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Soo I have end posting today and this is my case . Imagine you are my examiner and ask me all posible questions that come to your mind

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The second image analysis returned empty text - let me work with what I extracted from the first image plus my visual reading of both images. I can clearly see the case details from the images directly. Let me now act as your examiner.

🩺 END POSTING VIVA - Examiner Mode

Patient Summary I've read from your case:

Mayakara Swamy, 38M, Tea shop owner, Koramangala
Complaints: Irregular swelling on right lower limb (3 years) + pain (3 months) + wound (1 month)
HOPI: Insidious onset, gradually progressive swelling up to the knee, increases on standing/walking, relieved on lying down. Dull aching pain x 3 months. Wound on right lower limb x 1 month - open ulcer, s/o sclerotherapy done 3 years ago
Skin changes: Discoloration, lipodermatosclerosis, itching, progressive ulceration with discharge
Past Hx: No similar complaints, No comorbidities, No DM/HTN/Epilepsy
Family Hx: No significant family history
Social Hx: Smoking ~2-3 cigs/day x 20 years, Alcohol ~2 pegs/day
GPE: Conscious, cooperative, well oriented - BP 112/80, Pulse 76 bpm, Temp afebrile, RR 16 cpm - moderately nourished, Local examination pending

Alright, let's begin. I am your examiner. Answer each question as you would in the actual posting exam.

SECTION 1: HISTORY & PRESENTING COMPLAINT

Q1. You've noted an irregular swelling on the right lower limb for 3 years - what are the specific characteristics you would ask about to differentiate a venous, arterial, or lymphatic cause at the bedside history itself?

Q2. The patient is a tea shop owner who stands for prolonged periods. How does occupation contribute to the pathophysiology of his condition?

Q3. The swelling increases on prolonged standing and decreases on lying down - what is the specific term for this and what does it tell you about the likely diagnosis?

Q4. He had sclerotherapy 3 years ago. Can you comment on the significance of this in the context of his current presentation?

Q5. The wound appeared 1 month ago. What features in history would make you worried this is a venous ulcer versus an arterial ulcer versus a mixed ulcer?

SECTION 2: EXAMINATION

Q6. When you approach this patient for local examination of the right lower limb, describe the systematic order in which you will examine him - what do you look for on inspection alone?

Q7. What is lipodermatosclerosis and how would it appear on examination? Why does it occur?

Q8. How do you perform the Trendelenburg test and what are its two components? What does a positive test tell you?

Q9. Name and describe 3 other clinical tests you would perform in this patient to assess the venous system.

Q10. How would you assess the arterial supply of the limb before treating the ulcer, and why is this critical?

SECTION 3: INVESTIGATIONS

Q11. What is your first-line investigation for this patient? Describe what you would look for.

Q12. What does the CEAP classification stand for? What class do you think this patient falls into?

Q13. If you suspect deep venous involvement, what investigation would you order and what findings would suggest deep venous insufficiency?

Q14. What is the Ankle-Brachial Pressure Index (ABPI)? How do you calculate it, and what values indicate different disease states?

SECTION 4: DIAGNOSIS & PATHOPHYSIOLOGY

Q15. What is your most likely diagnosis? State it clearly.

Q16. Explain the pathophysiology of venous ulcer formation from the beginning - starting from venous hypertension all the way to ulceration.

Q17. What are the common sites for venous ulcers and why do they occur there specifically?

Q18. Why does the patient have night cramps? What is the mechanism?

SECTION 5: MANAGEMENT

Q19. Describe the complete management of this patient - both the ulcer and the underlying condition.

Q20. What is compression therapy? What types are available? What ABPI value is a contraindication to compression?

Q21. What are the surgical options for varicose veins with venous ulcer? Describe the procedure of Trendelenburg operation (High ligation and stripping).

Q22. What dressing would you apply to this ulcer and what properties should an ideal dressing have?

Q23. This patient smokes 2-3 cigarettes/day. How does smoking affect wound healing and what advice would you give?

SECTION 6: COMPLICATIONS & PROGNOSIS

Q24. What are the complications of varicose veins that you know of? Name at least 6.

Q25. What is Marjolin's ulcer? How would you suspect it in this patient and what would you do?

Q26. What is the risk of deep vein thrombosis in this patient, and what prophylaxis would you give perioperatively?

