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Question 1: Aortic Dissection (Stanford A)

Stem: A 60-year-old man presents to the emergency department with severe, “tearing” chest pain radiating to his back. A CT angiogram demonstrates a dissection flap originating in the ascending aorta and extending into the aortic arch.

Question: What is the most appropriate next step in management for this condition?

(A) Urgent surgical repair. (B) Aggressive medical management with beta-blockers. (C) Thoracic endovascular aortic repair (TEVAR). (D) Urgent transthoracic echocardiogram. (E) Systemic thrombolysis.

Correct Answer: (A) Urgent surgical repair.

Explanation:

  • Why (A) is correct: This is a Stanford Type A dissection (involving the ascending aorta). This is a surgical emergency with extremely high mortality due to the risk of rupture into the pericardium (causing cardiac tamponade), acute aortic regurgitation, or myocardial infarction (from coronary artery occlusion).
  • Why (B) is wrong: Aggressive medical management is the first-line treatment for uncomplicated Stanford Type B dissections (which only involve the descending aorta).
  • Why (C) is wrong: TEVAR is an endovascular (stent) option for complicated Stanford Type B dissections. It is not the primary treatment for Type A.
  • Why (D) is wrong: A CT angiogram is the gold standard for diagnosis. While an echo can show tamponade or aortic regurgitation, it is a diagnostic step, not the definitive management, and should not delay surgery.
  • Why (E) is wrong: Thrombolysis is absolutely contraindicated and would be fatal, as it would promote bleeding into the false lumen and pericardium.

Key Points: Stanford Type A Aortic Dissection

  • Definition: Any dissection that involves the ascending aorta (regardless of origin).
  • Management: Surgical emergency.
  • Key Complications:
    • Cardiac tamponade (most common cause of death).
    • Acute aortic regurgitation.
    • Myocardial infarction (coronary artery occlusion).
    • Stroke (carotid artery occlusion).

Question 2: Aortic Dissection (Stanford B)

Stem: A 68-year-old man with chronic hypertension presents with acute interscapular pain. A CT angiogram reveals a dissection flap beginning just distal to the left subclavian artery and extending down to the iliac bifurcation. The ascending aorta and arch are normal. The patient is haemodynamically stable with no signs of malperfusion.

Question: What is the most appropriate first-line management for this uncomplicated condition?

(A) Immediate open surgical repair. (B) Immediate thoracic endovascular aortic repair (TEVAR). (C) Aggressive medical management with blood pressure and heart rate control. (D) Surgical fenestration. (E) Catheter-directed thrombolysis.

Correct Answer: (C) Aggressive medical management with blood pressure and heart rate control.

Explanation:

  • Why (C) is correct: This is an uncomplicated Stanford Type B dissection (no involvement of the ascending aorta, no signs of rupture, and no organ malperfusion). The first-line treatment is medical, aiming to reduce aortic wall stress by lowering blood pressure (target SBP 100-120 mmHg) and heart rate (target <60 bpm), typically with IV beta-blockers.
  • Why (A) is wrong: Open surgery has high morbidity and is reserved for cases not amenable to endovascular repair.
  • Why (B) is wrong: TEVAR is reserved for complicated Type B dissections (e.g., persistent pain, rapid aortic expansion, malperfusion of the gut/kidneys/limbs, or rupture).
  • Why (D) is wrong: Fenestration (creating a hole in the flap) is a treatment for malperfusion, which this patient does not have.
  • Why (E) is wrong: Thrombolysis is contraindicated.

Key Points: Stanford Type B Aortic Dissection

  • Definition: Dissection confined to the descending aorta (distal to the left subclavian artery).
  • Management (Uncomplicated): Medical (IV beta-blockers, sodium nitroprusside).
  • Management (Complicated): Endovascular repair (TEVAR) is now the standard of care.

