Pressure ulcer management in disorders of the CNS

Pressure ulcers are localized areas of injury to skin and sub-adjacent structures that are due to sustained pressure and shear. There are now six pressure ulcer stages.² Stage I describes non-blanching erythema. Stage II breaches the epidermis to expose the dermis. Stage III pressure ulcers are full thickness, and reach the subcutaneous fatty layer. Stage IV ulcers breach fascia and involve muscle, joint capsule, or bone. Unstagable pressure ulcers (the “fifth” stage) have necrotic material that obscures the base. Some unstagable pressure ulcers are termed suspected deep tissue injury (DTI; the “sixth” stage) and have a decomposing base not yet demarcated.

External mechanical load causes internal response, the formation of the pressure ulcer.. The more the external load, the shorter time is necessary to form a pressure ulcer. External load causes axial pressure and shear (i.e., force or stress tangential to the skin). Shear stress has two deleterious effects: 1) causes deep tissue deformation (strain) and necrosis; 2) causes superficial friction to the stratum corneum, damaging the barrier function. Pressure ulcers form on buttocks, coccyx, sacrum trochanters, occiput, heels and other boney prominences. Absence of protective sensation increases risk, such as from spinal cord injury (SCI) or neuropathy.

Risk factors for pressure ulcers include: Activity and mobility restrictions, malnutrition, diminished capillary perfusion and increased skin moisture.²Risk factor intervention (e.g., promoting nutrition, repositioning, weight distribution, mobility) reduces incidence.

Two groups at high risk include the spinal cord injured and the elderly. For community-dwelling elderly, the incidence increases significantly with advancing patient age.³ From spinal cord injury (SCI) model systems data, the prevalence of pressure ulcers increases in time post-injury, from 11.5% one year post-injury, to 21% fifteen years post-injury.⁴

There are two mechanisms of pressure ulcer formation: top-down and bottom-up. Top-down formation involves pressure and shear damaging surface skin and the upper few millimeters of the sub-cutaneous layer: Stage I leads to Stage II to shallow stage III.

Ulcers also form from the bottom up. This occurs with suspected deep tissue injury (DTI). Sustained strain of muscle between the external load and a boney prominence forms the ulcer. Tissue death or infarction is complete within a few hours, but dead tissue takes up to a month to decompose completely. DTI is “suspected” because it can only be confirmed by observation through time as decomposition proceeds.

For DTI, three days after insult there is non-blanching erythema seen better in light-skinned individuals as red-purple or maroon rather than red, also called livido.After six days: Sloughing and blistering of the surface, with a dark base.Two weeks: Demarcation of black or yellow eschar.Three to four weeks: For the sacrum, a foul-smelling yellowish mass, and to the heel, black mummification. The uninitiated provider might mis-diagnose DTI as a pressure ulcer quickly evolving from stage II, to III, to IV.Follow the ulcer daily over several days to a week to confirm the diagnosis as DTI.

DTI can also be a marker of pre-terminal status. “Skin failure” is a phenomenon where DTI forms with greater frequency and severity near death.⁵

Pressure ulcers are associated with dementia, critical illness, pain, immobility, diabetes, atherosclerosis, end stage renal disease, medications (steroids, immunosupressants), smoking, upper or lower motor neuron disease, contractures, and non-adherence to treatments.⁶

Stage II-III pressure ulcers often present with cellulitis and stage IV with osteomyelitis. Pressure ulcers can erode into joint capsules causing septic arthritis. Ischial pressure ulcers can form fistulae to rectum or bladder. Pressure ulcers of the heel, if stage IV, may lead to ischemia infection and limb loss.

What dressings, topical ointments or antibiotics have been used? Has there been a recent decline in mobility, especially bed mobility? If no, are there re-positioning challenges, such as barriers to lying flat? Does the patient complain of pain worsened by pressure on the ulcer? If not, is the area insensate? Has patient unintentionally lost more than 10% of body weight in the last six months?² Is patient unable to communicate the problem due to speech or memory deficit?

General: Assess cachexia. One assesses cachexia by inspection as appearing pallid, frail, chronically ill. Assess body mass index (BMI), contractures, muscle strength, and range of motion, mental status, memory and cognitive impairment, muscle strength, contractures, pedal pulses sensory exam.

