Pressure Sores: Stages, Common Sites, Prevention and Treatment

A pressure injury is localised damage to the skin and underlying tissue, usually over a bony prominence (sacrum, heels), caused by disruption of blood supply, preventing oxygen and nutrients from reaching cells. "Pressure injury" is a more accurate term than "pressure ulcer" because some presentations are not open ulcers.

Incidence varies widely by setting: acute care 0.4–38%, long-term care 2.2–23.9%, home care 0–17%. About 25% of pressure ulcers are acquired intra-operatively.

Four mechanical forces operate together:

Pressure over a bony prominence → tissue deformation and ischaemia

Shear — head of bed elevated, torso slides down, transmitting force to the sacrum; stretches and angulates subcutaneous tissue

Friction — repeated movement of skin across sheets/clothing, which increases shear

Moisture — sweat, urine, faeces, bathing Together these cause thrombosis of small blood vessels, undermining then destroying skin. Loose, folded skin (loss of subcutaneous fat, dehydration) worsens shear.

The area of damage beneath the ulcer is often much larger than the visible ulcer — the "iceberg" effect — because pressure and shear are transmitted deep into subcutaneous tissue.

Pressure injuries are numerically staged 1, 2, 3 or 4 — using Arabic, not Roman, numerals — only if the depth of the wound can be visualised.

Stage 1 — Non-blanchable erythema of intact skin. Acute inflammatory response limited to epidermis. Irregular area of erythema, induration and oedema, which may feel firm or boggy. Redness persists beyond 30 minutes and does not blanch on pressure. In darker skin the colour may be red, blue or purple. Skin is unbroken.

Stage 2 — Partial-thickness loss. Inflammation extends through the dermis to the junction of subcutaneous fat. Appears as a blister, abrasion or shallow ulcer with distinct edges. Early fibrosis and pigment change occur.

Stage 3 — Full-thickness skin loss extending through subcutaneous fat, down to but not through the underlying fascia. Presents as a crater, often with undermining of adjacent tissue. Base may be infected with necrotic, foul-smelling tissue.

Stage 4 — Extension through deep fascia, with bone visible at the base. Undermining is even more common and sinus tracts may be present. Osteomyelitis and septic arthritis can occur.

Two additional categories when depth cannot be seen:

Unstageable pressure injury — wound base obscured by eschar and/or necrotic tissue; can be staged once debrided

Deep tissue pressure injury (DTPI) — skin intact but deep red, purple or maroon, or a haemorrhagic blister, indicating damage in deeper tissue

Special situations:

Medical device–related pressure injuries — from urinary catheters, rectal tubes, oxygen tubing, NIV masks; the wound conforms to the shape of the device. These ARE staged.

Mucous membrane pressure injuries must NOT be staged — only documented.

Reverse staging is inaccurate for assessing healing. Use the PUSH tool (Pressure Ulcer Scale for Healing), which scores size, exudate amount and tissue type and is sensitive to change over time.

More than 90% of pressure ulcers occur in the lower body — principally the sacral and coccygeal area, ischial tuberosities and greater trochanter, along with the heels.

Site varies with posture:

Risk factors: being bed- or chair-bound, unable 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 (i.e. an existing Stage 1 injury) and dry sacral skin. Advanced age itself is NOT an independent risk factor — it is the coexisting impairments in mobility, nutrition and skin health that matter.

Risk-assessment tools: Norton, Braden and Waterlow scales. Current recommendation is to apply a tool on admission to a facility and regularly thereafter. Because risk is multifactorial, multidisciplinary multifactorial intervention is effective — as with falls and delirium.

General principles of skin care in the immobile patient:

Identify patients at risk

Decrease pressure, friction and skin folding

Keep skin clean and dry; moisturise dry sacral skin

Avoid excessive bed rest — optimise and encourage function

Avoid over-sedation

Nutrition and hydration: 30–35 kcal/kg/day, protein 1–1.5 g/kg/day, fluid 1 mL/kcal; dietitian referral for those at risk

Support surfaces:

Non-powered — mattresses or overlays filled with air, water, gel or foam

Powered — mechanically vary the pressure beneath the patient, reducing the duration of applied pressure; far more costly

Specialised foam and sheepskin overlays reduce incidence compared with a standard hospital mattress; the choice between powered and non-powered is not clear

Mattress overlays on operating tables reduce postoperative pressure injuries

Repositioning: at least 2-hourly on a regular mattress, at least 4-hourly on a pressure-reducing mattress

Avoidability: Not all pressure injuries are avoidable, particularly at the end of life — but prevention protocols must be in place before concluding that an injury was unavoidable.

Stage-wise management. Overarching principle — managing the underlying contributing factors is more important than topical or adjunctive therapy. Standard local care of a healable ulcer must satisfy three criteria: moisture balance, bacterial balance and debridement.