Question 3: Endoleak (Type II)

Stem: A 75-year-old man is undergoing a 1-year follow-up CT angiogram after an endovascular repair (EVAR) of an abdominal aortic aneurysm (AAA). The scan shows the aneurysm sac has increased in diameter by 6 mm. There is a new small pocket of contrast within the sac, which appears to be filling retrogradely from a lumbar artery. The stent graft itself appears intact with no proximal or distal leaks.

Question: What type of endoleak is this?

(A) Type I (B) Type II (C) Type III (D) Type IV (E) Type V (Endotension)

Correct Answer: (B) Type II.

Explanation:

  • Why (B) is correct: This is the definition of a Type II endoleak. It is the most common type and involves retrograde flow from a branch vessel (most commonly the inferior mesenteric artery or a lumbar artery) back into the aneurysm sac.
  • Why (A) is wrong: Type I is a seal failure at the proximal (Ia) or distal (Ib) attachment site of the graft. It is high-pressure and requires urgent treatment.
  • Why (C) is wrong: Type III is a graft defect, either from disconnection of modular components (IIIa) or a fabric tear (IIIb).
  • Why (D) is wrong: Type IV is related to graft porosity (leakage through the graft fabric), which is very rare with modern grafts.
  • Why (E) is wrong: Type V (Endotension) is defined as sac expansion without a visible endoleak, thought to be due to pressure transmission through the thrombus.

Key Points: Endoleaks after EVAR

  • Type I: Seal failure (proximal or distal). High pressure.
  • Type II: Branch vessel (lumbar, IMA). Most common.
  • Type III: Graft defect (tear or separation). High pressure.
  • Type IV: Graft porosity (rare).
  • Type V: Endotension (sac growth with no visible leak).

Question 4: Popliteal Artery Aneurysm

Stem: A 67-year-old man presents with a pulsatile mass behind his right knee. An ultrasound confirms a 3 cm aneurysm of the popliteal artery.

Question: What is the most significant associated finding that must be screened for in this patient?

(A) A contralateral (left) popliteal artery aneurysm. (B) Marfan syndrome. (C) Mycotic infection. (D) Femoral arteriovenous fistula. (E) Buerger’s disease.

Correct Answer: (A) A contralateral (left) popliteal artery aneurysm.

Explanation:

  • Why (A) is correct: Popliteal artery aneurysms are the most common peripheral arterial aneurysm. They have a very strong association with being bilateral (50-70% of cases). They are also strongly associated with AAAs (40-50% of cases). Screening the other leg is essential.
  • Why (B) is wrong: Marfan syndrome is associated with aortic root aneurysms and dissection, not peripheral aneurysms.
  • Why (C) is wrong: A mycotic (infected) aneurysm is a rare cause, but the vast majority are atherosclerotic.
  • Why (D) is wrong: An AV fistula is a traumatic or iatrogenic connection, not an aneurysm.
  • Why (E) is wrong: Buerger’s disease (thromboangiitis obliterans) is an occlusive disease of small vessels, not an aneurysmal disease.

Key Points: Popliteal Artery Aneurysm

  • Associations: Strongest link is bilateral (50-70%). Also strongly linked to AAA (40-50%).
  • Risk: They are high-risk not for rupture, but for thrombosis or embolization, leading to acute limb ischemia.
  • Management: Elective repair is generally recommended for aneurysms >2 cm or if symptomatic.

Question 5: Subclavian Steal Syndrome

Stem: A 65-year-old woman complains of new-onset dizziness and vertigo that is only triggered when she performs vigorous work with her left arm. On examination, her left radial pulse is weak, and her blood pressure is 150/90 mmHg in the right arm but 110/70 mmHg in the left arm.

Question: A duplex ultrasound is most likely to show which finding?

(A) Retrograde (reversed) flow in the left vertebral artery. (B) Antegrade (normal) flow in both vertebral arteries. (C) Occlusion of the left internal carotid artery. (D) Severe stenosis of the right subclavian artery. (E) A large goitre compressing the carotid.

Correct Answer: (A) Retrograde (reversed) flow in the left vertebral artery.