Wound length and width and depth are measured in centimeters. Depth is the deepest point accessible. We also measure tunneling “by the clock” (e.g., 4 centimeters of tunneling at 6 o’clock; with noon toward the head).

Wound appearance and dimensions: The wound base itself is assessed for percentage of red, yellow and black.

Stage I has intact skin, which is non-blanching to pressure. Stage II exposes red and glistening dermis. Shallow stage III may have a yellow or white fibrous appearance and a depth of < 3-4 mm on the buttocks. For the buttocks, or ischium, deep stage III ulcers can extend through fatty layers several centimeters. Stage IV ulcers are cavernous, many centimeters deep. Muscle may be visible, bone palpable.

Watch for impaired bed mobility, weight shifts, transfers and ambulation. Watch for cognitive or communication deficit and be mindful of non-verbal signs of discomfort. Consider the location of the pressure ulcer as clues to formation:

1. Sacral ulcers: Supine positioning
2. Coccygeal ulcers: Supine positing or sacral sitting
3. Trochanteric ulcers: Lateral decubitus position
4. Ischial ulcers: Sitting
5. Heel or lateral ankle ulcers: External rotation while supine.
6. Malleoli, fibular head, lateral forefoot ulcers: Wheelchair leg rests, shoes.

Prealbumin (PAB) assesses processing of protein in the past two weeks. Albumin, C-reactive protein (CRP) and sedimentation rate are non-specific inflammatory markers of osteomyelitis which can be used to guide response to treatment only.

1. X-ray for osteomyelitis. Limited specificity of 50%. Where positive for erosion can make the diagnosis.
2. MRI for osteomyelitis. 95% sensitive and 88% specific and can localize the lesion anatomically.
3. Combined Indium WBC-bone scan where MRI is contraindicated. (Bone scan not good alternate, not specific).
4. Segmental arterial studies assess peripheral arterial disease (PAD): For heel ulcers.

The Braden scale is a valid, reproducible measure, which quantifies pressure ulcer risk. The classical Braden scale involves six sub-scales, each with four levels. The sub-scales are: 1) Insensitivity; 2) Mobility; 3) Activity; 4) Nutrition; 5) Moisture; 6) Friction and shear. The overall scale ranges from 6 to 24, with the highest score indicating lowest risk.7 The Norton risk assessment tool has five sub-scales and is also valid.

Stage II pressure ulcers heal within weeks, but stage IV ulcers may require 6-12 months to conservatively close. Healing rate slows with increasing disease burden, poor nutrition and/or inability to off-load.

Assess pressure support surfaces; assess bed, wheelchair, and caregiver support available.

Ask about recliner use: Recliners are notorious for pressure ulcer formation of the sacrum, as turning and positioning are difficult in one.

Wheelchair and cushions. Patients with stage III or IV ischial pressure ulcers (e.g., SCI patients) should empirically limit sitting 3-4 hours per day while ulcers are healing.² Of course, the benefits must be balanced against potential risks (e.g., depression, social isolation). One should consider a tilt-in-space wheelchair with an air villous or gel wheelchair cushion, solid seat and appropriate leg rests for tetraplegic patient with a stage III-IV buttocks pressure ulcer.

Specialty bed. For Stage I and II pressure ulcers, a passive foam or air overlay is recommended. For the patient with a stage III or IV sacral pressure ulcer, a low air loss “active” bed is appropriate. Turn and position every two hours.²

Assess for malfunctioning support surfaces (e.g., bed, wheelchair cushion).

All members of the inpatient rehabilitation team assist: Nursing (health promotion and teaching), PT (mobility) and OT (self care), ST (communication), nutritionist and psychologist (emotional adjustment). As function improves, healing occurs.

Outpatient staffing is often more limited to home health nursing (dressing changes and teaching) and PT for bed mobility and functional transfers.

Consultants: Referrals for osteomyelitis of the trunk or pelvis may include infectious disease, plastic or orthopedic surgery; for a heel pressure ulcer, vascular interventionist.

