Abdominal aortic aneurysm

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Most AAAs are infrarenal degenerative dilatations. Increasing diameter, rapid expansion, symptoms, smoking and individual anatomy influence rupture risk, while age, frailty, cardiorespiratory reserve and preferences influence the net benefit of repair.

Use the NHS screening measurement and surveillance pathway for screen-detected aneurysms. Incidental or symptomatic aneurysms still require clinical assessment and vascular referral; a screening interval must never be used to defer review of new pain.

For an unruptured AAA meeting a repair criterion, NICE offers open repair unless abdominal copathology, anaesthetic risk or medical comorbidity makes it unsuitable. Standard EVAR is considered for specified abdominal copathology or other person-specific reasons; when open repair is contraindicated, compare EVAR with conservative management.

Key points

AAA is an abdominal aortic diameter of 3.0 cm or more; most are asymptomatic until found by screening or incidental imaging.
In England, men are invited for one-off ultrasound in the screening year in which they turn 65; men older than 65 who have never been screened can self-refer.
Screening surveillance is annual for 3.0–4.4 cm and every 3 months for 4.5–5.4 cm aneurysms.
Refer an asymptomatic AAA of 5.5 cm or more to a regional vascular service, to be seen within 2 weeks.
NICE advises considering repair for a symptomatic AAA, an AAA at least 4.0 cm that grows by more than 1.0 cm in 1 year, or an asymptomatic AAA at least 5.5 cm.
A new painful or tender known AAA is an emergency even if the last diameter was below an elective threshold.
Ultrasound is the surveillance test; CT angiography is used for operative planning in people being evaluated for repair.
Smoking cessation, blood-pressure treatment and lipid/CVD risk management improve overall vascular prognosis, but no medicine substitutes for surveillance or indicated repair.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Age-related degenerative disease

Most infrarenal AAAs are multifactorial degenerative lesions involving loss of elastin and collagen strength, inflammation and impaired repair. Older men are affected most often, so age and male sex strongly influence pre-test probability.

Smoking and vascular risk

Current or previous smoking is strongly associated with AAA formation; continued smoking is also associated with faster expansion and rupture. Hypertension and coexistent coronary, cerebral or peripheral arterial disease identify a population with substantial shared vascular risk.

Familial or inherited susceptibility

A first-degree family history increases risk. Heritable connective-tissue aortopathy is less typical of an isolated infrarenal AAA but deserves consideration in unusually young patients or more widespread aortic disease.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Aortic wall weakening
Chronic inflammation and proteolytic activity degrade medial elastin and collagen. Smooth-muscle loss and impaired repair leave the infrarenal aorta progressively less able to resist pulsatile pressure.
2
Progressive dilatation
The weakened segment enlarges with each cardiac cycle. Smoking, blood pressure and individual anatomy influence growth, while mural thrombus may coexist without reliably protecting the wall.
3
Rising wall tension
All else being equal, increasing radius raises circumferential wall tension; local geometry, wall thickness and tissue strength also matter. This relationship contributes to the greater rupture concern with larger or rapidly growing aneurysms.
4
Leak or rupture
When wall stress exceeds residual strength, blood escapes into the retroperitoneum or peritoneal cavity. Concealed bleeding may briefly preserve pressure before major haemorrhage causes shock and collapse.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Incidental or screen-detected AAA

Usually asymptomatic; ultrasound or CT shows a maximum infrarenal aortic diameter of at least 3.0 cm.

Symptomatic intact AAARed flag

Persistent abdominal or back pain, focal tenderness or a new pulsatile sensation in a person with an AAA requires urgent vascular assessment.

Rupture or leakRed flag

Sudden severe abdominal/back/flank pain, syncope, pallor, shock or reduced consciousness; the classic triad is often incomplete.

Risk phenotype

Older age, male sex, current or previous smoking, family history and coexistent coronary, cerebrovascular or peripheral arterial disease increase pre-test probability.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Abdominal ultrasoundFirst step
Why
Confirm and measure AAA without radiation or contrast.
Interpretation and limitations
Use maximum anteroposterior inner-to-inner diameter in the NHS pathway: <3.0 cm no AAA; 3.0–4.4 cm small; 4.5–5.4 cm medium; at least 5.5 cm large.
02
CT angiography of aorta and access vessels
Why
Define anatomy for repair and investigate a stable symptomatic aneurysm.
Interpretation and limitations
Shows proximal neck, branches, iliac access, leak and rupture; do not let CT delay theatre in an unstable patient when the vascular team judges immediate treatment necessary.
03
FBC, U&E/eGFR, coagulation screen and group-and-save/crossmatch
Why
Assess anaemia, renal/contrast risk, coagulopathy and transfusion readiness.
Interpretation and limitations
Abnormalities modify resuscitation and procedural planning but do not rule out rupture.
04
ECG and cardiorespiratory assessment
Why
Estimate peri-operative risk for elective repair.
Interpretation and limitations
Use findings with functional status and comorbidity; extensive testing should be proportionate and should not delay emergency care.
05
Serial diameter comparison
Why
Detect expansion.
Interpretation and limitations
Growth greater than 1.0 cm in 1 year in an AAA at least 4.0 cm is a NICE criterion for considering repair; first confirm comparable technique and measurement plane.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Renal colic

Pain is usually colicky, radiates from loin to groin and may accompany haematuria. A tender or known aneurysm, syncope or haemodynamic disturbance should override this apparently benign pattern.

Acute aortic syndrome

Dissection more often begins in the thoracic aorta with abrupt chest or interscapular pain, pulse or neurological asymmetry and branch-vessel ischaemia; urgent aortic imaging defines the extent.