Explanation:

  • Why (A) is correct: This is the classic presentation of subclavian steal syndrome. There is a severe stenosis or occlusion of the proximal left subclavian artery (before the vertebral artery takeoff). When the arm exercises, it demands more blood. This “steals” blood by reversing flow down the left vertebral artery (drawing from the brain’s basilar artery), causing neurological symptoms.
  • Why (B) is wrong: Normal flow would not cause these symptoms.
  • Why (C) is wrong: Carotid occlusion would cause a stroke, not exertional vertigo in the arm.
  • Why (D) is wrong: The symptoms (arm claudication, pulse/BP difference) are on the left, so the pathology must be on the left.
  • Why (E) is wrong: A goitre would not cause these specific hemodynamic changes.

Key Points: Subclavian Steal Syndrome

  • Pathology: Occlusion of the proximal subclavian artery.
  • Haemodynamics: Blood flows up one vertebral artery, crosses over, and flows down the contralateral vertebral artery to supply the arm.
  • Symptoms: Neurological (dizziness, syncope) and/or arm claudication, triggered by arm exercise.
  • Sign: Unequal blood pressure (>15-20 mmHg difference) between arms.

Question 6: Fibromuscular Dysplasia (FMD)

Stem: A 34-year-old woman is investigated for new-onset, severe hypertension that is difficult to control. A CT angiogram of her renal arteries is performed. It demonstrates a “string of beads” appearance involving the mid and distal segments of the right renal artery.

Question: What is the most likely diagnosis?

(A) Atherosclerosis (B) Fibromuscular Dysplasia (FMD) (C) Polyarteritis Nodosa (PAN) (D) Takayasu’s Arteritis (E) Neurofibromatosis Type 1 (NF-1)

Correct Answer: (B) Fibromuscular Dysplasia (FMD).

Explanation:

  • Why (B) is correct: The combination of a young female patient, secondary hypertension, and the “string of beads” appearance is classic for FMD. This appearance is caused by alternating segments of stenosis (fibrous webs) and dilatation (aneurysms).
  • Why (A) is wrong: Atherosclerosis is the most common cause of renal artery stenosis overall, but it affects older patients and involves the ostium (origin) of the renal artery, not the mid/distal segments.
  • Why (C) is wrong: PAN causes multiple microaneurysms (“beading”) but in smaller visceral arteries (e.g., in the kidney parenchyma), not typically the main renal artery.
  • Why (D) is wrong: Takayasu’s is a large-vessel aortitis, causing long-segment wall thickening and stenosis, not a string of beads.
  • Why (E) is wrong: NF-1 can be associated with renal artery stenosis, but FMD is the classic cause of this specific angiographic sign.

Key Points: Fibromuscular Dysplasia (FMD)

  • Demographic: Classically young to middle-aged females.
  • Presentation: Secondary hypertension (renal artery) or stroke/TIA (carotid artery).
  • Classic Sign: “String of beads” on angiography.
  • Location: Affects mid-to-distal segments (unlike atherosclerosis, which is ostial).

Question 7: May-Thurner Syndrome

Stem: A 30-year-old woman, who is on the oral contraceptive pill, presents with her second episode of an unprovoked, swollen, and painful left leg. A duplex ultrasound confirms an extensive left iliofemoral DVT.

Question: Given the patient’s age and the exclusively left-sided nature of her DVT, what is the most likely underlying anatomical variant?

(A) Congenital absence of the IVC. (B) Compression of the left common iliac vein by the right common iliac artery. (C) Popliteal artery aneurysm. (D) Right-sided IVC. (E) Klippel-Trenaunay Syndrome.

Correct Answer: (B) Compression of the left common iliac vein by the right common iliac artery.

Explanation:

  • Why (B) is correct: This is the definition of May-Thurner Syndrome (or iliac vein compression syndrome). The left common iliac vein is compressed between the overriding right common iliac artery and the lumbar spine. This chronic compression promotes stasis and thrombus formation, explaining the strong predilection for DVTs to occur in the left leg.
  • Why (A) is wrong: IVC atresia would likely cause bilateral lower limb swelling and prominent collaterals.
  • Why (C) is wrong: A popliteal aneurysm would not cause an iliofemoral DVT.
  • Why (D) is wrong: A right-sided IVC is a normal variant and does not cause DVT.
  • Why (E) is wrong: This is a rare congenital syndrome involving port-wine stains, bony/soft tissue hypertrophy, and venous malformations, which is a much less common cause than May-Thurner.

Key Points: May-Thurner Syndrome

  • Pathology: Anatomical compression of the left common iliac vein by the right common iliac artery.
  • Presentation: The underlying cause for the majority of unprovoked left-sided iliofemoral DVTs, especially in younger women.

Question 8: Takayasu’s Arteritis

Stem: A 25-year-old Asian woman presents with bilateral arm claudication and absent radial pulses. A CT angiogram demonstrates marked, concentric wall thickening and long-segment stenosis of the aortic arch and its major branches (subclavian and carotid arteries).

Question: What is the most likely diagnosis?

(A) Giant Cell Arteritis (GCA) (B) Atherosclerosis (C) Buerger’s Disease (D) Takayasu’s Arteritis (E) Marfan Syndrome

Correct Answer: (D) Takayasu’s Arteritis.

Explanation:

  • Why (D) is correct: This is the classic “pulseless disease.” Takayasu’s is a large-vessel vasculitis that affects the aorta and its main branches. The key features are the young demographic (<40), female predominance, Asian ethnicity, and imaging findings of diffuse, long-segment wall thickening (aortitis).
  • Why (A) is wrong: GCA is also a large-vessel vasculitis but classically affects older patients (>50). While it can involve the aorta, Takayasu’s is the prime suspect in this age group.
  • Why (B) is wrong: Atherosclerosis is an intimal, plaque-forming disease and would be extremely unlikely to present this way in a 25-year-old.
  • Why (C) is wrong: Buerger’s disease affects the small-to-medium vessels of the distal extremities (hands and feet) and is associated with heavy smoking.
  • Why (E) is wrong: Marfan syndrome is a connective tissue disorder that causes aneurysms and dissection, not wall thickening and stenosis.

Key Points: Takayasu’s Arteritis

  • AKA: “Pulseless Disease.”
  • Pathology: Granulomatous large-vessel vasculitis.
  • Demographic: Young women (<40), often of Asian descent.
  • Imaging: Concentric mural thickening of the aorta and its major branches, leading to stenosis and occlusion.

Question 9: Intramural Haematoma (IMH)

Stem: A 72-year-old hypertensive man presents with acute, severe back pain. A non-contrast CT of the chest reveals a high-attenuation (60-70 HU) crescent within the wall of the descending aorta. There is no intimal flap or contrast-filled false lumen seen on the arterial phase.

Question: What is the most accurate diagnosis for this finding?

(A) Penetrating Atherosclerotic Ulcer (PAU) (B) Stanford Type B Dissection (C) Aortitis (D) Intramural Haematoma (IMH) (E) Saccular Aneurysm

Correct Answer: (D) Intramural Haematoma (IMH).

Explanation:

  • Why (D) is correct: This is the textbook definition of an IMH. It is part of the Acute Aortic Syndrome spectrum and is thought to be caused by a rupture of the vasa vasorum (the blood supply to the aorta itself), leading to a haematoma within the media. On non-contrast CT, this acute blood appears as a high-attenuation crescent. The key differentiator from dissection is the absence of an intimal flap.
  • Why (A) is wrong: A PAU is an outpouching of the lumen through a plaque. It can cause an IMH, but the finding itself is the IMH.
  • Why (B) is wrong: A dissection, by definition, must have an intimal flap separating a true and false lumen.
  • Why (C) is wrong: Aortitis is inflammatory wall thickening, which would be soft-tissue attenuation, not high-attenuation blood.
  • Why (E) is wrong: An aneurysm is a dilatation of all three layers; this is a haematoma within the wall.

