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Break in the continuity of the covering
epithelium with molecular death
(necrosis) – skin or mucous membrane.
Chronic ulcer > 6 weeks
Clinically and pathologically
 Clinically –
 Spreading ulcer
 Healing ulcer
 Callous or chronic ulcer
 Pathologically –
 Infective ulcers
 Non-infective ulcers
 Malignant ulcers
CLINICALLY
 Spreading ulcer
 Surrounding skin – inflamed
 Floor – slough
 Edge – inflamed and ragged
 No granulation tissue
 Healing ulcer
 Floor – healthy granulation tissue
 Edge – reddish with granulation
 Margin – bluish and growing
 Discharge – slight and serous
 Callous or chronic ulcer
 No tendency towards healing
 Floor – pale granulation tissue
 Discharge is scanty or absent
 Base, edge and skin is indurated
PATHOLOGICALLY
 Non-infective ulcers
 Venous ulcers (MC)
 Arterial ulcers
 Neurogenic ulcers (Trophic)
 Traumatic ulcers
 Associated with malnutrition
 Associated with systemic disease
 Miscellaneous
 Miscellaneous
 Vasculitis
 Hematological
 Emboli
 Drugs / Therapy
 Skin conditions
 Genetic conditions
 Infective ulcers
 Tuberculous
 Mycetoma
 Tropical
 Meleney’s
 Malignant ulcers
 Epithelioma (Squamous cell)
 Melanoma
 Rodent ulcer (Basal cell)
 Marjolin’s ulcer
Ulceration of the lower leg occurring as the result of
persistently elevated venous pressure and its secondary
effects on the microvascular system.
 Causes:
 Deep-vein valvular incompetence or post thrombotic
damage
 Incompetence superficial or communicating veins
 Elderly women
 Genetic ?
 Venous ulcers are the end result of superficial venous
insufficiency or the post-thrombotic syndrome (PTS)
 Associated skin changes –
Death of the skin following occlusion of its arterial blood supply.
 Atheroma of the abdominal and limb vessels is the single most
common cause of ischemic ulceration
 Three main causes:
 Extramural strangulation
 Mural thickening or accretion
 Intramural restriction of blood flow
 There is often considerable overlap, and the exact pathology is not
well defined
 Extramural causes
 Scar tissue and radio-dermatitis cause a fibrotic
strangulation of the arterioles
 Dermal sclerosis
 Compression by tumors
 Mural causes (speed of occlusion)
 Vasculitis – sudden
 Hypertension – slower
 Atherosclerosis
 Intramural causes (Microvascular occlusion)
 Change in blood viscosity
 Defective clotting mechanisms
 Peripheral arterial disease and poor peripheral circulation
 Atherosclerosis
 Buerger’s disease
 Raynaud’s disease
Neuropathic ulcer is a form of chronic ulceration, also known as
‘perforating ulcer’ which develops in anaesthetic skin.
 Characteristically neuropathic ulcers are –
 Painless
 persistent and uninflamed
 appearing on areas subject to trauma or pressure
 Causes
 Type II DM (most common)
 Leprosy
 Peripheral neuropathy
 Alcoholism
 Vitamin deficiencies
 Pernicious anemia
 Syringomyelia
 Tabes dorsalis
 Spinal dysraphism
 Spinal cord injury
 Hereditary sensory and autonomic neuropathies
 Neuropathic ulcers result from a distal polyneuropathy
encompassing motor, sensory and autonomic components
 Increased pressure under the metatarsal heads and heel – 90%
ulcers
 Autonomic neuropathy
 Loss of sweating, dryness with fissuring and cracking
 Changes in the normal microcirculatory autoregulation
 ‘Multifactorial’
 Neuropathy
 Macro and microvascular disease
 Infection
 Connective tissue abnormalities
 Hematological disturbances
 Neuropathic / Ischemic / Neuroischemic
 Any one factor may predominate
 Identification of the dominant factor
NEUROPATHY
 Glove and Stocking distribution of diabetic somatic sensory
neuropathy
 Somatic motor nerves
 Autonomic nervous system
Causes of neuropathy
 Metabolic factors
 Microvascular disease
 Effect of neuropathy
 Extrinsic neuropathic foot ulceration
 Intrinsic neuropathic foot ulceration
 Extrinsic – loss of somatic sensory
 Intrinsic – loss of somatic motor and autonomic
MICROVASCULAR DISEASE
 Structural changes in basement membrane
 Increased capillary permeability to albumin
 Absolute hyperperfusion Relative hypoperfusion
 Less ability to vasodilate and increase blood flow
 Endothelial dysfunction
MACROVASCULAR DISEASE
 Atherosclerosis – tibial and peroneal arteries
 Arteriosclerosis – calcification of the media
INFECTION
 Not generally the primary cause except ‘fungal’ infection
 Why increased propensity?
