Diagnosis of a Swelling - S. Das (A Manual on Clinical Surgery)

Step 1: What You Must First Determine

1. Where is the swelling arising from? - Skin? Subcutaneous tissue? Muscle? Vessel? Nerve? Bone?
2. What is the cause? - Congenital? Traumatic? Inflammatory? Neoplastic? Miscellaneous?

Step 2: Classification of Swellings by Cause

1. Congenital Swellings

• Generally present since birth: haemangioma, cystic hygroma, meningocele
• Some appear later in life but are still congenital: branchial cyst, dermoid cyst, thyroglossal cyst

2. Traumatic Swellings

• Develop immediately after trauma
• Examples: haematoma, fracture with displacement, dislocation, rupture of a muscle

3. Inflammatory Swellings

Exam tip from S. Das: Stress must be given to pain, redness, and heat. Also note: rapidly growing sarcomas (e.g. osteosarcoma) can mimic acute inflammatory swelling with pain, redness, swelling, and heat. The differentiating features in favour of acute inflammation are:

• Tenderness
• Brawny induration and oedema
• Fluctuation (= pus = inflammatory)
• Acute lymphadenitis in regional nodes
• Hectic fever (never in sarcoma)
• Leucocytosis (constant in inflammation, variable in sarcoma)

• Same signs as acute but in very subdued form
• Swelling dominates over pain, redness, heat
• Brawny induration and oedema are absent
• Can be difficult to differentiate from malignant growths - look for tenderness and fixity in malignant vs. history of occasional reduction in size in inflammatory (a tumour may be stationary but never recedes)

4. Neoplastic Swellings

Benign vs. Malignant Swellings - The Master Comparison Table

Key S. Das points:

• Benign tumours may undergo malignant transformation (commonest secondary change)
• Fibroadenoma of breast is called "Breast Mouse" due to free mobility
• Carcinoma = from epithelial cells; Sarcoma = from connective tissue
• Pain is absent in malignancy except osteosarcoma where pain precedes the swelling

Signs of Malignant Transformation in a Previously Benign Swelling

1. Sudden increase in size
2. Increased vascularity with rise of local temperature
3. Fixity and infiltration of surrounding structures (e.g. facial nerve in parotid tumour; hoarseness/dysphagia/dyspnoea in thyroid)
4. Secondary changes - increased pigmentation, ulceration, bleeding
5. Appearance of pain (late feature)
6. Involvement of regional lymph nodes
7. Appearance of distant metastasis

Step 3: How to Examine a Swelling (Local Examination)

A. Inspection

1. Site - Anatomical location
2. Size - Rough dimensions
3. Shape - Round, oval, lobulated, irregular
4. Surface - Smooth or nodular
5. Skin over the swelling - Normal, discoloured, redness, peau d'orange, dilated veins, punctum
6. Number - Single or multiple
7. Margin - Well-defined or ill-defined
8. Impulse on coughing - Present or absent

B. Palpation

1. Temperature - Warm (inflammation) vs. normal/cool
2. Tenderness - Acute inflammation; malignant tumours are NOT tender in early stages
3. Surface and edge - Smooth/rough, well-defined/ill-defined
4. Consistency:
   • Soft - Lipoma (characteristically soft with lobulated feel)
   • Firm - Fibroma, lymph node
   • Hard/Bony hard - Osteoma, calcified lesion
   • Fluctuant - Cyst, abscess (liquid content)
   • Rubbery - Lymphoma
5. Fluctuation test - Two-finger test (must be positive in two planes to confirm fluid)
6. Translucency - Shine a torch: positive = cystic hygroma, branchial cyst (fluid-filled); negative = dermoid (pultaceous material), lipoma, solid tumours
7. Compressibility and reducibility:
   • Compressible (refills on removing pressure) = lipoma, vascular swellings
   • Reducible = hernia, hydrocoele
8. Pulsatility:
   • Transmitted pulsation = aneurysm sac
   • Expansile pulsation = true aneurysm
9. Mobility:
   • Free mobility = benign (lipoma, fibroadenoma)
   • Fixity to skin = infiltrating malignancy, inflammatory adhesion
   • Fixity to deep structures = deep malignancy
10. Relations to skin: Pinch the skin over the swelling - free or attached
11. Relations to deep structures: Ask patient to contract underlying muscle - if swelling becomes less mobile = arising from/attached to deep structures
12. Regional lymph nodes - Always palpate draining lymph nodes
13. Impulse on coughing - Hernia, meningocele