RAPID FIRE ROUND 🔥

What nerve is at risk during stripping of the long saphenous vein?
What is the valve of Rosenmuller?
What is a blow-out perforator?
Name the Cockett perforators.
What is the difference between primary and secondary varicose veins?
At what ABPI would you absolutely NOT apply compression bandaging?

Good luck! Answer as many as you can - I'll give you feedback on each answer. Start with whichever question you feel most confident about, or go in order. 💪

Give me answers as well to all the questions

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Give me answers as well to all the questions

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Here are complete model answers to every question. Study these carefully - they are exam-standard responses.

COMPLETE VIVA ANSWERS - Varicose Veins with Venous Ulcer

SECTION 1: HISTORY & PRESENTING COMPLAINT

Q1. How to differentiate venous vs arterial vs lymphatic cause from history?

Feature	Venous	Arterial	Lymphatic
Onset	Gradual, insidious	Gradual or acute	Gradual
Swelling character	Pitting, soft, worse end of day	Minimal edema	Non-pitting, brawny
Pain	Dull aching, heaviness	Claudication, rest pain (severe)	Heaviness, no severe pain
Aggravated by	Standing, prolonged sitting	Walking (claudication)	Standing
Relieved by	Elevation of limb	Hanging limb down	Elevation
Skin changes	Pigmentation, eczema, lipodermatosclerosis	Pallor, atrophic, shiny, hair loss	Thickened, "peau d'orange"
Ulcer site	Gaiter area, medial malleolus	Tips of toes, pressure points	Rare
Night cramps	Yes	Severe rest pain at night	No

In this patient: Swelling worse on standing, relieved on lying down, insidious onset, associated pigmentation and lipodermatosclerosis = classical venous history.

Q2. How does occupation (tea shop owner, prolonged standing) contribute?

Prolonged standing increases ambulatory venous pressure in the lower limb. Normally, the calf muscle pump during walking reduces venous pressure from ~90 mmHg (standing) to ~30 mmHg (walking). In static standing, this pump mechanism is never activated. Result:

Persistent venous hypertension
Valve incompetence progressively worsens
Increased capillary hydrostatic pressure leads to protein-rich fluid leaking into interstitium = edema
Over time, leads to skin changes and ulceration
Occupations involving prolonged standing (barbers, surgeons, teachers, shop owners) are a well-recognized risk factor for varicose veins.

Q3. What is the term for swelling increasing on standing and reducing on lying down?

This is Dependent edema or Orthostatic edema. It indicates the edema is due to hydrostatic venous pressure rather than cardiac, renal, or hepatic causes. The fact that it relieves completely on lying down suggests it is not yet fibrotic (early-to-moderate stage). This is strongly suggestive of chronic venous insufficiency (CVI).

Q4. Significance of sclerotherapy 3 years ago?

Sclerotherapy was attempted as treatment for the varicose veins 3 years back, suggesting he had varicose veins even before the current presentation.
The fact that he now has a wound/ulcer suggests the sclerotherapy was either incomplete, the wrong veins were targeted, or there is underlying deep venous incompetence that sclerotherapy cannot fix.
Sclerotherapy works by injecting an irritant (e.g., sodium tetradecyl sulphate) into varicosed superficial veins, causing fibrosis and obliteration - but it only treats superficial incompetence.
If deep venous insufficiency is present, sclerotherapy alone will fail and the condition progresses.
Previous sclerotherapy can also cause skin changes and ulceration at injection sites.

Q5. History features to differentiate Venous vs Arterial vs Mixed ulcer?

Feature	Venous Ulcer	Arterial Ulcer	Mixed
Site	Medial gaiter area	Tips of toes, heel, pressure points	Variable
Pain	Mild, dull ache	Severe, worse at night	Moderate
History	Long-standing varicose veins, DVT	Smoking, DM, hypertension, claudication	Both
Skin around ulcer	Pigmented, lipodermatosclerosis	Pale, shiny, hairless, cold	Mixed
Bleeding on touch	Yes (bleeds freely)	No (ischemic, does not bleed)	Variable
Precipitating factor	Minor trauma	Minor trauma	Both
Relief	Elevation	Hanging limb down	Neither fully

In this patient: Medial limb, pigmentation, lipodermatosclerosis, preceded by varicose veins = venous ulcer. However, always check ABPI to rule out mixed component, especially since he smokes (atherosclerosis risk).

