14/15: Common Ulcerations and Case - Bennett Flashcards
define ulcer
- Lesion of the skin or mucous surface caused by superficial loss of tissue
- Usually associated with necrosis and inflammation
- Wound where the epidermis and part of the dermis is absent
Review Wagners Classification
Grade O – Intact skin (signs of inflammation, irritation, pre-ulcerative)
Grade I – Superficial (no sub Q involvement)
Grade II – Extends to tendon, capsule, bone (tracks)
Grade III – Associated with abscess, osteo, sepsis (clinical or radiographic signs of infection)
Grade IV – Gangrene of forefoot
Grade V – Gangrene of entire foot
Review UofT classification
Grade O – Intact Skin, Pre or post ulcerative site
Grade I – Ulcers are superficial wound through the epidermis/dermis
Grade II – Through tendon or capsule
Grade III – Through bone or into joints
Stage A – Clean
Stage B –Infection
Stage C – Ischemic
Stage D – Ischemic and infected
Review Knighton Classification
Grade I – Partial thickness (through epidermis)
Grade II – Full thickness (through dermis into sub Q)
Grade III – Full thickness (to tendon, ligament, bone, joint
Grade IV – Full thickness (associated abscess or osteo)
Grade V – Full thickness (necrosis)
Grade VI – Full thickness (ulcer with gangrene)
Review NPUAP classification
Stage I: Intact skin with non-blanchable redness of a localized area usually over a bony prominence. Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area
Stage II: Partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough. May also present as an intact or open/ruptured serum-filled blister.
Stage III: Full thickness tissue loss. Subcutaneous fat may be visible but bone, tendon or muscle are not exposed. Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunneling.
Stage IV: Full thickness tissue loss with exposed bone, tendon or muscle. Slough or eschar may be present on some parts of the wound bed. Often include undermining and tunneling.
Unstageable:Full thickness tissue loss in which the base of the ulcer is covered by slough (yellow, tan, gray, green or brown) and/or eschar (tan, brown or black) in the wound bed.
associated disease states for neuropathic ulcers (not just diabetes!)
Diabetes Peripheral nerve injury Alcoholism Anemia Tabes dorsalis Chemotherapy/radiation treatment Spina bifida
triad of diabetic ulcer
- neuropathy
- ischemia
- infection
etiology of diabetic ulcer
- Insulin not required for glucose uptake in neurons
- Therefore increased neuronal concentration in diabetics
- This prevents myo-inositol by competitive inhibition
- Low myo-inositol concentration in neurons results in abnormal cellular responses to receptor stimulation
- Impaired Na/K ATPase activity and nerve dysfunction
Glycation product, AGE’s cause …
Matrix overproduction
Focal thrombosis
Vasoconstriction
Diabetics are at risk for developing repetitive injuries that do not heal well due to:
Ischemia
Painless
Low resistance to pathogenic organisms
– Attenuated inflammatory response, impaired chemotaxis, inefficient bacterial-killing
—Infection increases the local tissue metabolism, burdening a tenuous blood supply, amplifying tissue necrosis
describe a neuropathic wound
- Absence of pain
- Ischemia (macrovascular and/or microvascular) may or may not be present which will alter appearance of ulcer bed
- Usually located in a weight bearing or pressure area
- Well circumscribed
clinical findings neuropathic ulcer
- Underlying bone pathology (rocker bottom, metatarsal deformity, sesamoid, hammertoe)
- Tissue is usually warm with a zone of hyperkeratotic tissue at the wound edges
- No pain
- Depth (depends on location, length of wound, infection)
- Base of fibrous-granular tissue
etiology venous ulceration
- Prolonged venous hypertension
- Incompetent valves
- Superficial Thrombophlebitis
- Deep vein thrombosis
- Calf muscle dysfunction
- Fibrin Cuff Hypothesis
- White Cell Hypothesis
describe fibrin cuff hypothesis
- Enlarged dermal capillaries, reduced capillary number, microvascular thrombosis, increased permeability of micro lymphatics
- Increased capillary permeability leads to extravasation of plasma proteins like fibrinogen which forms an insoluble fibrin cuff
- Fibrin cuff is a barrier to diffusion of oxygen and nutrients to overlying skin, therefore cell death and ulceration
describe white cell hypothesis
- Adhering leukocytes degranulate and release potent enzymes and reactive oxygen species that damage the capillaries and cause increased permeability and tissue damage
- Macromolecules like albumin bind or trap growth factors and matrix material, therefore are unavailable for tissue maintenance or repair
describe venous ulceration
- Usually present with presence of arterial flow
- Usually granulating bed (beefy red base)
- Painful
- Common by medial malleolus
- Associated with venous insufficiency (edema, hemosiderin deposition, induration)
describe varicose veins
- Dilated, tortuous superficial veins
- Increased deep venous pressure (venous hypertension)
- Increased distensibility of the venous walls
- Development of venous lakes [ blue, purple, compressible papules actually are dilated venules and capillaries ]
describe thrombophlebitis
- Great and lesser saphenous
- Presents as pain, swelling, warmth (more localized)
- Tender along the involved vein
- Often confused with cellulitis and infection
- Chronic recurrent bouts of inflammation along vein secondary to incompetent superficial veins
how do varicose veins lead to an ulcer? (sequence of events)
Varicose veins –> Thrombophlebitis –> Deep venous thrombosis –> Inoperative muscle pump –> Development of eczematous plaque –> Tissue hypoxic –> Minor trauma –> Development of the ulceration
clinical findings venous ulceration
Unilateral (medial ankle) Stasis pigmentation Chronic edema Fibrous-granular base Variable depth and size ****Irregular border (no hyperkeratotic rim) Variable pain Serous drainage (leakage)
treatment venous ulcer
- Culture and biopsy
- Treatment of underlying infection with appropriate antibiotic therapy
- Thorough exam (PADnet, etc)
Elevation - Regular debridement of wound
- control of inflammation
- compression therapy
key treatment venous wound
compression therapy
- During wound care and often
- Need a minimum of 30 mm Hg
- Unnaboot @ 30 mmHg
- Profore system @ 40 mmHg
describe an arterial ulcer
Signs of diminished circulation Usually painful * Well circumscribed Avascular wound bed More fibrotic base Any location on extremity, often where trauma has occurred
etiology of arterial ulcers
Narrowing lumen Can be worsened by a sudden thrombus (ischemic pain, blue toe, showering emboli) Absent pedal pulses Bruits Temperature Trophic skin changes Muscle atrophy Tissue necrosis