Pancreatitis or perforated viscus

Epigastric pain, vomiting, lipase elevation or peritonism supports an abdominal inflammatory or perforating process. These clues do not safely exclude a leaking AAA in an at-risk patient.

Acute mesenteric ischaemia

Severe pain out of proportion to early abdominal findings, metabolic acidosis or an embolic context suggests bowel ischaemia. CT angiography is useful when the patient is stable enough.

Musculoskeletal back pain

Pain reproducible with movement or palpation and no systemic disturbance is more supportive, but new persistent back pain over a known AAA still requires urgent vascular assessment.

Additional chapter-specific clues

Alternative diagnoses

Renal colic, pancreatitis, perforation, mesenteric ischaemia and musculoskeletal pain can mimic AAA pain; haemodynamic instability and vascular findings raise urgency.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01emergencySuspected ruptured or symptomatic AAAFirst stepSudden severe abdominal/back pain, collapse, shock, tenderness or new pain over a known AAA.

1First: ABC resuscitation, two large-bore IV lines, bloods/crossmatch, analgesia and immediate senior vascular/anaesthetic contact.
2Next: arrange direct transfer to a vascular centre; use CTA only if sufficiently stable and it will change immediate operative planning.
3EscalationEscalation: activate major haemorrhage and proceed to endovascular or open repair according to anatomy, physiology and vascular-team judgement.
4Avoid excessive crystalloid or attempts to normalise blood pressure before haemorrhage control; use a patient-specific permissive-resuscitation strategy led by the emergency/vascular team.

02screeningNHS screening resultAsymptomatic aortic diameter measured by screening ultrasound.

1First: <3.0 cm is not an AAA and leaves the routine screening pathway.
2Next: 3.0–4.4 cm enters annual ultrasound surveillance; 4.5–5.4 cm enters 3-monthly surveillance.
3EscalationEscalation: at 5.5 cm or more, refer to vascular surgery for assessment, normally within 2 weeks.
4At every size: explain rupture symptoms, support smoking cessation and address blood pressure and wider CVD risk.

03electiveConsidering repairSymptomatic AAA, rapid expansion or diameter at/above elective threshold.

1First: vascular review and CTA for anatomy, with assessment of fitness, life expectancy and patient goals.
2Next: consider repair if symptomatic, at least 4.0 cm with growth over 1.0 cm/year, or asymptomatic and at least 5.5 cm.
3Next: follow the NICE hierarchy: offer open repair unless abdominal copathology, anaesthetic risk or medical comorbidity contraindicates it; consider standard EVAR for specified abdominal copathology or other person-specific reasons, and compare EVAR with conservative management when open repair is contraindicated.
4EscalationEscalation: expedite if pain, tenderness or accelerated expansion develops; symptoms override the routine elective timetable.

04preventionRisk reduction during surveillanceConfirmed AAA below a repair threshold or repair deferred.

1First: record smoking status and offer evidence-based cessation support.
2Next: diagnose and treat hypertension and dyslipidaemia under NICE guidance; prescribe antiplatelet therapy only for a separate established indication.
3Next: encourage activity and weight management within symptoms and comorbidity.
4EscalationEscalation: re-refer sooner for new pain, rapid growth, threshold diameter or a material change in fitness/preferences.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Rupture and haemorrhagic shock

Wall failure produces massive internal bleeding, hypotension, organ hypoperfusion and high mortality. The classic combination of pain, shock and a pulsatile mass is often incomplete.

Distal thromboembolism or occlusion

Mural thrombus in an infrarenal aneurysm can embolise distally into iliac or lower-limb arteries, while extensive aorto-iliac thrombosis may cause acute limb ischaemia even without rupture.

Post-repair sac expansion

After endovascular repair, endoleak, graft migration or component failure can keep the sac pressurised and allow renewed enlargement or rupture, making long-term imaging adherence clinically important.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Record AAA diameter, measurement method and date so that growth is compared like-for-like.
Use annual ultrasound for 3.0–4.4 cm and 3-monthly ultrasound for 4.5–5.4 cm screen-detected AAAs.
At each contact ask about new abdominal/back pain, tenderness, syncope and functional decline.
Review smoking, clinic/standing blood pressure, lipids and suitability for NICE-directed vascular prevention.
After repair, follow the vascular service's graft-specific programme; EVAR requires ongoing imaging for endoleak, migration and sac enlargement.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Diameter is not the only trigger

Symptoms and confirmed rapid growth can justify considering repair below 5.5 cm.

Screening is sex- and age-specific

Routine NHS England invitations target men in their 65th year; this does not prevent diagnostic ultrasound in women or younger people with clinical suspicion.

A normal pulse examination is weak reassurance

Body habitus and examiner variability mean a non-palpable aorta cannot exclude AAA.

EVAR is not a discharge from follow-up

Late endoleak, migration and sac expansion are why imaging adherence matters.

Measurement language matters

Thresholds should be interpreted using the method specified by the pathway; apparent growth may reflect a change of plane or caliper convention.

11Common pitfallsFrequent interpretation and management errors.

01
Reassuring a patient with new pain because the most recent AAA was below 5.5 cm.
02
Ordering lengthy investigations before contacting vascular services in suspected rupture.
03
Applying the screening programme only to invited men and overlooking self-referral for previously unscreened men older than 65.
04
Starting aspirin solely because an AAA exists, without checking for another antiplatelet indication and bleeding risk.
05
Assuming EVAR is always preferable without discussing anatomy, fitness, reintervention and surveillance.