Localized skin and soft tissue injury over bony prominences from sustained pressure ± shear and friction.
Also known as: pressure injury, decubitus ulcer, bedsore, pressure sore
Overview
A pressure injury is localized damage to the skin and underlying soft tissue, typically over a bony prominence or related to a medical device, resulting from intense and/or prolonged pressure or pressure in combination with shear. Severity ranges from non-blanchable erythema (Stage 1) to full-thickness skin and tissue loss with exposed bone, muscle, or tendon (Stage 4) and unstageable, deep tissue, or mucosal subtypes.
Epidemiology
Common in hospitalized, long-term care, and home-care populations. Prevalence in acute hospitals ~5-15%, ICUs up to 25%, and long-term care 5-30%. Significant source of morbidity, mortality, and healthcare cost; one of the CMS hospital-acquired conditions for which Medicare withholds additional payment.
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Question 1DermatologyEasy
An 82-year-old woman with advanced dementia is bedbound at a long-term care facility and requires assistance for all activities. She is frequently incontinent of urine. On a routine skin inspection, a nurse finds a 4-cm full-thickness wound over the sacrum with visible subcutaneous fat and a small amount of yellow slough at the base; bone and tendon are not exposed. Which of the following is the most likely diagnosis?
APyoderma gangrenosum ulcer
BCalciphylaxis skin ulcer
CPilonidal sinus disease
DMoisture-associated dermatitis
EPressure (decubitus) ulcer
Reveal answer & full explanation
Correct answer: E — Pressure (decubitus) ulcer
APyoderma gangrenosum ulcer
BCalciphylaxis skin ulcer
CPilonidal sinus disease
DMoisture-associated dermatitis
EPressure (decubitus) ulcer✓
Why Pressure (decubitus) ulcer is correct
A full-thickness wound over the sacrum (a bony prominence) in an immobile, incontinent patient is the classic presentation of a pressure injury, driven by sustained pressure exceeding capillary closing pressure (>32 mmHg) plus shear and moisture.
Visible subcutaneous fat with slough but no exposed bone or tendon defines a Stage 3 pressure ulcer per the NPIAP 2016 staging system; immobility, dementia, and incontinence are core Braden Scale risk factors.
Why the others are wrong
Moisture-associated dermatitis — Incontinence-associated dermatitis causes diffuse, superficial erythema and erosion of the perineal and buttock skin with poorly defined edges; it does not produce a full-thickness wound exposing subcutaneous fat and slough over a bony prominence.
Pyoderma gangrenosum ulcer — A rapidly enlarging, very painful ulcer with a violaceous, undermined border, most often pretibial and associated with inflammatory bowel disease, rheumatoid arthritis, or hematologic malignancy; no associated disease is described, and a sacral wound in an immobile patient is explained by pressure.
Calciphylaxis skin ulcer — Calcific arteriolopathy seen mainly in end-stage kidney disease on dialysis, beginning as exquisitely painful retiform purpura that progresses to black necrotic eschar in fatty areas such as the thighs and abdomen; nothing in her history suggests kidney failure, and her wound sits over a bony prominence in an immobile patient.
Pilonidal sinus disease — the sacrococcygeal location makes it tempting, but pilonidal disease is a hair-driven inflammatory process of the natal cleft in young, often hirsute adults that presents as midline pits with a painful, draining abscess, not a full-thickness slough-based wound over a bony prominence in a bedbound, incontinent 82-year-old.
Additional high-yield points
Arterial (toes or lateral malleolus, diminished pulses), venous (medial malleolus, edema, hemosiderin staining), and diabetic neuropathic (plantar metatarsal heads, callus) ulcers are lower-extremity ulcers and do not belong in the differential of a sacral wound.
Question 2DermatologyMedium
An 82-year-old woman with advanced dementia is bedbound in a long-term care facility. On a routine skin check, a nurse notes a 4-cm area of intact skin over the sacrum that is deep maroon and non-blanchable, with surrounding skin that feels boggy and slightly cooler than adjacent tissue. The patient does not react to palpation of the area. Over the next 48 hours the discoloration darkens and a blood-filled blister forms. Which of the following best explains the findings?
AAutoantibody deposition along the dermoepidermal basement junction
BPressure-induced local ischemia exceeding capillary closing pressure
CMoisture and incontinence-associated maceration of the sacral skin
DSmall-vessel calcium-phosphate deposition with vascular thrombosis
EBacterial exotoxin-mediated necrosis of deep subcutaneous soft tissue
Reveal answer & full explanation
Correct answer: B — Pressure-induced local ischemia exceeding capillary closing pressure
AAutoantibody deposition along the dermoepidermal basement junction
BPressure-induced local ischemia exceeding capillary closing pressure✓
CMoisture and incontinence-associated maceration of the sacral skin
DSmall-vessel calcium-phosphate deposition with vascular thrombosis
EBacterial exotoxin-mediated necrosis of deep subcutaneous soft tissue
Why Pressure-induced local ischemia exceeding capillary closing pressure is correct
Pressure injuries arise when sustained external pressure over a bony prominence exceeds the capillary closing pressure (~32 mmHg), collapsing perfusion and producing local ischemia, endothelial injury, and microvascular thrombosis.
