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Vascular Surgery
Emergency Medicine
EMERGENCY

Abdominal Aortic Aneurysm (AAA)

High EvidenceUpdated: 2025-12-22

On This Page

Red Flags

  • Ruptured AAA triad: Abdominal/back pain + Hypotension + Pulsatile mass
  • Symptomatic/tender AAA (impending rupture)
  • Rapid expansion greater than 1cm per year
  • New onset lower limb ischaemia (embolisation)
  • Collapse in elderly male with flank pain
Overview

Abdominal Aortic Aneurysm (AAA)

1. Clinical Overview

Summary

Abdominal Aortic Aneurysm (AAA) is a permanent focal dilatation of the abdominal aorta to greater than 1.5 times its normal diameter, typically defined as greater than 3.0cm. The vast majority are infrarenal, degenerative, and associated with atherosclerosis. AAA is usually asymptomatic until rupture, which carries mortality exceeding 80%. The UK NHS AAA Screening Programme targets men aged 65 to detect and monitor aneurysms before catastrophic rupture.

Key Facts

  • Definition: Aortic diameter greater than 3.0cm (normal approximately 2.0cm)
  • Prevalence: 5-10% of men over 65; 1% of women
  • Mortality: Ruptured AAA carries greater than 80% overall mortality
  • Screening threshold: Intervention considered at 5.5cm diameter
  • Location: 95% are infrarenal
  • Key management: Surveillance for small; surgical repair (EVAR or open) for large or symptomatic

Clinical Pearls

The Triad: Suspect ruptured AAA in any patient with sudden abdominal or back pain, hypotension, and pulsatile abdominal mass. Do not delay for imaging if clinically obvious.

Permissive Hypotension: In suspected rupture, maintain systolic BP 80-100mmHg. Aggressive fluid resuscitation may dislodge the tamponading clot and cause exsanguination.

Renal Colic Mimic: Elderly men presenting with "renal colic" and haemodynamic instability must have AAA excluded. This is a common fatal misdiagnosis.

Why This Matters Clinically

AAA rupture is one of the most fatal surgical emergencies. Early detection through screening and elective repair before rupture transforms a condition with greater than 80% mortality into one with less than 5% operative mortality. Recognition of the atypical presentation mimicking renal colic saves lives.


2. Epidemiology

Incidence & Prevalence

  • Prevalence in screened population: 1.5% of men aged 65
  • Prevalence in men over 65: 5-10%
  • Prevalence in women: Less than 1% (6-fold lower)
  • Trend: Declining due to reduced smoking rates

Demographics

FactorDetails
AgePeak incidence 65-75 years; rare below 55
SexMale:Female ratio 6:1
EthnicityHigher in Caucasians than Asians
GeographyHigher in developed countries

Risk Factors

Non-Modifiable:

  • Age greater than 65
  • Male sex
  • Family history (first-degree relative with AAA increases risk 2-4 fold)
  • Connective tissue disorders (Marfan, Ehlers-Danlos)

Modifiable:

Risk FactorRelative Risk
Smoking5-8x (strongest risk factor)
Hypertension1.5-2x
Hyperlipidaemia1.5x
Peripheral vascular disease2x

3. Pathophysiology

Mechanism

Step 1: Atherosclerosis and Inflammation (The Trigger)

  • Initiation: Laminar flow disruption at the aortic bifurcation predisposes to injury.
  • Infiltration: LDL cholesterol infiltrates the subendothelium, oxidizing and recruiting monocytes/macrophages.
  • Inflammatory Soup: Activated macrophages release TNF-alpha, IL-1beta, and IL-6.
  • T-Cell Response: CD4+ T-helper 2 cells dominate, driving a chronic inflammatory state fundamentally different from standard occlusive atherosclerosis.