SECTION 2: EXAMINATION

Q6. Systematic inspection of the right lower limb:

Ask patient to stand. Inspect from groin to foot, front and back.

Look for:

Distribution of varicosities - Long saphenous (medial thigh/calf) vs short saphenous (posterior calf)
Saphena varix - Soft swelling at saphenofemoral junction in groin, disappears on lying down, has a cough impulse
Skin changes:
- Pigmentation (haemosiderin deposition) - brownish discoloration
- Lipodermatosclerosis - inverted champagne bottle appearance
- Atrophie blanche - white stellate scarring
- Varicose eczema/dermatitis
- Corona phlebectatica - fan-shaped intradermal veins at ankle
Ulcer: Site, size, shape, edge, floor, surrounding skin, depth, discharge, smell
Edema: Pitting or non-pitting, level
Limb color and hair loss: To assess arterial component
Dilated veins: Tortuosity, number, extent

Q7. What is lipodermatosclerosis (LDS)?

LDS is a chronic fibrotic process of the skin and subcutaneous fat in the gaiter region of the lower leg.
Appearance: The leg develops a characteristic inverted champagne bottle or inverted wine bottle shape - the ankle is constricted, the calf above is relatively normal. The skin is indurated, pigmented, thickened, and woody-hard on palpation.
Mechanism: Chronic venous hypertension → increased capillary hydrostatic pressure → extravasation of fibrin and red blood cells → haemosiderin deposition (pigmentation) → inflammatory cell infiltration → fibrosis of dermis and subcutaneous tissue → traps the skin
It is a CEAP C4b finding and indicates severe chronic venous disease.
Precedes ulceration in most cases.

Q8. Trendelenburg Test - Technique and Interpretation:

Technique:

Patient lies supine. Elevate the leg above heart level to empty the superficial veins completely (~45 degrees for 1-2 minutes).
Apply a tourniquet (or finger pressure) at the saphenofemoral junction (4 cm below and medial to the femoral pulse in the groin).
Ask the patient to stand up quickly.
Observe the veins for 30 seconds with tourniquet on, then release.

Interpretation - Two Components:

Part 1 (Tourniquet ON - standing):

Veins remain empty = Tourniquet has controlled the incompetent point = Saphenofemoral junction incompetence confirmed
Veins fill rapidly from below = Incompetent perforators below the tourniquet (tourniquet did not control filling)

Part 2 (Tourniquet RELEASED):

Veins fill rapidly from above (within 30 seconds) = Confirms sapheno-femoral incompetence (positive Trendelenburg)
Slow filling = Normal retrograde filling, not significant

Clinical significance: Identifies the level of incompetence, guiding surgical planning.

Q9. Three other clinical tests for venous assessment:

1. Perthe's Test (Deep vein patency test):

Apply tourniquet below knee while patient is standing
Ask patient to walk/exercise for 5 minutes
If deep veins are patent: superficial veins empty (muscle pump works)
If deep veins are obstructed: superficial veins engorge more (pain and worsening) = positive Perthe's = contraindication to surgery on superficial veins

2. Multiple Tourniquet Test (Fegan's / Three tourniquet test):

Three tourniquets applied at different levels (upper thigh, below knee, above ankle)
Patient stands
Filling between tourniquets identifies sites of incompetent perforators
The segment that fills indicates perforator incompetence at that level

3. Cough Impulse / Tap Test (Morrissey's / Percussion test):

Place one finger over the varicosity in the lower leg
Tap/percuss above the sapheno-femoral junction with other hand
A fluid thrill/impulse is felt = confirms continuity of the venous column = sapheno-femoral incompetence
Also: a cough causes a visible/palpable impulse along the long saphenous vein

Q10. Assessing arterial supply before treating ulcer:

This is critical because applying compression bandaging in the presence of arterial disease can cause limb ischemia and gangrene.