C. Auscultation

• Bruit = arteriovenous malformation, thyroid swelling (vascular)
• Bowel sounds = hernia containing bowel

Step 4: Differential Diagnosis - Swellings from Skin and Subcutaneous Tissue

Congenital Swellings

• Develops at lines of embryonic fusion
• Sites: outer angle of orbit (fronto-nasal + maxillary processes), behind pinna (post-auricular dermoid), below tongue (sublingual dermoid)
• Features: fluctuation positive, translucency negative (pultaceous material inside), round and smooth, margin yields to finger pressure and does NOT slip away (unlike lipoma)
• Free from skin AND deeper structures
• May produce bony indentation at margin
• Never gives impulse on coughing (except rare type extending intracranially)

• (a) Capillary (Strawberry) haemangioma - bright red/purple flat patches; pressure causes complete disappearance or blanching; commonly on the face/cheek
• (b) Cavernous haemangioma - compressible, bluish, soft; emptied on pressure and refills on release; may be on the face/forehead
• (c) Plexiform/Cirsoid haemangioma - from artery; pulsatile

Inflammatory Swellings

• Abscess: fluctuant, tender, warm, red; acute lymphadenitis in draining nodes; leucocytosis; hectic fever
• Lymph node (reactive): tender, soft, mobile; related to source of infection

Neoplastic Swellings

• Lipoma: Soft, lobulated, slips from under examining fingers ("slipping sign"), non-tender, translucent negative, fluctuation may be positive (pseudofluctuation), freely mobile
• Fibroma: Firm, smooth, mobile, non-tender
• Sebaceous cyst: Attached to skin (punctum visible), not attached to deep structures, fluctuant, NOT translucent
• Neurofibroma: Along course of a nerve; moves transversely but not longitudinally

Key Exam Points to Remember

1. 5 cardinal signs of inflammation - Rubor, Dolor, Calor, Tumor, Functio laesa
2. Fluctuation = fluid - Must test in two planes
3. Translucency - Positive in cystic hygroma; negative in dermoid (pultaceous content)
4. Lipoma slips under finger; dermoid cyst margin yields to finger
5. Pain in malignancy - Absent except osteosarcoma (pain precedes swelling)
6. Tumour never recedes in size - the most important differentiator from inflammatory swelling
7. Carcinoma = old patients; Sarcoma = young patients (general rule)
8. Benign = encapsulated, well-differentiated, no metastasis, no recurrence

Viva Questions & Answers: Swelling, Ulcers & Venous Ulcer

From S. Das - A Manual on Clinical Surgery

PART 1: SWELLING - VIVA QUESTIONS

A: (1) The anatomical layer from which the swelling arises - skin, subcutaneous tissue, muscle, vessel, nerve, or bone. (2) The cause - whether it is congenital, traumatic, inflammatory, neoplastic, or otherwise.

A: Rubor (redness), Dolor (pain), Calor (heat), Tumor (swelling), Functio laesa (loss of function). The most important ones to stress are pain, redness, and heat.

A: Both can present with pain, redness, swelling, and heat. Features favouring acute inflammation:

• Tenderness
• Brawny induration and oedema
• Fluctuation (= pus = inflammatory)
• Acute lymphadenitis in regional nodes
• Hectic fever (never in sarcoma)
• Leucocytosis (constant in inflammation, variable in sarcoma)

A: The most important differentiating feature is the history of occasional diminution in the size of the swelling - this goes in favour of inflammation. A tumour may be stationary for a long time but never recedes. Also look for tenderness and fixity (more in malignancy).

A: Carcinoma arises from epithelial cells and commonly affects older patients. Sarcoma arises from connective tissue and commonly affects young patients.

A: Osteosarcoma. Pain precedes the swelling.

A: Fibroadenoma of the breast. It is called so because of its extreme free mobility under the examining fingers.