Step 2: Extracellular Matrix (ECM) Degradation (The Weakening)

  • Elastolysis: The hallmark of AAA. Normal aorta is elastic; AAA aorta is rigid.
  • Enzymatic Destruction: Upregulation of Matrix Metalloproteinases (MMP-2 and MMP-9) overwhelms tissue inhibitors (TIMPs).
  • Elastin Fragmentation: Destruction of the tunica media lamellae leads to loss of recoil.
  • Collagen Turnover: Collagen subtypes shift from stable Type I to unstable Type III, reducing tensile strength.

Step 3: Vascular Smooth Muscle Cell (VSMC) Apoptosis

  • Loss of Cellularity: The media becomes acellular ("Medial Degeneration").
  • Phenotypic Switch: Remaining VSMCs switch from contractile to synthetic phenotype, producing inflammatory mediators instead of matrix.
  • Oxidative Stress: Reactive Oxygen Species (ROS) drive further apoptosis (programed cell death).

Step 4: Biomechanical Failure (The Expansion)

  • LaPlace's Law: Wall Tension ($T$) = Pressure ($P$) × Radius ($R$) / Wall Thickness ($h$).
  • The Vicious Cycle: As the radius ($R$) increases, Tension ($T$) increases. As the wall stretches, Thickness ($h$) decreases, further increasing Tension.
  • Asymmetry: Wall stress is highest at the shoulder of the aneurysm and the posterior wall, common sites for rupture.
  • Thrombus Role: Intraluminal Thrombus (ILT) is metabolically active, trapping neutrophils and increasing local hypoxia/proteolysis, weakening the wall further.

Step 5: Rupture Event

  • Critical Threshold: When Wall Stress > Wall Strength.
  • Trigger: Sudden spike in BP (coughing, straining) or progressive degradation.
  • Classification:
    • Free Rupture: Into peritoneal cavity -> Exsanguination -> Death in minutes.
    • Contained Rupture: Into retroperitoneum -> Tamponade effect -> "Window of opportunity" for survival.

Classification

TypeDefinitionClinical Features
True aneurysmInvolves all three layersMost common; fusiform shape
PseudoaneurysmContained by adventitia onlyPost-traumatic; unstable
FusiformCircumferential dilatation90% of AAAs
SaccularOutpouching from one sideHigher rupture risk
InfrarenalBelow renal arteries95% of cases
SuprarenalAbove or involving renals5%; more complex repair

Anatomical Considerations

  • The infrarenal aorta has fewer vasa vasorum and elastin, predisposing to aneurysm formation
  • Infrarenal location is important for EVAR; sufficient neck length (greater than 15mm) below renals is required for stent landing zone
  • Iliac arteries often involved (common iliac greater than 20mm is aneurysmal)

4. Clinical Presentation

Symptoms

Typical Presentation (Unruptured):

Symptomatic AAA (Impending Rupture):

Ruptured AAA:

Atypical Presentations:

Signs

Red Flags

[!CAUTION] Red Flags — Seek immediate vascular surgery input if:

  • Abdominal or back pain in patient with known AAA
  • Hypotension with pulsatile abdominal mass
  • New AAA tenderness on palpation
  • Collapse in elderly male with flank pain (do not assume renal colic)
  • Lower limb acute ischaemia with abdominal pulsatile mass

Asymptomatic (75%) — found incidentally on imaging or screening
Common presentation.
5. Clinical Examination

Structured Approach

General:

  • Haemodynamic status (BP, HR, capillary refill)
  • Signs of shock (pallor, sweating, confusion)
  • Peripheral pulses (may be reduced in rupture or embolisation)

Abdominal Examination:

  • Inspect for visible pulsation
  • Palpate gently for pulsatile expansile mass above umbilicus
  • Differentiate from transmitted pulsation (transmitted = pulsatile but not expansile)
  • Assess tenderness (suggests impending rupture)
  • Measure width of pulsation with two hands if possible

Peripheral Vascular:

  • Femoral, popliteal, posterior tibial, dorsalis pedis pulses
  • Look for concurrent peripheral aneurysms (popliteal present in 15% of AAA patients)