Pressure ulcer care has the benefit of several excellent guidelines over the years for prevention and managment. Two current guidelines are highly recommend:

1. National Pressure Ulcer Advisory Panel (NPUAP) guidelines²
2. Consortium for Spinal Cord Medicine Clinical Practice Guidelines¹

1. As a pressure ulcer heals, it continues to be referred to by the stage at which it initially presented.
2. Unstagable, Stage II-IV: Antibiotics for erythema <2cm beyond ulcer, increased pain, drainage or wound deterioration. It is useful to get semi-quantitative swab cultures by the Levine method and tailor antibiotics to sensitivities.2 Cultures are less helpful for peri-anal ulcers due to chronic contamination. Where there are systemic signs or symptoms of infection, consider inpatient admission.
3. Unstagable, Stage III-IV: Sharps debridement with pickups, scissors or curette. To reduce discomfort, premedicate, use topical anesthesia (e.g., viscous Lidocaine), and offer “time out” and redirection during the procedure. Alternatively, use enzymatic debridement with collagenase daily.
4. Unstagable or stage IV of the heel. Steps to preserve the limb include 1) revascularization; 2) appropriate surgical debridement; 3) antibiotics for osteomyelitis; 4) consideration of hyperbaric oxygen.⁹
5. Stage III-IV: Negative pressure therapy (NPT). Indication: When the pressure ulcer is debrided to about an 80% red base. Purpose: promotes granulation tissue formation.⁸ Endpoint: Granulation tissue fills most of the “dead space.” Contraindications: Untreated cellulitis, osteomyelitis, or exposed artery. Stage III-IV pressure ulcers in SCI. Reconstructive surgery might be the best option for relatively young SCI patients and in this group is often well tolerated and effective.
6. Stages II-IV nutritional requirements: Caloric: 30-35 Kcal/Kg/day body weight. Protein: 1.5 gram/Kg/day. Vitamin C 50 mg/day, Vitamin A 1000 IU/day and zinc 220 mg/day are also recommended.
7. Stage II- IV: Reduce pain by administering pain medications regularly (e.g., opiates and membrane stabilizing agents), off load, use moist wound dressings and avoid painful “wet to dry” dressings.
8. Stage III-IV with moderate or significant drainage: Alginate dressings, Minimal to moderate drainage consider foams or films
9. Stage II or shallow stage III with scant to minimal drainage: Foams or films, zinc oxide paste (which is relatively imperious to moisture and shear).

Wounds are assessed at least weekly. Key assessments include: Length, width, area , volume and serial photographs. Assessments are graphed versus time to illustrate healing rate. Supporting measures include drainage (e.g, scant, moderate), odor, tracking and undermining.

Guidelines:

1. Garber S, Biddle A, et al. Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury: A Clinical Practice Guideline for Health Care Professionals. Paralyzed Veterans of America; 2000.

2. National Pressure Ulcer Advisory Panel (NPUAP). Clinical Practice Guidelines for Prevention and Treatment, www.npuap.org; 2009.

References:

3. Margolis DJ, Bilker W, et al. The incidence and prevalence of pressure ulcers among elderly patients in general medical practice. Annals of Epidemiology. 2002;12(5): 321-325.

4. Chen YM, Devivo J, et al. Pressure ulcer prevalence in people with spinal cord injury: age-period-duration effects. Archives of Physical Medicine & Rehabilitation. 2005;86(6): 1208-1213.

5. Langemo DK, Brown G. Skin fails too: acute, chronic, and end-stage skin failure. Advances in Skin & Wound Care. 2006;19(4): 206-211.

6. Goldman RJ, Popescu A, et al. Prevention and management of chronic wounds. In: Braddom R, ed. Physical Medicine & Rehabilitation. Philadelphia, PA, Saunders Elsevier; 2007:685-708.

7. Bergstrom N, Braden B, et al. The Braden Scale for predicting pressure sore risk. Nurs Res. 1987:36:205-210.

8. de Leon JM, Barnes S, et al. Cost-effectiveness of negative pressure wound therapy for postsurgical patients in long-term acute care. Adv Skin Wound Care. 2009;22(3):122-127.

9. Goldman RJ. Hyperbaric oxygen therapy for wound healing and limb salvage: a systematic review. PM&R. 2009;1(5): 471-489.