 Intrinsic abnormalities of immune system
 Favorable environment
 Infection determines the outcome of lesion
 Polymicrobial in nature
CONNECTIVE TISSUE ABNORMALITIES
 Non-enzymatic glycosylation of proteins
 Advanced glycosylation end products
 Hemoglobin, collagen and keratin
 Rigid, inflexible and resistant to digestion
HEMATOLOGICAL DISTURBANCES
 RBCs are less deformable
 Tendency towards hypercoagubility
 Impaired WBC function
TUBERCULOUS ULCER
 Tuberculous chancre – Primary inoculation of the skin usually
following trauma in the non-immune host
 Tuberculosis verrucosa cutis – Primary infection in the immune
host
 Lupus vulgaris – Hematogenous, lymphatic or contiguous
spread but can occur following inoculation
 Scrofuloderma – Contiguous involvement of the skin overlying
tuberculosis in a deeper structure
 Metastatic tuberculous abscesses (tuberculous gumma) –
Hematogenous spread from a primary focus
 Erythema induratum of Bazin (Bazin’s disease) – Chronic
disorder characterized by recurrent hard subcutaneous
nodules over calves.
Erythema induratum
Tuberculous cutis
verrucosa
MYCETOMA FOOT / MADURAMYCOSIS
A localized chronic infection caused by various species
of fungi or actinomycetes, and characterized by the
formation of aggregates of the causative organisms
(grains) within abscesses.
 Fungi (eumycetoma) – Madurella mycetomatis (MC)
 Aerobic actinomycetes (actinomycetoma)
TROPICAL ULCERS
 Synergistic bacterial infection
 Following invasion of the skin by at least two organisms
 Fusobacterium spp.(F. ulcerans)
 Spirochetes or other anaerobic bacteria
 Develops at a site of potential trauma, a scratch, cut or insect
bite
 SCC develops after 10 years or more in some such cases.
MELENEY’S ULCER
Bacterial synergistic gangrene extending rapidly and has
a burrowing, bluish, undermined and painful edge.
 Symbiotic action of micro-aerophilic non hemolytic
streptococci and staphylococcus aureus
 De-novo – Ulcerative colitis
 Complicating previous ulcer
 Toxemia
BAZIN’S ULCER / ERYTHROCYANOID ULCER
 Erythrocyanoid frigida
 Exclusively women
 Predisposing factors
 Subcutaneous fat
 Thick ankle pad
 Poor arterial supply
 Sensitivity to extremes of temperature
YAWS
 Treponema Pertenue
 Bare-foot injury
 Painless ulcers
 Healing with tissue paper like scar
SQUAMOUS CELL CARCINOMA
A malignant tumor arising from the keratinocytes of the
epidermis
 Most common skin cancer
 Etiology
 sun exposure
 trauma
 Albinism
 Burn scars and thermal radiation
 ionizing radiation
 chronic inflammation
 chronic discoid lupus erythematosus
MALIGNANT MELANOMA
 Acral lentiginous melanoma (palmoplantar malignant
 melanoma)
 Commonest type of melanoma
 Sole of the foot, palm of the hand
 Etiology
 Genetic and ethnic
 Familial - autosomal dominant gene with incomplete
penetrance
 Environmental - intermittent sun exposure
 Melanocytic naevi
BASAL CELL CARCINOMA
 A malignant tumor that rarely metastasizes, composed of cells
similar to those in the basal area of the epidermis and its
appendages
 BCC in lower limb is uncommon
 Secondary to
 Lipodermatosclerosis
 Burn scars, vaccination scars
 Ionizing radiation
 Damage by sunlight
MARJOLIN’S ULCER
 SCC arising from long standing benign ulcer or scar
 MC – venous ulcer
 Slow growing, painless
MARTORELL’S ULCER
Association with longstanding, often poorly controlled,
hypertension, and healing response to specific
antihypertensive agents.