Special Tests

TestTechniquePositive FindingSensitivity/Specificity
Abdominal palpationTwo hands on either side of midline, feel for lateral expansionPulsatile expansile mass50-75% sensitivity for AAA greater than 5cm
Bedside ultrasoundFAST probe in midline, measure AP diameterDiameter greater than 3cm95%+ sensitivity in trained hands
Peripheral pulse examPalpate all lower limb pulsesAbsent pulses suggest embolisationN/A

6. Investigations

First-Line (Bedside)

  • Observations — Tachycardia, hypotension suggest rupture
  • ECG — Rule out cardiac cause; baseline before surgery
  • Bedside ultrasound — Rapid confirmation of AAA presence

Laboratory Tests

TestExpected FindingPurpose
FBCMay be normal initially; later Hb dropBlood loss assessment
Coagulation (PT/APTT)Check baselinePre-operative
Group and Save / CrossmatchHold 6-10 units packed red cellsPrepare for massive transfusion
U&EsBaseline creatinineRenal status pre-contrast/surgery
LactateElevated in shockMarker of tissue hypoperfusion

Imaging

ModalityFindingsIndication
UltrasoundAneurysm diameter; presence of thrombusScreening; surveillance; bedside in emergency
CT AngiogramPrecise size, morphology, relationship to renals, rupture confirmationPre-operative planning; suspected rupture (if stable)
MRAAlternative when CT contraindicatedAvoid in emergency
Plain X-rayCurvilinear calcification in aortic wallIncidental finding; not diagnostic

Diagnostic Criteria

  • AAA defined as aortic diameter greater than 3.0cm
  • Ruptured AAA diagnosed clinically (pain + hypotension + pulsatile mass) — do not delay for imaging if unstable

7. Management

Management Algorithm

           Abdominal Pain / Pulsatile Mass / Collapse
                        ↓
┌───────────────────────────────────────────────┐
│           IMMEDIATE ASSESSMENT (ED)           │
│  - Call: Vasc Surg + Anaesthetics + ED Senior │
│  - Access: 2 x Grey (16G) Cannulae            │
│  - Bloods: FBC, U&E, Clotting, X-match 6-10u  │
│  - Permissive Hypotension: Target SBP 80-90   │
└───────────────────────────────────────────────┘
                        ↓
┌───────────────────────────────────────────────┐
│           HAEMODYNAMIC STATUS?                │
├──────────────────────┬────────────────────────┤
│      UNSTABLE        │        STABLE          │
│ (SBP less than 90)   │ (SBP more than 100)    │
├──────────────────────┼────────────────────────┤
│          ↓           │           ↓            │
│  Bedside Ultrasound  │      CT Angiogram      │
│     (FAST Scan)      │    (Arterial Phase)    │
├──────────┬───────────┼───────────┬────────────┤
│   AAA    │  NO AAA   │    AAA    │   NO AAA   │
│ Confirmed│           │ Confirmed │            │
│    ↓     │    ↓      │    ↓      │    ↓       │
│ THEATRE  │ Medical   │ Assess    │ Medical    │
│  NOW     │ Cause     │ Anatomy   │ Cause      │
└────┬─────┴───────────┴────┬──────┴────────────┘
     │                      │
     ↓                      ↓
┌───────────────────────────────────────────────┐
│             INTERVENTION DECISION             │
│  1. EVAR Suitable? (Neck >15mm, Angulation)   │
│  2. Patient Fit? (Survival >6mo?)             │
│  3. Ruptured? (Emergency vs Urgent)           │
└───────────────────────────────────────────────┘
           ↓                        ↓
    ┌─────────────┐          ┌─────────────┐
    │    EVAR     │          │ OPEN REPAIR │
    │ (Endovasc)  │          │ (Laparotomy)│
    └─────────────┘          └─────────────┘

Acute/Emergency Management (Ruptured AAA)

Immediate Actions:

  1. Call vascular surgery team immediately
  2. Establish large-bore IV access (two 16G cannulae)
  3. Crossmatch 10 units packed red cells; activate massive transfusion protocol
  4. Permissive hypotension: target systolic 80-100mmHg
  5. Avoid excessive fluid resuscitation (risk of dislodging tamponade)
  6. Transfer directly to operating theatre if clinical diagnosis clear

Conservative Management

  • Best Medical Therapy (for all patients):
    • Smoking cessation (slows growth rate)
    • Blood pressure control (target less than 140/90)
    • Statin therapy (cardiovascular risk reduction)
    • Surveillance ultrasound as per size thresholds

Medical Management

Drug ClassDrugDoseDuration
StatinAtorvastatin20-80mg ODLifelong
AntihypertensiveACE inhibitor (e.g., Ramipril)Titrate to BP targetLifelong
AntiplateletAspirin75mg ODLifelong (cardiovascular protection)
Beta-blockerConsider if evidence of CVDVariableAs indicated

Surgical Management

Indications for Repair:

  • Diameter 5.5cm or greater (men); 5.0cm or greater often considered for women
  • Symptomatic AAA (any size)
  • Rapid growth (greater than 1cm per year)
  • Saccular morphology

Procedures:

ProcedureDescriptionMortalityReintervention
EVARStent graft via femoral arteries1-2%20% at 5 years
Open repairLaparotomy, aortic clamp, tube graft5-8%Less than 5%

Procedure Spotlight: EVAR (Endovascular Aneurysm Repair)

The Minimally Invasive Standard.

  • Indication: Anatomically suitable anatomy (Neck greater than 15mm long, less than 60° angulation, non-calcified access).
  • Anesthesia: Local (percutaneous) or General.
  • Steps:
    1. Access: Ultra-sound guided puncture of common femoral arteries causing Preclose technique (sutures placed before sheath).
    2. Wires: Stiff wires (Lunderquist) passed up to thoracic aorta.
    3. Main Body: Delivery system advanced. Stent deployed immediately below renal arteries ("Landing Zone").
    4. Gate Cannulation: Contralateral wire manipulated into the short leg of the main body.
    5. Limb Extension: Iliac limbs deployed to the iliac bifurcation.
    6. Modeling: Balloon inflation to seal all overlap zones.
  • Pros: Lower 30-day mortality (1.8% vs 4.3%), immediate mobilization, local anaesthetic possible.
  • Cons: Radiation exposure, contrast load, lifelong surveillance (endoleaks), higher re-intervention rate.

Procedure Spotlight: Open Surgical Repair

The Durability Gold Standard.

  • Indication: Unsuitable for EVAR, connective tissue disease, young fit patient.
  • Steps:
    1. Exposure: Midline laparotomy (from xiphisternum to pubis). Bowel reflected to right.
    2. Control: Dissection of Neck. "Blue Loops" around renal vein. Clamp placed on Aortic Neck (Infrarenal) and Iliacs.
    3. Aneurysmotomy: Sac opened longitudinally. Thrombus evacuated. Back-bleeding lumbar vessels oversewn.
    4. Grafting: Dacron tube graft (or Y-graft) sutured to healthy aorta with Prolene.
    5. Restoration: Clamps released ("Flush"). Check for bleeding. Sac closed over graft to protect bowel.
  • Pros: Durable (rarely fails late), no surveillance needed.
  • Cons: High physiological insult, risk of impotency/ischemia, prolonged recovery.

EVAR Anatomical Requirements (IFU):

  • Neck Length: >15mm healthy aorta below renals.
  • Neck Diameter: less than 32mm.
  • Neck Angulation: less than 60 degrees.
  • Access: Iliac arteries >7mm diameter, not heavily calcified/tortuous.