Stages 1–2: continue all preventive measures to stop progression. Clean with warm normal saline or water; avoid pressure and moisture; cover open wounds with an occlusive dressing chosen by wound condition, drainage and infection; use antibiotics very judiciously; manage pain. No single dressing has been shown superior to another.

Stage 3: debride necrotic tissue (autolytic, chemical, mechanical, sharp or surgical); irrigate 2–3 times daily; undermine and remove eschar if it conceals necrotic or infected tissue. Routine wound cultures are not warranted — they grow multiple organisms, miss anaerobes and reflect colonisation. Systemic antibiotics do not reach adequate concentration in the ulcer; reserve them for confirmed bacteraemia, sepsis, osteomyelitis or cellulitis.

Stage 4: tissue biopsy for routine and anaerobic culture; systemic antimicrobials are often necessary; surgical/plastic consultation for repair. If septic, use broad-spectrum cover for anaerobes, Gram-negatives and Staphylococcus aureus.

Diagnosing infection: increasing pain in a chronic wound is the strongest predictor (LR 11–20). The "classic signs" — purulent exudate, erythema, heat, oedema — and foul odour are NOT helpful. Use a quantitative swab by the Levine technique (rotate swab over a 1 × 1 cm area for 5 seconds with enough pressure to express fluid): positive LR 6.3, negative LR 0.47.

Adjunctive therapies (negative-pressure wound therapy, hyperbaric oxygen, laser, electrotherapy, electromagnetic therapy, therapeutic ultrasound): no good evidence that they improve healing.

Non-healable injuries / skin failure: where underlying conditions are irreversible or goals are comfort, prioritise reducing infection risk and controlling pain. Wounds appearing on bony prominences during overall decline are termed skin failure, not pressure injuries.

Documentation must include: type and duration; size as length × width × depth in cm; colour as percentage red (granulation) / yellow (slough) / black (eschar); exudate (serous, serosanguinous, sanguinous, purulent); odour assessed after cleaning; periwound tissue; and undermining.

Fourth edition of the International Pressure Injury Guideline (NPIAP/ EPUAP/PPPIA, 2025) — a rolling, online guideline. Partner organisations NPIAP, EPUAP and PPPIA are releasing the fourth edition with an expanded online format and staged release of chapters, plus refreshed quick-reference materials, governed by a Guideline Governance Group led by Professor Janet Cuddigan with over 240 clinical experts and consumer representatives using evidence-to-decision frameworks. Chapters live include Definition & Etiology, Preventive Skin Care, Nutrition, Repositioning, Support Surfaces, Seating, Heel Pressure Injuries and Device-Related Pressure Injuries, with Pressure Injury Risk and Skin & Tissue Assessment to follow.

The "2-hourly turn" is no longer mandatory. A meta-analysis of two RCTs in aged-care settings found 2-hourly repositioning was associated with a non-significant and counter-intuitively higher rate of pressure injuries than 3-hourly (1.3% vs 0.3%, RR 4.06, 95% CI 0.87–18.98). The guideline therefore suggests that either 2-hourly or 3-hourly repositioning may be used for most at-risk individuals, provided an appropriate pressure-redistribution support surface is in place (conditional recommendation, very low certainty). However, it suggests against routinely extending intervals to 4, 5 or 6 hourly, since a meta-analysis of five RCTs showed fewer injuries with 2-hourly turning (4.6% vs 5.7%, RR 0.89).

The harms of over-frequent turning are now formally recognised. A Cochrane review documented sleep disruption, musculoskeletal pain, wound pain and more injuries to care staff with shorter intervals. Staff compliance is higher at 3- and 4-hourly intervals (90–95%) than at 2-hourly (80%), and two economic analyses showed extending from 2-hourly to 3-hourly was more cost-effective when tolerated.

Positioning specifics with new evidence. 30-degree lateral positioning is suggested over greater angles (avoid the 90-degree lateral position), modified to 40 degrees in individuals with high BMI who cannot maintain it. Head-of-bed elevation should be kept at 30 degrees or lower — restricting elevation gave 68 fewer pressure injuries per 1,000 (11.1% vs 18.9%, OR 0.59, 95% CI 0.36–0.97) — but a lower head-of-bed increased ventilator-associated pneumonia (OR 2.15) and gastric reflux (OR 1.85), so clinical needs may override.

Micromovements for the haemodynamically unstable. It is now good practice to use frequent, small, incremental shifts (micromovements) in critically ill individuals too unstable for a regular repositioning regimen, with a trial of full body repositioning at least every 8 hours to see if regular turning can resume, allowing at least ten minutes for haemodynamic equilibrium after each position change.

