Overview
Ruptured Abdominal Aortic Aneurysm
Topic Overview
Summary
Ruptured abdominal aortic aneurysm (rAAA) is a catastrophic vascular emergency with mortality over 80% if untreated. The classic triad is sudden severe abdominal/back pain, hypotension, and pulsatile abdominal mass. However, patients may present with atypical features. Any patient with collapse and abdominal/back pain must have rAAA considered. Transfer to a vascular centre for emergency repair (open or EVAR) is time-critical. "Permissive hypotension" pre-operatively is recommended.
Key Facts
- Mortality: 80-90% overall (including pre-hospital deaths); 40-50% in those who reach surgery
- Classic triad: Abdominal/back pain + hypotension + pulsatile mass (only ~50% have all three)
- Treatment: Emergency surgery — open repair or EVAR
- Pre-op target: Permissive hypotension (SBP 70-90 mmHg) to limit ongoing haemorrhage
- Screening: UK AAA screening program for men at 65 reduces rupture mortality
Clinical Pearls
Classic triad present in only 50% — maintain high index of suspicion in any collapsed elderly patient
Do NOT give aggressive IV fluids — permissive hypotension (target SBP 70-90) limits haemorrhage
Time to theatre is the key determinant of survival — activate vascular surgery IMMEDIATELY
Why This Matters Clinically
Ruptured AAA is rapidly fatal without surgery. Fast recognition, resuscitation within limits (permissive hypotension), and immediate transfer to vascular surgery save lives. Misdiagnosis as renal colic, back pain, or MI is common and delays life-saving treatment.
Visual Summary
Visual assets to be added:
- CT angiogram showing rAAA with retroperitoneal haemorrhage
- Clinical algorithm for suspected rAAA
- Anatomy diagram of abdominal aorta and aneurysm
- EVAR vs open repair comparison
Epidemiology
Incidence
- Rupture incidence: 1-3% per year for AAA 5-6cm; 10-20% per year for over 7cm
- Emergency presentations: ~5,000-8,000 per year in UK
- Overall mortality: 80-90% (includes pre-hospital deaths)
- Hospital mortality: 40-60%
Demographics
- Age: Peak 65-80 years
- Sex: Male:Female = 6:1
- Smoking: Strongest modifiable risk factor
Risk Factors for AAA Development & Rupture
| Risk Factor | Notes |
|---|---|
| Age over 65 | Strongest risk factor |
| Male sex | 6× higher risk than females |
| Smoking | Current or ex-smoker |
| Family history | First-degree relative with AAA |
| Hypertension | Chronic |
| Atherosclerosis | Peripheral vascular disease, CAD |
| COPD | Independent risk factor |
| Connective tissue disorders | Marfan, Ehlers-Danlos |
AAA Screening (UK)
- Men offered one-time ultrasound at age 65
- Reduces rAAA mortality by up to 50%
Pathophysiology
Aneurysm Formation
- Degradation of elastin and collagen in aortic wall
- Chronic inflammatory process
- Wall weakening → progressive dilatation
- AAA defined as aortic diameter over 3cm (normal under 2cm)
Rupture Mechanics
- Wall stress exceeds tensile strength
- Rupture risk increases exponentially with diameter:
- Under 5cm: 1% per year
- 5-6cm: 3-5% per year
- Over 7cm: 20-40% per year
Types of Rupture
| Type | Features |
|---|---|
| Retroperitoneal | 80% of ruptures; tamponade effect may allow transient stability |
| Free intraperitoneal | Massive haemorrhage; rapid cardiovascular collapse |
| Aortocaval fistula | Rare; high-output cardiac failure |
| Aortoenteric fistula | GI bleeding; can present as haematemesis/melaena |
"Contained Rupture"
- Retroperitoneal haematoma contained by psoas/spine
- Patient may be transiently haemodynamically stable
- Provides window for surgical intervention
Clinical Presentation
Classic Triad (Only ~50% Have All Three)
| Feature | Sensitivity |
|---|---|
| Abdominal/back pain | 75-90% |
| Hypotension | 50-60% |
| Pulsatile abdominal mass | 25-50% |
Typical Presentation
Atypical Presentations (Common Misdiagnoses)
Red Flags for rAAA
| Feature | Action |
|---|---|
| Age over 50 with sudden back/abdominal pain + collapse | High suspicion |
| Known AAA | Assume ruptured until proven otherwise |
| Hypotension | Do NOT delay for tests if unstable |
| Pulsatile mass | Immediate vascular referral |
Sudden onset severe abdominal or back pain
Common presentation.
May radiate to flanks, groin, or legs
Common presentation.
Collapse or syncope
Common presentation.
Signs of shock (pallor, tachycardia, altered mental status)
Common presentation.