Disposition

  • Admit if: Ruptured or symptomatic AAA (emergency theatre)
  • Discharge if: Screened asymptomatic AAA with appropriate surveillance arranged
  • Follow-up: Per size thresholds; 1-3 monthly for large AAA; post-EVAR requires lifelong CT surveillance

8. Complications

Immediate (Minutes-Hours)

ComplicationIncidencePresentationManagement
RuptureVariableSudden pain, collapse, shockEmergency surgery
Intraoperative haemorrhage5-10%HypotensionSurgical control, transfusion
Cardiac events5%Chest pain, arrhythmiaStandard ACS management

Early (Days)

  • Renal failure: Contrast nephropathy or suprarenal clamping (5-10%)
  • Bowel ischaemia: Inferior mesenteric artery ligation; look for bloody diarrhoea (2-5%)
  • Lower limb ischaemia: Thromboembolism; may require embolectomy
  • Graft infection: Rare but devastating; presents with fever and sepsis

Late (Weeks-Months)

Endoleaks (Post-EVAR)

The "Achilles Heel" of EVAR.

TypeCauseDescriptionManagement
Type 1Seal FailureBlood flows around the top (1a) or bottom (1b) of the stent. High pressure.URGENT FIX: Extension cuff or ballooning. Risk of rupture.
Type 2RetrogradeBack-bleeding from lumbar or IMA vessels into the sac. Low pressure.Watch: Treat only if sac expands >5mm (Embolization).
Type 3Fabric FailureTear in the fabric or disconnection of modules. High pressure.URGENT FIX: Relining the graft.
Type 4PorosityBlood oozing through graft pores (historical grafts).Self-limiting: Resolves once anticoags reverse.
Type 5EndotensionPressure transmission without visible leak.Debated: Relining or conversion to open if sac expands.
  • Aortoenteric fistula: Late presentation with haematemesis / melaena; often fatal
  • Incisional hernia: Post-open repair (10-20%)
  • Sexual dysfunction: Pelvic nerve damage (open repair)

9. Prognosis & Outcomes

Natural History

  • AAA growth rate approximately 2-3mm per year
  • Risk of rupture increases exponentially with size:
    • Less than 4cm: Less than 0.5% per year
    • 4-5cm: 1% per year
    • 5-6cm: 5-10% per year
    • Greater than 6cm: 10-25% per year
  • Rupture carries greater than 80% overall mortality (50% die before reaching hospital)

Outcomes with Treatment

VariableEVAROpen Repair
30-day mortality1-2%5-8%
5-year survival65-70%65-70%
Reintervention rate15-20%Less than 5%
Aneurysm-related mortalitySimilar long-termSimilar long-term

Prognostic Factors

Good Prognosis:

  • Early detection through screening
  • Elective repair before rupture
  • Smoking cessation
  • Good cardiac function (low anaesthetic risk)
  • EVAR-suitable anatomy

Poor Prognosis:

  • Rupture before surgery
  • Advanced age (greater than 80)
  • Significant comorbidities (cardiac, renal, respiratory)
  • Suprarenal extension
  • Post-operative complications (renal failure, bowel ischaemia)

10. Evidence & Guidelines

Key Guidelines

  1. NICE NG156 (2020) — Abdominal aortic aneurysm: diagnosis and management. Recommends EVAR or open based on individual assessment; surveillance thresholds. NICE NG156
  2. NAAASP (UK NHS Screening Programme) — Men invited for screening in year they turn 65. Surveillance thresholds: less than 3cm discharge, 3-4.4cm annual, 4.5-5.4cm 3-monthly. NHS AAA Screening
  3. ESVS Guidelines (2019) — European Society for Vascular Surgery clinical practice guidelines on management of AAA. Threshold 5.5cm; consideration of 5.0cm in women.

Landmark Trials

UK Small Aneurysm Trial (1998) — Early surgery versus surveillance for 4.0-5.5cm AAAs

  • 1090 patients randomised
  • Key finding: No benefit to early surgery for small aneurysms
  • Clinical Impact: Established 5.5cm as the threshold for intervention

EVAR-1 Trial (2004, updated 2010) — EVAR versus open repair for elective AAA

  • 1082 patients randomised
  • Key finding: Lower 30-day mortality with EVAR (1.8% vs 4.3%), but benefit lost by 2 years; higher reintervention with EVAR
  • Clinical Impact: EVAR is preferred for high-risk patients; open repair remains valid for fit patients

