Decubitus Ulcer

A localised area of tissue damage, ranging from superficial skin changes to full thickness necrosis extending to muscle and bone, caused by sustained, unrelieved pressure over a bony prominence.

It most commonly occurs in patients with reduced mobility, impaired sensation, or significant comorbidity impairing tissue perfusion and healing capacity.

It is a largely preventable condition where the primary clinical priority is prevention through systematic risk assessment and pressure relief. Established ulcers are managed through a combination of pressure offloading, wound care, and treatment of any associated infection or underlying contributing factor.

Pathophysiology and risk factors

• Sustained pressure exceeding capillary closing pressure over a bony prominence causes local tissue ischaemia.
• Tissue damage progresses in many cases from the deep tissue adjacent to bone outward toward the skin surface.
• The visible external skin change therefore frequently underestimates the true extent of underlying tissue damage, particularly in more severe injuries.
• Risk factors include:
  • immobility, from any cause including critical illness, neurological impairment, or advanced frailty
  • impaired sensation (spinal cord injury, peripheral neuropathy, reduced consciousness)
  • malnutrition
  • incontinence with associated moisture and skin maceration
  • impaired tissue perfusion from vascular disease, diabetes or oedema
• Common sites reflect typical positions of sustained pressure: the sacrum, heels, ischial tuberosities and, in patients lying on their side, the greater trochanter and lateral malleolus.

• Staging systems classify decubitus ulcers by depth and tissue involvement:
  • stage one: non blanchable erythema of intact skin
  • stage two: partial thickness skin loss with exposed dermis, presenting as a shallow open ulcer or intact or ruptured blister
  • stage three: full thickness skin loss with visible subcutaneous fat, though without exposed bone, tendon or muscle
  • stage four: full thickness tissue loss with exposed bone, tendon or muscle, frequently with undermining and tunnelling
• Unstageable ulcers are obscured by slough or eschar, preventing accurate assessment of the true depth of tissue involvement.
• Deep tissue pressure injury describes intact or non intact skin with a localised area of persistent, non blanchable deep red, maroon or purple discolouration, reflecting damage to underlying soft tissue.
• It may evolve to reveal the true extent of injury over subsequent days despite optimal treatment.
• Signs of local infection include increasing pain, erythema extending beyond the ulcer margin, purulent discharge, malodour and delayed healing. Systemic features of sepsis occur in more severe cases.
• Actively assess for infection at every review, given the significant risk of progression to osteomyelitis, particularly in deep, longstanding ulcers overlying bone.

• Diagnosis and staging are clinical, based on careful visual inspection and assessment of the wound.
• A structured, validated risk assessment tool (such as the Waterlow or Braden scale) should be used systematically in at risk patients, to identify those requiring enhanced preventive measures before an ulcer develops.
• Assessment for underlying osteomyelitis is warranted for any deep, chronic, non healing ulcer, particularly with exposed or palpable bone.
• A positive probe to bone test has reasonable predictive value for underlying osteomyelitis in this context.
• Magnetic resonance imaging is the investigation of choice where this complication is suspected. Bone biopsy provides definitive microbiological and histological confirmation where required.
• Wound swab culture has limited utility for guiding antibiotic therapy in the absence of clinical signs of infection, as chronic wounds are universally colonised with bacteria.
• It should be reserved for wounds with clear clinical evidence of infection.
• Deep tissue sampling obtained at debridement gives more reliable microbiological information than surface swabbing alone.
• Nutritional assessment is an important component of overall evaluation, given the significant impact of nutritional status on both ulcer development risk and subsequent healing capacity.
• It includes relevant blood tests, such as albumin, which is an imperfect marker because it behaves as a negative acute phase reactant, together with a broader clinical nutritional assessment.

• Pressure relief and offloading is the fundamental cornerstone of both prevention and treatment.
• It is achieved through regular repositioning (typically at least every two hours for at risk immobile patients, according to individualised risk assessment) and specialist pressure redistributing support surfaces and mattresses.
• For specific sites such as the heel, dedicated offloading devices eliminate pressure entirely from the affected area.
• Wound care principles include maintenance of a moist wound healing environment, with a dressing selected according to the wound's characteristics: exudate level, presence of slough or necrotic tissue, and depth.
• Hydrocolloid, foam or alginate dressings are commonly used according to these characteristics.
• Regular reassessment adjusts the dressing choice as the wound evolves through the healing process.
• Debridement of necrotic tissue or slough is essential to support healing and to allow accurate assessment of the true wound depth and extent.
• Options are sharp surgical debridement, autolytic debridement (using an appropriate moisture retentive dressing to support the body's own enzymatic breakdown of necrotic tissue), or other modalities according to the clinical context and available expertise.
• Nutritional optimisation is an essential component of full management, supporting the underlying physiological capacity for wound healing.
• It includes adequate protein and calorie intake and correction of any specific identified deficiency.
• Manage any contributing factor, such as incontinence (with appropriate skin protection and moisture management) or oedema.
• Antibiotic therapy is reserved for wounds with clear clinical evidence of infection (rather than colonisation alone) or confirmed osteomyelitis, with the regimen guided by deep tissue or bone culture results where obtained.
• Topical antiseptic or antimicrobial dressings are considered for localised, superficial infection or heavily colonised wounds impeding healing progress.
• Surgical intervention, including formal debridement, and, for extensive stage four ulcers not responding to conservative measures, flap reconstruction, is considered in appropriate patients with adequate physiological reserve to tolerate surgery, through multidisciplinary discussion involving plastic surgery, tissue viability specialists and the wider clinical team.
• Systematic, structured prevention is the single most effective strategy for reducing the substantial morbidity, and associated mortality risk in severe cases, of this largely preventable condition.
• It comprises regular skin inspection, appropriate risk assessment and proactive implementation of pressure relieving measures in every identified at risk patient.