24]

Classification

Types of AAA

Specific types of AAA are: [4] [5]

• Congenital: while medial degeneration occurs naturally with age, it is accelerated in patients with

bicuspid aortic valves and Marfan's syndrome.

• Infectious: infection of the aortic wall (mycotic aneurysm) is a rare

aetiology. Staphylococcusand Salmonella are the most common pathogens. Chlamydia pneumoniae has been

postulated as an infectious aetiology for conventional aneurysms.

• Inflammatory: the aetiology of inflammatory AAAs remains controversial. This variant is characterised by

an abnormal accumulation of macrophages and cytokines in diseased tissue. Pathologically there is

perianeurysmal fibrosis, thickened walls, and dense adhesions.

ScreeningScreening may reduce the incidence of aortic rupture, especially if applied to high-risk groups.

[8] [60] [61] [62] Current recommendations include: [47]

• One-time ultrasound screening for AAA is recommended for all men aged ≥65 years. Screening men as

early as 55 years is appropriate for those with a family history of AAA.

• Re-screening patients for AAA is not recommended if an initial ultrasound scan performed on patients

aged ≥65 years demonstrates an aortic diameter of 2.6 cm.

• Surveillance imaging at 12-month intervals is recommended for patients with an AAA of 3.5 to 4.4 cm in

maximum diameter.

• Surveillance imaging at 6-month intervals is recommended for those patients with an AAA between 4.5

and 5.4 cm in maximum diameter.

• Follow-up imaging at 3 years is recommended for those patients with an AAA between 3.0 and 3.4 cm in

maximum diameter.

• Follow-up imaging at 5-year intervals is recommended for patients whose maximum aortic diameter is

between 2.6 and 2.9 cm.

These recommendations are based on a meta-analysis of published data regarding the use of screening

programmes to detect AAA compiled and summarised by the United States Preventative Services Task Force

(USPSTF), several randomised trials, and the concept that screening for AAA and surgical repair of large AAAs

































(≥5.5 cm) in men aged 65 to 75 years who have ever smoked leads to decreased AAA-specific

mortality. [4] [47] [63] [64] [65] [49] [66] [67] [68] [69] [70] [71] [B Evidence]

While the USPSTF argues against screening in women, some authors argue that in certain subgroups of women

at increased risk of AAA (i.e., age ≥65 years with a positive history of smoking or family history of AAA)

screening should be considered with one-time ultrasound. [1][4] [44] [47] [63] [72]

History & examinationKey diagnostic factorshide all

presence of risk factors (common)

• Key risk factors include cigarette smoking, family history, increased age, male sex for prevalence

and female sex for rupture, and congenital/connective tissue disorders.palpable pulsatile abdominal mass (uncommon)

• Aneurysm palpation on clinical examination has been shown to be sensitive only in thin patients

and those with AAA >5 cm (sensitivity and specificity of 68% and 75%, respectively). [1] [48]

Other diagnostic factorshide all

abdominal, back, or groin pain (uncommon)

• However, patients are usually asymptomatic and their aneurysm is detected incidentally.

hypotension (uncommon)

• Patients with ruptured aneurysm present with the triad of abdominal and/or back pain, pulsatile

abdominal mass and hypotension.

Risk factorshide all

Strong

cigarette smoking

• This is the risk factor most strongly associated. [1] [7] [11] [26] [27]

• Active cigarette smoking is independently associated with histological high-grade tissue

inflammation. [28]

• The duration of smoking is significantly associated with an increased risk in a linear dose-response

relationship. Each year of smoking increases the relative risk by 4%. [27] hereditary/family history

• Studies support a familial aggregation of and genetic predisposition to

AAA. [1] [4] [7] [25] [29] [30] [31] [32] [33] [34] [35]

• The age- and sex-adjusted relative risk to a first-degree relative of an AAA patient is 11.6% and a

history of AAA in a parent confers the same excess risk. [32]

• The overall prevalence of AAA in siblings of AAA patients is 8 times that observed among control

cohort. [33] First-degree relatives have been shown to have an AAA in 15% to 28% of

cases. [3] [34] [35] increased age

• Prevalence increases with age. [1] [11]



























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• Most frequently diagnosed in men >55 years of age and rupture rarely occurs before 65 years of

age.

• AAA is discovered approximately 10 years later in women. [7] [36] [37]

male sex (prevalence)

• AAAs are 4 to 6 times more prevalent in men than women. [1] [7] [11]

female sex (rupture)

• Female sex increases risk of rupture. [4] [34] [38]

congenital/connective tissue disorders

• Aortic degeneration is accelerated in patients with bicuspid aortic valves, Marfan's syndrome, and

during pregnancy. [4]

• Marfan's syndrome specifically is associated with cystic medial necrosis of the aorta secondary to

an autosomal dominant anomaly in fibrillin type 1, a structural protein that directs and orients elastin

in the developing aorta.[39] [40] As a result, the mature aorta demonstrates abnormal elastic

properties, progressive stiffening, and dilation. [4] [41]

Weak

hyperlipidaemia

• Lipoproteins are elevated in patients with AAA independent of cardiovascular risk factors and

extent of atherosclerosis. [3] [4] [7]

• AAA patients have significantly lower levels of apolipoprotein AI and HDL cholesterol than matched

controls with aorto-iliac occlusive disease. [1] [3]

• High serum total cholesterol is a relatively weak risk factor for AAA, whereas high HDL cholesterol

was strongly associated with a low risk of AAA. [11] [37] COPD

• This is attributed to tobacco-induced elastin degradation. [3] [4] [7]

• Studies suggest that the association between reduced respiratory function and AAA may be due to

the activation of inflammation and haemostasis in response to injury.[42]atherosclerosis (i.e., CAD, peripheral arterial occlusive disease)

• CAD is an independent associated risk factor. [1] [26]

HTN

• HTN is an independent risk factor. [1] [7] [11]

• There is a significant relation between systolic BP and AAA in women and a significant association

with ever-use antihypertensive medication and AAA risk for both sexes. [11] [37] increased height

• Increased height is an independent associated risk factor, although after adjustment for age and

sex the association was no longer significant. [1] [26] [43] central obesity

• While obesity is generally not considered a risk factor, one study of more than 12,000 men

demonstrated an independent association between central obesity and AAA. [37]




























































































































non-diabetic

• Diabetes is negatively associated with AAA. [34] [26] [37]

Diagnostic tests1st tests to order hide all

Test

abdominal ultrasound

Definitive test (sensitivity and specificity of 92% to 99% and nearly 100%, respectively). [1] [2] [4] [ [8] [4

The ultrasound is performed perpendicular to the aortic axis as oblique views may overestimate the true

diameter . [4]

Intra-observer correlation may be better near the aortic bifurcation than in the proximal infrarenal aorta.

