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.
Try two board-style Pressure Ulcers questions
Real questions from the FirstPassPA bank, with the full explanation. Pick an answer — no signup, no email.
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. Pedal pulses are 2+ bilaterally, and there is no plantar callus or lower-extremity edema. Which of the following is the most likely diagnosis?
AVenous insufficiency ulcer
BDiabetic neuropathic ulcer
CPressure (decubitus) ulcer
DArterial insufficiency ulcer
Reveal answer & full explanation
Correct answer: C — Pressure (decubitus) ulcer
AVenous insufficiency ulcer
BDiabetic neuropathic ulcer
CPressure (decubitus) ulcer✓
DArterial insufficiency 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
Arterial insufficiency ulcer: ischemic ulcers sit on distal extremities (toes, lateral malleolus) with punched-out borders and diminished pulses; this patient has 2+ pedal pulses and a sacral location.
Venous insufficiency ulcer: occurs at the medial malleolus with hemosiderin staining and lower-extremity edema, neither of which is present here.
Diabetic neuropathic ulcer: forms on the plantar surface over a metatarsal head with surrounding callus; the sacral location and absent callus exclude it.
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. A deep tissue pressure injury is diagnosed. Which of the following best explains the findings?
ABacterial exotoxin-mediated necrosis of deep subcutaneous soft tissue
BSmall-vessel calcium-phosphate deposition with vascular thrombosis
CAutoantibody deposition along the dermoepidermal basement junction
DPressure-induced local ischemia exceeding capillary closing pressure
Reveal answer & full explanation
Correct answer: D — Pressure-induced local ischemia exceeding capillary closing pressure
ABacterial exotoxin-mediated necrosis of deep subcutaneous soft tissue
BSmall-vessel calcium-phosphate deposition with vascular thrombosis
CAutoantibody deposition along the dermoepidermal basement junction
DPressure-induced local ischemia exceeding capillary closing pressure✓
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 afebrile localized lesion over a pressure point is not infectious necrosis.
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.
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.
🔒 Free preview limit reached
Keep reading — start your free trial
You've read your 2 free diagnosis previews. Create your free account to unlock the full Pressure Ulcers (Decubitus) outline — plus all 514 diagnoses, 6,500+ board-style questions, flashcards, and an AI tutor. Your 7-day free trial includes everything, and there's no credit card required.
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 (must be debrided to stage)
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; consider arginine and zinc supplementation in malnourished patients with Stage 3-4 ulcers (NUTRIS-PI and OUR trials)
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 culture-directed prolonged IV antibiotics (typically 6 weeks) 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)
OUR trial — Cereda E et al. A nutritional formula enriched with arginine, zinc, and antioxidants for the healing of pressure ulcers: a randomized trial (Ann Intern Med 2015)
Practice Dermatology questions on FirstPassPA
Turn this outline into retention. 6,500+ board-style questions with an AI tutor that explains every answer — free to start, no card required.
Educational use only. This outline is a study aid for PA students and is not medical advice or a substitute for clinical judgment. FirstPassPA is an independent study tool and is not affiliated with, endorsed by, or sponsored by NCCPA or PAEA. PANCE® and PANRE® are registered trademarks of the National Commission on Certification of Physician Assistants; End of Rotation™ is a program of the Physician Assistant Education Association.