GC199 Pulsating Abdominal Mass Aortic Aneurysm
An abdominal aortic aneurysm is a pathological dilation of the aorta (≥3 cm) that typically presents as a pulsatile, expansile midline abdominal mass with a risk of life-threatening rupture.
Pulsating Abdominal Mass — Aortic Aneurysm
This lecture, delivered by Prof. Stephen W.K. Cheng from the Division of Vascular Surgery, is a comprehensive tour of aneurysms — what they are, why they form, how they present, how to investigate and manage them, and what goes wrong if you miss them. The centrepiece is the Abdominal Aortic Aneurysm (AAA), the most common true arterial aneurysm, which is a silent killer: most patients are asymptomatic until it ruptures, and an unoperated rupture carries 100% mortality [1].
Learning objectives (inferred from lecture outline):
- Define aneurysm and classify by form, structure, and aetiology.
- Understand the pathology and natural history of AAA.
- Recognise clinical presentation (intact vs. ruptured).
- Perform focused physical examination of AAA.
- Select and interpret investigations (USS, CT, AXR).
- Understand indications and options for surgical treatment (open vs. endovascular repair/EVAR).
- Recognise and manage complications of AAA surgery — early and late.
- Understand the management of ruptured AAA as a surgical emergency.
- Appreciate screening evidence and the small-AAA trial.
- Understand advanced endovascular concepts (fenestrated/branched grafts, endoleaks).
Core Concepts and Mechanisms
An aneurysm is a PERMANENT, localised DILATATION of an ARTERY by ≥50% increase in diameter. [1]
High Yield Definition
Three critical words in the GC slide definition: Permanent (not transient spasm-related dilation), Localised (not diffuse ectasia of the entire vessel), Artery (venous dilations are varicosities, not aneurysms). The 50% threshold means that if the normal aorta is 2 cm, any focal dilation ≥ 3 cm qualifies as aneurysmal [1][2].
Why does this matter? Arteries are pressurised tubes. If a segment's wall weakens and dilates, the wall tension increases according to LaPlace's Law (Wall tension = Pressure × Radius). So once an aneurysm starts, dilation begets more wall tension, which begets more dilation — a positive feedback loop that explains why aneurysms progressively expand and eventually rupture.
| Form | Description | Key Point |
|---|---|---|
| Fusiform | Symmetrical dilation involving the entire circumference | Most AAAs are fusiform |
| Saccular | Asymmetric outpouching from one side of the artery wall | Think mycotic/infected aneurysms |
What the classification diagrams show: spindle (fusiform) vs localized outpouching (saccular) vs slit-like dissecting channel; separately, true wall vs false/pseudoaneurysm with laminated thrombus contained by compressed fibrous tissue. [1]
| Type | Layers Involved | Example |
|---|---|---|
| True aneurysm | All 3 layers — intima, media, adventitia | Most AAAs |
| False (pseudo) aneurysm | Wall made of extravascular connective tissue only; no true arterial wall | Anastomotic aneurysm, traumatic, femoral artery post-catheterisation |
Why this distinction matters: A true aneurysm still has some structural wall integrity. A pseudoaneurysm is essentially a contained leak — the "wall" is just fibrous tissue, making it inherently more unstable and prone to rupture.
Etiology is multi-factorial: Mechanical (degeneration, BP), Enhanced proteolytic activity (elevated MMP), Genetic (Marfan's, Ehlers-Danlos IV), Autoimmune, Infection. [1]
| Category | Mechanism | Example |
|---|---|---|
| Atherosclerotic/degenerative | Chronic inflammation → elastin/collagen degradation | 95% of AAAs |
| Mechanical | Hemodynamic stress, especially at bifurcations | Infrarenal aorta (turbulent flow) |
| Proteolytic | Elevated matrix metalloproteinases (MMP-2, MMP-9) destroy extracellular matrix | All AAAs |
| Genetic/connective tissue | Defective structural proteins | Marfan's (fibrillin-1), Ehlers-Danlos IV (type III collagen) |
| Autoimmune/inflammatory | Inflammatory infiltrate in adventitia | Inflammatory AAA (~5%) |
| Infective (mycotic) | Direct bacterial invasion of vessel wall | Salmonella, Staphylococcus, syphilis |
Anastomotic aneurysms are a specific type that occurs at the junction of a graft and native artery — a late complication of prior aortic surgery [1].
Rupture, Thrombosis, Embolism, Infection, Pressure effects [1]
Why each matters:
- Rupture: The feared outcome; risk is proportional to size (LaPlace's Law).