Shear deforms deeper tissue and disrupts perforating vessels, so necrosis often begins in muscle near bone and progresses outward, explaining the deep maroon, non-blanchable discoloration and blood-filled blister of a deep tissue pressure injury over the sacrum in an immobile patient.
The boggy texture and temperature change reflect early deep-tissue damage beneath still-intact skin.
Why the others are wrong
Bacterial exotoxin-mediated necrosis of deep subcutaneous soft tissue - describes necrotizing soft-tissue infection, which presents with rapidly spreading pain out of proportion, systemic toxicity, crepitus, or gas; this localized lesion over a pressure point in a patient without systemic toxicity is not infectious necrosis.
Small-vessel calcium-phosphate deposition with vascular thrombosis - is the mechanism of calciphylaxis, seen in dialysis or CKD patients as exquisitely painful retiform purpura with eschar; it is not pressure-localized and would be accompanied by deranged calcium-phosphate metabolism.
Autoantibody deposition along the dermoepidermal basement junction - is the mechanism of bullous pemphigoid, which produces widespread tense bullae on inflamed or urticarial skin, not a single non-blanchable maroon patch confined to a weight-bearing bony prominence.
Moisture and incontinence-associated maceration of the sacral skin - incontinence-associated dermatitis is common in bedbound long-term care residents and is a classic mimic of a sacral pressure injury, but it is a top-down injury of the epidermis that produces diffuse, ill-defined erythema with maceration and superficial erosion over the perineum, buttocks, and gluteal cleft, not a localized non-blanchable maroon patch of intact skin with boggy deeper tissue and a blood-filled blister over a bony prominence.
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Sustained external pressure exceeding capillary closing pressure (>32 mmHg) leads to local ischemia, endothelial injury, and microvascular thrombosis. Shear forces deform deeper tissues and disrupt perforating vessels. Reperfusion injury, inflammation, and tissue necrosis follow, beginning in muscle near bone and progressing outward (deep tissue injury). Moisture, friction, and inflammation amplify damage.
Clinical presentation
Symptoms
Pain over a bony prominence in patients with intact sensation
Often absent in patients with impaired sensation, leading to late presentation
Discharge, malodor, surrounding cellulitis if infected
Systemic signs (fever, leukocytosis) if osteomyelitis or sepsis develops
Signs / physical exam
Stage 1: intact skin with non-blanchable erythema over a bony prominence
Stage 2: partial-thickness loss of dermis presenting as an open shallow ulcer or intact/ruptured serum-filled blister
Stage 3: full-thickness tissue loss with visible subcutaneous fat; bone, tendon, and muscle not exposed; may have slough or eschar; tunneling/undermining possible
Stage 4: full-thickness loss with exposed bone, tendon, or muscle; high osteomyelitis risk
Unstageable: full-thickness loss obscured by slough or eschar (stage is revealed once slough or eschar is removed; stable, dry eschar on the heel or an ischemic limb should not be removed)
Deep tissue pressure injury: persistent non-blanchable deep red, maroon, or purple discoloration; may progress to dark blood-filled blister or open wound
Classic findings
Non-blanchable erythema or full-thickness ulcer over sacrum, ischium, heel, or greater trochanter in an immobile patient.
Differential diagnosis
Arterial (ischemic) ulcer — Distal extremity (toes, lateral malleolus), punched-out borders, diminished pulses, pale base, painful; ABI low
Venous stasis ulcer — Medial malleolus, irregular borders, hemosiderin staining, edema; ABI normal
Calciphylaxis — Painful retiform purpura with eschar in dialysis or CKD patients; not pressure-related; calcium-phosphate elevations
Pyoderma gangrenosum — Violaceous undermined border, IBD or RA association, pathergy
Marjolin ulcer (SCC in chronic wound) — Non-healing chronic ulcer with raised, indurated edges or new nodularity; biopsy
Moisture-associated skin damage (incontinence-associated dermatitis) — Diffuse erythema and erosion of perineum/buttocks, not localized over bony prominence; treat with barrier and continence care
Diagnostic workup
Diagnostic criteria
Diagnosis is clinical, staged per current National Pressure Injury Advisory Panel (NPIAP) 2016 staging system. Document stage, dimensions, undermining/tunneling, exudate, surrounding tissue, and signs of infection at each evaluation.
