• Areas of Concern heading
  • Areas of concern Autonomic Dystrifexlia Link
  • Areas of concern Neurogenic Bladder link
  • Areas of concern Neurogenic Bowel link
  • Areas of concern Pressure Ulser link
  • Areas of concern Respiratory complications link
  • Health promotion and maintenance link
  • resources link

Pressure Ulcers

  • Pressure ulcers are a frequent, costly, and potentially life-threatening complication of spinal cord injury
  • Pressure ulcers can have a major impact on quality of life
  • Prevention, early detection, and treatment are key. Family physicians therefore play a critical role
  • Daily skin checks, regular pressure redistribution, and offloading play an important role in the prevention of pressure ulcers
  • Pressure ulcers often start in the dermis before breakdown is visible in the epidermis
  • Treatment of pressure ulcers is best done through a multidisciplinary team approach that includes a physician, wound care nurse, physiotherapist/occupational therapist, and other specialists as required
  • Clarifying the goals of care early on is important (i.e., healing, maintenance, palliation)

Definition

Pressure Ulcers: Pressure ulcers are lesions caused by unrelieved pressure, or pressure in combination with shear and/or friction, resulting in damage of underlying tissue. They usually occur over bony prominences and in North America are classified by stages according to the degree of tissue damage.

The pressure ulcer staging classification is intended to describe the severity of tissue damage. Accurate staging is essential because allowable services, supplies/ equipment, and treatment options are often linked to the severity of the pressure ulcer. A pressure ulcer can progress to a greater stage but reverse staging (describing a healing pressure ulcer as a lesser stage) is incorrect practice.

Stage

Illustration

(click/touch to enlarge)

Description
Suspected deep tissue injury

suspected deep tissue injury image

Purple or maroon localised area of discoloured intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer, or cooler as compared to adjacent tissue.

Stage I

stage 1 deep tissue injury

Intact skin with non-blanchable redness of a localised area usually over a bony prominence. Darkly pigmented skin may not have visible blanching; its colour may differ from the surrounding area.
Stage II

stage 2 deep tissue injury

Full thickness tissue loss. Subcutaneous fat may be visible but bone, tendon, or muscle are not exposed. Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunnelling.
Stage III

stage 3 deep tissue injury

Full thickness tissue loss. Subcutaneous fat may be visible but bone, tendon, or muscle are not exposed. Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunnelling.
Stage IV

stage 4 deep tissue injury

Full thickness tissue loss with exposed bone, tendon or muscle. Slough or eschar may be present on some parts of the wound bed. Often include undermining and tunnelling.
Unstageable

unstageable deep tissue injury

Full thickness tissue loss in which the base of the ulcer is covered by slough (yellow, tan, gray, green, or brown) and/or eschar (tan, brown, or black) in the wound bed.

Content from National Pressure Ulcer Advisory Panel (revised 2007, www.npuap.org).

Incidence and prevalence

Annual incidence rate of pressure ulcers ranges from 20-31%. Prevalence ranges from 10.2-30% (www.scireproject.com).

Most common sites for pressure ulcers are bony prominences such as the sacrum, ischial tuberosities, and heels/feet.

7-8% of those who develop pressure ulcers will die from related complications (e.g., sepsis, osteomyelitis) (Richards et al., 2004).

Richards, J.S., Waites, K., Chen, Y.Y., Kogos, K., & Schumitt, M.M. (2004). The epidemiology of secondary conditions following spinal cord injury. Topics in Spinal Cord Injury Rehabilitation, 10, 15-29.

Pathophysiology

pressure ulcer pathophysiology
  • Development of pressure ulcers is a multifactorial process that is not completely understood.
  • Pressure ulcers are thought to be the result of inadequate tissue perfusion, impaired lymphatic function, and mechanical tissue destruction.
  • Pressure (direct sustained pressure and repetitive moderate pressure), shear forces, and/or friction cause blood vessels to collapse resulting in tissue ischemia and thrombotic occlusion of the capillary vasculature.
  • Nutritional deficiencies, moisture, and altered skin properties resulting from spinal cord injury increase susceptibility to ischemia.
  • Impaired perfusion (ischemia) can lead to inflammation and necrosis.
  • Cells die as a result of prolonged necrosis. As muscle cells require more oxygen, cell death happens quicker in muscle tissue and damage is not initially seen on the surface.
  • Bacterial colonisation of an ulcer contributes to necrosis and may lead to infection.

Signs and symptoms

Ulcers are often not recognised until the ulcer has significantly progressed or has become infected when pressure is of greater intensity and duration. Cell death happens quicker in muscle cells than skin cells so frequent skin checks are important to identify subtle underlying tissue changes.

Extra vigilance is required with patients with darker skin. The typical redness or other colour changes associated with pressure ulcers are less visible. Therefore, compare the area of skin alteration with an adjacent or opposite area of the body.

When assessing the ulcer, the following should be observed:

  • Anatomic location and stage (see Pressure Ulcer >> Definition).
  • Size: Length, width, depth in cms? Increasing or decreasing?
  • Undermining or tunnelling/sinus tracts: Absent or present (check size with probe)?
  • Wound edges: Attached or not attached? Maceration?
  • Peripheral tissue: Colour changes? Edema or induration? Cellulitis?
  • Odour: Absent or present?
  • Exudate: Colour, consistency, and amount?
  • Wound bed: Granulation, hypergranulation, friable, necrotic tissue, avascular?
  • Pain: Type, location, quantity (use a scale)?

