Ulcer

Introduction
• An ulcer is a break in the continuity of the covering epithelium,
either skin/mucous membrane due to molecular death.

• Part of an ulcer
1. Margin
• It may be regular/irregular.
• It may be rounded/oval.

2. Edge
• Edge is the one which connects floor of the ulcer to the margin.
• Different edges are :
 Introduction
Sloping edge
• It is seen in a healing ulcer.
• Its inner part is red because of red, healthy granulation tissue.
• Its outer part is white due to scar/fibrous tissue.
• Its middle part is blue due to epithelial proliferation.

Undermined edge
• It is seen in a tuberculous ulcer.
• Disease process advances in deeper plane (in subcutaneous tissue)
whereas (skin) epidermis proliferates inwards.

Punched out edge

• It is seen in a gummatous (syphilitic) ulcer & trophic ulcer.
• It is due to endarteritis.
 Introduction
Raised & beaded edge (pearly white) is seen in a rodent ulcer (BCC).
• Beads are due to proliferating active cells.

Everted edge (rolled out edge)

• It is seen in a carcinomatous ulcer due to spill of the proliferating
malignant tissues over the normal skin.

3. Floor
• It is the one which is seen.
• Floor may contain discharge, granulation tissue/slough.

4. Base
• Base is the one on which ulcer rests.
• It may be bone/soft tissue.
 Introduction
• Induration of an ulcer
• Induration is a clinical palpatory sign which means a specific type
of hardness in the diseased tissue.
• It is obvious in well-differentiated carcinomas.
• It is better felt in squamous cell carcinoma.
• It is also observed in long standing ulcer with underlying fibrosis.
• It is absent/less in poorly differentiated carcinomas & malignant
melanoma.
• Less indurated carcinoma is more aggressive.
 Introduction
• Induration of an ulcer
• Specific types of indurations are observed in venous disease &
chronic deep venous thrombosis.
• Brawny induration is a feature of an abscess.
• Induration is felt at edge, base & surrounding area of an ulcer.
• Induration at surrounding area signifies the extent of disease
(tumor).
• Outermost part of the indurated area is taken as the point from
where clearance of wide excision is planned.
 Classification
• Classification 1 (clinical)
1. Spreading ulcer
• Here edge is inflamed, irregular & edematous.

• It is an acute painful ulcer, floor does not contain healthy granulation

tissue (or granulation tissue is absent) but with profuse purulent
discharge & slough; surrounding area is red & edematous.

• Regional (draining) lymph nodes are enlarged & tender due to

inflammation.

• There will be associated fever, pain, impairment of functions with local

tissue destruction & with little evidence of regeneration.
 Classification
• Classification 1 (clinical)
2. Healing ulcer
• Edge is sloping with healthy pink/red healthy granulation tissue with
scanty/minimal serous discharge in the floor; slough is absent;
regional lymph nodes may/may not be enlarged but when enlarged
always non-tender.

• Surrounding area does not show any signs of

inflammation/induration; base is not indurated.

• 3 zones are observed in healing ulcer.

• Innermost red & zone of healthy granulation tissue; middle bluish

zone of growing epithelium; outer whitish zone of fibrosis & scar
formation.
 Classification
3. Non – healing ulcer
• It may be a chronic ulcer depending on the cause of the ulcer, here edge
will be depending on the cause –
• Punched out (trophic)
• Undermined (tuberculous)
• Rolled out (carcinomatous ulcer),
• Beaded (rodent ulcer)
• Floor contains unhealthy granulation tissue & slough, &
serosanguineous/purulent/body discharge; regional draining lymph
nodes may be enlarged but non-tender.
 Classification
3. Callous (stationary) ulcer
• It is also a chronic non-healing ulcer, floor contains pale unhealthy,
flabby, whitish yellow granulation tissue & thin scanty serous
discharge/often with copious serosanguinous discharge, with indurated
non-tender edge; base is indurated, nontender & often fixed .
• Ulcer does not show any tendency to heal.
• It lasts for many months to years.
• Tissue destruction is more with absence of or only minimal
regeneration.
• Induration & pigmentation may be seen in the surrounding area.
• There is no/less discharge.
• Regional lymphnodes may be enlarged, are firm/hard & nontender.
• It is callousness towards healing; word callous means – insensitive &
cruel; & also it means hard skinned.
 Classification
• Classification 2 (Based on duration)
• Acute ulcer– duration is <2 weeks.
• Chronic ulcer – duration is >2 weeks.

• Classification 3 (pathological)
1. Specific ulcers
• Tuberculous ulcer
• Syphilitic ulcer – It is punched out, deep, with “wash-leather” slough in
the floor & with indurated base.
• Actinomycosis
• Meleney’s ulcer
 Classification
2. Malignant ulcers
• Carcinomatous ulcer
• Rodent ulcer
• Melanotic ulcer

3. Non specific ulcers

• Traumatic ulcer : It may be mechanical, physical, chemical common.

• Arterial ulcer : Atherosclerosis, TAO (Thromboangitis obliterans).

• Venous ulcer : Gravitational ulcer, post phlebitis ulcer

 Classification
• Trophic ulcer/Pressure sore

• Infective ulcers : Pyogenic ulcer

• Tropical ulcers : It occurs in tropical countries.