- Thrombosis: Slow flow within the aneurysm sac → mural thrombus → can occlude the vessel or embolise distally.
- Embolism: Fragments of mural thrombus or atherosclerotic debris break off → distal ischaemia (trash foot, blue toe syndrome).
- Infection: Mural thrombus is an excellent culture medium.
- Pressure effects: Large aneurysm compresses adjacent structures (ureter → hydronephrosis; duodenum → obstruction; vertebral bodies → erosion/back pain; IVC → venous congestion).
Abdominal Aortic Aneurysm (AAA) — Slide-by-Slide Detail
Loss of elastin and smooth muscle cells, disruption of extracellular matrix, deposition of adventitial collagen, wall thickening, inflammatory infiltrate. [1]
From first principles: The normal aortic wall is an elastic artery with abundant elastin (media) allowing it to recoil during diastole. In AAA:
- Elastin is degraded by MMPs → wall loses recoil.
- Smooth muscle cells undergo apoptosis → wall loses contractile tone.
- Collagen is deposited (adventitia tries to compensate) but is stiffer, not elastic → dilates progressively.
- Chronic inflammatory infiltrate (macrophages, lymphocytes) sustains the proteolytic environment.
Expansion follows LaPlace's law: ~5 mm/year. Risk of rupture at 5 years: < 5 cm = 20%; > 5 cm = 50% (10% per year). [1]
| AAA Size | Annual Rupture Risk | 5-Year Rupture Risk |
|---|---|---|
| < 5 cm | Low (~1–3%/year) | ~20% |
| > 5 cm | ~10%/year | ~50% |
| > 6 cm | 10–20%/year | Very high |
| > 8 cm | 30–50%/year | Almost certain |
From Maksim Surgery Notes [2]: Size-based rupture risk guides the threshold for intervention.
High Yield
The lecture uses a 5 cm threshold for discussion of surgical intervention. Some recent guidelines use 5.5 cm for men and 5.0 cm for women, but for exam purposes, use the GC lecture framing: ≥ 5 cm is the threshold for considering surgery [1].
Asymptomatic: incidental, PULSATILE abdominal MASS. Symptomatic: PAIN = impending rupture. [1]
Exam Trap
Any AAA with pain must be treated as a surgical emergency until proven otherwise — pain suggests impending rupture or contained leak. Never reassure a symptomatic AAA patient. This is the single most important clinical message from this lecture [1].
The lecture slide on survival shows that:
- Intact AAA repair: 3–5% operative mortality.
- Ruptured AAA repair: > 50% operative mortality.
- Unoperated ruptured AAA: 100% mortality.
This stark contrast is why elective repair of large AAAs (≥ 5 cm) is recommended.
Clinical Approach
Confirm AAA: Mass above umbilicus, Expansile pulsation. Extent of AAA: Size, Upper border, Lower border. Cardiovascular: Pulses, heart, BP. [1]
Step-by-step approach:
- Inspection: Visible pulsation in the epigastrium (thin patients).
- Palpation:
- Mass above the umbilicus [1] — the aortic bifurcation is at L4 (umbilical level), so an infrarenal AAA sits between the costal margin and umbilicus.
- Expansile pulsation [1] — place both hands on either side of the mass; they should be pushed apart with each pulse beat. This distinguishes an expansile mass (aneurysm) from a mass that is merely transmitted pulsation (e.g., a mass sitting on the aorta, like a pancreatic tumour, which pushes your hands forward but not apart).
- Size: Estimate transverse diameter between your hands.
- Upper border: Can you get above it? If yes → infrarenal. If no → suprarenal or thoracoabdominal.
- Lower border: Can you get below it? If yes → no iliac involvement.
- Tenderness: Tender = possible expansion/impending rupture.
- Cardiovascular assessment: Heart sounds, peripheral pulses (femoral, popliteal, dorsalis pedis, posterior tibial), BP in both arms, look for signs of distal embolisation (blue toes, livedo reticularis).
- Other aneurysms: Palpate femoral and popliteal arteries for aneurysms.
