Decubitus (Pressure) Ulcers


Bedsores otherwise known as pressure ulcers and decubitus ulcers  are injuries to skin and underlying tissue resulting from prolonged pressure on the skin.

Decubitus ulcers most often develop on skin that covers bony areas of the body, such as the heels, ankles, hips and tailbone.

  • They are localized physical manifestation of changes in blood supply to the skin, usually manifesting over bony areas.
  • They result from pressure or pressure in combination with friction/shear
  • They may occur in institutional or home settings
  • They can be a useful indicator of quality of care.

Risk factors for decubitus ulcer

The following are the risk factors for decubitus ulcer:

  1. Age (higher risk in older patients)
  2. Decreased serum albumin (3-fold increase in risk)
  3. Emergency admission (up to 36-fold
    increase in risk in patients admitted for surgical indications)
  4. Faecal incontinence (up to 3-fold increase in risk)
  5. Fractures (up to 5-fold increase in risk)
  6. Number of days in bed
  7. Number of days without nutrition

In older persons with functional limitations (bed-or chair-bound):

  1. Decreased body weight (2-fold increase in risk)
  2. Dry skin
  3. Immobility or reduced mobility
  4. Lymphopaenia (5-fold increase in risk)

Facility dependent factors

  1. Ambulation difficulties
  2. Diabetes mellitus
  3. Faecal incontinence
  4. Feeding difficulties
  5. History of cerebrovascular accident (5 fold increase in risk)
  6. Male gender

Stages of decubitus ulcer

Stage I

  1. Intact skin
  2. Non-blanchable erythema
  3. May be painful, warm or cool, firm or soft, compared to adjacent skin
  4. May be missed in darkly pigmented skin

Stage II

  1. Ulcer extends through epidermis
  2. No slough
  3. May present as blister with intact or ruptured blister
  4. Does not include other skin breaches e.g. excoriation, maceration, tape burns or
    dermatitis associated with incontinence

Stage III

  1. Full thickness loss of tissue
  2. Subcutaneous fat may be visible
  3. Bone, tendon, muscle not exposed
  4. Tunneling, undermining may be present
  5. Depth varies by anatomical location

Stage IV

  1. Full thickness tissue loss
  2. Slough present
  3. Depth varies by anatomical location
  4. May extend to muscle, fascia, joint capsule
  5. Bone/or muscle may be exposed or palpable
  6. Tunneling, undermining frequent
  7. May be associated with osteitis or osteomyelitis


  1. Full thickness tissue loss
  2. Depth obscured by slough and/or eschar in the wound bed
  3. Adherent, dry, intact eschar on the heel is protective and should not be removed

Suspected deep tissue injury

  1. Localized area of discoloured skin
  2. Initial boggy swelling
  3. May become blood-filled blister
  4. May be cooler or warmer than

surrounding skin

Symptoms and Clinical features of decubitus ulcer

  1. Skin lesions at different stages (as noted above)
  2. Signs of wound infection:
    • Erythema around edges of wound
    • Enlarging wound
    • Foul odour
    • Friable granulation tissue
    • Increased necrotic tissue
    • Increasing pain
    • Marked oedema
    • Purulent exudate
    • Tunneling
    • Warmth
    • Wound breakdown

Differential diagnoses

  • Arterial ulcers
  • Diabetic ulcers
  • Venous ulcers

Complications of decubitus ulcer

  1. Secondary wound infection
  2. Systemic Inflammatory Response
  3. Osteomyelitis


  • Levine’s technique for obtaining wound swabs:
    • Cleanse wound with 0.9% saline
    • Rotate a swab over a 1-cm square area of viable wound tissue (not necrotic tissue or wound exudate)
    • Apply enough pressure to get fluid from beneath the wound surface
  • Tissue biopsy
    • Wound contamination is not synonymous with wound infection
    • Culture of wound surface exudates is not useful to diagnose wound infection
    • Cultures obtained using Levine’s technique give results comparable to those from tissue specimens

Treatment for decubitus ulcer

Treatment objectives

  • Achieve wound healing
  • Prevent secondary wound infection

Non-drug treatment

1. Remove debris from wound

  • Clean wound using 0.9% saline or
    lactated Ringer’s solution at each
    dressing change
  • Antiseptic solutions may be cytotoxic
  • Contraindicated in patients with ulcers in lower extremities who have arterial disease