Clinical assessment:

Palpate peripheral pulses: dorsalis pedis, posterior tibial, popliteal, femoral
Capillary refill time
Skin temperature, color
Buerger's test (if arterial disease suspected)

Investigations:

Ankle-Brachial Pressure Index (ABPI) using hand-held Doppler - gold standard bedside test
Duplex Doppler - to assess both arterial and venous flow
CT angiography / MR angiography if revascularization is planned

SECTION 3: INVESTIGATIONS

Q11. First-line investigation:

Duplex Ultrasound Scanning (DUS)

Non-invasive, no radiation, cheap, reproducible
What to assess:
- Direction of flow in superficial and deep veins
- Presence of reflux (reflux >0.5 seconds = significant)
- Site and level of incompetence: SFJ, SSJ, perforators
- Deep vein patency (rule out DVT or post-thrombotic syndrome)
- Diameter of LSV/SSV (guides choice of ablation technique)
- Perforator incompetence (>3.5 mm diameter perforator with outward flow = incompetent)

For the ulcer specifically:

ABPI measurement (hand-held Doppler)
Wound swab if infected
Biopsy if malignancy suspected (Marjolin's)

Q12. CEAP Classification:

C = Clinical (C0-C6) E = Etiology (Congenital, Primary, Secondary) A = Anatomic (Superficial, Perforator, Deep) P = Pathophysiology (Reflux, Obstruction, Both)

Class	Description
C0	No visible signs
C1	Telangiectases / reticular veins
C2	Varicose veins
C3	Edema
C4a	Pigmentation or eczema
C4b	Lipodermatosclerosis or atrophie blanche
C5	Healed venous ulcer
C6	Active venous ulcer
C6r	Recurrent active venous ulcer

This patient: C6 (active ulcer) or C6r (recurrent, given sclerotherapy history), Ep (primary etiology), As/Ap (superficial ± perforator), Pr (reflux)

Q13. Deep venous involvement - investigation and findings:

Investigation: Duplex ultrasound (first-line for deep veins)

For obstruction: look for non-compressibility, absent flow, echogenic thrombus
For reflux: >1 second reflux in deep veins = deep venous insufficiency

Findings suggesting deep venous insufficiency:

Reflux in common femoral vein, popliteal vein, or tibial veins
Dilated deep veins
Post-thrombotic changes: thickened valve leaflets, intraluminal echoes, irregular walls
Reduced venous flow augmentation on calf compression

If DVT suspected acutely:

D-dimer (screening)
Venogram (gold standard, rarely done now)

Significance: If deep veins are involved, surgical treatment of superficial veins alone is insufficient and may actually be contraindicated (Perthe's test positive).

Q14. Ankle-Brachial Pressure Index (ABPI):

Definition: Ratio of systolic BP at ankle to systolic BP at brachial artery.

How to calculate:

Patient lies supine for 10 minutes
Measure brachial systolic BP (both arms, use higher)
Measure ankle systolic BP using hand-held Doppler at posterior tibial and dorsalis pedis (use higher)
ABPI = Ankle systolic pressure / Brachial systolic pressure

Interpretation:

ABPI	Significance
>1.3	Calcified vessels (DM/elderly) - falsely elevated, unreliable
1.0 - 1.2	Normal
0.8 - 1.0	Mild arterial disease (compression safe)
0.5 - 0.8	Moderate arterial disease (modified compression only, 30 mmHg)
<0.5	Severe arterial disease - NO compression - revascularize first
<0.3	Critical ischemia - limb threatening

For this patient's ulcer management:

ABPI >0.8: standard full compression (35-40 mmHg) is safe
ABPI 0.5-0.8: modified compression (30 mmHg) may be used
ABPI <0.5: compression is absolutely contraindicated - Bailey and Love's, p.1062

SECTION 4: DIAGNOSIS & PATHOPHYSIOLOGY

Q15. Most likely diagnosis:

Primary varicose veins of the right lower limb (Long saphenous system) with chronic venous insufficiency, complicated by venous (varicose) ulcer at the gaiter region.

Supporting features: 38-year-old male, prolonged standing occupation, insidious onset, progressive swelling to knee level, reduces on lying down, preceded by sclerotherapy, skin changes (lipodermatosclerosis, pigmentation), ulcer at typical site.