Key Points: Intramural Haematoma (IMH)

  • Part of: Acute Aortic Syndrome (along with dissection and PAU).
  • Pathology: Haemorrhage into the aortic media without an intimal flap.
  • CT Finding: High-attenuation crescent in the aortic wall on non-contrast CT.
  • Risk: Can progress to a classic dissection or rupture.

Question 10: Penetrating Atherosclerotic Ulcer (PAU)

Stem: An 80-year-old man with extensive peripheral vascular disease presents with severe back pain. A CT angiogram demonstrates a focal, crater-like outpouching of the descending aortic lumen that projects beyond the aortic wall. This lesion arises from a heavily calcified and ulcerated atherosclerotic plaque.

Question: What is the most likely diagnosis?

(A) Aortic Dissection with thrombus (B) Saccular Aneurysm (C) Intramural Haematoma (IMH) (D) Penetrating Atherosclerotic Ulcer (PAU) (E) Mycotic Aneurysm

Correct Answer: (D) Penetrating Atherosclerotic Ulcer (PAU).

Explanation:

  • Why (D) is correct: This is the definition of a PAU. It is an ulceration of an atherosclerotic plaque that erodes through the internal elastic lamina into the media. On CTA, this appears as a contrast-filled, “crat-like” outpouching associated with severe atherosclerosis. It often has an associated IMH.
  • Why (B) is wrong: A true saccular aneurysm involves all three layers of the aortic wall and is not necessarily associated with a single plaque. A PAU is a specific entity arising from a plaque.
  • Why (C) is wrong: An IMH is the haematoma in the wall, which is often caused by a PAU, but the PAU is the primary lesion described here.
  • Why (A) is wrong: There is no dissection flap described.
  • Why (E) is wrong: A mycotic aneurysm is an infected aneurysm, often saccular, but is not associated with calcified plaque and usually occurs in a different clinical context (e.g., endocarditis, sepsis).

Key Points: Penetrating Atherosclerotic Ulcer (PAU)

  • Part of: Acute Aortic Syndrome.
  • Pathology: Ulceration of an atheromatous plaque that penetrates the internal elastic lamina.
  • Location: Almost always in the descending aorta (due to high plaque burden).
  • Imaging: A focal, contrast-filled outpouching in an area of severe plaque.
  • Risk: High risk of rupture; often associated with IMH.

Question 11: Acute Limb Ischemia

Stem: A 78-year-old woman with known atrial fibrillation, who is not anticoagulated, presents with a 3-hour history of a “perishingly cold,” painful, and pulseless right leg. A CT angiogram is performed.

Question: What is the most likely finding?

(A) Diffuse, concentric wall thickening of the femoral artery. (B) A large popliteal aneurysm with laminated thrombus. (C) An abrupt “meniscus sign” filling defect in the common femoral artery, with minimal collateral vessels. (D) Long-segment, calcified, occlusive disease in all calf vessels with extensive “corkscrew” collaterals. (E) Popliteal artery compression by the medial head of gastrocnemius.

Correct Answer: (C) An abrupt “meniscus sign” filling defect in the common femoral artery, with minimal collateral vessels.

Explanation:

  • Why (C) is correct: This describes a classic acute embolic occlusion. The source is the left atrium (due to atrial fibrillation). An embolus lodges at a bifurcation (like the common femoral), causing an abrupt cut-off with a “meniscus” shape. The lack of collaterals is what makes it a limb-threatening emergency.
  • Why (A) is wrong: This describes vasculitis, which is not the correct diagnosis.
  • Why (B) is wrong: A popliteal aneurysm can cause acute thrombosis, but an embolic occlusion from AFib is more likely and presents with this classic cut-off.
  • Why (D) is wrong: This describes chronic peripheral arterial disease, where the body has had years to develop collateral vessels. This patient would have claudication, not an acute “6 P’s” presentation.
  • Why (E) is wrong: This is popliteal artery entrapment syndrome, a rare cause of claudication in young athletes.