IMPROVE Trial (2014) — EVAR versus open for ruptured AAA

  • 613 patients
  • Key finding: No difference in 30-day mortality (35% both groups); EVAR associated with shorter hospital stay
  • Clinical Impact: EVAR is a viable option for ruptured AAA in suitable anatomy

RESCAN Study (2013) — Meta-analysis of AAA screening

  • 127,891 men screened
  • Key finding: Screening reduces AAA-related mortality by 45% at 13 years
  • Clinical Impact: Justifies national screening programmes

Evidence Strength

InterventionLevelKey Evidence
InterventionLevelKey Evidence
-----------------------------------
Screening men at 651aMASS / RESCAN: Reduced AAA mortality by 42%. NNS = 700.
5.5cm repair threshold1bUK Small Aneurysm Trial: Survival identical for surveillance vs early surgery for 4.0-5.5cm.
EVAR for elective repair1bEVAR-1: 1/3 lower 30-day mortality. Benefit lost by 4 years due to re-interventions/aneurysm rupture.
EVAR unfit patients1bEVAR-2: No survival benefit of EVAR over medical therapy in unfit patients.
Ruptured: EVAR vs Open1bIMPROVE: 30-day mortality similar (~35%). EVAR patients go home faster and have better QoL.
Permissive hypotension2bMAP less than 70 mmHg associated with improved survival in trauma/rupture.

11. Patient/Layperson Explanation

What is an Abdominal Aortic Aneurysm?

Your aorta is the main blood vessel that carries blood from your heart down through your belly to your legs. Think of it like the main water pipe in your house. An aneurysm is a bulge in the wall of this pipe, like a weak spot in a balloon. If it gets too big, it could burst, which is very dangerous.

Why does it matter?

Most aneurysms cause no symptoms and are found by screening or by chance. However, if an aneurysm bursts, it causes massive internal bleeding. Unfortunately, many people do not survive a burst aneurysm. The good news is that if we find an aneurysm before it bursts, we can monitor it and fix it before it becomes dangerous.

How is it treated?

  1. Watching and waiting: For small aneurysms (less than 5.5cm), we do regular scans to check if it is growing. Most grow slowly.
  2. Lifestyle changes: Stopping smoking is the single most important thing you can do. We also control blood pressure and cholesterol.
  3. Keyhole surgery (EVAR): If the aneurysm is big enough to need fixing, we often use a stent inserted through a small cut in the groin. This is less invasive.
  4. Open surgery: Sometimes we need to do a larger operation through the belly to replace the weak part with a new tube. This is more major but very effective.

What to expect

  • If you are having regular scans, you will come to the hospital every few months to a year for an ultrasound.
  • If you have keyhole surgery, you may go home in 1-3 days and need rest for a few weeks. You will need CT scans for life to check the stent.
  • If you have open surgery, expect to stay in hospital for about a week and take 2-3 months to fully recover.

When to seek help

Call 999 or go to A&E immediately if you experience:

  • Sudden severe pain in your belly or back
  • Feeling faint or collapsing
  • Any new symptoms if you have a known aneurysm
  • Your tummy feels tender over the aneurysm

12. References

Primary Guidelines

  1. National Institute for Health and Care Excellence. Abdominal aortic aneurysm: diagnosis and management (NG156). 2020. NICE NG156
  2. Wanhainen A, et al. European Society for Vascular Surgery (ESVS) 2019 Clinical Practice Guidelines on the Management of Abdominal Aorto-iliac Artery Aneurysms. Eur J Vasc Endovasc Surg. 2019;57(1):8-93. PMID: 30528142