A: Place two fingers of one hand on opposite sides of the swelling. Press one side - if the other finger is lifted = fluctuation positive. Must be tested in two planes at right angles. A positive fluctuation indicates fluid content (cyst or abscess).

A: Shine a torch/light against the swelling in a darkened room - if light passes through, translucency is positive. Positive in: cystic hygroma, branchial cyst (clear fluid). Negative in: dermoid cyst (pultaceous material), lipoma, solid tumours.

A: A lipoma is soft, lobulated, non-tender, fluctuant (pseudofluctuation), and shows the characteristic slipping sign - the swelling slips from under the examining fingers. This helps differentiate it from a dermoid cyst (whose margin yields to pressure and does NOT slip away).

A: A dermoid cyst that develops at the lines of embryonic fusion. Common sites:

• Outer angle of orbit (fronto-nasal and maxillary processes)
• Behind the pinna (post-auricular dermoid)
• Below the tongue in midline (sublingual dermoid)
• Features: fluctuation +ve, translucency -ve (pultaceous content), margin yields to pressure (does not slip), free from skin and deep structures, may show bony indentation at the margin.

A: (1) Sudden increase in size, (2) Increased vascularity with rise of local temperature, (3) Fixity and infiltration of surroundings, (4) Ulceration, bleeding, increased pigmentation, (5) Appearance of pain (late feature), (6) Involvement of regional lymph nodes, (7) Distant metastasis.

A:

• Transmitted pulsation - the swelling receives pulse from an adjacent artery (e.g. aneurysm sac - pulsates but does not expand)
• Expansile pulsation - the swelling itself expands in all directions with each pulse = true aneurysm

A: Ask the patient to contract the underlying muscle. If the swelling becomes less mobile or disappears, it is arising from or attached to deep structures/muscle. If it remains the same or becomes more prominent, it is superficial to the muscle.

PART 2: ULCER - VIVA QUESTIONS

A: An ulcer is a break in the continuity of an epithelial surface (skin or mucous membrane) with loss of substance, that does not tend to heal.

A: Every ulcer is described by:

1. Edge - sloping/shelving (healing/venous), undermined (TB/pressure), punched-out (syphilis/arterial/trophic), rolled/everted (carcinoma), raised and pearly (rodent ulcer)
2. Margin - the junction between the ulcer edge and the surrounding skin
3. Floor - the base you see (granulation tissue, slough, bone, tendon)
4. Base - what the floor rests on (indurated in carcinoma, fixed to bone in TB)
5. Discharge - type and amount
6. Depth - shallow vs deep
7. Surroundings - pigmentation, oedema, induration, varicosities, eczema

A:

1. Spreading ulcer - floor covered with profuse offensive slough, no granulation tissue; edge is inflamed, oedematous, ragged; painful; regional lymph nodes enlarged/tender
2. Healing ulcer - floor shows pinkish/red healthy granulation tissue; edge reddish with granulation; margin bluish with growing epithelium; discharge slight and serous
3. Callous/Chronic ulcer - no tendency to heal; floor has pale granulation tissue; may show wash-leather slough (gummatous ulcer); discharge scanty/absent; base and edge considerably indurated

A: (A) Non-specific:

1. Traumatic (mechanical, physical, chemical)
2. Arterial (atherosclerosis, Buerger's, Raynaud's)
3. Venous (varicose/postphlebitic/gravitational)
4. Neurogenic/Trophic (bedsore, perforating ulcer)
5. Associated with malnutrition (tropical ulcer - Vincent's organisms)
6. Associated with systemic disease (gout, diabetes, anaemia, avitaminosis, rheumatoid arthritis)
7. Special types: Bazin's ulcer, Martorell's ulcer

(B) Specific: Tuberculous, syphilitic, soft sores, actinomycosis, Meleney's ulcer

(C) Malignant: Epithelioma, Marjolin's ulcer, rodent ulcer, malignant melanoma

A: Raised, rolled, everted (or "proliferative and everted"). The floor is covered by necrotic slough and the base is hard due to infiltration.