Key Points: Acute Limb Ischemia (Embolus)

  • Clinical: The 6 P’s (Pain, Pallor, Pulselessness, Paresthesia, Paralysis, Perishingly cold).
  • Source: Most commonly cardiac (e.g., AFib, post-MI thrombus).
  • Imaging:
    • “Meniscus sign”: A sharp, convex cut-off of the contrast column.
    • No/Poor Collaterals: This is the key difference from chronic disease.

Question 12: Pulmonary AVM / HHT

Stem: A 38-year-old woman is investigated for dyspnoea and small strokes (TIAs). She has a history of recurrent, severe nosebleeds (epistaxis) and has small red macules on her lips and fingertips. A CT angiogram of the chest reveals a 3 cm nodular lesion in the right lower lobe, which is fed by a large, dilated pulmonary artery branch and drained by a large pulmonary vein.

Question: What is the most likely underlying syndrome?

(A) Marfan Syndrome (B) Neurofibromatosis Type 1 (C) Tuberous Sclerosis (D) Hereditary Haemorrhagic Telangiectasia (HHT) (E) Birt-Hogg-Dubé Syndrome

Correct Answer: (D) Hereditary Haemorrhagic Telangiectasia (HHT).

Explanation:

  • Why (D) is correct: This is the classic triad for HHT (also known as Osler-Weber-Rendu syndrome). The triad is: 1) Telangiectasias (the red spots), 2) Recurrent epistaxis, and 3) Arteriovenous Malformations (AVMs). The lung lesion is a classic pulmonary AVM. The strokes are paradoxical emboli that pass through the AVM (bypassing the lung filter) and go to the brain.
  • Why (A) is wrong: Marfan syndrome is associated with aortic root disease.
  • Why (B) is wrong: NF-1 is associated with neurogenic tumours.
  • Why (C) is wrong: Tuberous sclerosis is associated with lymphangioleiomyomatosis (LAM) and renal angiomyolipomas.
  • Why (E) is wrong: Birt-Hogg-Dubé is associated with lung cysts, pneumothorax, and renal tumours.

Key Points: Hereditary Haemorrhagic Telangiectasia (HHT)

  • AKA: Osler-Weber-Rendu Syndrome.
  • Pathology: Autosomal dominant disorder causing abnormal blood vessel formation.
  • Clinical: Epistaxis, skin/mucosal telangiectasias.
  • Imaging: AVMs are the key finding. Most common in the lungs, liver, and brain.
  • Complication: Pulmonary AVMs create a right-to-left shunt, leading to paradoxical emboli (stroke).

Question 13: Chronic DVT

Stem: A 55-year-old man with “post-thrombotic syndrome” in his left leg undergoes a duplex ultrasound. The left popliteal vein is non-compressible. Which of the following features would most specifically indicate chronic DVT rather than acute DVT?

(A) The vein is distended to twice the size of the artery. (B) The thrombus within the vein is anechoic (black). (C) The vein is narrow, fibrosed, and contains echogenic linear webs (synechiae). (D) There is an absence of flow on Doppler. (E) The vein is compressible.

Correct Answer: (C) The vein is narrow, fibrosed, and contains echogenic linear webs (synechiae).

Explanation:

  • Why (C) is correct: These are the classic features of chronic DVT. The acute clot organizes, retracts, and becomes part of the vein wall. This leaves behind a narrowed, fibrosed, and often echogenic vein. The linear webs are remnants of the recanalized thrombus.
  • Why (A) is wrong: A distended vein is a sign of acute DVT, as the new clot expands the vessel.
  • Why (B) is wrong: An anechoic thrombus is a sign of acute DVT (fresh blood clot). Chronic clot is echogenic (bright).
  • Why (D) is wrong: Absence of flow can be seen in both, but complete occlusion is more typical of an acute event. Chronic DVT often has some partial (trickle) recanalized flow.
  • Why (E) is wrong: A compressible vein is a normal finding and rules out DVT in that segment.