 Bilateral superficial painful ulceration
 Presence of peripheral pulses
 Absence of atherosclerosis
 Subendothelial hyaline degeneration
 Smooth muscle hyperplasia
TRAUMATIC ULCERS
 Mechanical injury
 Rat bite
 Physical e.g. burns, electrical or X-ray
 Chemical e.g. caustics
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classification.pptx

  • 2. Break in the continuity of the covering epithelium with molecular death (necrosis) – skin or mucous membrane. Chronic ulcer > 6 weeks
  • 3. Clinically and pathologically  Clinically –  Spreading ulcer  Healing ulcer  Callous or chronic ulcer  Pathologically –  Infective ulcers  Non-infective ulcers  Malignant ulcers
  • 4. CLINICALLY  Spreading ulcer  Surrounding skin – inflamed  Floor – slough  Edge – inflamed and ragged  No granulation tissue  Healing ulcer  Floor – healthy granulation tissue  Edge – reddish with granulation  Margin – bluish and growing  Discharge – slight and serous
  • 5.  Callous or chronic ulcer  No tendency towards healing  Floor – pale granulation tissue  Discharge is scanty or absent  Base, edge and skin is indurated
  • 6. PATHOLOGICALLY  Non-infective ulcers  Venous ulcers (MC)  Arterial ulcers  Neurogenic ulcers (Trophic)  Traumatic ulcers  Associated with malnutrition  Associated with systemic disease  Miscellaneous
  • 7.  Miscellaneous  Vasculitis  Hematological  Emboli  Drugs / Therapy  Skin conditions  Genetic conditions
  • 8.  Infective ulcers  Tuberculous  Mycetoma  Tropical  Meleney’s  Malignant ulcers  Epithelioma (Squamous cell)  Melanoma  Rodent ulcer (Basal cell)  Marjolin’s ulcer
  • 9.
  • 10. Ulceration of the lower leg occurring as the result of persistently elevated venous pressure and its secondary effects on the microvascular system.  Causes:  Deep-vein valvular incompetence or post thrombotic damage  Incompetence superficial or communicating veins  Elderly women  Genetic ?
  • 11.  Venous ulcers are the end result of superficial venous insufficiency or the post-thrombotic syndrome (PTS)
  • 12.  Associated skin changes –
  • 13.
  • 14. Death of the skin following occlusion of its arterial blood supply.  Atheroma of the abdominal and limb vessels is the single most common cause of ischemic ulceration  Three main causes:  Extramural strangulation  Mural thickening or accretion  Intramural restriction of blood flow  There is often considerable overlap, and the exact pathology is not well defined
  • 15.  Extramural causes  Scar tissue and radio-dermatitis cause a fibrotic strangulation of the arterioles  Dermal sclerosis  Compression by tumors  Mural causes (speed of occlusion)  Vasculitis – sudden  Hypertension – slower  Atherosclerosis
  • 16.  Intramural causes (Microvascular occlusion)  Change in blood viscosity  Defective clotting mechanisms  Peripheral arterial disease and poor peripheral circulation  Atherosclerosis  Buerger’s disease  Raynaud’s disease
  • 17.
  • 18. Neuropathic ulcer is a form of chronic ulceration, also known as ‘perforating ulcer’ which develops in anaesthetic skin.  Characteristically neuropathic ulcers are –  Painless  persistent and uninflamed  appearing on areas subject to trauma or pressure
  • 19.  Causes  Type II DM (most common)  Leprosy  Peripheral neuropathy  Alcoholism  Vitamin deficiencies  Pernicious anemia  Syringomyelia  Tabes dorsalis  Spinal dysraphism  Spinal cord injury  Hereditary sensory and autonomic neuropathies
  • 20.  Neuropathic ulcers result from a distal polyneuropathy encompassing motor, sensory and autonomic components  Increased pressure under the metatarsal heads and heel – 90% ulcers
  • 21.  Autonomic neuropathy  Loss of sweating, dryness with fissuring and cracking  Changes in the normal microcirculatory autoregulation
  • 22.
  • 23.
  • 24.  ‘Multifactorial’  Neuropathy  Macro and microvascular disease  Infection  Connective tissue abnormalities  Hematological disturbances  Neuropathic / Ischemic / Neuroischemic  Any one factor may predominate  Identification of the dominant factor
  • 25. NEUROPATHY  Glove and Stocking distribution of diabetic somatic sensory neuropathy  Somatic motor nerves  Autonomic nervous system Causes of neuropathy  Metabolic factors  Microvascular disease
  • 26.
  • 27.  Effect of neuropathy  Extrinsic neuropathic foot ulceration  Intrinsic neuropathic foot ulceration  Extrinsic – loss of somatic sensory  Intrinsic – loss of somatic motor and autonomic
  • 28.