Q16. Pathophysiology of venous ulcer formation:

Valve incompetence (congenital, acquired, or post-DVT) at saphenofemoral junction or perforators
Blood refluxes from deep to superficial system → venous hypertension in superficial veins
High venous pressure transmitted to capillaries → increased capillary hydrostatic pressure
Fluid, proteins (including fibrin), and red blood cells leak into interstitium
Pericapillary fibrin cuffs form around capillaries → act as barrier to O2 and nutrient diffusion
Red blood cell extravasation → breakdown → haemosiderin deposition → skin pigmentation
Leukocyte trapping: WBCs accumulate in capillaries, become activated → release proteolytic enzymes, reactive oxygen species, cytokines → tissue damage
Fibroblast senescence: fibroblasts become abnormal, unable to respond to growth factors
Minor trauma to the already-compromised skin → ulceration
Growth factors are inhibited → poor wound healing → chronic non-healing ulcer

(Bailey & Love's, p.1060)

Key accepted mechanism: Ambulatory venous hypertension is the only universally accepted underlying cause of venous ulceration.

Q17. Common sites for venous ulcers and why:

Site: The gaiter region - the area between the ankle and the lower third of the calf, specifically the medial aspect above the medial malleolus (most common).

Why:

The medial malleolus overlies the medial group of perforating veins (Cockett's perforators) - these are the most commonly incompetent perforators
When these perforators become incompetent, high-pressure blood from the deep system is transmitted directly to the skin here
This area has thin skin and poor subcutaneous tissue, making it vulnerable
The long saphenous vein runs medially, making medial side more prone
Lateral ulcers occur over the short saphenous territory (posterior calf perforators)

Q18. Why does the patient have night cramps?

Mechanism:

Venous congestion in the limb leads to tissue hypoxia in muscles
Accumulation of lactic acid and metabolic byproducts in muscle due to poor venous drainage
This triggers involuntary muscle contractions = cramps
Night cramps in varicose veins are thought to be due to altered electrolyte balance (potassium, magnesium) at the muscle cell level due to chronic venous stasis
They typically occur at night because: during the day, walking helps venous return; at night when lying flat, while venous congestion reduces, muscles may cramp during relaxation/stretch phase

Treatment: Elevation of foot end of bed, compression stockings in daytime, quinine sulphate 300 mg at night.

SECTION 5: MANAGEMENT

Q19. Complete management of this patient:

Step 1: Assessment

Full clinical examination + ABPI
Duplex ultrasound (map veins, identify incompetence, check deep veins)
Blood investigations: CBC, RBS, RFT, coagulation profile
Wound swab if infected

Step 2: Conservative (all patients, first-line)

Limb elevation above heart level
Graduated elastic compression stockings (Class II: 25-35 mmHg) - worn from morning to night
Avoid prolonged standing, regular walks to activate calf muscle pump
Smoking cessation (this patient smokes - critical)
Wound care/dressing of ulcer
Treat infection if present (antibiotics)
Pentoxifylline 400 mg TDS as adjunct to compression

Step 3: Ulcer management

Cleanse with saline
Debridement of slough
Appropriate dressing (see Q22)
Four-layer compression bandaging (ideal interface pressure 35-40 mmHg, if ABPI >0.8)
Treat surrounding eczema with mild topical steroid + emollients

Step 4: Treatment of underlying venous disease (definitive)

Endovenous thermal ablation (EVLA - Endovenous Laser Ablation or RFA - Radiofrequency Ablation) - first choice if eligible
Sclerotherapy (Foam sclerotherapy) - for smaller veins or recurrences
Surgery: High ligation + stripping + avulsions (Trendelenburg + Babcock's operation)
SEPS (Subfascial Endoscopic Perforator Surgery) - for incompetent perforators in patients with ulcers

Q20. Compression therapy:

Types:

Elastic stockings (graduated compression stockings):
- Class I: 14-17 mmHg (mild varicose veins)
- Class II: 18-24 mmHg (moderate, edema)
- Class III: 25-35 mmHg (severe, post-ulcer)
- Class IV: >35 mmHg (lymphedema)
Compression bandaging:
- Short stretch bandages (inelastic): Zinc oxide impregnated (Viscopaste/Unna boot)
- Four-layer bandaging: Wool + crepe + elastic + cohesive = 35-40 mmHg
Intermittent pneumatic compression (IPC): Sequential pneumatic cuffs, useful when patient cannot tolerate bandages
Stockinette with compression: Two-layer hosiery

Contraindications to compression:

ABPI <0.5 (absolute) - Bailey & Love's, p.1062
Acute heart failure
Acute DVT (relative, though now used with DVT socks)
Peripheral neuropathy (relative)
Active infection / gangrene

Q21. Surgical options + Trendelenburg operation:

Surgical options for varicose veins with ulcer:

High ligation + stripping (Trendelenburg + Babcock's operation)
Multiple avulsion phlebectomy (stab avulsions)
SEPS (Subfascial Endoscopic Perforator Surgery)
Endovenous Laser Ablation (EVLA) / Radiofrequency Ablation (RFA) - modern day preference

Trendelenburg Operation (High ligation and Stripping):

Position: Supine, leg slightly abducted and externally rotated.

