Pressure injuries

A pressure injury is localised damage to skin and underlying tissue, usually over a bony prominence or under a medical device, caused by intense or prolonged pressure, or pressure combined with shear. It is largely preventable and reflects both external load and the tolerance of the tissue.

Clinical relevance. Pressure injuries cause pain, infection, osteomyelitis, sepsis, prolonged admission and death, and are a marker of care quality.

Mechanisms. Sustained pressure compresses capillaries and causes ischaemia and reperfusion injury. Shear distorts deep tissue. Moisture, friction and a warm microclimate reduce skin tolerance. Malnutrition, poor perfusion, diabetes, neuropathy, oedema, age, and corticosteroid or vasopressor use reduce tolerance further.

Common sites. Sacrum, heels, ischial tuberosities, greater trochanters, occiput, scapulae, elbows, malleoli, ears, and any skin under a device.

Stages.

• Stage 1: intact skin with non-blanchable erythema.
• Stage 2: partial thickness loss with exposed dermis (a shallow pink or red open ulcer, or an intact or ruptured serum filled blister). No slough or eschar.
• Stage 3: full thickness skin loss with visible fat. Slough or eschar may be present. Undermining or tunnelling may be present. No fascia, muscle, tendon, ligament, cartilage or bone exposed.
• Stage 4: full thickness loss with exposed or palpable fascia, muscle, tendon, ligament, cartilage or bone.
• Unstageable: full thickness loss with the base obscured by slough or eschar.
• Deep tissue pressure injury: persistent deep red, maroon or purple discolouration, or a blood filled blister, over intact or non-intact skin.
• Medical device related and mucosal pressure injuries are classified by the same stages (mucosal injury is not staged).

Key distinctions. Do not reverse stage a healing ulcer: a healing stage 3 injury remains a stage 3 injury. Separate pressure injury from moisture associated skin damage, which is diffuse, shallow, irregular, perianal or in skin folds, and without necrosis.

History. Mobility, sensation, continence, nutrition and hydration, previous injury, length of surgery or ICU stay, vasopressors, steroids, diabetes, peripheral vascular disease, smoking, spinal cord injury, and use of devices (splints, oxygen tubing, collars, catheters). Onset, pain, drainage and previous treatments.

Risk assessment.

• Braden scale (total 6 to 23): 18 or less is at risk, 15 to 18 mild, 13 to 14 moderate, 10 to 12 high, 9 or less very high.
• Waterlow score: 10 or more at risk, 15 or more high, 20 or more very high.
• Norton score: 14 or less at risk.

Examination.

• Inspect all skin, including bony prominences, heels and under devices, at admission and each day in at risk patients. Palpate for warmth, induration, bogginess, oedema.
• Blanching test with a finger or transparent disc. In darker skin tones, colour change is less reliable, so rely on temperature, oedema, firmness and pain.
• Wound: site, length, width, depth, stage, tissue type (granulation, slough, eschar), exudate, odour, edges, undermining, tunnelling, surrounding skin. Probe for bone.
• Infection: increasing pain, warmth, spreading erythema, purulence, odour, friable granulation, delayed healing, crepitus.
• Perfusion: pedal pulses, capillary refill, ankle brachial index for lower limb injuries.

Red flags.

• Spreading cellulitis, crepitus or necrosis suggesting necrotising infection.
• Fever, rigors or hypotension.
• Exposed or probe-positive bone.
• Sinus tract.
• New autonomic dysreflexia in a spinal injury patient.
• Pain out of proportion.
• Rapid deterioration.

Special groups. Spinal cord injury (high recurrence), paediatrics (occiput, devices), obese patients (skin folds), palliative patients (Kennedy terminal ulcer, rapidly developing sacral injury near death), and people with dark skin (early injury is missed).

Other skin breakdown.

• Moisture associated skin damage (incontinence associated dermatitis), skin tear, friction blister, contact dermatitis.
• Arterial ulcer, venous ulcer, diabetic neuropathic foot ulcer.
• Thermal or chemical burn, particularly in people with sensory loss.

Infection. Cellulitis, necrotising fasciitis, herpes simplex sacral ulcer, tuberculous or fungal ulcer, osteomyelitis (a complication and a mimic).

Inflammatory and vascular. Pyoderma gangrenosum, vasculitic ulcer, cryoglobulinaemia, calciphylaxis, warfarin skin necrosis, purpura fulminans, sickle cell leg ulcer, bullous pemphigoid, pemphigus.

Malignant. Squamous cell carcinoma, Marjolin ulcer (malignant change in a chronic wound), and ulcerating primary or metastatic skin tumours.

Drug eruptions. Stevens-Johnson syndrome and toxic epidermal necrolysis.

Other. Bruising or haematoma over bone, and deep tissue injury, which can resemble a bruise. Deliberate injury or neglect.

Diagnosis and staging are clinical. Investigations assess complications and healing barriers.

First line. Stage and measure, and photograph with consent. Full blood count, CRP, ESR, urea, creatinine, electrolytes, glucose and HbA1c, albumin (reflects inflammation more than nutrition), and nutritional screening.