2. Remove necrotic tissue

  • Autolytic methods (hydrogels or moisture retaining dressings)
  • Chemical debridement
  • Sharp debridement
  • Close dead spaces in wound
  • Pack tunnels and undermining loosely with moist gauze dressings

Adjunct treatment to facilitate wound healing

  • Electrical therapy
  • Electromagnetic therapy
  • Laser therapy
  • Ultrasound therapy
  • Vacuum-assisted closure
  • Prevent further injury
  • Avoid pressure on wound
  • Chair cushions for sitting
  • Keep heels off pressure
  • Pressure-reducing mattresses
  • Reposition every 2 hours (or more
    frequently, depending on host factors)

Support wound healing process

  • Adequate protein intake, unless
    contraindicated by renal disease: 1.25 – 1.5g/kg/day)
  • Adequate calorie intake (30 – 35 kcal/kg/day)
  • Avoid exposure to cold (causes
    vasoconstriction and impaired tissue perfusion)
  • Correct deficiencies e.g. of vitamin C and zinc

Drug treatment


Give appropriate pain medicines 30 minutes before wound procedures


Topical antibiotics: Indicated for ulcers:

  • With 21 million CFU/g of tissue
  • That grow any level of ß-haemolytic
  • Which are clean but fail to heal after 2-4 weeks of optimal care
  • Limit use to avoid tissue toxicity and development of resistance
  • Spectrum should cover Gram-negative,
  • Gram-positive and anaerobic organisms

Systemic antibiotics: Indicated if there is evidence of:

  • Cellulitis
  • Localized infection
  • Systemic Inflammatory Response Syndrome (SIRS)
  • Osteomyelitis

Superficial wound with localized signs of infection; no signs of SIRS or osteomyelitis

  • Amoxicillin/clavulanate
  • Clindamycin
  • Clindamycin plus ciprofloxacin.

Superficial to deep wound with SIRS

  • Clindamycin plus ciprofloxacin
  • Clindamycin plus ceftriaxone
  • Vancomycin (for MRSA)
    • Given for 2-4 weeks

Deep tissue involvement with SIRS,
osteomyelitis and/or threat to limb or life

  • Clindamycin plus ceftriaxone
  • Clindamycin plus gentamicin
  • Vancomycin (for MRSA)
    • Given for 2-12 weeks; prolonged oral treatment required for bone and joint infections after initial intravenous therapy

Surgical Therapy

  • This involves direct wound closure
  • It is suitable for a select group of patients e.g. those with spinal cord injury, deep Stage III/ IV decubiti
    • High risk of recurrence if factors contributing to ulcers are not corrected

Notable adverse drug reactions

  • Vancomycin may be oto- and nephrotoxic; it may also cause blood dyscrasias, rashes, Steven-Johnson’s syndrome, toxic epidermal necrolysis; muscle spasm, pain, phlebitis, vasculitis, severe hypotension and flushing of the upper body (‘red man’ syndrome) are otherpossible complications. It’s use should be restricted to cases of MRSA).

Prevention of decubitus ulcer

  • Address potentially modifiable risk
    factors e.g. dry skin, immobility,
    nutritional factors, etc.
  • Incidence can be reduced up to 30% with aggressive prevention/ intervention strategies
  • A multi-disciplinary wound team is an asset, where available

Pressure relief

  • Improve mobility (‘bed is bad’)
  • Frequent turning (interval may be
    reduced from traditional 2 hours
    depending on host risk factors)
  • Pressure-relieving devices


  • To redistribute local pressure over a wider area
  • Foam mattresses
  • Devices containing air, gel or water


  • Redistribute pressure over wider body area e.g.:
  • Alternating pressure pads
  • Air suspension devices
  • Air-fluid surfaces
  • Use power sources

Nutritional Interventions in decubitus ulcer

  • Increase daily caloric intake to 30
    kcal/kg/day for malnourished patients
  • Achieve daily protein intake between 1.2-1.5 g/kg/day
    • Current evidence does not support routine supplementation with vitamin C or zinc unless in those with demonstrated deficiency
    • High serum zinc levels may interfere with healing and with metabolism of copper

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