A: A squamous cell carcinoma arising from the margin of a long-standing venous ulcer (or from the scar of burns, lupus vulgaris, chronic sinus). Features suggesting malignant transformation: edge becomes raised and everted, base becomes hard, pain may appear. Biopsy is mandatory to confirm.

A: Basal cell carcinoma. Edge is raised, pearly, and rolled with visible telangiectases. It is locally invasive ("rodent" = eats locally) but NEVER metastasizes. Common on face above a line joining angle of mouth to the ear (S. Das).

A: A painless ulcer occurring at pressure points due to loss of sensation (peripheral neuropathy - e.g. diabetes, leprosy). It occurs at the ball of the foot (under metatarsal heads) and heel. Painless despite deep penetration (may expose tendon/bone). Also called perforating ulcer.

PART 3: VENOUS ULCER - VIVA QUESTIONS (Your Case)

A: The basic cause is abnormal venous hypertension in the lower third of the leg. The main pathway of venous drainage of ankle skin in erect posture is via the ankle perforating veins. When the valves of these perforating veins are damaged, local venous hypertension results. This is aggravated by obstructed main deep veins. Post-canalisation of thrombosed deep veins leads to destruction of valves of the deep veins, which is the main contributing cause for ankle venous hypertension.

A: Varicose ulcer, post-thrombotic ulcer, gravitational ulcer. S. Das says the term "varicose ulcer" is not fully justified because varicose veins may or may not be present - the real cause is venous hypertension due to perforator/deep vein valve incompetence.

A: Medial aspect of the lower third of the leg (above the medial malleolus). They are never seen above the junction of the middle and upper thirds of the leg.

A: Age group 40 to 60 years. Women are affected far more often than men.

A:

• Site: Medial aspect, lower third of leg (above medial malleolus)
• Shape/size: Any shape and size
• Edge: Sloping, pale purple-blue in colour
• Margin: Thin and blue (growing epithelium)
• Floor: Pale granulation tissue
• Depth: Shallow and flat - never penetrates the deep fascia (key feature)
• Discharge: Seropurulent with occasional trace of blood
• Base: Fixed to deeper structures
• Surrounding skin: Pigmentation, induration, tenderness (signs of chronic venous hypertension); scars of previous ulcers; eczema
• Varicose veins: May or may not be present in the proximal limb
• Lymph nodes: Inguinal lymph nodes enlarged only if ulcer is infected
• Pain: Painful initially; becomes painless once chronic

A: As quoted by S. Das: "The ulcer is painful in the beginning but once it settles down and becomes chronic it becomes painless." This is in contrast to arterial ulcer which is always painful.

A:

• Doppler ultrasound - to assess venous reflux and deep vein patency; identify incompetent perforators
• Duplex scan - gold standard for venous mapping
• ABPI (Ankle Brachial Pressure Index) - to rule out arterial component before applying compression (ABPI <0.8 = significant arterial disease; compression contraindicated)
• Venography - if surgery planned
• Blood tests - FBC (anaemia), blood sugar (diabetes), ESR, renal/liver function
• Wound swab - if signs of infection
• Biopsy - MANDATORY if Marjolin's ulcer is suspected (raised, everted edge; hard base)

A:

Conservative (mainstay):

1. Elevation of the limb - reduces venous hypertension
2. Four-layer compression bandaging - the single most effective treatment; reduces venous hypertension
3. Regular dressing - clean the ulcer; debride slough
4. Treat surrounding eczema - mild topical steroid
5. Treat infection if present - antibiotics based on swab culture
6. Treat underlying cause - anaemia, diabetes, malnutrition

Surgical:

1. Skin grafting (split-thickness skin graft) - for large, non-healing ulcers after the wound bed is clean
2. Surgery for varicose veins - stripping of long saphenous vein, ligation of incompetent perforators (Linton's operation)
3. Pinch grafting - for small ulcers

For Marjolin's ulcer - wide local excision + skin graft; lymph node dissection if nodes involved

A: Marjolin's ulcer - squamous cell carcinoma developing from the margin of a long-standing venous ulcer. It should be suspected when the edge of the ulcer becomes raised and everted and the base becomes hard. Biopsy is mandatory to confirm.