Unfortunately, ultrasound offers little utility in imaging aneurysms close to the origins of, or proximal to, t

arteries. [4] [51] [52]

Tests to consider hide all

Test

ESR/CRP

Suggests inflammatory AAA.

FBC

Recommended if infectious AAA suspected.

blood cultures

Recommended if infectious AAA suspected.

CT

May demonstrate blood within the thrombus (crescent sign), low thrombus-to-lumen ratio retroperitonea

discontinuity of the aortic wall, or extravasation of contrast into the peritoneal cavity, which are all signs o

rupture. [7] [53]

Also useful in diagnosing aortic aneurysms close to the origins of, or proximal to, the renal arteries. [4] [5

MRI/magnetic resonance angiography (MRA)

Preoperative study of choice for operative strategy if a patient has an iodinated contrast allergy.

































































aortography

Adjunctive modality for preoperative planning.

Differential diagnosis

Condition

Differentiating

signs/symptoms Differentiating tests

Diverticulitis• Obstipation;

abdominal pain is

more common

and typically

localises to the

left lower

quadrant.

• No pulsatile

abdominal mass

on clinical

examination.

Instead,

abdominal or

• Stool guaiac testing may be trace positive.

• Leukocytosis may be present.

• CT scan will demonstrate a normal-calibre aorta and

possibly diverticula, inflammation of the pericolic fat or

other tissues, bowel-wall thickness >4 mm, or a

peridiverticular abscess. [54]









perirectal

"fullness" may be

appreciated.

Fever is possible.

[54]

Renal colic• Severe

abdominal pain

that starts in the

flank and

radiates

anteriorly to the

groin.

• Associated with

nausea, emesis,

haematuria,

dysuria, and

urinary frequency

or urgency. [55]

• Urinalysis positive for blood and may demonstrate

crystals and/or evidence of infection.

• Ultrasound and CT scan will demonstrate a normal-

calibre aorta and possibly ureteral or renal stones.[55]

Irritable bowelsyndrome (IBS)

• Intermittent

abdominal

discomfort with

flares lasting 2 to

4 days.

• Associated

symptoms may

include bloating,

stool frequency,

and abnormal

defecation.

• Women aged 20

to 40 years are

affected more

often than men.

• On examination,

most patients

• Imaging modalities are often inconclusive, but will

demonstrate a normal-calibre aorta.

















appear anxious,

although general

examination is

usually normal.

There may be

poorly localised

abdominal

tenderness to

palpation. [56]

Inflammatory

bowel disease• Abdominal pain

is often "crampy"

and left-sided.

Patients typically

suffer fromdiarrhoea (bloody

and non-bloody),

urgency of

defecation, and

tenesmus.

• Extra-intestinal

manifestations

are common in

Crohn's disease.

• Abdominal

examination may

demonstrate

abnormal bowel

sounds, detection

of an abdominal

mass, and pain

on palpation.

Mucocutaneous

lesions may be

visible. Peri-anal

fistulae, fissures,

or abscesses

may be present

• Anaemia is common.

• Radiographical imaging (i.e., ultrasound or CT scan) will

demonstrate a normal-calibre aorta.

• Endoscopic evaluation with biopsy shows typical lesions

of ulcerative colitis or Crohn's disease. [57]











on rectal

examination. [57]

Appendicitis• Pain is typically

periumbilical with

localisation to theright lower

quadrant.

• Associated

nausea, emesis,

and anorexia are

common.

• Patients are

classically febrile

with tenderness

in the right lower

quadrant or

rebound

tenderness on

abdominal

examination.

• Leukocytosis and sterile pyuria on urinalysis is common.

• Imaging with ultrasound or CT scan will demonstrate a

normal-calibre aorta with an inflamed appendix or

evidence of perforation.

Ovarian torsion• Women suffer

sudden,

continuous, non-

specific pain in

the lower

abdomen;

nausea and

emesis are

common.

Patients may

demonstrate

fever on clinical

examination and

an adnexal mass

may be palpable.

[58]

• Leukocytosis may be present. Ultrasound will

demonstrate a normal calibre aorta and possible

reduced or absence of adnexal vascular flow. [58]

















GI haemorrhage• Patients

presenting with

haemorrhagic

shock may mimic

aortic rupture. A

history of

previous GI

bleed,

haematemesis,

melaena, or

bright red blood

per rectum is

common.

• Historical risk

factors for GI

malignancy or

peptic ulcer

disease may be

elicited.

• On rectal

examination

gross blood maybe visible or

coffee ground

haematemesis

may be returned

with nasogastric

tube placement.

• Stool is likely to be guaiac positive.

• Endoscopic evaluation may demonstrate the luminal

bleeding source along with mucosal ulcerations, polyps,

or tumour.

• Radiographical imaging with ultrasound or CT scan will

demonstrate a normal calibre aorta.

Splanchnic

artery

aneurysms/acuteocclusion

• Acute embolic or

thrombotic

occlusion of the

splanchnic

vessels results in

a marked

disparity between

acute

• Leukocytosis, haemoconcentration, and systemic

acidosis are common with acute splanchnic vessel

occlusion. Elevated levels of serum amylase, inorganic

phosphorous, creatinine phosphokinase, and alkaline

phosphatase may accompany frank bowel infarction.

• Angiography is diagnostic and potentially therapeutic in

the case of vascular occlusion.



excruciating mid-

abdominal pain

and a paucity of

early physical

findings.

• Patients typically

suffer

unremitting,

intense mid-

abdominal pain

with nausea and

vomiting that

might be

accompanied by

explosive

diarrhoea.

• Most splanchnic

artery aneurysms

are

asymptomatic

until rupture. [59]

• Ultrasound and CT scan will demonstrate a normal-

calibre aorta and will diagnose any splanchnic artery

aneurysms. [59]

•

Step-by-step diagnostic approachPatients most commonly lack any symptoms and their aneurysm is noted onphysical examination or radiographic studies performed for other reasons.