  • 29. MICROVASCULAR DISEASE  Structural changes in basement membrane  Increased capillary permeability to albumin  Absolute hyperperfusion Relative hypoperfusion  Less ability to vasodilate and increase blood flow  Endothelial dysfunction MACROVASCULAR DISEASE  Atherosclerosis – tibial and peroneal arteries  Arteriosclerosis – calcification of the media
  • 30. INFECTION  Not generally the primary cause except ‘fungal’ infection  Why increased propensity?  Intrinsic abnormalities of immune system  Favorable environment  Infection determines the outcome of lesion  Polymicrobial in nature
  • 31.
  • 32. CONNECTIVE TISSUE ABNORMALITIES  Non-enzymatic glycosylation of proteins  Advanced glycosylation end products  Hemoglobin, collagen and keratin  Rigid, inflexible and resistant to digestion
  • 33. HEMATOLOGICAL DISTURBANCES  RBCs are less deformable  Tendency towards hypercoagubility  Impaired WBC function
  • 34.
  • 35. TUBERCULOUS ULCER  Tuberculous chancre – Primary inoculation of the skin usually following trauma in the non-immune host  Tuberculosis verrucosa cutis – Primary infection in the immune host  Lupus vulgaris – Hematogenous, lymphatic or contiguous spread but can occur following inoculation
  • 36.  Scrofuloderma – Contiguous involvement of the skin overlying tuberculosis in a deeper structure  Metastatic tuberculous abscesses (tuberculous gumma) – Hematogenous spread from a primary focus  Erythema induratum of Bazin (Bazin’s disease) – Chronic disorder characterized by recurrent hard subcutaneous nodules over calves.
  • 38. MYCETOMA FOOT / MADURAMYCOSIS A localized chronic infection caused by various species of fungi or actinomycetes, and characterized by the formation of aggregates of the causative organisms (grains) within abscesses.  Fungi (eumycetoma) – Madurella mycetomatis (MC)  Aerobic actinomycetes (actinomycetoma)
  • 39.
  • 40. TROPICAL ULCERS  Synergistic bacterial infection  Following invasion of the skin by at least two organisms  Fusobacterium spp.(F. ulcerans)  Spirochetes or other anaerobic bacteria  Develops at a site of potential trauma, a scratch, cut or insect bite  SCC develops after 10 years or more in some such cases.
  • 41.
  • 42. MELENEY’S ULCER Bacterial synergistic gangrene extending rapidly and has a burrowing, bluish, undermined and painful edge.  Symbiotic action of micro-aerophilic non hemolytic streptococci and staphylococcus aureus  De-novo – Ulcerative colitis  Complicating previous ulcer  Toxemia
  • 43.
  • 44. BAZIN’S ULCER / ERYTHROCYANOID ULCER  Erythrocyanoid frigida  Exclusively women  Predisposing factors  Subcutaneous fat  Thick ankle pad  Poor arterial supply  Sensitivity to extremes of temperature
  • 45. YAWS  Treponema Pertenue  Bare-foot injury  Painless ulcers  Healing with tissue paper like scar
  • 46.
  • 47. SQUAMOUS CELL CARCINOMA A malignant tumor arising from the keratinocytes of the epidermis  Most common skin cancer  Etiology  sun exposure  trauma  Albinism  Burn scars and thermal radiation  ionizing radiation  chronic inflammation  chronic discoid lupus erythematosus
  • 48. MALIGNANT MELANOMA  Acral lentiginous melanoma (palmoplantar malignant  melanoma)  Commonest type of melanoma  Sole of the foot, palm of the hand  Etiology  Genetic and ethnic  Familial - autosomal dominant gene with incomplete penetrance  Environmental - intermittent sun exposure  Melanocytic naevi
  • 49.
  • 50. BASAL CELL CARCINOMA  A malignant tumor that rarely metastasizes, composed of cells similar to those in the basal area of the epidermis and its appendages  BCC in lower limb is uncommon  Secondary to  Lipodermatosclerosis  Burn scars, vaccination scars  Ionizing radiation  Damage by sunlight
  • 51.
  • 52. MARJOLIN’S ULCER  SCC arising from long standing benign ulcer or scar  MC – venous ulcer  Slow growing, painless
  • 53.
  • 54. MARTORELL’S ULCER Association with longstanding, often poorly controlled, hypertension, and healing response to specific antihypertensive agents.  Bilateral superficial painful ulceration  Presence of peripheral pulses  Absence of atherosclerosis  Subendothelial hyaline degeneration  Smooth muscle hyperplasia
  • 55. TRAUMATIC ULCERS  Mechanical injury  Rat bite  Physical e.g. burns, electrical or X-ray  Chemical e.g. caustics