Clinical Examination
Key Findings
Vital Signs:
- Tachycardia
- Hypotension (may be normotensive in contained rupture)
- Altered mental status
Abdominal Examination:
- Pulsatile epigastric/periumbilical mass (may not be palpable if obese or small aneurysm)
- Abdominal tenderness
- Abdominal distension (free blood)
- Peritonism (if free rupture)
Peripheral Signs:
- Mottled extremities
- Cool peripheries
- Weak/absent femoral pulses (rare)
Differential Diagnosis
| Condition | Distinguishing Features |
|---|---|
| Renal colic | Haematuria, normal exam, younger patient |
| Perforated viscus | Peritonism, free air on CXR |
| Acute pancreatitis | Raised amylase/lipase, different risk factors |
| Acute MI | ECG changes, troponin elevation |
| Mesenteric ischaemia | Acidosis, lactate, often AF |
Investigations
Haemodynamically Unstable Patient
- No time for imaging — proceed directly to theatre if clinical suspicion high
- Bedside ultrasound to confirm AAA (if available and rapid)
- Activate vascular team, arrange OR
Haemodynamically Stable (Contained Rupture Suspected)
| Investigation | Findings |
|---|---|
| CT angiogram | Gold standard — shows aneurysm, rupture site, retroperitoneal haematoma |
| Bedside USS | Confirms AAA presence (not rupture) |
| FBC | May show low Hb (or normal if acute) |
| Group & Save / Crossmatch | 10 units RBC |
| U&E, LFTs | Baseline |
| Coagulation | Baseline |
| ABG/VBG | Lactate, acidosis |
IMPORTANT
- Do NOT delay surgery for investigations in unstable patients
- Fluid resuscitation should be minimal (permissive hypotension)
Classification & Staging
By Haemodynamic Status
| Status | Management |
|---|---|
| Class I (Stable) | CT aortogram, planned repair if ruptured |
| Class II (Transient responder) | Rapid imaging, urgent repair |
| Class III (Non-responder) | Direct to theatre, resuscitative surgery |
Hardman Index (Mortality Prediction)
| Risk Factor | Points |
|---|---|
| Age over 76 | 1 |
| Creatinine over 200 μmol/L | 1 |
| Hb under 90 g/L | 1 |
| Ischaemic ECG changes | 1 |
| Loss of consciousness | 1 |
- 0-1: Survival ~60-70%
- 2: Survival ~40%
- 3+: Survival under 20% (futility consideration)
Management
Pre-Hospital / ED Resuscitation
Permissive Hypotension:
- Target SBP 70-90 mmHg (conscious patient)
- Avoid aggressive fluid boluses — increases haemorrhage
- Large-bore IV access × 2
Transfusion:
- Activate massive transfusion protocol
- O-negative if waiting for crossmatch
- Balanced ratio RBC:FFP:Platelets = 1:1:1
Analgesia:
- Avoid sedation/opioids that drop BP further
- Low-dose morphine if needed
Surgical Repair Options
| Method | Advantages | Disadvantages |
|---|---|---|
| EVAR | Lower immediate mortality, less physiological stress, faster recovery | Not suitable for all anatomy; endoleak risk |
| Open repair | Suitable for all, durable | Higher perioperative mortality, longer recovery |
EVAR vs Open in rAAA
- Meta-analyses show similar 30-day mortality
- EVAR preferred in anatomically suitable patients
- Open repair for unsuitable anatomy or aortoiliac occlusion
Post-Operative Care
- ICU admission
- Manage coagulopathy, hypothermia, acidosis ("lethal triad")
- Anticipate complications: AKI, ischaemic colitis, multi-organ failure
Complications
Immediate
- Death (perioperative mortality 40-50%)
- Massive haemorrhage
- Cardiac arrest
Post-Operative
- Ischaemic colitis: Inferior mesenteric artery ligation
- Acute kidney injury: Suprarenal clamping, contrast, hypoperfusion
- Abdominal compartment syndrome
- Multi-organ failure
- Lower limb ischaemia: Embolisation
- Spinal cord ischaemia (rare in infrarenal)
Long-Term (EVAR)
- Endoleak: Type I, II, III, IV
- Aneurysm sac expansion
- Graft infection
- Need for re-intervention
Prognosis & Outcomes
Mortality
| Stage | Mortality |
|---|---|
| Pre-hospital death | 50-60% |
| Reach hospital alive → die before surgery | 10-20% |
| Operative mortality (open) | 40-50% |
| Operative mortality (EVAR) | 30-40% |
| Overall survival | 10-20% |
Long-Term Survival (Survivors)
- 5-year survival after repair: ~50%
- Depends on comorbidities, age, post-op complications
Futility Considerations
- Hardman Index 3+ suggests extremely poor prognosis
- Shared decision-making with family if patient unlikely to survive
Evidence & Guidelines
Key Guidelines
- NICE AAA Screening Programme
- ESVS Guidelines on AAA Management (2019)
- Vascular Society of Great Britain and Ireland (VSGBI) Outcomes
Key Trials
- IMPROVE Trial: EVAR vs open repair for rAAA — similar 30-day mortality, better QoL with EVAR
- EVAR-1 and EVAR-2: Elective repair trials informing approach
Patient & Family Information
What is a Ruptured AAA?
An abdominal aortic aneurysm (AAA) is a bulge in the main blood vessel (aorta) in your tummy. If it bursts (ruptures), it causes life-threatening internal bleeding and needs emergency surgery.
Warning Signs
- Sudden, severe pain in the tummy or back
- Collapse or fainting
- Feeling sweaty, faint, or unwell
Treatment
- Emergency surgery to repair the blood vessel
- Some patients are suitable for keyhole surgery (EVAR)
- Surgery is high-risk but life-saving
Screening
- In the UK, men are offered a one-time ultrasound scan at age 65 to check for AAA
Resources
References
Primary Guidelines
- 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
- NHS AAA Screening Programme. aaa.screening.nhs.uk
Key Trials
- 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
- Hardman DT, et al. Ruptured abdominal aortic aneurysms: who should be offered surgery? J Vasc Surg. 1996;23(1):123-129. PMID: 8558722