HistoryTypical symptoms include abdominal, back, and groin pain. Medical history isdirected towards risk factors:

•

Development (i.e., hyperlipidaemia, connective tissue disorder, COPD, and HTN) [1] [3] [4] [7] [11] [26] [41] [42]

• Expansion (i.e., previous cardiac or renal transplant, previous stroke, advanced age (>70 years), and

severe cardiac disease) [44] [45]

• Rupture (i.e., female sex, previous cardiac or renal transplant, HTN). [7] [43] [44] [46]

A history of cigarette smoking increases a patient's risk of AAA development,expansion, and rupture. [7] [26] [27] [28] [44] A history of previous abdominal










































































surgery or previous endovascular aortic aneurysm repair can be elicited aswell as family history of AAA.

Physical examinationThe abdomen can be palpated for a pulsatile abdominal mass and abdominal

tenderness. Physical examination should include an assessment of femoraland popliteal arteries in all patients with a suspected AAA as an AAA ispresent in 62% of patients with a popliteal aneurysm and in 85% of patientswith a femoral artery aneurysm. [44] [45] [47]

Aneurysm palpation on clinical examination has only been shown to besensitive in thin patients and those with AAA >5 cm with an overall sensitivityand specificity of 68% and 75%, respectively. [1] [48]

Ruptured aneurysm presents with the triad of abdominal and/or back pain,pulsatile abdominal mass, and hypotension.

The presence of fever may increase suspicion for infectious AAA in theappropriate clinical setting.

Key testsUltrasonography is the initial method of choice for AAA detection (sensitivityand specificity of 95% and nearly 100%, respectively). Once the diagnosis ismade, further imaging with CT, MRI, or magnetic resonance angiography(MRA) is used for anatomical mapping to assist with operative planning (open

or endovascular). [7] [49] Aortography is helpful when the proximal aneurysm margin is juxta- or suprarenal, there is a clinical history indicative of lower-extremity arterialocclusive disease, there is suspicion of renovascular disease evidenced byuncontrolled HTN or azotaemia, or if the patient has had previous aorticintervention. [1]

Elevated ESR and CRP support a diagnosis of possible inflammatory AAA.Leukocytosis and a relative anaemia on FBC with positive blood cultures arerecommended if infectious AAA is suspected.

Predictors of rupture risk including AAA expansion rate, increase inintraluminal thrombus thickness, wall stiffness, wall tension, and peak AAAwall stress. [47] [50]

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Diagnostic guidelinesNorth Americashow all

The care of patients with an abdominal aortic aneurysm: the Society for Vascular Surgery practiceguidelines (external link)

Published by: Society for Vascular SurgeryLast published: 2009

Summary

Provides recommendations for patient evaluation and risk of rupture in AAA, and for selecting surgical or

endovascular intervention, peri- and intra-operative strategies, follow-up, and treatment of complications.

Case history #1 A 70-year-old man presents to his primary care physician for a healthmaintenance examination. He has been feeling well and in his usual state of good health. His medical history is notable for mild HTN and he has a 100-pack-year tobacco history. On clinical examination, there is a palpable

pulsatile abdominal mass.

Case history #2 A 55-year-old man with a history of HTN (well controlled with medication) andtobacco use presents to his primary care physician with a 2-day history of constant and gnawing hypogastric pain. [4] The pain has been steadilyworsening in intensity. He believes the pain radiates to his lower back andboth groins at times. While he cannot identify any aggravating factors (suchas movement), he feels the pain improves with his knees flexed. There is a

palpable pulsatile mass just left of midline below the umbilicus. He isimmediately referred for definitive management, but during transfer becomeshypotensive and unresponsive.

Other presentationsThe triad of abdominal pain, weight loss, and elevated ESR suggestsinflammatory AAA. [4] A tender, palpable pulsatile mass on examination andelevated CRP may also be present. [5] Abdominal or back pain with fever is

suggestive of mycotic or infectious AAA. Typically there is history of arterialtrauma, IV drug abuse, local or concurrent infection, bacterial endocarditis, or impaired immunity. Osteomyelitis of the thoracic or lumbar spine maydevelop. Anaemia, leukocytosis, and positive blood cultures arecommon. [6] Diagnosis may be aided by complications of unrupturedaneurysms, including distal embolisation, acute thrombosis, or symptomscaused by ureterohydronephrosis. [7]

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Treatment Options

Patient group

Treatment

line Treatmenthide all

ruptured AAA 1st standard resuscitation measures

• The airway is managed with supplemental oxygen and

endotracheal intubation.

• A central venous catheter is inserted.

• Monitoring requires insertion of an arterial catheter and urinary

catheter.

• A target systolic BP of 50 to 70 mmHg and withholding fluids is

advocated preoperatively. [112] [117] [118]

• Aggressive fluid replacement may cause dilutional and

hypothermic coagulopathy and secondary clot disruption from

increased blood flow, increased perfusion pressure, and

decreased blood viscosity thereby exacerbating

bleeding. [112] [108] [117] [118] Infusing more than 3.5 L of

fluid preoperatively may increase the relative risk of

death. [108]

plus

[?]

urgent surgical repair

• Endovascular AAA repair (EVAR) is the most efficacious test

for repair, aortoiliac anatomy permitting; otherwise, traditional

open repair is performed.

[1] [108] [109] [110] [111] [112] [113] [B Evidence]

• Operative mortality for open repair is 48%. [114] Despite

frequent prolonged ICU and hospital lengths of stay, around

60% survive with long-term survival similar to that of the

general population. Data support cost effectiveness. [114]

[115] [116]

plus

[?]

perioperative antibiotic therapy

• Antibiotic therapy is indicated for patients undergoing

emergency repair of ruptured AAA to cover gram-positive and

gram-negative organisms and prevent graft infection.

• Broad-spectrum antibiotic coverage is tailored to patient clinical

presentation and cultures, and in accordance with local

protocols.





































































Patient group

Treatment


ruptured AAA1st standard resuscitation measures





catheter.





increased blood flow, increased perfusion pressure, anddecreased blood viscosity thereby exacerbating



death. [108]

symptomatic, but not

ruptured AAA

1st semi-urgent surgical repair

• Aorto-iliac anatomy permitting, endovascular AAA repair

(EVAR) may be offered to these patients.

• Urgent traditional open repair of symptomatic unruptured AAAs

carries increased morbidity and mortality with a rate between

that of ruptured AAA repair and elective repair. [1] [137] EVAR

in this setting demonstrates promising results with lower first-

month mortality. [1] [113]

• Co-morbid diseases are medically optimised and beta-blockade

instituted preoperatively. [1]

plus

[?]

preoperative cardiovascular risk reduction

• Beta-blockers should be used perioperatively to reduce

morbidity and mortality as supported by a reduced risk of inhospital death among high-risk patients undergoing major

non-cardiac surgery when given perioperatively. [1] [101]

[102] [103] [104] [105] [47] Preoperative guidelines recommend

beta-blockade before AAA repair in all patients unless

contraindicated. [1] [44] [124] [125] [A Evidence]

• A short-acting beta-blocker such as metoprolol allows for

dosing adjustment within a few days. Atenelol and propanolol






























































Patient group

Treatment


ruptured AAA1st standard resuscitation measures





catheter.





increased blood flow, increased perfusion pressure, anddecreased blood viscosity thereby exacerbating



death. [108]

have also been used. [1] [106]

• Doses should be started days to weeks before elective surgery,

with a target heart rate of <65 beats per minute. [47] [107]

• Clinical data also support the notion that statins, alpha-2

antagonists, and calcium channel blockers reduce perioperative

cardiac morbidity and death.[47]

plus

[?]


• Perioperative antibiotic therapy is given. Broad-spectrum

antibiotic coverage is necessary, in accordance with local

protocols.

Acute



















Patient group

Treatment


incidental finding:

asymptomatic smallAAA

1st surveillance

• For AAA detected as an incidental finding, repair is deferred

until the theoretical risk of rupture exceeds the estimated risk of

operative mortality. Generally, repair is indicated in patients

with large asymptomatic AAA (e.g., with a diameter exceeding

5.5 cm in men or 5.0 cm in women in the US), although

treatment decisions based on greater size may differ in other

countries (e.g., UK). [1] [4] [73] [74] [75] [76] [77]

• Current guidelines suggest that surveillance with selective

repair is most appropriate for older male patients with

significant co-morbidities. Young, healthy patients, and

especially women, with AAA between 5.0 and 5.4 cm may

benefit from early repair. [47] [4] [73] [75] [74] [76] [B Evidence]

• Monitor infra-/juxtarenal AAAs measuring 4.0 to 5.4 cm in

diameter with ultrasonography (USS)/CT every 6 to 12

months. [4] [A Evidence]

• AAAs <4.0 cm require USS every 2 to 3 years. [4] [B Evidence]

plus

[?]

aggressive cardiovascular risk management

• Patients should be encouraged to stop smoking and offered

drug therapy to assist with this if needed.• Beta-blockers may be used to reduce the rate of aneurysm

expansion, [47] [4] [102] [103] [104] [B Evidence] although

clinical trials have not supported this. Regardless, their use

clearly decreases mortality from other cardiovascular disease

and is associated with a reduced risk of in-hospital death

among high-risk patients undergoing major non-cardiac surgery

when given perioperatively. [1] [101] [102] [103] [104] [105] [47]

• Other modifiable cardiovascular risk factors (such as

hyperlipidaemia) can be treated, and statins may be considered

to reduce the risk of AAA enlargement.[47]




incidental finding:1st elective surgical repair











































































































Patient group

Treatment


incidental finding:


1st surveillance







countries (e.g., UK). [1] [4] [73] [74] [75] [76] [77]










large AAA • Generally, repair is indicated in patients with large

asymptomatic AAA (e.g., with a diameter exceeding 5.5 cm in

men or 5.0 cm in women in the US), although treatment

decisions based on greater size may differ in other countries

(e.g., UK). Repair of aneurysms ≥5.5 cm offers a survival

advantage.[1] [74] [75] [76] [77]

• Young, healthy patients, and especially women, with AAA

between 5.0 and 5.4 cm may benefit from early

repair . [47] [4] [73] [75] [74] [76] [B Evidence]

• Data suggest that in patients with large AAAs (ranging from 5 to

5.5 cm) undergoing elective repair, EVAR is equivalent to open

repair in terms of overall survival, although the rate of

secondary interventions is higher for EVAR. [85] [86] [A

Evidence] EVAR also reduces AAA-related mortality (but not

longer-term overall survival) in patients unsuitable for open

repair . [87] [A Evidence]

• Patients with greater risk of perioperative morbidity and

mortality (i.e., COPD, multiple previous abdominal operations)




























































Patient group

Treatment


incidental finding:


1st surveillance







countries (e.g., UK). [1] [4] [73] [74] [75] [76] [77]










may benefit from a less invasive approach, aorto-iliac anatomy

permitting. Younger, healthier patients may benefit from thedurability of a traditional open repair. Reasons for deferring

care may include terminal illness (i.e., cancer) such that life

expectancy is <6 to 12 months and patient choice.

plus

[?]

preoperative cardiovascular risk reduction

• Beta-blockers should be used perioperatively to reduce

morbidity and mortality as supported by a reduced risk of

inhospital death among high-risk patients undergoing major

non-cardiac surgery when given perioperatively. [1] [101]

[102] [103] [104] [105] [47] Preoperative guidelines recommendbeta-blockade before AAA repair in all patients unless

contraindicated. [1] [44] [124] [125] [ A Evidence]

































































Patient group

Treatment


incidental finding:


1st surveillance







countries (e.g., UK). [1] [4] [73] [74] [75] [76] [77]













plus

[?]




protocols.

endovascular repair

leak requiring

treatment

1st corrective procedure

• Endoleak is persistent blood flow outside the graft and within

the aneurysm sac. [126] [127] Risk following endovascular repair (EVAR) is 24%. [126] Endoleak is not a complication

following open repair. There are 5 types of endoleak and

management is dependant upon type.

• Type I: repair is indicated upon discovery (endovascular

extension grafts or conversion to open repair if

necessary). [47] View image View image



























Patient group

Treatment


incidental finding:


1st surveillance







countries (e.g., UK). [1] [4] [73] [74] [75] [76] [77]










• Type II: treatment remains controversial and is advocated

either if persistent at 6 to 12 months or when aneurysm sac

size increases. [129] [130] [131] [132] Treatment of choice is

transarterial coil embolisation, although laparoscopic ligation of

collateral branches, direct percutaneous translumbar puncture

of the sac, translumbar embolisation, and transcatheter

transcaval embolisation have been

reported. [127] [129] [130] [133] [131] [134] [135] [136]

• Type III: repair is indicated upon discovery (endovascular stent

graft extension). [130] [47]

• Type IV: these leaks are uncommon with newer stent grafts

and are self-limited, requiring no treatment. [130] [47]

• Type V: there is no standardised method to measure

endotension or consensus on indicated therapy in the absence

of aneurysm enlargement; however, treatment of endotension

to prevent aneurysm rupture is suggested in selected patients

with continued aneurysm expansion. [127] [47]

plus preoperative cardiovascular risk reduction






























































Patient group

Treatment


incidental finding:


1st surveillance







countries (e.g., UK). [1] [4] [73] [74] [75] [76] [77]










[?] • Beta-blockers should be used perioperatively to reduce

morbidity and mortality as supported by a reduced risk of

inhospital death among high-risk patients undergoing major non-cardiac surgery when given perioperatively. [1] [101]

[102] [103] [104] [105] [47]







antagonists, and calcium channel blockers reduce perioperativecardiac morbidity and death.[47]

plus

[?]




protocols.

Ongoing













































Treatment approachPatients presenting with a ruptured aneurysm require emergent repair, andfor patients with symptomatic aortic aneurysms, repair is indicated regardlessof diameter. [4] For AAA detected as an incidental finding, repair is deferred

until the theoretical risk of rupture exceeds the estimated risk of operativemortality. Generally, repair is indicated in patients with large asymptomatic AAA (e.g., with a diameter exceeding 5.5 cm in men or 5.0 cm in women inthe US), although treatment decisions based on greater size may differ inother countries (e.g., UK).[1] [4] [73] [74] [75] [76] [77]

Types of repair Open repair:

•

The conventional open repair ensues through a retroperitoneal (RP) or transperitoneal incision. Withproximal and distal aortic control obtained, the aneurysm is opened, back-bleeding branch arteries are ligated,

and a prosthetic graft is sutured from normal proximal aorta to normal distal aorta (or iliac segments). Once flow

is restored to the bilateral iliac arteries the aneurysm sac is closed over the graft. [78]

• Although advocates of a RP approach claim various physiological benefits, including reductions in fluid

losses, cardiac stress, postoperative pulmonary complications, and severity of ileus, randomised prospective

studies have generated conflicting results. A retroperitoneal approach should be considered for patients in which

aneurysmal disease extends to the juxtarenal and/or visceral aortic segment, or in the presence of an

inflammatory aneurysm, horseshoe kidney, or hostile abdomen. [47] [79] [80]

• Straight tube grafts are recommended for repair in the absence of significant disease of the iliac

arteries. [47]

• The proximal aortic anastomosis should be performed as close to the renal arteries as possible. [47] It is

recommended that all portions of an aortic graft should be excluded from direct contact with the intestinal

contents of the peritoneal cavity. [47]

• Re-implantation of a patent inferior mesenteric artery (IMA) should be considered under circumstances

that suggest an increased risk of colonic ischaemia (i.e., associated coeliac or superior mesenteric artery

occlusive disease, an enlarged meandering mesenteric artery, a history of prior colon resection, inability to

preserve hypogastric perfusion, substantial blood loss or intraoperative hypotension, poor IMA backbleeding

when graft open, poor Doppler flow in colonic vessels, or should the colon appear ischaemic). [47] [81]

• This repair is effective and durable; 5-year survival rates after intact aneurysm repair average 60% to

75%. [4]

• Complications include cardiac and pulmonary events, mesenteric ischaemia, renal failure, bleeding,

wound and graft infection, spinal cord ischaemia/paraplegia, embolisation/limb ischaemia, and late graft

complications (i.e., aortoenteric fistula and aortic pseudoaneurysm). [1] [4] [82]

• The operative mortality associated with open repair averages 2% to 7%; this has prompted a movement

towards less-invasive technique and endovascular AAA repair. [4] [83] [84]























































































Endovascular repair (EVAR):

• EVAR is progressively replacing open repair for the treatment of infrarenal AAA, and now accounts for

more than 50% of all AAA repairs in the US. [47]

• Data suggest that in patients with large AAAs (ranging from 5 to 5.5 cm) undergoing elective repair,

EVAR is equivalent to open repair in terms of overall survival, although the rate of secondary interventions ishigher for EVAR. [85] [86] [ A Evidence] EVAR also reduces AAA-related mortality (but not longer-term overall

survival) in patients unsuitable for open repair.[87] [A Evidence]

• EVAR involves the transfemoral endoluminal delivery of a covered stent graft into the aorta, thus sealing

off the aneurysm wall from systemic pressures, preventing rupture, and allowing for sac shrinkage.View

imageView image

• Additional complications may include endoleak, graft occlusion, and graft migration with aortic neck

expansion. [4]

• Studies support that EVAR offers patients an early perioperative mortality benefit (0% to 1.7%) with

decreased hospital length of stay and blood product utilisation. [1] [4] [88] [89] [90] The advantage is lost with

longer follow-up, and no advantage with respect to all-cause mortality or quality of life has been

demonstrated. [1] [4] [91] [92] [93] [94]

• Late re-interventions related to AAA are more common after EVAR but are balanced by an increase in

laparotomy-related re-interventions (i.e., incisional hernia repair) and hospitalisations after open surgery. [95]

• Multivariate meta-regression analysis showed that rates of operative mortality, postoperative rupture,

and total number of endoleaks have all fallen significantly demonstrating a low mortality and a gradual reduction

in vascular morbidity and mortality associated with endovascular repair since it was first introduced. [96]

• As an adjunct to EVAR, bilateral hypogastric artery occlusion may be acceptable in certain anatomical

situations for patients at high risk for open surgical repair. Buttock claudication and erectile dysfunction may

occur in up to 40% of patients after unilateral embolisation - these symptoms may persist in 11% to 13% of

patients following bilateral occlusion. [47] [97] [98] Newer techniques, including use of iliac branch graft devices

for preservation of the internal iliac arteries, are emerging and are more commonly used in some centres. [99]

Treatment of co-existing cardiac diseaseWhile a substantial number of patients suffering from AAA also haveunderlying coronary artery disease, non-invasive stress testing should beconsidered for patients with a history of ≥3 clinical risk factors (i.e., CAD,

congestive heart failure, cerebrovascular accident, diabetes mellitus, chronicrenal insufficiency) and an unknown or poor functional capacity (MET <4) thatare undergoing endovascular repair (EVAR) or open surgical repair, if it willchange management. While routine coronary revascularisation by coronaryartery bypass grafting (CABG) or percutaneous transluminal coronaryangioplasty (PTCA) prior to elective vascular surgery in patients with stablecardiac symptoms does not appear to significantly alter the risk of postoperative MI or death or long-term outcome, coronary revascularisation is



























































































indicated for those patients who present with acute ST elevation MI, unstableangina, or stable angina with left main coronary artery or 3-vessel disease, aswell as those patients with 2-vessel disease that includes the proximal leftanterior descending artery and either ischaemia on non-invasive testing or anejection fraction <0.5. [47]

Perioperative managementRegarding blood transfusion: [47]

• Preoperative autologous blood donation may be beneficial for patients undergoing open aneurysm

repair.

• Cell salvage or an ultrafiltration device is recommended if large blood loss is anticipated or the risk of

disease transmission from banked blood is considered high.

•

Intraoperative blood transfusion is recommended for a haematocrit <30% in the presence of ongoingblood loss.

• If the intraoperative haematocrit is <30% and blood loss is ongoing, consider use of FFP and platelets in

a ratio with packed blood cells of 1:1:1.

Pulmonary artery catheters should not be used routinely in aortic surgery,unless there is a high risk for a major haemodynamicdisturbance. [47] Central venous access is recommended for all patientsundergoing open aneurysm repair. [47] DVT prophylaxis consisting of

intermittent pneumatic compression and early ambulation are recommendedfor all patients undergoing open repair or EVAR. [47] [100]

Preoperative cardiovascular risk reduction:

• Beta-blockers should be used perioperatively to reduce morbidity and mortality as supported by a

reduced risk of inhospital death among high-risk patients undergoing major non-cardiac surgery when given

perioperatively. [1] [101] [102] [103] [104] [105] [47] A short-acting beta-blocker such as metoprolol allows for

dosing adjustment within a few days. Atenelol and propanolol have also been used. [1] [106] Doses should be

started days to weeks before elective surgery, with a target heart rate of <65 beats per minute. [47] [107]

• Clinical data also support the notion that statins, alpha-2 antagonists, and calcium channel blockers

reduce perioperative cardiac morbidity and death. [47]

Antibiotic cover:

• Antibiotic therapy is indicated for patients undergoing elective and emergent repair of ruptured AAA to

cover gram-positive and gram-negative organisms (i.e., Staphylococcus aureus, Staphylococcus epidermidis,

and enteric gram-negative bacilli) and prevent graft infection.



































































• Broad-spectrum antibiotic coverage is tailored to patient clinical presentation and cultures, and in

accordance with local protocols.

Ruptured AAAPatients with the triad of abdominal and/or back pain, pulsatile abdominal

mass, and hypotension warrant immediate resuscitation and surgicalevaluation as repair offers the only potential cure. [4] View image [BEvidence] However, most patients with rupture will not survive to reachtheatre. Overall mortality is about 90%; [4] mortality in those that reach theoperating suite is 50%. [47] EVAR is the most efficacious test for repair, aortoiliac anatomy permitting;otherwise, traditional open repair isperformed. [1] [108] [109] [110] [111] [112] [113] [B Evidence] Operativemortality for open repair is 48%. [114] Despite frequent prolonged ICU and

hospital lengths of stay, around 60% survive with long-term survival similar tothat of the general population. Data support costeffectiveness. [114] [115] [116]

Supportive treatment of ruptured AAAStandard resuscitation measures are initiated immediately. This includes:

• Airway management (supplemental oxygen or endotracheal intubation)

• Intravenous access (central venous catheter)

• Arterial catheter

• Notify anaesthetic, ICU, and operating teams

• Urinary catheter

• Hypotensive resuscitation: aggressive fluid replacement may cause dilutional and hypothermic

coagulopathy and secondary clot disruption from increased blood flow, increased perfusion pressure, and

decreased blood viscosity thereby exacerbating bleeding.[112] [108] [117] [118] Infusing more than 3.5 litres of fluid preoperatively may increase the relative risk of death. [108] A target systolic BP of 50 to 70 mmHg and

withholding fluids is advocated preoperatively. [112] [117] [118]

• Blood product (packed red cells, platelets, and fresh frozen plasma) availability and transfusion for

resuscitation, severe anaemia, and coagulopathy.

Symptomatic but not ruptured























































































In patients with symptomatic aortic aneurysms, repair is indicated regardlessof diameter. [4] [C Evidence] The development of new or worsening pain mayherald aneurysm expansion and impending rupture. Repair is undertakenwithin 24 hours; co-morbid diseases are medically optimised and beta-blockade instituted preoperatively. [1]

Incidental finding of small AAAFor AAA detected as an incidental finding, repair is deferred until thetheoretical risk of rupture exceeds the estimated risk of operative mortality.Generally, repair is indicated in patients with large asymptomatic AAA (e.g.,with a diameter exceeding 5.5 cm in men or 5.0 cm in women in the US),although treatment decisions based on greater size may differ in other countries (e.g., UK). [1] [4] [73] [74] [75] [76] [77] Current evidence andguidelines suggest that surveillance with selective repair is most appropriate

for older male patients with significant co-morbidities. Young, healthypatients, and especially women, with AAA between 5.0 and 5.4 cm maybenefit from early repair. [4] [47] [73] [74] [75] [76] [119] [B Evidence]

• While long-term survival was equivalent in the United Kingdom Small Aneurysm Trial (UKSAT) and the

Aneurysm Detection and Management (ADAM) trial for both immediate surgery and surveillance groups, a trend

towards a beneficial effect of early surgery was observed in both studies in the younger patient and for those

with larger aneurysms [47] [75] [74] [76] [77]

• The observation that EVAR is associated with reduced perioperative mortality prompted the Comparison

of surveillance vs endografting for small aneurysm repair (CAESAR) and Positive impact of endovascular

options for treating aneurysm early (PIVOTAL) trials in an effort to compare immediate EVAR with surveillance

and selective EVAR, but neither trial has been designed to determine whether immediate EVAR might be

beneficial or harmful for specific AAA size ranges or age subgroups. [47] [120]

Additionally, elective repair should be considered for patients that presentwith a saccular aneurysm. [47]

Medical goals for asymptomatic small aneurysms include:

1. Surveillance:

• Monitor infra-/juxtarenal AAAs measuring 4.0 to 5.4 cm in diameter with ultrasonography (USS)/CT

every 6 to 12 months. [4] [ A Evidence]


• Consider expansion rates, as some advocate that expansion of 4 to 8 mm over 12 months suggests

instability. [1]