OSCE Tip
In an OSCE, demonstrate expansile pulsation by placing one hand on each side of the mass. Say: "I am checking whether this is an expansile pulsation, which would suggest an aortic aneurysm, rather than a transmitted pulsation from a mass overlying the aorta." This is a discriminator between AAA and other central abdominal masses [1][3].
| Investigation | Role | Key Points |
|---|---|---|
| Plain X-ray (AXR) | Calcifications in the aortic wall outline the aneurysm | Eggshell calcification; not sensitive (only visible if calcified) [1] |
| Ultrasound | Screening / Diagnosis / Surveillance | Non-invasive, no radiation, cheap. Measures AP and transverse diameter. Best for surveillance of small AAAs [1] |
Visual recognition: plain films with curvilinear rim calcification outlining the aneurysm; ultrasound showing a round dilated aortic lumen; CT panels for suprarenal extent and associated iliac aneurysms — imaging answers “how big, how high, what else?” before open vs EVAR planning. [1] | CT scan with contrast | Preoperative assessment (gold standard for anatomy) | Shows size, extent (supra/infrarenal), relationship to renal/iliac arteries, mural thrombus, retroperitoneal haematoma in rupture [1] | | CT Angiography (CTA) | Planning EVAR | Assesses neck length, angle, iliac access | | MRA/DSA | Rarely used | DSA reserved for intervention |
Ultrasound for screening and surveillance. CT scan for preoperative planning. [1]
Symptoms: Any symptoms = urgent. Size: 5 cm (approx). Medical risk: Associated diseases. Life expectancy: Not a contraindication. Age: Not a contraindication. [1]
Decision framework:
Risk of OPERATION vs. Risk of RUPTUREAll AAA > 5 cm should be operated on unless patient is medically unfit (operative mortality > risk of rupture) or has limited life expectancy. [1]
| Factor | Explanation |
|---|---|
| Symptoms | Any symptom (pain, tenderness, embolisation) → urgent surgery regardless of size |
| Size ≥ 5 cm | Elective repair indicated |
| Size 4.0–5.5 cm | Surveillance (USS every 6 months) — supported by UK Small Aneurysm Trial [1] |
| Age | Not a contraindication for surgery [1]; even 90-year-olds can be treated (usually with EVAR) [5] |
| Medical fitness | Cardiac disease is the biggest concern — major cause of perioperative death = MI [1] |
General: Blood tests, ECG, CXR. Cardiac: Cardiac assessment / intervention. Preparations: Monitors, blood. Major operative mortality = myocardial infarction. [1]
Why cardiac assessment?
- AAA patients share atherosclerotic risk factors with coronary artery disease.
- Aortic cross-clamping during open repair causes massive afterload increase → myocardial stress.
- De-clamping causes sudden preload drop and reperfusion → arrhythmias, hypotension.
- Hence, pre-op stress testing (e.g., dobutamine stress echo) is standard in elective cases.
Surgical Treatment [1]
Procedure:
- Midline laparotomy or retroperitoneal approach.
- Cross-clamp aorta above and below the aneurysm.
- Open the aneurysm sac.
- Sew in a Dacron inlay graft (tube graft if disease limited to aorta; bifurcated graft if iliac arteries involved).
- Close the aneurysm sac over the graft (to separate graft from duodenum — prevents aortoenteric fistula).
Open repair options: Tube graft (infrarenal only) or Aorto-iliac bifurcated graft (if iliacs involved). [1]
Endovascular Repair: Aortic stent graft [1]
Principle: A covered stent (fabric-covered metal frame) is inserted via the femoral arteries under fluoroscopic guidance, deployed within the aneurysm to exclude it from the circulation. Blood flows through the stent; the aneurysm sac is depressurised and eventually thromboses.
EVAR Critical Anatomical Requirements [1]:
| Parameter | Requirement | Why |
|---|---|---|
| Neck length | > 1.5 cm | Adequate landing zone for seal |
| Neck diameter | < 32 mm | Standard stent grafts cannot seal in very wide necks |
| Neck angle | < 45° | Severe angulation prevents good seal |
| Access vessel (iliac) diameter | > 7 mm | Device must fit through |
| Iliac tortuosity | Minimal | Severe tortuosity impedes delivery |
| Preserve internal iliac arteries | When possible | Loss of bilateral IIA → buttock claudication, pelvic ischaemia, colonic ischaemia |
EVAR Selection Criteria — High Yield
The lecture specifically lists neck length > 1.5 cm, neck diameter < 32 mm, neck angle < 45°, and iliac access diameter > 7 mm as EVAR requirements [1]. These are commonly tested as discriminators in MCQs.
30-day mortality: EVAR 1.7% vs. Open 4.7%. 4-year aneurysm-related mortality: EVAR 4% vs. Open 7%. [1] (EVAR-1 trial)
| EVAR | Open Repair | |
|---|---|---|
| 30-day mortality | 1.7% | 4.7% |
| 4-year aneurysm-related mortality | 4% | 7% |
| Durability | Requires lifelong surveillance (endoleaks) | Definitive |
| Reintervention rate | Higher | Lower |
| Hospital stay | Shorter | Longer |
| Suitability | Requires favourable anatomy | No anatomical restrictions |
Important nuance: EVAR has lower peri-operative mortality but requires lifelong CT surveillance for endoleaks and may need reintervention. Long-term all-cause mortality may converge between EVAR and open repair.
Types I, II, III, IV endoleaks [1]
| Type | Source | Significance | Management |
|---|---|---|---|
| I | Inadequate seal at proximal (Ia) or distal (Ib) attachment site | High pressure → high rupture risk | Re-intervention required (extension cuff, conversion to open) |
| II | Retrograde flow from branch vessels (lumbar, IMA) into sac | Most common; usually benign | Observe; intervene if sac expands |
| III | Fabric tear or junction between graft components | High pressure → rupture risk | Re-intervention required |
| IV | Porosity of graft fabric (early, self-limiting) | Benign | Self-resolves |
Operative Complications [1]
General: Cardiac (clamp/declamp), Respiratory. Specific: Haemorrhage, Bowel ischaemia, Impotence, Renal failure, Distal embolism, Paraplegia. [1]
| Complication | Mechanism | Key Detail |
|---|---|---|
| Cardiac (MI) | Aortic clamping → massive afterload ↑; declamping → sudden preload drop + reperfusion | Major cause of operative mortality [1] |
| Respiratory | Atelectasis, pneumonia, prolonged ventilation | Exacerbated by midline laparotomy |
| Haemorrhage | Anastomotic bleeding, back-bleeding from lumbar arteries | |
| Bowel ischaemia | Ligation of IMA, hypoperfusion of sigmoid colon | Most common segment affected: sigmoid colon (watershed area) |
| Impotence | Damage to hypogastric plexus during dissection around aortic bifurcation | |
| Renal failure | Suprarenal clamping, embolisation, hypoperfusion | |
| Distal embolism (Trash foot) | Manipulation dislodges thrombus/atheromatous debris → showers distally | Trash foot = multiple areas of digital ischaemia with palpable pedal pulses [1] |
| Paraplegia | Spinal cord ischaemia from occlusion of artery of Adamkiewicz (T9–L2) | More common in thoracoabdominal repairs |
Graft infection, Anastomotic aneurysm, Graft-duodenal fistula [1]
| Complication | Presentation | Management |
|---|---|---|
| Graft infection | Fever, bacteraemia, CT showing peri-graft fluid/gas | Explantation + extra-anatomic bypass ± long-term antibiotics |
| Anastomotic aneurysm | Pulsatile mass at anastomotic site, years later | Surgical repair |
| Graft-duodenal (aortoenteric) fistula | Herald GI bleed (small haematemesis) followed by massive haemorrhage | Must suspect in any patient with prior aortic graft + GI bleeding — endoscopy, CT → urgent surgery |
Exam Classic
A patient with a history of previous AAA repair who presents with GI bleeding — always consider aortoenteric fistula before attributing it to peptic ulcer disease. The classic pattern is a "herald bleed" (small, self-limiting bleed) followed by catastrophic haemorrhage [1].
Ruptured AAA [1]
Retroperitoneal, Intraperitoneal (Free), Into duodenum (GI bleeding), Into IVC (Heart failure) [1]
| Site | Outcome | Clinical Features |
|---|---|---|
| Retroperitoneal (most common) | Contained rupture — tamponaded by retroperitoneum; buys time | Severe back/flank pain, haemodynamically may stabilise transiently |
| Intraperitoneal (free) | Exsanguination, rapidly fatal | Sudden cardiovascular collapse, rigid distended abdomen |
| Into duodenum | Primary aortoenteric fistula | Massive GI haemorrhage |
| Into IVC | Aortocaval fistula | Acute high-output heart failure, continuous abdominal bruit, lower limb oedema |
PAIN (abdomen/back) + MASS (pulsatile, may be masked) + SHOCK (transient/profound) [1]
High Yield — The Classic Triad
Pain + Pulsatile Mass + Shock = Ruptured AAA until proven otherwise. This triad is the foundation of the clinical diagnosis. Note: the mass may be "masked" by obesity, abdominal distension, or a contained retroperitoneal haematoma [1].
Only 1 in 3 reaches hospital. Surgical emergency. Immediate diagnosis – operation. Operative mortality > 50%. Overall mortality > 80%. [1]
Treat hemorrhagic shock: Large bore IV, Cross match blood / FFP. Immediate operation. Do not waste time in investigations. [1]
Step-by-step emergency management:
- ABC: Secure airway, large-bore IV access × 2.
- Volume resuscitation: Crossmatch blood (at least 6 units pRBC + FFP). Use a permissive hypotension strategy (target SBP ~80–90 mmHg) — aggressive fluid resuscitation before aortic control can disrupt a contained haematoma and convert contained rupture to free rupture.
- Do NOT waste time on investigations if diagnosis is clinically clear [1].
- Immediate transfer to operating theatre for aortic control (clamp or endovascular balloon occlusion).
- In a modern vascular centre, urgent CT scan may be obtained if the patient is haemodynamically stable enough and diagnosis is uncertain, to plan for EVAR vs. open repair [6].
Cardiac, Respiratory, Renal failure (shock), Bleeding tendency (massive transfusion), Paralytic ileus (retroperitoneal hematoma), Jaundice (bleeding + transfusion) [1]
| Complication | Mechanism |
|---|---|
| Renal failure | Pre-renal (shock) + suprarenal clamping |
| Bleeding tendency / DIC | Massive transfusion → dilutional coagulopathy, hypothermia |
| Paralytic ileus | Retroperitoneal haematoma irritates gut |
| Jaundice | Haemolysis from massive transfusion + hepatic hypoperfusion |
| Colonic ischaemia | Post-op bloody mucus per rectum = ischaemic colitis of sigmoid (IMA ligation + hypotension) |
High aortic clamp → Proximal hypertension, Critical ischaemic time (visceral/renal), Vital branches, Spinal ischaemia. Treatment: Bypass, Reimplant visceral arteries. [1]
These are far more complex than infrarenal AAAs because clamping above the renal arteries causes:
- Renal ischaemia → acute kidney injury.
- Visceral ischaemia → mesenteric infarction.
- Spinal cord ischaemia → paraplegia (artery of Adamkiewicz).
- Proximal hypertension → cardiac strain.
Treatment: Open repair requires reimplantation of visceral arteries (coeliac trunk, SMA, renal arteries). Endovascular options include fenestrated and branched stent grafts [1].
Fenestrated and Branched Stent Grafts [1]
- Fenestrated graft: Has holes (fenestrations) aligned with the origins of renal/visceral arteries, allowing blood flow to these branches while excluding the aneurysm.
- Branched graft: Has dedicated limbs that are deployed into visceral/renal arteries.
- These are used when the aneurysm extends to involve the renal arteries (juxtarenal/pararenal/suprarenal).
Screening Evidence [1]
AAA screening in men over 65 reduces aneurysm-related mortality. [1]
- Multicentre Aneurysm Screening Study: Invited men ≥ 65 years for one-time USS screening.
- Result: Significant reduction in AAA-related mortality in the screened group (~ 42% reduction at 4 years).
- Lindholdt 2008: Confirmed both AAA-related and possibly all-cause mortality reduction with screening [1].
Small AAA (4.0–5.5 cm): Surveillance is as good as early surgery. [1]
- N = 1,090 patients with AAAs 4.0–5.5 cm randomised to early surgery vs. USS surveillance.
- Result: No survival benefit of early surgery for small AAAs → surveillance with regular USS until the aneurysm reaches ≥ 5.5 cm (or becomes symptomatic/rapidly expanding).
Endovascular repair is increasingly used for leaking/ruptured aneurysms in centres with appropriate expertise and equipment [1].
Advantages: Avoids laparotomy, can be faster to achieve aortic control via endovascular balloon occlusion. But requires favourable anatomy and CT planning (if patient is stable enough).
Exam Intelligence
| Trap | Why Students Get It Wrong | Correct Answer |
|---|---|---|
| "Transmitted pulsation" vs. "Expansile pulsation" | Students confuse masses overlying the aorta with AAA | Expansile = hands pushed apart; transmitted = mass pushed anteriorly only |
| Age as contraindication to surgery | Instinct says "too old for surgery" | Age is NOT a contraindication [1]. Even 90-year-old patients can undergo EVAR [5] |
| Investigating a clearly ruptured AAA | Students pick "CT scan" | Do not waste time on investigations — go to OR [1]. Exception: stable patient in modern vascular centre |
| Size threshold for elective repair | Confusion between 5.0 and 5.5 cm | GC lecture uses 5 cm; many guidelines use 5.5 cm for men. Use GC framing for exam [1] |
| Post-op bloody stool after AAA repair | Students think surgical haemorrhage | Think ischaemic colitis of sigmoid colon (IMA ligation + shock) — confirm with flexible sigmoidoscopy [5] |
| EVAR as "cure" | Students think EVAR is definitive | EVAR requires lifelong surveillance for endoleaks [1] |
| Type II endoleak | Students think all endoleaks need intervention | Type II (from lumbar/IMA branches) is usually benign — observe unless sac expands [1] |
| Condition | Distinguishing Features |
|---|---|
| AAA | Expansile pulsation, above umbilicus, non-tender (if intact) |
| Mass overlying aorta (e.g., pancreatic tumour, lymphoma) | Transmitted pulsation only (not expansile) |
| Tortuous aorta (elderly, hypertensive) | No true dilation on USS |
| Horseshoe kidney | Midline mass, does not pulsate |
- Aortic dissection vs. AAA: Dissection = tear in intima creating a false lumen; Aneurysm = dilation of all layers without a flap. Treatment is completely different (dissection: medical ± surgical depending on Stanford type; AAA: surgical) [8].
- Ruptured AAA as DDx of acute abdomen: Always consider in elderly patients with abdominal pain + shock. Other DDx includes perforated viscus, mesenteric ischaemia, acute pancreatitis [9].
- Interventional radiology: Stent grafts for AAA are covered in GC 014 [10]. The principle is that a fabric-covered stent excludes the aneurysm from circulation, reducing wall tension to zero.
- Abdominal examination: In OSCE/clinical exam, AAA is a recognised finding — palpate for expansile pulsation in the epigastrium [3][11].
High Yield Summary
-
Definition
- Aneurysm = permanent, localised dilation of artery ≥ 50% of normal diameter.
-
AAA key facts
- M > F, 97% infrarenal, 95% associated atherosclerosis, 20% have associated peripheral aneurysms.
-
Natural history
- Expands ~5 mm/year (LaPlace's law). Rupture risk < 5 cm = 20% at 5 years; > 5 cm = 50% at 5 years.
-
Clinical triad of rupture
- Pain (abdomen/back) + Pulsatile mass (may be masked) + Shock.
-
Physical exam
- Expansile pulsation above umbilicus; get above/below mass; check cardiovascular system and peripheral pulses.
-
Investigations
- USS for screening/surveillance; CT with contrast for preoperative planning.
-
Surgery threshold
- ≥ 5 cm or symptomatic. Age is NOT a contraindication. Operative mortality: intact 3–5%, ruptured > 50%, unoperated rupture = 100%.
-
Treatment
- Open repair (aneurysmectomy + inlay graft) vs.
- EVAR (stent graft).
- EVAR has lower 30-day mortality (1.7% vs. - 4.7%) but requires lifelong surveillance for endoleaks.
- EVAR requires neck ≥ 1.5 cm, diameter < 32 mm, angle < 45°, iliac access > 7 mm.
-
Ruptured AAA
- Treat shock, crossmatch blood/FFP, immediate operation. Do NOT waste time on investigations (unless in modern vascular centre with stable patient).
-
Post-op complications
- Cardiac (MI — #1 killer), bowel ischaemia (bloody stool = sigmoid ischaemic colitis, confirm with sigmoidoscopy), renal failure, trash foot, paraplegia. Late: graft infection, anastomotic aneurysm, aortoenteric fistula.
- Screening
- USS for men > 65 reduces AAA-related mortality (MASS trial). Small AAAs (4.0–5.5 cm) → surveillance (UK Small Aneurysm Trial).
Active Recall - Lecture Notes
[1] GC 199. Pulsating abdominal mass aortic aneurysm.pdf [2] Maksim Surgery Notes.pdf (Vascular surgery, Section 7.1) [3] MBBS Final MB (Surgery) (Felix PY Lai).pdf (Vascular Diseases, AAA section; Abdominal examination) [4] Ryan Ho GI.pdf (Central abdominal pain — Ruptured AAA) [5] 2017 Fourth Summative SAQ.pdf (Question 6) [6] 2020 Fourth Summative Assessment MCQ paper.pdf (Question 70) [7] 2021 Fourth Summative Assessment MCQ.pdf (Question 69, EMQ Section III) [8] Block A - Sudden severe chest pain_ acute myocardial infarction; aortic dissection.pdf [9] Maksim Medicine Notes.pdf (Section 7.1, GI clinical approach) [10] GC 014. How can interventional radiology help patient management.pdf [11] abdominal exam (MBBS IV) (student version).pdf
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