Fellowship of the Royal College of Surgeons (FRCS) Vascular Surgery Syllabus

What are the four main causes of acute mesenteric ischaemia?

(1) SMA embolism (most common, often cardiac/AF source), (2) SMA thrombosis (on pre-existing atheroma), (3) non-occlusive mesenteric ischaemia (low-flow states), and (4) mesenteric venous thrombosis.

What is the typical presentation of renal artery stenosis and its commonest cause?

Resistant or accelerated hypertension, 'flash' pulmonary oedema, and progressive renal impairment (especially after ACE inhibitor/ARB). The commonest cause is atherosclerosis; in younger women, fibromuscular dysplasia.

What is the definition of an abdominal aortic aneurysm (AAA)?

A permanent focal dilatation of the abdominal aorta to $\geq 3$ cm, or more than $1.5\times$ the expected normal diameter. Most are infrarenal and true aneurysms involving all three vessel-wall layers.

What are the UK threshold diameters for elective AAA repair?

Repair is generally offered when the aneurysm is $\geq 5.5$ cm in diameter, expands by $>1$ cm per year, or becomes symptomatic. Below these thresholds the rupture risk is lower than the operative risk.

What is the UK AAA screening programme and its surveillance intervals?

Single abdominal ultrasound for men in the year they turn 65. Surveillance: $3.0\text{–}4.4$ cm rescanned yearly; $4.5\text{–}5.4$ cm rescanned every 3 months; $\geq 5.5$ cm referred for repair consideration.

What is the classic triad of a ruptured AAA?

Sudden severe abdominal/back (flank) pain, hypotension/shock, and a pulsatile expansile abdominal mass. A stable patient may go to CT angiography; an unstable patient with known/suspected AAA goes straight to theatre.

Compare EVAR and open repair for AAA in terms of early and late outcomes.

EVAR has lower perioperative mortality and shorter recovery but requires lifelong surveillance and has higher rates of reintervention and endoleak; the early survival advantage is lost over time. Open repair is more durable with fewer late reinterventions but higher initial morbidity/mortality.

What is an endoleak and what are the five types?

Persistent blood flow within the aneurysm sac outside the EVAR graft. Type I: graft attachment-site leak (proximal/distal). Type II: retrograde flow from branch vessels (e.g. lumbar, IMA) — commonest. Type III: graft defect/junctional separation. Type IV: graft fabric porosity. Type V: endotension (sac expansion without visible leak).

What defines a thoracoabdominal aortic aneurysm and what is the Crawford classification?

An aneurysm involving both the thoracic and abdominal aorta. Crawford types: I (descending thoracic to upper abdominal, above renals), II (extensive — from subclavian to aortic bifurcation, highest risk), III (distal thoracic to abdominal), IV (entirely abdominal, including visceral segment).

What is the most feared complication of thoracoabdominal aneurysm repair and how is it mitigated?

Spinal cord ischaemia causing paraplegia (from interruption of intercostal/segmental arteries supplying the artery of Adamkiewicz). Mitigation: CSF drainage, maintaining higher perfusion pressure, reimplantation of segmental arteries, and distal aortic perfusion/staged repair.

At what diameter is repair of a descending thoracic aortic aneurysm typically considered, and what is the favoured technique?

Repair is generally considered at $\geq 5.5\text{–}6$ cm (or $\geq 6$ cm) for degenerative descending thoracic aneurysms, lower in connective tissue disorders. TEVAR (thoracic endovascular aneurysm repair) is favoured when anatomy is suitable.

What is the most common peripheral arterial aneurysm, and why is bilateral assessment and AAA screening important?

The popliteal artery aneurysm. It is bilateral in ~$50\%$ of cases and associated with AAA in up to ~$30\text{–}50\%$, so the contralateral popliteal and the aorta should always be imaged.

What is the main risk of a popliteal artery aneurysm and its threshold for repair?

Unlike AAA, the main risk is thrombosis/distal embolisation causing acute limb ischaemia (rather than rupture). Repair is generally considered at $\geq 2$ cm, or if symptomatic/containing thrombus.

What is the commonest visceral (splanchnic) artery aneurysm and when is it especially important to treat?