Key Points: Acute vs. Chronic DVT (Ultrasound)

  • Acute DVT:
    • Vein: Distended.
    • Thrombus: Anechoic or hypoechoic.
    • Flow: Often completely occlusive.
  • Chronic DVT:
    • Vein: Normal size or narrowed.
    • Thrombus: Echogenic (bright), calcified.
    • Wall: Thickened.
    • Flow: Synechiae (webs), collaterals, partial recanalization.

Question 14: Carotid Artery Stenosis (NASCET)

Stem: A 70-year-old man presents with a transient ischemic attack (TIA). A CT angiogram of his neck is performed. The diameter of the most severe stenosis in the proximal left internal carotid artery (ICA) is 2 mm. The diameter of the normal distal cervical ICA (used as the reference) is 6 mm.

Question: According to the NASCET criteria, what is the calculated percentage of stenosis?

(A) 33% (B) 50% (C) 67% (D) 75% (E) 83%

Correct Answer: (C) 67%.

Explanation:

  • Why (C) is correct: The NASCET (North American Symptomatic Carotid Endarterectomy Trial) criteria are the standard for measuring carotid stenosis.
    • Formula: % Stenosis = (1 – [Stenosis Diameter / Distal ICA Diameter]) x 100
    • Calculation: (1 – [2 mm / 6 mm]) x 100
    • (1 – 0.33) x 100 = 0.666… x 100 = 66.7% (or 67%)
  • Why (A) is wrong: 33% would be the ratio of the stenosis to the distal vessel (2/6), not the percentage of stenosis.
  • Why (B), (D), (E) are wrong: These are incorrect calculations.

Key Points: Carotid Stenosis Measurement (NASCET)

  • NASCET Criteria: Compares the stenotic segment (S) to the normal distal cervical ICA (D).
  • Formula: (D – S) / D or 1 – (S / D)
  • Significance: This method is preferred over the “ECST” or “Common Carotid” method.
  • Management: Symptomatic patients with >70% stenosis (or 50-69% in some cases) benefit from carotid endarterectomy or stenting.

Question 15: Impending AAA Rupture

Stem: A 77-year-old man with a known 6 cm AAA presents to the ED with acute, severe abdominal pain and hypotension. A non-contrast CT is performed.

Question: Which of the following findings is the most specific sign of an unstable or acutely rupturing aneurysm?

(A) A large volume of intramural thrombus. (B) Extensive circumferential calcification of the aortic wall. (C) A high-attenuation crescent within the mural thrombus. (D) Bilateral common iliac artery aneurysms. (E) An associated popliteal artery aneurysm.

Correct Answer: (C) A high-attenuation crescent within the mural thrombus.

Explanation:

  • Why (C) is correct: The “high-attenuation crescent” sign on a non-contrast CT is the most specific sign of an unstable aneurysm or impending rupture. It represents an acute haematoma that has dissected into the mural thrombus or the aortic wall itself.
  • Why (A) is wrong: A large thrombus burden is common in large, stable aneurysms and is not itself a sign of instability.
  • Why (B) is wrong: Calcification is a chronic process and does not signify acute rupture. A focal breach in the calcification would be a sign, but “extensive calcification” is not.
  • Why (D) & (E) are wrong: These are common associated findings with AAA but do not indicate acute instability.

Key Points: Signs of AAA Instability / Rupture

  • High-attenuation crescent sign (on non-contrast CT).
  • Retroperitoneal haematoma (frank rupture).
  • Focal discontinuity of intimal calcification (“broken rind” sign).
  • Draped aorta sign (the posterior aortic wall conforms to the shape of the vertebral body, indicating posterior wall rupture).
  • Thrombosed-lumen-to-outer-wall distance > 10 mm.

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