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

24 sample cards from the Vascular Surgery deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. 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.

2. 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.

3. 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).

4. 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.

5. 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.

6. 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.

7. 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.

8. 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.

9. 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.

10. 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.

11. 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.

12. 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.

13. 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.

14. 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.

15. 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.

16. 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.

17. 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 $<0.9$.

18. 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.

19. 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.

20. 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.

21. 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.

22. 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.

23. 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.

24. 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.

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