The splenic artery aneurysm. It is more common in women and treatment is recommended in pregnancy or women of childbearing age, if symptomatic, if $>2$ cm, or if a pseudoaneurysm, because of high rupture mortality in pregnancy.

What is the DeBakey classification of aortic dissection?

Type I: originates in ascending aorta and extends beyond the arch. Type II: confined to the ascending aorta. Type III: originates in the descending aorta distal to the left subclavian (IIIa above diaphragm, IIIb extending below).

What is the Stanford classification of aortic dissection and how does it guide management?

Type A involves the ascending aorta (regardless of origin) — usually a surgical emergency due to risk of tamponade, aortic regurgitation and coronary involvement. Type B is confined to the descending aorta (distal to left subclavian) — usually managed medically unless complicated.

What is the initial medical management of aortic dissection?

Aggressive impulse control: reduce systolic BP to ~$100\text{–}120$ mmHg and heart rate $<60$ bpm to lower aortic wall shear stress ($\frac{dP}{dt}$). First-line is an IV beta-blocker (e.g. labetalol/esmolol), adding a vasodilator if needed, with strong analgesia.

What is the CEAP classification used for in venous disease?

Clinical, Etiological, Anatomical, Pathophysiological classification of chronic venous disorders. Clinical grades C0–C6: C0 none, C1 telangiectasia/reticular veins, C2 varicose veins, C3 oedema, C4 skin changes (pigmentation, eczema, lipodermatosclerosis), C5 healed ulcer, C6 active venous ulcer.

What is the primary pathophysiology of varicose veins and which clinical test localises reflux?

Incompetent venous valves causing reflux and venous hypertension in the superficial system. The Trendelenburg (tourniquet) test localises the level of incompetence; duplex ultrasound is the definitive investigation to map reflux (e.g. saphenofemoral/saphenopopliteal junction).

What are the NICE-recommended treatment options for symptomatic varicose veins, in order of preference?

1st line: endothermal ablation (radiofrequency or endovenous laser). 2nd line: ultrasound-guided foam sclerotherapy. 3rd line: surgery (high tie and stripping/ligation). Compression hosiery is used only if interventional treatment is unsuitable.

What are the components of Virchow's triad for venous thromboembolism?

(1) Venous stasis, (2) endothelial/vessel wall injury, and (3) hypercoagulability. These three factors describe the contributors to pathological thrombus formation.

What is the Wells score used for and how does it direct DVT investigation?

It estimates clinical pre-test probability of DVT. Score $\geq 2$ = DVT likely → proximal leg vein ultrasound (within 4 h, or D-dimer + interim anticoagulation if delayed). Score $\leq 1$ = unlikely → D-dimer; if positive, proceed to ultrasound.

What is the first-line anticoagulation for confirmed DVT/PE per current NICE guidance, and the usual treatment durations?

First-line is a DOAC (apixaban or rivaroxaban). Duration: at least 3 months; provoked VTE with a resolved transient factor typically 3 months, while unprovoked or ongoing risk factors are reviewed for long-term/indefinite anticoagulation.

What are the indications for an IVC filter in VTE?

Recurrent PE despite adequate anticoagulation, or VTE with an absolute contraindication to anticoagulation. Retrievable filters are preferred and should be removed once anticoagulation can safely be (re)started.

What is the underlying mechanism and typical location of a venous ulcer?

Sustained venous hypertension (from valvular incompetence or post-thrombotic obstruction) causes capillary leakage, fibrin cuffing and tissue damage. Ulcers are typically shallow, exudative, with irregular borders over the gaiter area, classically the medial malleolus.

What is the cornerstone of venous ulcer management and what must be checked first?

Graduated multilayer compression bandaging (e.g. four-layer) after confirming adequate arterial supply with ABPI (compression is safe if $\text{ABPI} \geq 0.8$). Wound care, leg elevation, and treatment of underlying superficial reflux aid healing and prevent recurrence.

How do venous, arterial and neuropathic (diabetic) ulcers differ in typical site and appearance?

Venous: gaiter area/medial malleolus, shallow, exudative, irregular margin. Arterial: distal/pressure points/toes, 'punched-out', deep, painful, dry. Neuropathic: over pressure/weight-bearing points (e.g. metatarsal heads), painless, surrounded by callus.

What distinguishes primary from secondary lymphoedema, and what is the diagnostic imaging test?

Primary lymphoedema arises from intrinsic lymphatic developmental abnormality (e.g. Milroy disease, lymphoedema praecox/tarda); secondary results from an external insult (filariasis worldwide, or surgery/radiotherapy/malignancy in developed countries). Lymphoscintigraphy is the diagnostic imaging test.

What is the mainstay of lymphoedema management?

Decongestive lymphatic therapy: skin care, manual lymphatic drainage, multilayer compression bandaging/garments, and exercise. Surgery (e.g. lymphaticovenous anastomosis, debulking) is reserved for selected refractory cases. Treating/preventing cellulitis is important.

What is the preferred type and order of arteriovenous access for haemodialysis?

An autogenous arteriovenous fistula is preferred (lowest infection/thrombosis rates and best patency). Order: radiocephalic (Brescia–Cimino) first, then brachiocephalic, then brachiobasilic transposition; a prosthetic AV graft is used when no suitable vein exists; tunnelled catheters are last resort.

What is the typical maturation time of a radiocephalic fistula and the 'rule of 6s'?

It usually takes ~$6\text{–}8$ weeks to mature. The rule of 6s for a usable fistula: flow $>600$ mL/min, diameter $>6$ mm, depth $<6$ mm below the skin, by ~6 weeks.

What is dialysis-associated steal syndrome and how does it present?

Diversion of arterial blood through the AV access shunts flow away from the distal hand, causing distal ischaemia: hand pain, coldness, pallor, paraesthesia, and in severe cases tissue loss. It may require banding, DRIL procedure, or ligation.

What are the 'hard' and 'soft' signs of vascular injury in trauma?

Hard signs (mandate intervention): pulsatile/expanding haematoma, active arterial haemorrhage, absent distal pulses, palpable thrill/audible bruit, signs of distal ischaemia. Soft signs: history of haemorrhage, non-expanding haematoma, proximity wound to major vessel, nerve deficit, ABPI $<0.9$.

What is the injured-extremity Doppler index used in trauma and its significance?

The injured extremity index (ankle pressure of injured limb divided by uninjured arm pressure). A value $<0.9$ suggests significant arterial injury and warrants CT angiography or surgical exploration.

In a mangled limb with combined orthopaedic and vascular injury, what is the usual order of repair?

Control haemorrhage first, then restore perfusion early (often a temporary vascular shunt), perform skeletal stabilisation, then definitive vascular repair, with a low threshold for prophylactic fasciotomy to prevent compartment syndrome from reperfusion.

What are the components of the diabetic foot pathological triad?

Peripheral neuropathy (sensory, motor and autonomic), peripheral arterial disease (ischaemia), and immunopathy/susceptibility to infection. Together they predispose to ulceration, infection and amputation.

What is a Charcot foot and how does it present acutely?

Charcot neuroarthropathy — progressive destruction of bones and joints in a neuropathic (well-perfused) foot. Acutely it presents as a red, hot, swollen foot, often without significant pain, that can be mistaken for cellulitis/infection; it can collapse into a 'rocker-bottom' deformity.

What classification grades diabetic foot ulcers, and what does it assess?

The University of Texas (and the older Wagner) classification. The University of Texas system grades ulcer depth (0–3) and stages for infection and ischaemia (A–D), better predicting outcome than Wagner, which grades depth/gangrene 0–5.

What is the principle of antibiotic and surgical management of an infected diabetic foot?

Urgent broad-spectrum antibiotics (guided by deep tissue/bone cultures), surgical drainage/debridement of dead tissue, offloading pressure, optimising glycaemic control, and revascularisation if ischaemic. Osteomyelitis may require prolonged antibiotics and/or bone resection.

What is Buerger's angle and what does it indicate in chronic limb ischaemia?

The angle to which the leg must be raised (supine) before it goes pale due to inadequate arterial pressure. An angle $<20^\circ$ indicates severe ischaemia; on dependency the foot becomes red (reactive hyperaemia/sunset foot) — a positive Buerger's test.