A:

• Pigmentation (haemosiderin deposition - brownish discolouration)
• Induration (lipodermatosclerosis)
• Tenderness of surrounding skin
• Eczema/dermatitis
• Oedema of the ankle
• Scars of previous healed ulcers
• Varicose veins in the proximal limb (may or may not be present)

A: First diagnosis = venous ulcer (most common cause of leg ulcer, on medial side, sloping edge, pale granulation floor, surroundings with pigmentation/eczema). Confirm with:

• Doppler/duplex ultrasound for venous reflux
• ABPI to rule out arterial component
• Biopsy only if malignant transformation is suspected

A: A test to identify incompetent saphenofemoral junction and perforators. The limb is elevated to empty veins, then the saphenofemoral junction is occluded with a tourniquet, and the patient stands. If veins fill from below while junction is occluded = incompetent perforators. If veins fill rapidly on releasing the tourniquet = saphenofemoral incompetence. Incompetent perforators are the primary cause of venous hypertension leading to venous ulcers.

Quick-Fire Summary for the Viva Table

Management of Venous Ulcer in a Diabetic Patient (10 Years Duration)

Why Diabetes Makes a Venous Ulcer Worse

"Long duration of diabetes (>10 years) is a known risk factor associated with foot ulceration and adverse outcomes." - Fitzpatrick's Dermatology

Step 1: Assessment First (Before Any Treatment)

History

• Duration of ulcer, previous episodes, prior treatment
• Symptoms of arterial disease: intermittent claudication, rest pain, cold feet
• Symptoms of neuropathy: numbness, tingling, burning
• Diabetes control: HbA1c, current medications (insulin/oral), diet compliance
• Signs of infection: fever, increased discharge, smell, red streaking

Investigations - Mandatory in a Diabetic

1. ABPI (Ankle Brachial Pressure Index) - CRITICAL before applying any compression
   • ABPI > 0.8 = safe to compress
   • ABPI 0.5-0.8 = mixed ulcer (venous + arterial) - modified/reduced compression only
   • ABPI < 0.5 = significant arterial disease - compression is CONTRAINDICATED
2. Doppler/Duplex ultrasound - assess venous reflux, identify incompetent perforators, check deep vein patency
3. Blood glucose (fasting + postprandial) + HbA1c - key marker of long-term control
4. Complete blood count - anaemia (impairs healing), leucocytosis (infection)
5. Renal function tests - diabetic nephropathy affects fluid balance and drug dosing
6. Wound swab for culture and sensitivity - diabetic wounds frequently polymicrobial
7. X-ray of the foot/leg - rule out osteomyelitis if ulcer is deep
8. Serum albumin/protein - nutritional status affects healing
9. Biopsy - if edge becomes raised/everted/hard (suspect Marjolin's ulcer)
10. Semmes-Weinstein 10g monofilament test - assess protective sensation in the foot

Step 2: Management - The ABCDE Framework

A - Address Diabetes First (Glycaemic Control)

• Target HbA1c < 7% (53 mmol/mol)
• If on oral hypoglycaemics - optimize dose or switch to insulin during active ulcer phase (better control with insulin)
• High blood glucose feeds bacteria and impairs every stage of wound healing
• "The risk of a foot ulcer increases in nearly direct proportion to every 1% increase in HbA1c"
• Involve endocrinologist/physician for co-management

B - Wound Bed Preparation (Local Ulcer Care)

• Remove all necrotic tissue, slough, and callus from the ulcer margin
• Sharp surgical debridement under anaesthesia if needed (diabetics may not feel pain)
• Enzymatic debridement (collagenase) for ongoing maintenance
• Maggot therapy (larval therapy) in resistant cases

• Moist wounds heal 3x faster than dry wounds
• Dressings of choice:
  • Alginate dressings (for exudative ulcers)
  • Hydrocolloid dressings (for low-to-moderate exudate, promotes autolytic debridement)
  • Foam dressings (for moderate exudate)
  • Silver-containing dressings (if infection/biofilm suspected)
  • Avoid dry gauze packing - delays healing