Early mobilisation is now an evidence-based pressure injury intervention. A meta-analysis of six RCTs and six comparative studies showed early mobilisation significantly reduced pressure injuries (5.2% vs 6.9%, RR 0.75, 95% CI 0.61–0.92) — 17 fewer per 1,000. It also prevented ICU-acquired weakness (RR 0.49), deep vein thrombosis (RR 0.16) and pneumonia (RR 0.39), with a small increase in falls. The staged protocol is: passive range of movement → dangling limbs → sitting out of bed → standing → walking, 2–3 times daily as tolerated.

Wearable movement sensors — a conditional new option. Three studies of body-worn movement sensors showed a non-significant lower rate of pressure injuries (0.7% vs 6.9%, RR 0.15, 95% CI 0.02–1.08); sensors are suggested to help evaluate repositioning needs where resources permit, but must complement rather than replace clinical judgement, and may not detect offloading at the head, ears, elbows and heels.

Prophylactic dressings and refined skin assessment. The 2025 Preventive Skin Care chapter suggests a multilayered soft silicone foam dressing on the sacrum and heels for individuals at high risk, where resources permit (conditional, very low certainty), and specifies that skin assessment must include the scalp and under hair, using wide-toothed combs and moisturising products for curly, textured or tightly coiled hair to allow visual inspection. Subepidermal moisture (SEM) measurement and skin temperature are now recommended within skin assessment, as SEM detects inflammation and tissue damage predictive of Stage 1 and greater injuries, especially at the sacrum, and high-resolution ultrasound is valuable for deep tissue injury, particularly in darker skin tones.

Device-related injuries are a growing share of the burden. In acute care, medical device–related pressure injuries account for more than 30% of all hospital-acquired pressure injuries, largely from prolonged prone positioning with ventilation devices in the mouth and nose; sedation, oedema and increased skin moisture are contributory.

Indian data — lower prevalence but more advanced disease. A point-prevalence study in a north Indian tertiary hospital using the EPUAP minimum data set found an overall prevalence of 7.8%, with the sacrum and heel most commonly affected and, strikingly, Grade III ulcers being the commonest presentation (42.8%) — indicating late detection. ICU prevalence was 24.3%, and injuries were more frequent in patients hospitalised more than a month. An earlier Varanasi study found a prevalence of 4.94%, with anaemia, malnutrition and diabetes as key risk factors and morbidity in long-stay neurology wards as high as 40.9%. Practical Indian implications: home-based bedbound care is the dominant setting, caregiver education is the single highest-yield intervention, and low-cost foam or sheepskin overlays with disciplined repositioning outperform expensive powered mattresses that most families cannot afford.

"Pressure injury" is preferred to "pressure ulcer" — not all are open ulcers.

Four forces: pressure, shear, friction, moisture.

Shear occurs when the head of the bed is elevated and the torso slides down onto the sacrum.

Damage below the ulcer is larger than the visible ulcer.

Stage 1 = non-blanchable erythema, intact skin, persisting beyond 30 minutes.

Stage 2 = partial thickness — blister, abrasion or shallow ulcer.

Stage 3 = full thickness through fat, down to but not through fascia — crater with undermining.

Stage 4 = through deep fascia, bone visible — sinus tracts, osteomyelitis.

Unstageable = base obscured by eschar; DTPI = intact skin, deep purple/ maroon or haemorrhagic blister.

Device-related injuries ARE staged; mucosal injuries are NOT.

Never reverse-stage — use the PUSH tool (size, exudate, tissue type).

>90% occur in the lower body: sacrum/coccyx, ischial tuberosity, greater trochanter (plus heels).

Risk tools: Norton, Braden, Waterlow — on admission and regularly.

Advanced age is NOT an independent risk factor.

Nutrition target: 30–35 kcal/kg, protein 1–1.5 g/kg, fluid 1 mL/kcal.

Turn 2-hourly on a regular mattress, 4-hourly on a pressure-reducing mattress (now individualised — 2 or 3 hourly both acceptable).

30-degree lateral position; head-of-bed ≤30 degrees.

Increasing pain is the best predictor of chronic wound infection (LR 11–20) — classic signs and odour are unhelpful.

Levine technique = swab rotated over 1 × 1 cm for 5 seconds.

Systemic antibiotics only for bacteraemia, sepsis, osteomyelitis or cellulitis — not for routine Stage 3 ulcers.

Managing underlying causes beats any dressing — no single dressing is superior.

Not all pressure injuries are avoidable, especially at the end of life — but the prevention protocol must be in place first.

Falls are multifactorial — an acute trigger acting on accumulated chronic impairments; medications are the most modifiable factor.

Progressive balance and functional exercise has the strongest evidence of any fall-prevention intervention; technology and scoring tools are adjuncts.

A fragility fracture requires both a fall and fragile bone — and the effectiveness of fracture prevention increases with advancing age.

In pressure injuries, correcting the underlying contributing factors matters more than the choice of dressing or any adjunctive therapy.