Key Trials

  1. The UK Small Aneurysm Trial Participants. Mortality results for randomised controlled trial of early elective surgery or ultrasonographic surveillance for small abdominal aortic aneurysms. Lancet. 1998;352(9141):1649-55. PMID: 9853436
  2. EVAR Trial Participants. Endovascular versus open repair of abdominal aortic aneurysm. N Engl J Med. 2010;362(20):1863-71. PMID: 20382983
  3. IMPROVE Trial Investigators. Endovascular or open repair strategy for ruptured abdominal aortic aneurysm: 30 day outcomes from IMPROVE randomised trial. BMJ. 2014;348:f7661. PMID: 24418950
  4. Cosford PA, Leng GC. Screening for abdominal aortic aneurysm. Cochrane Database Syst Rev. 2007;(2):CD002945. PMID: 17443519

Further Resources

  • NHS AAA Screening Programme: nhs.uk/conditions/abdominal-aortic-aneurysm-screening
  • British Heart Foundation: bhf.org.uk
  • Circulation Foundation: circulationfoundation.org.uk
13. Examination Focus

The "Vascular Status" Station

1. Inspection (End of Bed)

  • Patient: Cachectic? Painful? (Rupture). Connective tissue features (Marfanoid)?
  • Abdomen: Visible pulsation (thin patients). Scars (Previous laparotomy/EVAR).
  • Legs: Mottling, dusky toes (Trash foot - embolisation).

2. Palpation of the Aorta

  • Technique: Patient flat, hips flexed (relax abs). Use two hands.
  • Start: Xiphisternum. Move inferiorly.
  • Differentiate:
    • Pulsatile: Movement occurs.
    • Expansile: Hands move apart (The key sign of aneurysm).
  • Limits: Bifurcation is at the Umbilicus (L4). So palpate above the umbilicus.

3. The Trap: "Mass Assessment"

  • A pulsatile mass is NOT always an aneurysm.
  • Differentials:
    • Thin patient (normal aorta).
    • Mass transmitted pulsation (Pancreatic tumor, pseudocyst, lymph nodes) - Hand moves up/down, not apart.
    • Tortuous aorta.

4. Check Distal Perfusion

  • Blue Toe Syndrome: Micro-emboli from the aneurysm sac showering the toes. Palpable pulses but necrotic toes.
  • Popliteal Aneurysms: "Widened" popliteal pulse. 50% of popliteal aneurysms have an AAA. 15% of AAAs have a popliteal aneurysm.

Viva Questions:

  • Q: Who gets screened for AAA in the UK?
    • A: Men in their 65th year are invited for a one-off ultrasound. Women are not (low prevalence).
  • Q: Define an Aneurysm.
    • A: Permanent focal dilatation of an artery >50% of its normal diameter (>3cm for Abdominal Aorta).
  • Q: What is the risk of rupture at 6cm?
    • A: Approximately 10-20% per year.
  • Q: Why do we not operate on 4cm aneurysms?
    • A: The risk of surgery (approx 3-5%) exceeds the risk of rupture (less than 1%).
  • Q: What is the primary cause of death after elective AAA repair?
    • A: Myocardial Infarction. (AAA is a marker of systemic vascular disease).

Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists for emergency situations.

Last updated: 2025-12-22

At a Glance

EvidenceHigh
Last Updated2025-12-22
Emergency Protocol

Red Flags

  • Ruptured AAA triad: Abdominal/back pain + Hypotension + Pulsatile mass
  • Symptomatic/tender AAA (impending rupture)
  • Rapid expansion greater than 1cm per year
  • New onset lower limb ischaemia (embolisation)
  • Collapse in elderly male with flank pain

Clinical Pearls

  • **The Triad**: Suspect ruptured AAA in any patient with sudden abdominal or back pain, hypotension, and pulsatile abdominal mass. Do not delay for imaging if clinically obvious.
  • **Permissive Hypotension**: In suspected rupture, maintain systolic BP 80-100mmHg. Aggressive fluid resuscitation may dislodge the tamponading clot and cause exsanguination.
  • **Renal Colic Mimic**: Elderly men presenting with "renal colic" and haemodynamic instability must have AAA excluded. This is a common fatal misdiagnosis.
  • "Window of opportunity" for survival.
  • **Red Flags — Seek immediate vascular surgery input if:**

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines