Pressure ulcers — staging and management

Definition. Localised injury to skin and/or underlying tissue, usually over a bony prominence, resulting from sustained pressure, or pressure in combination with shear. The current NPUAP/NPIAP term is "pressure injury", which better reflects that damage can occur under intact skin.

Pathogenesis. Sustained pressure exceeding capillary closing pressure causes tissue ischaemia. Shearing forces — for example when the head of the bed is elevated and the torso slides down, transmitting force to the sacral area — stretch and angulate subcutaneous tissues, leading to thrombosis of small blood vessels and destruction of skin from beneath. Friction from repeated movement across sheets increases shear, and both are worsened by the loose, folded skin that is common in the elderly from loss of subcutaneous tissue and dehydration. Moisture from bathing, sweat, urine and faeces compounds the damage.

Sites. More than 90% of pressure ulcers occur in the lower body — mainly the sacral and coccygeal areas, the ischial tuberosities and the greater trochanter; also heels, malleoli and occiput. Critically, the area of damage beneath the ulcer can be much larger than the visible ulcer, because pressure and shear are transmitted to deeper subcutaneous tissues.

Risk factors. Being bed- or chair-bound, inability to reposition without assistance, difficulty with ambulation, history of stroke, faecal incontinence, low body weight, lymphopenia, difficulty with independent feeding, impaired nutritional intake, non-blanchable erythema of intact skin (a Stage 1 injury), and dry sacral skin. Advanced age has NOT been identified as an independent risk factor — it is the coexisting impairments in mobility, nutrition and skin health that create risk.

Risk assessment. Commonly used tools are the Braden, Norton and Waterlow scales. Current recommendation: apply a risk-assessment tool on admission to a facility and regularly thereafter. Because pressure injury shares risk factors with falls, incontinence and functional dependence, multifactorial interventions delivered by a multidisciplinary team are effective, just as for other geriatric syndromes.

Staging (NPIAP). Stage 1 — acute inflammatory response limited to the epidermis; intact skin with non-blanchable erythema persisting more than 30 minutes; may look red, blue or purple in darker skin; skin unbroken; often over a bony prominence. Stage 2 — extension through the dermis to the junction of subcutaneous fat; a blister, abrasion or shallow ulcer with distinct edges. Stage 3 — full-thickness loss through subcutaneous fat, down to but not through fascia; presents as a crater with undermining; base often necrotic and foul-smelling. Stage 4 — extension through deep fascia, with bone, tendon or muscle visible; extensive undermining and sinus tracts; osteomyelitis and septic arthritis may be present. Unstageable — base obscured by slough or eschar. Deep tissue pressure injury — persistent non-blanchable deep red, maroon or purple discolouration, or a blood-filled blister.

Staging rules the examiner will test. Medical device-related pressure injuries are staged, and often conform to the shape of the device. Pressure injuries of mucous membranes are NOT staged — they are documented only. Reverse staging is inaccurate for assessing healing; instead use the validated PUSH tool (Pressure Ulcer Scale for Healing), which scores size, exudate amount and tissue type and is sensitive to change over time.

Prevention — the highest-yield section. Identify patients at risk; decrease pressure, friction and skin folding; regular repositioning; use support surfaces — non-powered (foam, gel, air or water overlays and mattresses) or powered (alternating-pressure surfaces, which are far more costly); keep skin clean and dry; avoid excessive bed rest — optimise and encourage function; avoid over-sedation; and provide adequate nutrition and hydration: 30–35 kcal/kg/day, protein 1–1.5 g/kg/day and fluid 1 mL/kcal.

Management of Stage 1 and 2. Apply all preventive measures to stop progression, plus intensive local skin care. Clean with warm normal saline or water; avoid pressure and moisture; cover open wounds with an occlusive dressing selected on the basis of granulation and necrotic tissue, type and amount of drainage, surrounding tissue and evidence of infection; prevent further injury and infection, using antibiotics very judiciously; and manage the associated pain. No single local technique is superior to another — the important factor is the attention the skin receives, above all relief from pressure.

Management of Stage 3 and 4. Debride necrotic tissue — autolytic, chemical/enzymatic, mechanical, sharp or surgical; undermine and remove eschar if it is hiding necrotic or infected tissue; irrigate and cleanse two to three times daily and dress the wound. Stage 3 — routine wound swabs are not warranted (they grow multiple organisms, miss anaerobes and reflect colonisation, not infection); systemic antimicrobials do not reach adequate concentration in the ulcer and should be reserved for confirmed bacteraemia, sepsis, osteomyelitis or cellulitis. Stage 4 — take a tissue or bone biopsy for aerobic and anaerobic culture, give systemic antimicrobials, and obtain surgical consultation for possible flap repair. Manage pain at every stage.

The EPUAP/NPIAP/PPPIA International Clinical Practice Guideline and its subsequent implementation updates recommend prophylactic multilayer silicone foam dressings over the sacrum and heels in high-risk patients (strong evidence for prevention in ICU and emergency transport), repositioning every 2–4 hours matched to the support surface and the individual rather than a rigid 2-hourly rule, and sub-epidermal moisture (SEM) measurement to detect impending damage before visible erythema appears.

On adjunctive therapies, the current evidence base is clear: high-protein oral nutritional supplements enriched with arginine, zinc and antioxidants accelerate healing of Stage 2–4 ulcers, whereas there is insufficient evidence for hyperbaric oxygen, topical oxygen or biological dressings, and only limited evidence for platelet-derived growth factor. Preventing pressure injury and managing the underlying causes — rather than focusing on topical dressings — remains what is most likely to be effective.