• It is callous type of ulcer, e.g. Vincent’s ulcer

• Ulcers due to chilblains & frostbite (cryopathic ulcer).

• Martorell’s hypertensive ulcer.

• Bazin’s ulcer

• Diabetic ulcer
 Classification
• Ulcers due to leucaemia, polycythemia, jaundice, collagen diseases,
lymphoedema.

• Cortisol ulcers are due to long time application of cortisol (steroid)

creams to certain skin diseases.

• These ulcers are callous ulcers last for long time & require excision &
skin grafting.
 Wagner’s Grading/classification of ulcer

• Grade 0 – Preulcerative lesion/healed ulcer

• Grade 1 – Superficial ulcer
• Grade 2 – Ulcer deeper to subcutaneous tissue exposing soft
tissues/bone
• Grade 3 – Abscess formation underneath/osteomyelitis
• Grade 4 – Gangrene of part of the tissues/limb/foot
• Grade 5 – Gangrene of entire one area/foot
 Stages of ulcer healing

1. Stage of extension – Ulcer floor is covered with slough, purulent

discharge & inflamed edge & margin.

2. Stage of transition – Floor shoes separated slough, healthy

granulation tissue, serous discharge.

3. Stage of repair – Fibrosis, collagen deposition, scar formation

occurs.
 Granulation tissue
• It is proliferation of new capillaries & fibroblasts intermingled with RBCs
& WBCs with thin fibrin cover over it.

• Types
• Healthy granulation tissue
• It occurs in a healing ulcer.
• It has got sloping edge.
• It bleeds on touch.
• It has got serous discharge.
• 5 Ps of granulation tissue – Pink, punctate hemorrhages, pulseful,
painless, pin head granulation.
• Skin grafting takes up well with healthy granulation tissue.
• Streptococci growth in culture should be less than 105/gram of tissue
before skin grafting
 Granulation tissue
• Unhealthy granulation tissue
• It is pale with purulent discharge.
• Its floor is covered with slough.
• Its edge is inflamed & edematous.
• It is a spreading ulcer.

• Unhealthy, pale, flat granulation tissue

• It is seen in chronic nonhealing ulcer (callous ulcer).

• Exuberant granulation tissue (Proud flesh)

• It occurs in a sinus/ulcer wherein granulation tissue protrudes out of
the sinus opening/ulcer bed like a proliferating mass.
• It is commonly associated with a retained foreign body in the sinus
cavity.
 Granulation tissue
• Sprouting granulation – tissue of sinus.

• Pyogenic granuloma
• It is a type of exuberant granulation tissue.
• Here granulation tissue from an infected wound/ulcer bed protrudes
out, presenting as a well-localised, red swelling which bleeds on
touching.
• Differential diagnosis – Papilloma, skin adnexal tumors.
• Treatment – Antibiotics, excision & sent for biopsy.
 Granulation tissue
• Different discharges in an ulcer (as well as from sinus)
a. Serous – In healing ulcer
b. Purulent - In infected ulcer
c. Bloody – Malignant ulcer, healing ulcer from healthy granulation
tissue
d. Seropurulent
e. Serosanguinous – Serous & blood
f. Serous with Sulphur granules – Actinomycosis
g. Yellowish – Tuberculous ulcer
 Investigations for an ulcer
• Study of discharge – Culture & sensitivity, AFB study, cytology.

• Wedge biopsy – Biopsy is taken from the edge because edge contains
multiplying cells.
• Usually 2 biopsies are taken.
• Biopsy taken from the center may be inadequate because of central
necrosis.
• X-ray of the part to look for periostitis/osteomyelitis.
• FNAC (Fine needle aspiration cytology) of the lymph node.

• Chest X-ray, Mantoux test in suspected case of tuberculous ulcer.

• Hemoglobin, ESR, total WBC count, serum protein estimation
(albumin).
 Assessment of an ulcer
• Causes of an ulcer should be found – diabetes/venous/arterial/infective.

• Clinical type should be assessed

• Assessment of wound is important – anatomical site, size & depth of the

wound, edge of the wound, mobility, fixity, induration, surrounding
area, local blood supply.

• Wound perimeter may be useful in assessing this

• Wound imaging is done by tracing it on a transparent acetate sheet at

regular intervals.
 Assessment of an ulcer

• Presence of systemic features, regional nodal status, function of the

limb/part, joint movements, distal pulse, sensations should be
assessed.

• Severity of infection should be assessed – culture of discharge

• Specific investigations like wedge biopsy, X-ray of part, blood sugar,

arterial/venous doppler, angiogram.
 Management of an ulcer

• Cause should be found & treated.

• Correction of the anemia, deficiencies like of protein & vitamins.
• Proper investigation as needed.
• Transfusion of the blood if required.
• Control the pain & infection.
• Rest, immobilization, elevation, avoidance of repeated trauma.

• Care of the ulcer by debridement, ulcer cleaning & dressing.

• Desloughing is done either mechanically/chemically.
• Mechanically it is done using scissor by excising the slough.
• Hydrogen peroxide which releases nascent oxygen is used as chemical
agent.
 Management of an ulcer

• Acriflavine is antiseptic & irritant & so desloughs the area & promotes
granulation tissue formation.

• Eusol (Edinburgh University Solution) which contains sodium

hypochlorite releases nascent chlorine which forms a water soluble
complex with slough to dissolve it.

• Use of povidone iodine in ulcer cleaning is controversial (open wound is

not suitable, it is mainly for cleaning the surgical field prior to incision).

• Maggots if present in the wound will cause crawling sensation & are
removed using turpentine solution.

• Removal of the exuberant granulation tissue is also required when

present.
 Management of an ulcer

• Ulcer cleaning & dressing is done daily/twice daily/once in 2-3 days

depending on the type of ulcer & type of dressing used.
• Normal saline is ideal for ulcer cleaning.
• Various dressings are available.

• Films (opsite/semipermeable polyurethane),

• hydrocolloids (duoderm),
• hydrogels (polyethylene oxide with water),
• hydroactives (nonpectin-based polyurethane matrix),
• foams (polyurethane hydrophilic/hydrophobic non –occlusive),
• impregnates (non-adherent fine mesh impregnated with antibacterials),
• calcium alginates etc.
 Management of an ulcer
• Topical antibiotics for infected ulcers are not essential but like
framycetin, silver sulphadiazine, mupirocin may be used.

• Vacuum assisted closure (VAC) therapy

• It is by creation of negative pressure (25-200 mmHg),
continuous/intermittent over the wound surface.

• It causes reduced fluid in the interstitial space, reduce edema, increases

the cell proliferation & protein matrix synthesis, promotes formation of
healthy granulation tissue.

• Sterile foam is placed over the ulcer bed covering widely, tube drain
with multiple holes is kept within it & end of the tube comes out
significantly away, foam is sealed airtight using a sterile adhesive film.
 Management of an ulcer
• Tube is connected to suction system.

• Suction is maintained initially continuously later intermittently.

• Redressing is done only after 4-7 days.

• Therapy using infrared/short wave/ultraviolet rays to decrease the ulcer

size is often used but their benefits are not proved.

• Amnion to promote re-epithelization, chorion to promote granulation

tissue formation is also often used.

• Antibiotics are not required once healthy granulation tissues are

formed.
 Management of an ulcer
• Maggot debridement therapy
• It is used as biotherapy (but not commonly) by placing cultured live
disinfected maggots.

• Maggots are larvae of the green bottle fly, also known as the green
blowfly (Lucilia sericata).

• They act by dissolving & engulfing dead necrotic tissues, they may
reduce the bacterial content in the wound.

• They can inhibit many bacteria including MRSA (methicillin resistant

bacteria), anaerobic & aerobic bacteria.

• They secrete proteolytic enzymes to have mechanical effects, secretion

of ammonia alters the pH in the ulcer bed which inhibits bacterial
growth.
 Management of an ulcer
• Maggot debridement therapy
• They increase the granulation tissue formation also.

• Once ulcer granulates, defect is closed with secondary suturing, skin

graft/flaps.

• Autologous bone marrow monocytes injection into the ulcer area is

new concept by Professor Sribatsa Mohapatra but yet to confirm.
 Management of an ulcer
• Debridement of an ulcer
• It is removal of devitalized tissue
• Small ulcers are debrided in the ward
• Large ulcers are debrided in operation theatre under general anesthesia
• All dead, devitalized, necrotic tissues are removed
• Slough should be separated adequately before debridement
• Often devitalised tissue separates on its own by autolysis
• Enzymes like collagenase are used for debridement
• Hydrotherapy & dressings are mechanical nonselective method of
debridement.
 Management of an ulcer
• Dressing of an ulcer is done
• To keep ulcer moist
• To keep surrounding skin dry
• To reduce pain
• To soothen the tissue
• To protect the wound
• As an absorbent for the discharge

• Note - Debridement can be surgical, mechanical, autolytic/enzymatic.

 Management of an ulcer
• Ulcer dressings
• Cotton dressing – cheap but traumatic

• Paraffin dressing

• Polyurethane dressings used in clean wounds

• Alginates (seaweed) dressing used when there are heavy exudates

• Type 1 collagen dressings caused hemostasis, proliferation of fibroblasts

& improve the blood supply

• Foam dressings are highly absorbent, decrease the wound maceration

& reduce the frequency of dressing – hydrophilic polyurethane foam
 Management of an ulcer
• Hydrocolloid dressing help in separation of slough & autolysis of dead
tissues.

• Transparent film dressings are waterproof, permit oxygen & water

vapour across & prevent contamination.

• Hydrogel dressings used for clean wound

 Causes of formation of chronic/nonhealing ulcer

• Local causes
• Recurrent infection
• Trauma, presence of foreign body/sequestrum
• Absence of rest & immobilization
• Poor blood supply, hypoxia
• Edema of the part
• Loss of sensation
• Periostitis/osteomyelitis of the underlying bone
• Fibrosis of the surrounding soft tissues
• Lymphatic diseases
 Causes of formation of chronic/nonhealing ulcer

• General/specific causes
• Anemia, hypoproteinemia
• Vitamin deficiencies
• Tuberculosis, leprosy
• Diabetes mellitus, hypertension
• Chronic liver/kidney diseases
• Steroid therapy locally/systemically
• Cytotoxic chemotherapy/radiotherapy
• Malignancy
 Traumatic ulcer

• Such ulcer occurs after trauma.

• It may be mechanical – dental ulcer along the margin of the tongue due
to tooth injury; physical - like by electrical burn; chemical - like by alkali
injury.

• Such ulcer is acute, superficial, painful & tender.

• Secondary infection/poor blood supply of the area make it chronic &

deep.

• Footballer’s ulcer is a traumatic ulcer occurring over the shin of males

due to direct knocks on the shin.

• It is staphylococcal infection with a chronic & deep ulcer.

 Traumatic ulcer

• Traumatic ulcers can occurs anywhere in the body due to trauma.

• Trauma causes infection, necrosis, fasciitis, crush injury, endarteritis of

the skin leading into formation of large/deep nonhealing ulcer.

• Treatment depends on size & extent of ulcer.

• Regular dressing, later skin grafting is done.

 Trophic ulcer (pressure sore/decubitus ulcer)

• Pressure sore is tissue necrosis & ulceration due to prolonged

pressure.

• Blood flow to the skin stops once external pressure becomes more
than 30 mmHg (more than capillary occlusive pressure) & this causes
tissue hypoxia, necrosis & ulceration.

• It is more prominent between bony prominence & an external surface.

• It is due to:
• Impaired nutrition
• Defective blood supply
• Neurological deficit
 Trophic ulcer (pressure sore/decubitus ulcer)
• Sites
• Over the ischial tuberosity
• Sacrum
• In the heel
• In relation to heads of metatarsals
• Over the shoulder
• Occiput

• Due to the presence of neurological deficit, trophic ulcer is also called as

neurogenic/neuropathic ulcer.

• Initially it begins as callosity due to repeated trauma & pressure, under

which suppuration occurs & gives way through a central hole which
extends down into the deeper plane up to the underlying bone as
perforating ulcer. (penetrating ulcer).
 Factors causing pressure sore

• Normal stimulus to relive the pressure is absent in anaesthetized patient.

• Nutritional deficiencies worsens the necrosis.

• Inadequate padding over the bony prominences in malnourished

patients.

• Urinary incontinence in paraplegia patient causes skin soiling maceration

-infection-necrosis.
 Neurological causes
• Diabetic neuropathy
• Peripheral neuritis
• Tabes dorsalis
• Spina bifida
• Leprosy
• Spinal injury
• Paraplegia
• Peripheral nerve injury
• Syringomyelia

• Investigations
• Study of discharge, blood sugar, biopsy from the edge, X-ray of the part,
X-ray spine.
 Staging of pressure sore

• Non blanching erythema – early superficial ulcer

• Partial thickness skin loss – late superficial ulcer

• Full thickness skin loss extending into subcutaneous tissue but not
through fascia – early deep ulcer

• Full thickness skin loss with fascia & underlying structures like
muscle/tendon/bone etc. – late deep ulcer
 Treatment

• Causes should be treated.

• Nutritional supplementation
• Rest, antibiotics, slough excision, regular dressings.

• Vacuum - assisted closure (VAC)

• It is the creation of intermittent negative pressure of minus 125 mmHg
to promote formation of healthy granulation tissue.

• Negative pressure reduces tissue edema, clears the interstitial fluid &
improves the perfusion, increases the cell proliferation & so promotes
the healing.

• A perforated drain is kept over the foam dressing covered over the
pressure sore.
 Treatment

• Vacuum - assisted closure (VAC)

• It is sealed with a transparent adhesive sheet.
• Drain is connected to required vacuum apparatus.
• Once ulcer granulates well, flap cover/skin grafting is done.
• Excision of the ulcer & skin grafting.
• Flaps-local rotation/other flaps (transposition flaps).
• Cultured muscle interposition.

• Proper care
• Change in position once in 2 hours
• Lifting the limb upwards for 10 seconds once in 10 minutes
• Nutrition
 Treatment

• Use of water bed/air bed/air fluid floatation bed & pressure dispersion
cushions to the affected area;
• Urinary & fecal care
• Hygiene
• Psychological counselling.
• Regular skin observation
• Keeping skin clean & dry (using regular use of talcum powder)
• Oil massaging of the skin & soft tissues using clean, absorbent porous
clothing
• Control & prevention of sepsis helps in the management.
 Ulcer due to chilblains

• It is due to exposure to intense cold causing blisters & ulcerations in the

feet.
• These ulcers are superficial.
• It is due to excessive cutaneous arteriolar constriction.
• The condition is also called as perniosis.
 Ulcer due to frostbite

• It is due to exposure of a part to wet cold below the freezing point (cold
wind).
• There is arteriolar spasm, denaturation of proteins & cell destruction.
• It leads to gangrene of the part.
• Ulcers here are always deep.
 Martorell’s Ulcer (1945)

• It is seen in hypertensive patients often with atherosclerosis.

• It is seen in calf.
• Often it is bilateral & painful.
• Necrosis of calf skin occurs with sloughing away & formation of deep,
punched out ulcers extending into the deep fascia.
• There is sudden obliteration of the arterioles of the calf skin.
• All peripheral pulses are present.
• It takes months to heal.

• Treatment
• Once ulcer granulates well, skin grafting with lumbar sympathectomy is
done.
 Arterial/ischemic ulcer
• It is common in toes, feet/legs; often can occur in upper limb digits.

• It is due to poor supply following blockage of the digital/medium sized

arteries.

• Atherosclerosis & TAO (Thromboangiitis obliterans) are common causes

in lower limb.

• Cervical rib, Raynaud’s phenomenon & vasculitis are common causes in

upper limb.

• Ulcer initially occurs after trauma, soon becomes nonhealing, spreading

with scanty granulation tissue.

• Ulcer is very painful, tender & often hyperesthetic.

 Arterial/ischemic ulcer
• Digits may often be gangrenous.
• Intermittent claudication, rest pain are common.
• Other features of ischemia are obvious in the adjacent areas.
• They are pallor, dry skin, brittle nail, patchy ulcerations & loss of hair.
• Ulcer is usually deep, destructs the deep fascia, exposing tendons,
muscles & underlying bone.
• Dead tendons look pale/greenish with pus over it.

• Management
• Specific investigations like arterial doppler, angiogram, lipid profile &
blood sugar are done.
• Treatment is done accordingly drugs like vasodilators, arterial surgeries
may be needed.
 Bairnsdale ulcer
• It is chronic, irregular, undetermined ulcer due to Mycobacterium
ulcerations infection.

• Deep severe form, with extensive dermal necrosis is called as ‘Buruli

ulcer’.

• Discharge study will show acid- fast bacilli.

• Anti tuberculous drugs resolve the ulcer usually.

• Skin grafting may be required later.

 Carcinomatous ulcer (Epithelioma, squamous cell carcinoma)

• It arise from pickle cell layer of skin.

• It may initially begin as a nodule/ulcer; but later forms an ulcerative
lesion with rolled out/everted edge.
• Floor contains necrotic content, unhealthy (tumor) granulation tissue &
blood.
• Ulcer bleeds on touch & is vascular & friable.

• Induration is felt at the base & edge.

• It is usually circular/irregular in shape.
• Initially ulcer is mobile but becomes nonmobile once it infiltrates into
deeper tissues.
• The typical foul smell is due to necrotic material, infection & release of
polyamides from the tumor cells.
 Carcinomatous ulcer (Epithelioma, squamous cell carcinoma)

• Hard, discrete regional lymph nodes are often palpable, initially mobile
but later become fixed.

• Lymph nodes can fungate eventually.

• Ulcer & lymph nodes are initially pain-less; but becomes painful &
tender once there is deeper infiltration/secondary infection.

• Systemic spread is rare.

• It is a locoregional malignant disease.

• Verrucous carcinoma is exophytic, locally malignant well differentiated

squamous cell carcinoma without lymphatic spread.
 Carcinomatous ulcer (Epithelioma, squamous cell carcinoma)

• Management
• Wedge biopsy ▲; FNAC of regional lymph nodes are the investigations.

• Treated with wide local excision with skin grafting & regional lymph
node block dissection.
 Marjolin’s ulcer (Rene Marjolin, 1828, Paris)

• It is slow growing locally malignant lesion – a very well differentiated

squamous cell carcinoma occurring in an unstable scar of long duration.

• It is commonly seen in chronic venous ulcer scar.

• Often it is observed in burns scar & scar of previous snake bite.

• Lesion is ulcerative/proliferate.

• Edge may be everted/may not be.

• It is painless as scar does not contain nerve fibrils.

 Marjolin’s ulcer (Rene Marjolin, 1828, Paris)

• It does not spread into lymphatics as scar is devoid of lymphatics.

• Induration is felt at the edge & base.

• There is marked fibrosis also.

• Once lesion spreads into adjacent normal skin, it can spread into
regional lymph nodes behaving like squamous cell carcinoma.

• Managed by wedge biopsy & wide local excision & grafting.

 Rodent ulcer
• It is ulcerative form of basal cell carcinoma which is common in face.

• Ulcer shows central area of dry scab with peripheral raised active &
beaded (pearly white) edge.

• Often floor is pigmented.

• It erodes into deeper plane like soft tissues, cartilages & bones hence
the name – rodent ulcer.

• As lymphatics are blocked early in the disease by large tumor cells, it

does not spread to regional lymph nodes.

• Blood spread is absent.

• It is only locally malignant.

 Rodent ulcer

• It is common in face, rarely can it occur over tibia, external genitalia,

mucocutaneous junction.

• It does not occur in mucosa.

• Management
• Wedge biopsy, CT scan of the part to see the depth, wide excision.
 Melanotic ulcer
• It is ulcerative form of melanoma.
• It can occur in skin as de novo/in a pre-existing mole.
• Ulcer is pigmented often with a halo around.
• Ulcer is rapidly growing, often with satellite nodules & ‘in-transit’
lesions.
• It is very aggressive skin tumor arising from melanocytes.
• It spreads rapidly to regional lymph nodes which are pigmented.
• Blood spread to liver, lungs, brain & bones is common.
• It can occur in mucosa, genitalia & eye.
• It is a systemic malignant disease.
 Melanotic ulcer

• Management
• Excision biopsy (usually incision biopsy is not done), FNAC lymph node,
US abdomen.

• Treatment is wide local excision, regional node block dissection,

chemotherapy.
 Diabetic ulcer

• Causes
• Increased glucose in the tissue precipitates infection.
• Diabetic microangiopathy which affects microcirculation.
• Increased glycosylated hemoglobin decreases the oxygen dissociation.
• Increased glycosylated tissue protein decreases the oxygen utilization.
• Diabetic neuropathy involving all sensory, motor & autonomous
components.
• Associated atherosclerosis.
 Diabetic ulcer
• Diabetic angiopathy may be macro-angiopathy (thickening of the
basement membrane of vessels & capillaries).

• Sepsis in diabetes
• Cellulitis, deep seated abscess, ulcer formation, gangrene foot,
osteomyelitis of metatarsals, septicemia, multiorgan dysfunction
syndrome can occur faster in diabetes.

• Phagocytic activity in diabetes is reduced significantly; granulocyte

mobilization is reduced in diabetic ketoacidosis.

• Neuropathy, angiopathy, high tissue glucose level, associated smoking,

hypertension, hyperlipidemia, reduced immunity increases the chances
of sepsis in diabetics.

• Polymicrobial & fungal infections are common.

 Diabetic ulcer

• Sites
• Foot-plantar aspect – is the most common site
• Leg
• Upper limb, back, scrotum, perineum
• Diabetic ulcer may be associated with ischemia
• Ulcer is usually spreading & deep

• Investigation
• Blood sugar both random & fasting
• Urine ketone bodies
• Discharge for culture & sensitivity
• X-ray of the part to see osteomyelitis.
• Arterial Doppler of the limb; glycosylated hemoglobin estimation
 Diabetic ulcer

• Problems with diabetic ulcer

• Neuropathy, in foot – clawing of toes, hammer toe (due to intrinsic
muscle paralysis)
• Multiple deeper abscesses; osteomyelitis of deeper bones are common
• Reduced leukocyte function; resistant infection; spreading cellulitis.
• Arterial insufficiency
• Septicemia; diabetic ketoacidosis.
• Associated cardiac diseases like ischemic heart disease.
 Diabetic ulcer

• Treatment
• Control of diabetes using insulin.
• Antibiotics
• Nutritional supplements
• Regular cleaning, debridement, dressing
• Once granulates, the ulcer is covered with skin graft/flap.
• Revascularization procedure is done by
endarterectomy/thrombectomy/balloon angioplasty/arterial bypass
graft.
• But if distal vessels are involved then success rate is less.
• Toe/foot/leg amputation
• Microcellular rubber (MCR) shoes to prevent injuries; care of foot.
 Meleney’s ulcer (postoperative synergistic gangrene)

• It is commonly seen in postoperative wound in abdomen & chest wall

like empyema drainage/after surgery for peritonitis.

• It is an acute rapidly spreading ulcer with destruction & deep burrowing

of subcutaneous tissues.

• Occasional symbiotic infection may develop in leg/hand.

• This can be as de novo association of ulcerative of colitis/on a pre

existing venous ulcer.
 Meleney’s ulcer (postoperative synergistic gangrene)

• Etiology
• It is common in old age & immunosuppressed individuals & after
surgery for infected cases.

• It is caused by microaerophilic streptococci, Staphylococcus aureus &

anaerobes.

• Sites
• It is common in abdomen & thorax.
• It begins in wound margin & spreads rapidly.
• It can also occur in other areas of skin.
• Infection is severe, often with endarteritis of the skin leading to ulcer &
destruction.
 Meleney’s ulcer (postoperative synergistic gangrene)

• Clinical features
• Features of toxemia.
• Spreading painful ulcer with discharge.
• Abundant granulation tissue with purple & red zones.

• Management
• Random blood sugar is checked, if diabetic it has to be controlled.
• Antibiotics
• Blood transfusion, critical care.
• Adequate excision of dead tissues until it bleeds.
• Once healthy granulation tissue is formed skin grafting is done.
 Lupus vulgaris (‘Lupus’ wolf)

• It is cutaneous tuberculosis which occurs in young age group.

• Commonly seen on face, hand & forearm; starts as typical apple-jelly

nodule with congestion of skin around.

• Eventually a superficial ulcer with undermined edge is formed.

• Glass slide pressed firmly on the diseased area to eliminate the

surrounding hyperemia causes clinically obvious apple-jelly appearance.

• The ulcer is active & destruction occurs at the periphery with healing
takes place at the center.

• Often lesion extends into nose & oral cavity involving the mucosa.
 Lupus vulgaris (‘Lupus’ wolf)

• Due to lymphatic obstruction facial edema can occur.

• Long-standing lupus vulgaris can turn squamous cell carcinoma.

• Investigation
• ESR, discharge study, biopsy, chest X-ray.

• Treatment
• Anti tuberculous drugs
• If complete healing does not occur, then excision & skin grafting is
required.
 Tuberculous Ulcer

• It is due to Mycobacterium tuberculosis.

• It is usually due to cold abscess later forming ulcer in the neck, chest
wall, axilla & groin.

• It can also be primary tuberculosis of the skin (commonly in face).

• Ulcer can be single/multiple; oval/rounded; with undermined edge

(due to progression of disease outwards underneath & healing inwards
in skin), painless with caseating material on the floor.
 Tuberculous Ulcer

• Ulcer is usually not deep.

• Regional lymph nodes may be enlarged matted, firm & nontender.

• Tuberculosis ulcer is usually painless except on the tongue.

• Management
• Discharge study for epithelioid cells (modified histiocytes), AFB, edge
biopsy, anti tuberculous drugs.
 Bazin’s disease (Erythrocyanosis frigida/Erythema induratum)

• It is localised area of fat necrosis with chronic ischemia of ankle skin

affecting exclusively adolescent girls.

• It may be due to tuberculosis.

• It is observed in girls with more/thick subcutaneous fat around ankle.

• Bluish pink leg which becomes bluish mottling in extreme cold season.

• On warming, skin turns bright red & painful which is typical due to
hyperemia.
 Bazin’s disease (Erythrocyanosis frigida/Erythema induratum)

• In these patients performing arteries perfusing the skin around the

ankle are small/poor/not existing causing ischemia of skin around ankle
which becomes hyperesthetic ischemia of skin around ankle which
becomes hyperesthetic & sensitive for temperature alteration.

• Symmetrical, purple nodules develop in ankles & lower leg which later
break down forming multiple, small, painful, superficial ulcers often with
ankle edema & pigment scars.

• Treatment is antitubercular drugs & lumbar sympathectomy.

 Tropical ulcer

• It is endemic in monsoon hit humid tropics with repeated epidemics but

sporadic in subtropics.

• Trauma/insect bite leads into infection exclusively in the lower part of

the leg & foot.

• It is an acute ulcerative lesion of the skin observed in tropical regions

like Africa, India & South America.

• It is associated with lower socioeconomic group, anemia & malnutrition

& vitamin deficiency.

• It is commonly caused by fusobacterium fusiformis (Vincent’s

organisms) & Borrelia vincentii.
 Tropical ulcer

• There are abrasions, redness, papule & pustule formation, acute

regional lymphadenitis & severe pain.

• Pustule bursts in 3 days with necrobiosis & phagedena causing a

spreading painful ulcer with an undermined edge, brownish floor &
serosanguineous discharge.

• Spreading stops in few weeks with ulcer persisting for many months to
years.

• Eventually a chronic, large nonhealing/callous ulcer forms with

persistent pain, profuse serosanguineous discharge, extremely
unpleasant odour, long existing firmly adherent slough in the floor
without any obvious constitutional symptoms.
 Tropical ulcer
• During healing it causes a slight pigmented, parchment like round scar.

• Often destruction is progressive without cessation (phagedena) to

extend into entire soft tissues of foot & leg inviting amputation.

• Phagedena (Greek – to eat) is also seen in chancroid & cancrum oris.

• Note – Phagedena is destruction without proliferation.

• Occasionally squamous cell carcinoma can develop in it.

• Treatment
• Improvement in nutrition, penicillin, metronidazole, Eusol dressing, skin
grafting at a later date.
 Venous ulcer (gravitational ulcer)

• It is common around ankle (gaiter’s zone) due to ambulatory chronic

venous hypertension.

• It is due to varicose veins (long saphenous vein/short saphenous

vein/perforators) or post phlebitis limb.

• Post phlebitis limb consists of veins that is been partially recanalized

following deep venous thrombosis which causes increased venous
pressure around ankle through perforators.

• Varicose veins are common in females.

• 50% of venous ulcer are due to varicose veins; 50% are due to post
phlebitis limb (previous DVT).
 Venous ulcer (gravitational ulcer)

• Pain, discomfort, pigmentation, dermatitis, lipodermatosclerosis,

ulceration, periostitis, ankle joint ankylosis, talipes equinovarus
deformity & Marjolin’s ulcer are the problems of varicose veins & later
of venous ulcer.

• Ulcer is initially painful; but once chronicity develops it becomes

painless.

• Ulcer is often vertically oval; commonly locate on the medial side;

occasionally on lateral side; often on both sides of the ankle; but never
above the middle 3rd of the leg.

• Floor is covered with pale/often without any granulation issue.

• When well granulated, edge is sloping.

 Venous ulcer (gravitational ulcer)

• Induration & tenderness is seen often at the base of an ulcer.

• Venous ulcer is vertically oval with sloping edge & will not penetrate
deep fascia.

• Inguinal lymph nodes (vertical group) are often enlarged.

• Ulcer often attains very large size which is nonhealing, indolent &
callous.

• Ulcer heals on rest & treatment; but reforms again.

• Scar ring is common due to repeated healing & recurrent ulcer

formation.

• This unstable scar of long duration may lead into squamous cell
carcinoma (Marjolin’s ulcer).
 Venous ulcer (gravitational ulcer)

• Management
• Venous Doppler, regular dressing, skin grafting, specific treatment for
varicose veins.
 Syphilitic ulcer

• Nowadays it is rare entity.

• It is caused by Treponema pallidum bacterium.
• It is sexually transmitted disease.

• It is named as ‘Syphilis’ after a shepherd named Syphilus who acquired

the disease as was written in a poem by Francastorius of Verona.

• Many clinical lesions are observed in different stages of syphilis.

• John Hunter inoculated himself with syphilis organism to study the

clinical features & effect.
• After 24 years of inoculation, he died from rupture of syphilitic aortic
aneurysm at the age of 65.
 Syphilitic ulcer

• Genital chancre (hard/Hunterian chancre) is painless, hard, button like,

indurated, nonbleeding ulcer, usually seen in corona/frenum of penis,
often on lips, breasts & anal region, appears 4 weeks after initial
infection in 1st stage of the disease (primary syphilis).