• Diabetics: infection spreads rapidly and can progress to cellulitis, fasciitis, or osteomyelitis
• Surface colonisation: clean with antiseptic (povidone-iodine or chlorhexidine)
• Clinical infection (warmth, pus, odour, erythema): systemic antibiotics based on wound swab C&S
• Empirical: cover Gram +ve (Staphylococcus, Streptococcus) + anaerobes
  • Amoxicillin-clavulanate OR Clindamycin + Ciprofloxacin
• Osteomyelitis: prolonged antibiotics (4-6 weeks); surgical debridement of dead bone

C - Compression Therapy (Core of Venous Ulcer Treatment)

• Only if ABPI > 0.8 (always check in diabetics - they have accelerated atherosclerosis)
• Four-layer compression bandage - the gold standard for venous ulcer healing
  • Layer 1: Orthopaedic wool (padding)
  • Layer 2: Crepe bandage (smoothing)
  • Layer 3: Elastic bandage (compression)
  • Layer 4: Cohesive bandage (retention)
  • Applies approximately 40 mmHg at ankle
• Changed every 1-2 weeks (or sooner if heavily exudating)
• If ABPI 0.5-0.8: reduced/modified compression (23-25 mmHg) with close monitoring
• Contraindicated if ABPI < 0.5: treat arterial component first

D - Elevation and Off-loading

• Elevate the limb above heart level when resting - reduces venous hypertension, reduces oedema
• Encourage ankle exercises (calf pump activation - improves venous return)
• Off-loading / pressure relief:
  • Diabetics must avoid prolonged standing and walking on an active ulcer
  • Specially fitted diabetic footwear or total contact casting if trophic component present
  • Avoid tight footwear (poor vision in diabetics means footwear injuries are common)

E - Eliminate Underlying Causes & Systemic Support

• High-protein diet (1.2-1.5 g/kg/day) - protein is essential for collagen and granulation tissue
• Vitamin C supplementation (collagen synthesis)
• Zinc supplementation (if deficient - common in diabetics)
• Iron supplementation for anaemia

• Compression + elevation (as above)
• If cardiac/renal cause: diuretics (with care in renal impairment)

• Pentoxifylline (400 mg TDS) - proven adjunct in venous ulcers; improves microcirculation; particularly useful when arterial component also present in diabetics

• Diabetics are hypercoagulable; if immobile, LMWH prophylaxis

Step 3: Surgical Management (When Conservative Fails)

Indications for Surgery

• Ulcer not responding to 12 weeks of adequate conservative management
• Large ulcer (>2 cm diameter)
• Significant incompetent perforators/saphenofemoral incompetence confirmed on Doppler

Surgical Options

• Split-thickness skin graft (STSG) - most commonly used
  • Harvest from thigh; graft applied to clean granulating ulcer bed
  • Requires good wound bed preparation first
  • In diabetics: check blood glucose is controlled (ideally HbA1c < 8%) for graft take
• Pinch grafting - for small ulcers

• Ligation and stripping of long saphenous vein (reduces superficial venous hypertension)
• Linton's operation - subfascial ligation of incompetent perforators (open method)
• SEPS (Subfascial Endoscopic Perforator Surgery) - minimally invasive, preferred in diabetics (reduces wound complications)
• Must be done AFTER the ulcer heals (operating on infected ground risks poor healing)

• VAC (Vacuum-Assisted Closure / Negative Pressure Wound Therapy) - especially useful in deep, infected, or post-surgical wounds in diabetics
• Bilayered living skin equivalents (Apligraf) - shown to improve healing rates in chronic diabetic ulcers that fail standard care
• Recombinant PDGF (Becaplermin) - modest benefit if used with adequate debridement and infection control

Step 4: Prevention and Follow-up (Critical in Diabetics)

• Strict glycaemic control permanently - most important long-term measure
• Graduated compression stockings (Class II, 23-32 mmHg) after ulcer heals - prevents recurrence
• Foot care education: daily inspection of feet, proper nail care, appropriate footwear
• Regular podiatry review
• Monitor for signs of malignant transformation (Marjolin's ulcer) in long-standing cases - biopsy any change in ulcer characteristics
• Regular wound review every 1-2 weeks during active treatment

Summary Table - Special Considerations in Diabetic Venous Ulcer