Steps:

High ligation (Trendelenburg's ligation):
- Groin incision (below inguinal ligament, over saphenofemoral junction)
- Expose long saphenous vein (LSV) at its junction with femoral vein
- Ligate and divide all 5-6 tributaries of LSV at the SFJ (superficial epigastric, superficial iliac circumflex, superficial external pudendal, anterolateral thigh vein, posteromedial thigh vein)
- Flush ligation at the femoral vein (within 5mm) to prevent recurrence
- Do NOT accidentally ligate the femoral vein
Stripping (Babcock's operation):
- Make a second incision at knee level (where LSV is accessible)
- Pass an internal or external Babcock stripper (invagination stripper) from groin to knee
- Strip the LSV from groin to knee (NOT below knee - risk of saphenous nerve damage)
- The vein invaginates on itself as it is pulled out
Multiple stab avulsions:
- Small stab incisions over marked varicose tributaries
- Avulse veins using phlebectomy hooks
- Leave all incisions open or close with Steri-strips
Perforator ligation:
- If incompetent perforators identified, ligate through separate incisions or via SEPS

Nerve at risk: Saphenous nerve runs with LSV below knee → stripping only done above knee to avoid injury.

Q22. Dressing for venous ulcer + properties of ideal dressing:

Ideal dressing properties (moist wound healing):

Maintains moist environment (promotes epithelialization)
Allows gaseous exchange (O2, CO2)
Provides thermal insulation (37°C optimal)
Impermeable to bacteria
Non-adherent (painless removal)
Absorbs excess exudate
Non-toxic, non-allergenic
Cost-effective
Easy to use
Conformable to wound shape

Dressing choices based on ulcer state:

Ulcer State	Dressing
Clean, granulating	Non-adherent dressings (Mepitel, Adaptic)
Highly exudative	Foam dressings (Mepilex), Alginate dressings (Kaltostat)
Sloughy, necrotic	Hydrogel (Intrasite gel), Hydrocolloid (Duoderm)
Infected	Silver-containing dressings (Aquacel Ag), Iodine (Inadine)
Epithelializing	Thin hydrocolloid, simple non-adherent

Then apply four-layer compression bandaging over the dressing.

Q23. Smoking and wound healing - advice to patient:

How smoking impairs wound healing:

Vasoconstriction (nicotine) → reduces tissue perfusion → tissue hypoxia
Carboxyhemoglobin (CO) → binds Hb, reduces O2 delivery to tissues
Inhibits WBC function → impaired immune response → increased infection risk
Impairs collagen synthesis → weak scar formation
Reduces growth factor activity (VEGF, PDGF) → poor angiogenesis
Increases oxidative stress → free radical damage to healing tissue
Increases platelet aggregation → thrombosis risk in small vessels

Advice:

Counsel strongly on smoking cessation
Refer to cessation clinic / quit line
Nicotine replacement therapy (patch, gum, lozenge)
Pharmacotherapy: Varenicline (Champix) or Bupropion
Explain risk clearly: patients who continue smoking have significantly higher ulcer recurrence rates and surgical complications

SECTION 6: COMPLICATIONS & PROGNOSIS

Q24. Complications of varicose veins (at least 6):

Mnemonic: HE BLEED

Haemorrhage - rupture of varicosities (can be torrential, especially in elderly)
Eczema / Varicose dermatitis - itchy, scaly rash
Bleeding into tissues - bruising, haemosiderin pigmentation
Lipodermatosclerosis - fibrosis of skin and subcutaneous tissue
Edema - ankle swelling
Erysipelas / Cellulitis - recurrent skin infections
DVT - deep vein thrombosis (especially with thrombophlebitis)
Thrombophlebitis - painful inflammation of varicose vein segment
Ulceration (venous leg ulcer) - most serious chronic complication
Saphena varix - dilation at saphenofemoral junction
Marjolin's ulcer - squamous cell carcinoma in chronic ulcer

Q25. Marjolin's ulcer:

Definition: A squamous cell carcinoma (or rarely basal cell carcinoma) arising in a chronic longstanding wound/ulcer. Originally described in burn scars by Jean Nicholas Marjolin.

