KEY NOTES CHAPTER 6: LOWER LIMB - Pressure Ulcers. Flashcards
What is the epidemiology of pressure ulcers?
- Develop in 3-14% of hospitalised patients.
- Associated with fivefold increased mortality in the elderly.
• Tend to occur in:
∘ The old
∘ The hospitalised
∘ The young neurologically impaired.
Define pressure ulcer.
Definition: a localised injury to the skin and/or underlying tissue, usually over a
bony prominence, as a result of pressure or pressure in combination with shear.
The microclimate (moisture and temperature) also contributes.
Where can pressure ulcers occur?
∘ Sacrum ∘ Heel ∘ Ischium ∘ Elbow ∘ Malleolus ∘ Trochanter ∘ Knee ∘ Scapula ∘ Occiput. ∘ With medical devices, e.g. nasogastric tubes, CPAP.
What is the pathogenesis?
• Pressure ulcers are initiated by extrinsic factors and propagated by intrinsic factors.
Extrinsic factors
- Pressure
- Shear
- Friction
Intrinsic factors
- General
- Local
How does pressure cause pressure ulcers?
• Prolonged pressure -> tissue ischaemia -> necrosis and ulceration.
• Low pressure over long time = high pressure over a short period.
• Necrosis first occurs in tissues closest to the bone, usually muscle. Skin necrosis occurs late.
∘ Results in a characteristic cone-shaped wound - degree of skin loss is the tip of the iceberg.
What is shear and friction?
Shear
• Mechanical stress applied parallel to the skin’s surface.
∘ Skin moves in the opposite direction to bone.
• Less pressure is required to occlude blood vessels.
Friction
• Opposes movement of one surface against another.
• When a patient is dragged across a surface, or ill-fitting shoes.
• Loss of epidermis may initiate or accelerate pressure ulceration.
What intrinsic factors propagate the development of pressure ulcers?
General • Old age • Immobility • Acute illness or terminal illness • Impaired nutrition or hydration ∘ Low lean body mass ∘ Anaemia • Impaired perfusion ∘ Diabetes ∘ Smoking ∘ Peripheral vascular disease ∘ Use of vasopressors.
Local • Local ischaemia or fibrosis • Decreased sensation • Loss of autonomic control • Skin moisture ∘ Excessively dry or moist skin both contribute to pressure ulceration ∘ Urinary and faecal incontinence • Infection.
How do the European Pressure Ulcer Advisory Panel (EPUAP) and American National Pressure Ulcer Advisory Panel (NPUAP) categorise pressure ulcers?
Category I: Non-blanchable erythema
• Intact skin with non-blanchable redness of a localised area, usually over a bony prominence.
• Discolouration, warmth or induration may be indicators in individuals with dark skin.
Category II: Partial thickness
• Partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound
bed, without slough.
Category III: Full thickness skin loss
• Subcutaneous fat may be visible but bone, tendon or muscle are not exposed.
Category/Stage IV: Full thickness tissue loss
• Exposed bone, tendon or muscle. Slough or eschar may be present.
How are patients risk assessed for pressure ulcers?
∘ Norton score (1962)
∘ Waterlow score (1985)
∘ Braden score (1987)
Describe the Waterlow scoring system
- Updated in 2005 based on new research.
- Most widely used risk assessment tool in UK.
- Patients are scored on these factors:
∘ BMI ∘ Skin type and risk areas ∘ Sex and age ∘ Appetite and weight loss ∘ Continence ∘ Mobility ∘ Special risks - Tissue malnutrition, neurological deficit, major surgery or trauma, medications.
- Scores 10+ - at risk
- Scores 15+ - high risk
- Scores 20+ - very high risk
How are pressure ulcers prevented?
- Skin care (emollients, barrier areas, clean and dry skin regularly, remove particulate matter from beneath patient)
- Urinary or faecal diversion
- Nutrition
- Positioning (avoid bony prominences, pillows)
- Repositioning (bed bound 2hrly, seated every 15-30mins.)
- Pressure dispersion (alternating-pressure mattresses)
- Pressure awareness (patient and carer education)
What is the treatment for pressure ulcers?
Non-operative 1 Optimise the patient • Nutrition • Comorbidities, e.g. diabetes or anaemia • Smoking cessation • Medication review • Exclude malignancy • Patient education.
2 Treat the wound pathology
• Improve blood flow, e.g. angioplasty
• Provide compression therapy for venous insufficiency
• Minimise friction, shear and pressure on the wound.
3 Optimise the local healing environment • Bedside debridement of eschar • Treatment of infection ∘ Cellulitis: simple antibiotics ∘ OM: extensive orthopaedic surgery • Maintain adequate wound hydration • Consider negative pressure wound therapy.
What are the indications for reconstructive surgery?
Indications for reconstructive surgery
• Patients should be fully investigated:
∘ Imaging may reveal a dislocated hip or OM.
• Predisposing factors should be corrected if possible.
• Preventative measures in place pre-operatively to prevent recurrence postoperatively.
• Deteriorating conditions are not candidates for reconstruction.
• Patients expected to increase their mobility are treated conservatively (ulcers will improve)
• Surgery is best suited to:
∘ Well-motivated, young patients
∘ Clinically stable conditions
∘ Compliant
What are the principles of surgery?
- Adequate wound excision, including:
∘ Surrounding scar
∘ Underlying bursa - delineate with methylene blue staining
∘ Bone and soft tissue calcifications. - Obliteration of dead space.
- Reconstruction with durable skin.
- Flaps should not be wasted:
readvancable flaps should be used. Territories of future potential flaps should not be violated. - Flaps are designed as large as possible.
- Suture lines should lie away from pressure areas.
- Large drains are empirically left in place for at least 2 weeks post-operatively.
How are sacral pressure sores reconstructed?
• Occur in supine patients.
• Can be reconstructed with the gluteus maximus musculocutaneous flap.
∘ Quoted recurrence rate: 16%.
• Can be designed as a rotation or V-to-Y advancement flap.
• The muscle’s greater trochanter insertion can be divided in non-ambulatory patients.
∘ This increases flap mobility.
• Lumbosacral flaps, based on regional perforating vessels, can also be used.
• Use of the superior gluteal artery perforator flap is also described.