Infection and bone.

• Swab culture only when clinical infection is present, after cleansing, using a deep tissue technique. Superficial swabs show colonisation.
• Blood cultures in sepsis.
• Probe-to-bone test: positive suggests osteomyelitis. ESR over 70 mm/h supports it.
• MRI is the best imaging test. Plain radiographs are insensitive early. Bone biopsy for culture and histology is the reference test and is directed by the surgical or infection team.
• CT for gas or deep collections, ultrasound for collections.

Perfusion. Ankle brachial index for heel and lower limb wounds: under 0.5 or a toe pressure under 30 mmHg indicates ischaemia that limits healing, and over 1.3 indicates non-compressible vessels, so use toe pressure instead.

Biopsy. For ulcers not healing after 12 weeks of optimised care, atypical appearance, or suspected malignancy.

Limitations. Stage 1 and deep tissue injury are easily missed in dark skin. Wound swabs overdiagnose infection. Albumin is not a nutrition marker.

Offloading.

• Reposition every 2 to 4 hours depending on support surface and tolerance, at 30 degree tilt, avoiding 90 degree side lying and direct lying on trochanters or the injury.
• Head of bed 30 degrees or less except for meals.
• Float heels with pillows or devices. Limit sitting time, with pressure redistributing cushions and shifting weight.
• Avoid ring or donut cushions and avoid massaging bony prominences.
• High specification foam mattress for at risk patients. Alternating pressure or low air loss mattress for stage 3 to 4, unstageable injury, or high risk patients.
• Protect skin under devices and rotate or pad them.

Skin and moisture. Gentle pH balanced cleansing, barrier products, prompt continence care, and prophylactic silicone foam dressings over sacrum and heels in high risk patients.

Nutrition. Energy 30 to 35 kcal/kg daily, protein 1.25 to 1.5 g/kg daily (adjust for kidney disease), fluid about 30 mL/kg daily. Treat deficiencies when proven. Evidence for routine arginine, zinc and vitamin C supplements is limited.

Wound care.

• Cleanse with saline or potable water. Remove non-viable tissue by sharp or autolytic debridement by a trained clinician, but do not debride stable dry eschar on an ischaemic heel.
• Dressings to maintain moist wound healing: hydrocolloid or foam for stage 2, foam, alginate or hydrofibre for exudate, hydrogel for dry necrosis. Topical antiseptics (silver, iodine, honey) for local infection.
• Negative pressure therapy for clean stage 3 and 4 wounds after debridement, when offloading is secure.

Analgesia. Paracetamol 1 g orally 30 to 60 minutes before dressing changes and every 6 hours as needed; maximum 4 g daily (3 g if weight under 50 kg, malnutrition, alcohol excess or liver disease); monitor liver tests with prolonged use. Avoid NSAIDs in older adults.

Systemic antibiotics. Only for spreading cellulitis, systemic signs, or osteomyelitis.

• Amoxicillin with clavulanic acid, oral 500/125 mg every 8 hours or IV 1.2 g every 8 hours, for 5 to 7 days for soft tissue infection; maximum 3.6 g IV daily; monitor liver tests and diarrhoea; reduce frequency in kidney impairment (eGFR 10 to 30 mL/min: oral every 12 hours or IV 1.2 g then 600 mg every 12 hours).
• Add MRSA cover when risk factors or prior MRSA: doxycycline 100 mg orally every 12 hours for 5 to 7 days (maximum 200 mg daily; take upright with water to avoid oesophagitis; avoid in pregnancy), or vancomycin IV with dosing adjusted to kidney function and levels in severe infection.
• Osteomyelitis: bone biopsy directed therapy, usually 6 weeks, under specialist infection care.

Surgery. Flap reconstruction for selected stage 3 and 4 injuries after nutrition, offloading, infection control and smoking cessation are addressed. Debridement of infected bone.

Monitoring. Measure and photograph weekly. A reduction of about 30% in area over 2 to 4 weeks predicts healing. If healing stalls, reassess for infection, ischaemia, nutrition, inadequate offloading, adherence, and malignancy.

Special groups. In spinal cord injury, assess seating and coordinate with a spinal unit. In palliative care, aim for comfort and pressure relief.

Referral and escalation. Tissue viability for stage 3 and 4 or non-healing injuries. Plastic surgery for reconstruction, vascular surgery for ischaemia, orthopaedics or infection specialists for osteomyelitis, dietitian, and occupational therapy for seating. Report new stage 3 or 4 injuries through safeguarding and incident systems when neglect is suspected.

Admission criteria. Sepsis, spreading or necrotising infection, osteomyelitis, stage 3 to 4 injury needing surgical debridement, inability to offload at home, uncontrolled pain, or neglect.

Discharge and safety netting. Discharge with the right support surface and equipment, a repositioning plan, trained carers, and community nursing review. Patients and carers are told to return for fever, spreading redness, offensive discharge, new black tissue, or increasing pain.