In this patient - suspect if:

Ulcer is not healing despite adequate treatment >3 months
Edge becomes raised, everted, heaped up, rolled
Base becomes hard, warty, fungating
Foul smell out of proportion
Painless ulcer that was previously painful (loss of sensation as nerve invasion occurs)
Regional lymph node enlargement

Management:

Biopsy - punch biopsy or incisional biopsy from the edge
Histopathology confirms: well-differentiated squamous cell carcinoma
Wide local excision with adequate margins (2 cm)
Split skin grafting to cover the defect
Regional lymph node dissection if nodes involved
Radiotherapy/chemotherapy for advanced disease

Note: Marjolin's ulcer has a poor prognosis - it is aggressive, metastasizes rapidly via lymphatics, and has high recurrence rates.

Q26. DVT risk and perioperative prophylaxis:

DVT risk in this patient:

This patient already has venous insufficiency (stagnant blood, Virchow's triad)
Perioperative immobility increases risk further
Smoking adds to hypercoagulability
Use Caprini or Wells score to quantify risk

Virchow's Triad (predisposing factors):

Stasis - immobility, venous insufficiency
Endothelial damage - surgical trauma
Hypercoagulability - post-op state, smoking, malignancy

Perioperative prophylaxis:

Mechanical: Graduated elastic stockings (TED stockings), Intermittent pneumatic compression (IPC) intraoperatively, early ambulation post-op
Pharmacological:
- LMWH: Enoxaparin 40 mg SC once daily (starting 12 hrs before surgery or 6-8 hrs post-op)
- Continue for 7-10 days post-op (or until fully mobile)
- If high risk: continue for 28 days
Hydration: Adequate IV fluids perioperatively
Early mobilization: Most important - walk patient on same day as surgery if possible

RAPID FIRE ANSWERS 🔥

1. Nerve at risk during stripping of LSV? The saphenous nerve (sensory branch of femoral nerve) - runs alongside the LSV below the knee. This is why stripping is only done from groin to knee, not below. Injury causes numbness/paraesthesia along the medial side of the leg and dorsum of foot.

2. Valve of Rosenmuller? The terminal valve (valve of Rosenmuller) is the valve at the saphenofemoral junction, just before the long saphenous vein drains into the femoral vein. Incompetence of this valve is the most common cause of primary varicose veins.

3. Blow-out perforator? A blow-out perforator is an incompetent perforating vein where the valve has completely failed, allowing high-pressure blood from the deep system to blow outward into the superficial system. On examination, there is a localized bulge/blowout of the overlying skin and a fascial defect is palpable. The largest perforator defects are responsible for ulcer formation.

4. Cockett's perforators? The Cockett perforators (medial lower leg perforators) are 3 in number:

Cockett I: 6 cm above medial malleolus
Cockett II: 13.5 cm above medial malleolus
Cockett III: 18.5 cm above medial malleolus

They connect the posterior arch vein (tributary of LSV) to the posterior tibial veins. Their incompetence is directly responsible for medial malleolar venous ulcers - the most common site.

5. Primary vs Secondary varicose veins?

	Primary	Secondary
Cause	Intrinsic valve weakness/congenital	Consequence of another disease
Common causes	Heredity, prolonged standing, pregnancy	DVT, AV fistula, pelvic tumour, pregnancy
Deep veins	Normal	Often involved
Perthe's test	Negative (deep veins patent)	Positive (deep veins obstructed)
Surgery	Appropriate	May be contraindicated

6. ABPI at which you absolutely CANNOT apply compression? ABPI < 0.5 (or absolute ankle pressure < 60 mmHg) = absolute contraindication to compression bandaging. Revascularization must be done first. (Bailey & Love's, p.1062)

Sources: Bailey & Love's Short Practice of Surgery 28th Ed, Pye's Surgical Handicraft 22nd Ed, Harrison's Principles of Internal Medicine 22nd Ed (2025)

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