2. Control modifiable risk factors for expansion and rupture:











































































































• Smoking cessation - nicotine-replacement therapy, nortriptyline, and bupropion, or

counselling. [1] [7] [11] [26] [27] [121] [122] [123]

• Beta-blockers may be used to reduce the rate of aneurysm expansion, [47] [4] [102] [103] [104] [B

Evidence] although clinical trials have not supported this. Regardless, their use clearly decreases mortality from

other cardiovascular disease and is associated with a reduced risk of in-hospital death among high-risk patients

undergoing major non-cardiac surgery when given perioperatively. [1] [101] [102] [103] [104] [105] [47]

3. Aggressively manage other cardiovascular disease.

• Other modifiable cardiovascular risk factors (such as hyperlipidaemia) can be treated, and statins may

be considered to reduce the risk of AAA enlargement. [47]

• Clinical data also support the notion that statins, alpha-2 antagonists, and calcium channel blockers

reduce perioperative cardiac morbidity and death. [47]

Incidental finding of large AAA

Generally, repair is indicated in patients with large asymptomatic AAA (e.g.,with a diameter exceeding 5.5 cm in men or 5.0 cm in women in the US),although treatment decisions based on greater size may differ in other countries (e.g., UK). Repair of aneurysms ≥5.5 cm offers a survivaladvantage. [1] [74] [75] [76] [77] Elective repair should be also considered for patients that present with a saccular aneurysm. [47] Data suggest that in patients with large AAAs (ranging from 5 to 5.5 cm)undergoing elective repair, EVAR is equivalent to open repair in terms of overall survival, although the rate of secondary interventions is higher for

EVAR. [85] [86] [A Evidence] EVAR also reduces AAA-related mortality (butnot longer-term overall survival) in patients unsuitable for open repair. [87] [AEvidence]Elective repair in asymptomatic patients allows for preoperative assessment,cardiac risk stratification, and medical optimisation of other co-morbidities.CAD remains the leading cause of early and late mortality after AAA repair.Preoperative guidelines recommend beta-blockade before AAA repair in allpatients unless contraindicated. [1] [44] [124] [125] [A Evidence] The 2005 American College of Cardiology/American Heart Association

Practice Guidelines state: "once an infrarenal aortic aneurysm reaches anappropriate size for graft replacement, a choice must be made between atraditional open operation or endovascular repair. Like all other aspects of aneurysm management, this decision requires a balanced judgement of relative risks." [4]

EVAR leak










































































































































Endoleak is persistent blood flow outside the graft and within the aneurysmsac. [126] [127] Risk following EVAR is 24%. [126] Endoleak is not acomplication following open repair. There are 5 types of endoleak.

Type I:

•

Leak at the attachment site (proximal/distal end of the endograft or iliac occluder); usually immediate,but delayed leaks may occur.View image

• Repair is indicated upon discovery (endovascular extension grafts or conversion to open repair if

necessary). [47] View image View image

Type II:

• Patent branch leak.View image

• Spontaneous resolution may occur, although persistence may result in sac growth. [128]

• If a type II endoleak or other abnormality of concern is observed on contrast-enhanced CT imaging at 1

month after EVAR, postoperative imaging at 6 months is recommended. [47]

• Treatment remains controversial and is advocated either if persistent at 6 to 12 months or when

aneurysm sac size increases. [129] [130] [131] [132]

• Treatment of choice is transarterial coil embolisation, although laparoscopic ligation of collateral

branches, direct percutaneous translumbar puncture of the sac, translumbar embolisation, and transcatheter

transcaval embolisation have been reported. [127] [129] [130] [133] [131] [134] [135] [136]

Type III:

• Graft defect with leak through fabric tears, graft disconnection, or disintegration of the fabric.[126] [127]

• Repair is indicated upon discovery (endovascular stent graft extension). [130] [47]

Type IV:

• Leak from graft wall porosity. [126] [127]

• These leaks are uncommon with newer stent grafts and are self-limited. [130] [47]

Type V:

• Endotension is increased intrasac pressure after EVAR without visualised endoleak on delayed contrast

CT scans.

•

There is no standardised method to measure endotension or consensus on indicated therapy in theabsence of aneurysm enlargement; however, treatment of endotension to prevent aneurysm rupture is

suggested in selected patients with continued aneurysm expansion. [127] [47]

Emerging treatments

Doxycycline or roxithromycin
















































































































Doxycycline is a non-specific inhibitor of matrix metalloproteinases (MMP)that promote degradation of collagen and elastin and are integral toaneurysm formation. [1] [14] Targeted gene disruption of MMP-9 in micesuppresses the development of experimental AAA and both MMP-2 and -9are necessary to induce experimental AAA formation in

mice. [138] [139] [140] Animal models have shown that continuous periaorticinfusion of doxycycline lowers the effective dose, and can effectivelysuppress experimental AAAs serving as a prototype for adjuvant treatmentmodalities that complement endovascular AAA exclusion and may inhibitprogressive expansion of aortic aneurysms. [1] [141] [142] One clinical trialhas found that prolonged administration of doxycycline for 6 months is safeand well tolerated by patients with small asymptomatic AAAs and isassociated with a gradual reduction in plasma MMP-9 levels.[1] [143] Another small randomised trial assessing the ability of doxycycline to inhibit the

growth of aortic aneurysms noted no growth in doxycycline-treated patients at6 and 12 months.[144] [145] Further studies are needed to evaluate the long-term effects of doxycycline on the rate and extent of aneurysm growth andthe potential use of plasma MMP-9 levels as a biomarker of aneurysmdisease progression, but there appear to be sufficient preliminary data tosupport a large prospective randomised trial of doxycycline to preventaneurysm expansion.[144] At this time, however, insufficient data exist torecommend use of doxycycline or roxithromycin. [47] [146]

Treatment guidelinesEuropehide all

Endovascular stent-grafts for the treatment of abdominal aortic aneurysms (external link)Published by: National Institute for Health and Clinical Excellence

Last published: 2009

Summary

Provides an appraisal of the use of grafts in the treatment of AAA.

Laparoscopic repair of abdominal aortic aneurysm (external link)Published by: National Institute for Health and Clinical Excellence


Summary

These guidelines make recommendations on the laparoscopic repair of AAA. Recommendations

are made on who should carry out the procedure, and the information given to patients and their

Trust.