Pocket Assessment Card

Causative factors

Pressure ulcers are usually the result of multiple contributing and confounding factors. The result the pressure has on the skin is influenced by its intensity and duration, as well as the tissue tolerance to the pressure.

Risk factors for pressure ulcers

  • Demographics
    • Advanced age
    • Male gender
    • Lower educational level
    • Unemployed
  • Physical
    • Inability to feel pain
    • Decreased level of activity
    • Moisture (e.g., urinary and faecal incontinence)
    • Friction and shear (e.g., spasticity, slides down chair/bed)
    • Poor nutrition and/or hydration
    • Muscle atrophy
    • Low BP
    • Increased co-morbidities
    • Inappropriate equipment
  • Psychological
    • Depression/anxiety
    • Cognitive impairment
    • Substance abuse (inc. smoking)

The Braden Scale is often used to assess risk for pressure ulcer development. The higher the risk the more preventative measures should be instituted.

Management and recommendations

It is important to clarify the goals of care early on (i.e., healing, maintenance, palliation).

Prevention

  • Provide patient and family with information around early recognition and treatment (e.g., Pressure Ulcers: What you should know)
  • Encourage daily skin checks, especially of Areas at Risk, to facilitate early detection
  • Inform about the need for regular repositioning and optimal positioning evidence icon. Shift weight in wheelchair every 15 minutes and reposition in bed every 2 hours
  • Keep skin clean, dry, and supple
  • Recommend skin barrier products if exposure to excessive moisture cannot be avoided
  • Verify adequate transfer techniques and equipment
  • Facilitate acquisition of adequate equipment and support surfaces (e.g., chair, bed, car) and regular seating/positioning assessment
  • Promote smoking cessation
  • Teach importance of good nutrition and hydration
  • Instruct to keep head of bed less than 30 degrees unless contraindicated

There is level 3 evidence that 1-2 minutes of pressure relief must be sustained to raise tissue oxygen to unloaded levels.

There is level 4 evidence to support position changes to reduce pressure at the ischial tuberosities.

Investigations

  • If impaired healing capacity suspected: Haemoglobin
  • If infection suspected: CBC, ESR, C-reactive protein, culture and sensitivity of wound (ensure wound is well irrigated and culture sample is from deeper tissue)
  • If nutrition impairment suspected: Body weight, albumin, transferrin, and pre-albumin in 1-2 weeks
  • If osteomyelitis suspected: X-ray, bone scan, or MRI of adjacent bone
  • If chronic wound is not healing despite best practices: Consider referral for a tissue biopsy to rule out the presence of an underlying malignancy (e.g., Marjolin ulcer)

General management

  • Implement strategies to mitigate or remove contributing factors
  • Refer to local Community Care Agency wound program, which will have own evidence-informed wound protocol, or local wound management clinic/wound specialist
  • Ask patient to take regular photographs to monitor wound progression
  • Cleanse with non-cytotoxic solution or wound cleanser (e.g., sterile water, normal saline) and avoid antiseptic agents (e.g., hydrogen peroxide, rubbing alcohol)
  • For wounds with potential to heal, debride areas with devitalised tissue (except for heel pressure ulcers). See Methods of Pressure Ulcer Debridement
  • For wounds with potential to heal, use wound dressing products that keep ulcer wound bed moist but surrounding skin dry (except for heel pressure ulcers). For a summary of major dressings, see Product Picker Dressing Selection Guide
  • Monitor wound healing every 2-4 weeks (stages of wound healing)
  • Change treatment if no response after 2-4 weeks or signs and symptoms of infection
  • Surgical referral if stage 4 or deep stage 3 with tunnelling/sinus tracts
  • Consider biophysical agents in conjunction with wound specialist (e.g., electrical stimulation , ultrasound, phototherapy, negative pressure wound therapy, hyberbaric oxygen)
  • Consider biologic agents (e.g., skin substitute, extracellular matrix scaffolds, molecular and cellular regulators)
  • Consider enhanced foods or oral supplements between meals if calorie/protein deficiency suspected.
  • Consider vitamin and mineral supplements if deficiencies suspected (expert opinion). Daily multivitamin and Vitamin C (500mg BID). If the pressure ulcer is draining large amounts of exudation and/or the patient has poor nutritional intake, consider two to four weeks of 40mg of elemental zinc daily (e.g., Zinc Sulphate 220mg). Adequate protein and hydration, unless contraindicated, are also necessary for wound healing.

Follow-up

  • Preventative measures are key as there is a high rate of recurrence among patients with spinal cord injury (see Management and recommendations)
  • Ask patient to bring photographs of wound, documentation from wound care nurse, and dressings to appointments
  • Coordinate services and plan appointments on days dressings need changing
  • Ask patient to keep a log of pressure ulcer history so healthcare team members can be informed and remain vigilant
  • Provide patient education (e.g., Pressure Ulcers: What you should know)

References

Consortium for Spinal Cord Medicine. (2000). Pressure Ulcer prevention and treatment following spinal cord injury: A clinical practice guideline for health-care professionals. Washington, DC: Paralyzed Veterans of America.

Richards, J.S., Waites, K., Chen, Y.Y., Kogos, K., & Schumitt, M.M. (2004). The epidemiology of secondary conditions following spinal cord injury. Topics in Spinal Cord Injury Rehabilitation, 10(1), 15-29.