Labs
CBC, BMP, prealbumin/albumin, glucose/HbA1c, vitamin D
Wound culture not routinely indicated for surface colonization; quantitative cultures and bone biopsy for suspected osteomyelitis
Blood cultures if systemic infection
Braden Scale or other validated risk assessment on admission and at intervals
Imaging
Plain radiograph for suspected osteomyelitis (early changes can be subtle)
MRI is most sensitive for osteomyelitis and soft tissue extension
Bone biopsy with culture and histology is the diagnostic gold standard for osteomyelitis
Diagnostic algorithm
Stage
Findings
Key Management
Stage 1
Intact skin, non-blanchable erythema over bony prominence
Pressure redistribution; barrier; reposition q2h
Stage 2
Partial-thickness loss; shallow open ulcer or intact/ruptured serum blister
Hydrocolloid or foam dressing; offload
Stage 3
Full-thickness loss; subcutaneous fat visible; no exposed bone/tendon/muscle
Debride to visualize and stage (except stable heel eschar)
Deep tissue injury
Intact or non-intact skin with persistent non-blanchable deep red/maroon/purple
Offload; monitor for evolution to Stage 3-4
NPIAP pressure injury staging (2016) and key management priorities.
Treatment
First-line
Pressure redistribution: turn and reposition every 2 hours (every 4 hours on appropriate support surfaces), heel offloading with pillows or boots, head of bed ≤30° when possible
High-specification support surfaces (foam, air-fluidized beds) for at-risk patients and those with existing ulcers
Nutrition optimization: protein 1.2-1.5 g/kg/day, adequate calories, hydration; offer high-calorie, high-protein oral supplements enriched with arginine, zinc, and antioxidants to patients with Stage 2 or greater injuries who are malnourished or at risk of malnutrition (NPIAP/EPUAP/PPPIA 2019; Cereda et al., Ann Intern Med 2015)
Moisture management: skin barriers, prompt cleansing after incontinence
Wound care: gentle cleansing with normal saline; choose dressing by wound characteristics — hydrocolloid for clean Stage 2; alginate or foam for moderate exudate; hydrogel for dry/necrotic; antimicrobial silver or iodine dressings for critical colonization
Debridement of necrotic tissue: sharp (most effective), autolytic, enzymatic (collagenase), or mechanical; do NOT debride stable, dry eschar on the heel without ischemic evaluation
Treat infection: cellulitis with oral antibiotics (cephalexin, dicloxacillin; broaden for MRSA or polymicrobial wounds); osteomyelitis with prolonged culture-directed antibiotics (typically about 6 weeks; IV or highly bioavailable oral agents) and surgical debridement
Second-line / adjunct
Negative-pressure wound therapy (NPWT) for Stage 3-4 wounds with significant tissue loss
Surgical reconstruction (flap closure) for select Stage 3-4 wounds in appropriate candidates with controlled comorbidities and modifiable risk factors
Pain control with acetaminophen, NSAIDs (if appropriate), opioids for dressing changes
Multidisciplinary team approach (wound care nursing, nutrition, PT/OT, plastic surgery)
Complications
Local infection, cellulitis, abscess
Osteomyelitis (Stage 3-4 wounds especially over sacrum, ischium, heels)
Bacteremia and sepsis
Marjolin ulcer (squamous cell carcinoma in chronic non-healing pressure ulcers)
Pain, depression, prolonged hospitalization, mortality (up to 60,000 deaths annually in the US attributed to pressure-injury complications)
Increased cost and length of stay; medicolegal exposure
PANCE pearls
The best treatment is prevention: routine risk assessment (Braden Scale), turning schedule, pressure redistribution surfaces, skin inspection, moisture management, and nutrition.
Heel pressure injuries are common and often missed — keep heels off the bed entirely with pillows or offloading boots.
Stable, dry, intact eschar on an ischemic heel should be left in place ('don't soften, don't debride') until perfusion is established.
Do not use Stage 1 or Stage 2 staging for healing or reverse staging; once a higher stage is reached, document as 'healing Stage 4' rather than 'Stage 2'.
Persistent non-healing ulcers with rolled or indurated borders should be biopsied to exclude Marjolin (SCC).
Osteomyelitis is diagnosed by bone biopsy, not surface swab; treat with prolonged culture-directed antibiotics and surgical debridement.
References
NPIAP 2019 — National Pressure Injury Advisory Panel. Prevention and Treatment of Pressure Ulcers/Injuries: Clinical Practice Guideline (NPIAP/EPUAP/PPPIA 2019)
AHRQ — Preventing Pressure Ulcers in Hospitals: A Toolkit for Improving Quality of Care (AHRQ 2014)
Cereda 2015 — Cereda E, Klersy C, Serioli M, Crespi A, D'Andrea F; OligoElement Sore Trial Study Group. A nutritional formula enriched with arginine, zinc, and antioxidants for the healing of pressure ulcers: a randomized trial (Ann Intern Med 2015;162(3):167-174)
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