• Shotty painless, firm, discrete groin lymph nodes may get enlarged along
with genital chancre.

• Suppuration in these nodes will not occur.

• Extragenital chancres in lips & breasts show enlarged neck/axillary

nodes which are inflamed, painful & also often may be matted.
 Syphilitic ulcer

• During 2nd stage (secondary syphilis) white, thickened mucous patches

appear commonly in the mouth like small, circular, superficial snail track
ulcers.

• Also there appears raised, flat, hypertrophied & warty like epithelium at
mucocutaneous junctions (mouth, genitalia) called as condyloma lata.

• Generalized, shotty, hard, discrete, painless lymph nodes are palpable,

epitrochlear & suboccipital nodes in particular are enlarged.

• Epitrochlear nodes are felt 1-2 cm above the medical epicondyle (It is
also enlarged in non-Hodgkin’s lymphoma/NHL).
 Syphilitic ulcer
• Iritis, arthritis, hepatitis (massive liver in syphilis is called as hepar
lobatum), meningitis, syphilitic osteitis with ‘ivory’ sequestrum, coppery
red skin rash, moth-eaten alopecia are other features of 2nd syphilis.

• In tertiary/late stage syphilis gummatous ulcer develops.

• It is deep, punched out, painless, nontender ulcer with wash leather

slough in the floor, with ‘silvery tissue paper’ like scar around & occurs
over the subcutaneous bones like tibia, sternum, skull, palate/other
area.

• It is also can occur over the tongue, anterior aspect of the scrotum.
• It is due to delayed hypersensitivity reaction with endarteritis obliterans
& vasculitis.
 Syphilitic ulcer
• Perforation of nasal septum/palate can occur.
• Clutton’s joint & Sabre tibia are often seen.
• Lymph nodes are not affected in tertiary syphilis.

• Neurosyphilis (tabes dorsalis), aneurysm of arch of aorta are other

features of tertiary syphilis.

• Tabes dorsalis presenting as generalized paralysis of insane is often

called latent tertiary/quaternary syphilis.

• Long quiescent asymptomatic period from secondary to tertiary is called

as latent syphilis.

• Secondary syphilitic stage shows plenty of circulating Treponema

spirochaetes in blood where as in tertiary stage spirochaetes are
less/absent.
 Soft chancre/sore/ducrey’s ulcer/chancroid/Bubo

• These multiple irregular genital ulcers appear 3 days after infection with
Hemophilus ducrey’s as a venereal disease.

• They are acute painful, tender, nonindurated ulcers.

• Floor shows yellowish slough with purulent discharge.

• Edge is edematous & inflamed.

• Acute regional lymphadenitis with suppuration presenting as tender,

soft/firm swelling is common.

• Such soft fluctuant inguinal swelling is termed as bubo.

• Treatment is by drugs like co-trimoxazole, erythromycin, cipro floxacillin,

ceftriaxone; aspiration of bubo.
 Climatic bubo/tropical bubo

• It is due to lymphogranuloma inguinale, a venereal spreading organism.

• In LGV, lesion of primary genital stage is small, painless & commonly

unnoticed.

• Lesion of secondary stage develops in 2 weeks.

• In males inguinal lymph nodes; in female intrapelvic & pararectal nodes

are involved.

• Suppuration of inguinal nodes eventually occurs leading into discharging

sinuses.

• Frei intradermal test becomes positive in 6 weeks & remains positive for
life time.
 Climatic bubo/tropical bubo

• In tertiary stage, eye, joint, meninges may get involved after many years.

• Repeated chronic inflammation, lymphatic blockage, scar-ring can cause

rectal stricture & vulval elephantiasis (esthiomene) in females.

• Treatment is tetracycline for 3 weeks.

 Other ulcer

• Ulcer can occur, in various parts like over shin, legs, feet, face, chest
wall, in various disease like anemia, polycythemia, sickle cell disease,
hereditary spherocytosis, leukemia, vasculitis, autoimmune disease, like
RA, Paget’s disease of bone (deep, nonmobile, fixed to bone; common
in tibia), ulcerative colitis, etc.

• Treponema pertenue causing yaws (Frambesia) can have multiple

painless ulcers in leg & feet due to walking with bare foot (organism
enters through abrasion) which heals spontaneously leaving a tissue
paper like scar.

• Poor hygiene & dressings can cause multiple, small, red often scabbed
staphylococcus aureus ulcers on the skin over the leg & feet which is
often recurrent & disturbing.
 Other ulcer

• Buruli ulcer – It is chronic ulcer caused by Mycobacterium ulcerans (acid

fast bacillus).

• Initially it forms a subcutaneous nodule later forming non-caseous

necrosis showing slow healing with severe scarring.

• Veld sore – It is cutaneous diphtheria through the skin causing vesicles

with a straw colored fluid; once vesicles rupture chronic tender shallow
ulcers will form.

• Delhi boil (Oriental sore) – Here Leishmania tropica infection causes

indurated papules on the face & exposed body parts causing indolent
chronic ulcer which heals producing an ugly pigmented scar.