Stent-graft placement in abdominal aortic aneurysm (external link)Published by: National Institute for Health and Clinical Excellence


Summary

These guidelines make recommendations on the information clinicians should ensure patients

understand about the procedure and the potential risks involved. The guidelines also advise on



































http://guidance.nice.org.uk/TA167

http://guidance.nice.org.uk/IPG229

















http://guidance.nice.org.uk/TA167





patient selection for the procedure.

North Americahide all

The care of patients with an abdominal aortic aneurysm: the Society for Vascular Surgerypractice guidelines (external link)

Published by: Society for Vascular Surgery


Summary

Provides recommendations for patient evaluation and risk of rupture in AAA, and for selecting

surgical or endovascular intervention, peri- and intra-operative strategies, follow-up, and treatment

of complications.

ACC/AHA 2007 guidelines on perioperative cardiovascular evaluation and care for noncardiacsurgery (external link)

Published by: American College of Cardiology (ACC)/American Heart Association (AHA)


Summary

Recommendations are made about preoperative non-invasive evaluation of left ventricular function,

preoperative resting 12-lead ECG, non-invasive stress-testing before non-cardiac surgery,preoperative coronary revascularisation with CABG or percutaneous coronary intervention, beta-

blocker medical therapy, and statin therapy.

ACC/AHA 2005 practice guidelines for the management of patients with peripheral arterialdisease (lower extremity, renal, mesenteric, and abdominal aortic) (external link)

Published by: American College of Cardiology (ACC)/American Heart Association (AHA)


Summary

Recommendations are made about aortic aneurysm rupture, screening high-risk populations, BP

control and beta-blockade, and an overview of management.

MonitoringIn patients with small aneurysms, monitor infra-/juxtarenal AAAs measuring4.0 to 5.4 cm in diameter with ultrasonography (USS)/CT every 6 to 12months. [4] [A Evidence] AAAs <4.0 cm require USS every 2 to 3 years. [4] [BEvidence] Consider expansion rates, as some advocate expansion of 4 to 8mm over 12 months suggests instability. [1]

As late aneurysm formation may be noted in approximately 1%, 5%, and 20%of patients at 5, 10, and 15 years after open repair, respectively, follow-up

non-contrast CT imaging at 5-year intervals is recommended. [47] Previous recommendations regarding post-endovascular repair (post-EVAR)surveillance included CT imaging at 1, 6, and 12 months postoperatively andyearly thereafter to evaluate for late graft complications (i.e., migration,occlusion, and endoleak). [44] However, more recent concerns regarding thefrequent use of CT scanning, cost, and cumulative radiationexposure/potential lifetime cancer risk have resulted in a shift towards colour



http://my.americanheart.org/professional/StatementsGuidelines/ByTopic/TopicsA-C/ACCAHA-Joint-Guidelines_UCM_321694_Article.jsp







































duplex ultrasound imaging for surveillance. Current recommendations includecontrast-enhanced CT imaging at 1 and 12 months during the first year following EVAR. If neither endoleak nor AAA enlargement is documentedduring first year after EVAR, colour duplex ultrasonography is suggested asan alternative to CT imaging for annual postoperative surveillance with non-

contrast CT imaging every 5 years. [47] Antibiotic prophylaxis of graftinfection is required prior to bronchoscopy, gastrointestinal or genitourinaryendoscopy, and any dental procedure that may lead to bleeding. [47] Generalised sepsis, groin drainage, pseudoaneurysm formation, or ill-definedpain after open repair or EVAR should prompt evaluation of graftinfection. [47] GI bleeding after open repair or EVAR should promptevaluation of an aortoenteric fistula. [47]

Patient InstructionsPatients should be educated on the importance of smoking cessation(including counselling and pharmacotherapy as needed), and blood pressureand cholesterol control.

ComplicationsComplicationhide all Timeframe Likelihood

ureteral obstruction

Ureteric obstruction is related to encasement of the ureters in an

inflammatory perianeurysmal fibrosis of unresolved aetiology rather thansecondary to aneurysm compression. [148] Most often, ureteral

compression is associated with inflammatory aortic aneurysm. Extensive

retroperitoneal adhesions may result in ureteral obstruction in 18% of

patients. The inferior vena cava may become involved as well. [149]

long term low

functional gastric outlet obstruction

Duodenal obstruction is a consequence of compression of the duodenum

in its fixed retroperitoneal course between the aneurysmal aorta and the

superior mesenteric artery. [148]

long term low

distal embolisation

Incidence is 3% to 29%, most commonly affecting the digits (blue toe

syndrome). There is a 5% incidence of distal embolisation resulting in

limb-threatening ischaemia, digital ischaemia, and calf myonecrosis. [150]

variable low




































PrognosisThe natural course involves slow and steady growth with ultimate progressionto rupture. Most patients with rupture will not survive to reach the operatingtheatre; overall mortality is around 90%. [4] Given the morbidity and mortality

associated with surgical intervention, repair is typically deferred until thetheoretical risk of rupture exceeds the estimated risk of operative mortality.The majority of patients undergoing open repair remain without significantgraft-related complications during the remainder of their lives (0.4% to 2.3%incidence of late graft-related complications). [1] [147] Five-year survival ratesafter intact aneurysm repair average 60% to 75%. Those undergoingendovascular repair are more likely to have a delayed complication andrequire re-intervention.

Ultrasound of a 3.8 cm x 4.2 cm AAA














CT scan of a ruptured AAA

Various endovascular stent grafts used for endovascular repair (EVAR)



Endovascular repair (EVAR)



Type I endoleak at the distal left iliac anastomosis (leak encircled)



Extension stent graft deployed for the same type I endoleak (encircled)



Resolution of the type I endoleak resolved after extension deployed

Type II endoleak (encircled) discovered on follow-up CTEmail

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Ultrasound of a 3.8 cm x 4.2 cm AAA

University of Michigan, specifically the cases of Dr Upchurch reflecting the Departments of Vascular Surgery and

Radiology

CT scan of a ruptured AAA


Radiology

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Various endovascular stent grafts used for endovascular repair (EVAR)


Radiology

Endovascular repair (EVAR)


Radiology



Type I endoleak at the distal left iliac anastomosis (leak encircled)


Radiology



Extension stent graft deployed for the same type I endoleak (encircled)


Radiology



Resolution of the type I endoleak resolved after extension deployed


Radiology



Type II endoleak (encircled) discovered on follow-up CT


Radiology

Documents

Aneur Abd Aorte