Pressure Ulcers and Diabetic Ulcers

Pressure Ulcers (Bedsores/Decubitus)

  • Pressure ulcers, bedsores, and decubitus ulcers are all terms referring to the same condition: localized tissue necrosis (death) caused by unrelieved pressure, or pressure combined with shearing. Decubitus is Latin for lying down ulcer.
  • Shearing involves micro-tearing of tissue below the subcutaneous layer due to combined pressure and movement.
  • Pressure ulcers result from tissue ischemia caused by external pressure (e.g., bed surface) and the body's internal structures.
  • These ulcers typically occur over bony prominences but can develop anywhere.
  • High-risk patients include those with spinal cord injuries or impaired sensation, making them unaware of pressure-related warnings.
  • Hospitalized patients who aren't moved frequently and residents of long-term care facilities are also at risk.
  • Pressure sores can also result from prolonged sitting (e.g., in a wheelchair without a good cushion) or external devices like braces or casts.
  • Healthcare workers prevent pressure ulcers by turning patients, rolling them, and teaching weight-shifting and pressure-relieving techniques.
  • However, pressure ulcers are not always preventable.
  • They commonly occur where bone and an external surface compress the skin, cutting off circulation.
  • Affected areas vary by body position but commonly include:
    • Shoulder
    • Back of the head
    • Elbow
    • Lower back
    • Sacrum
    • Heels
  • Approximately 15% of hospitalized patients develop pressure ulcers.
  • The cost to treat a facility-acquired decubitus ulcer is approximately $43,000, which the facility cannot bill to insurance.
  • The approximate annual cost in the U.S. is $11 billion.
  • Proper patient positioning and movement are crucial in preventing pressure ulcers.
  • A pressure ulcer is a wound caused by unrelieved pressure and shear forces that cause micro damage to the subcutaneous tissues.
  • Prolonged pressure and shear effects are worsened at bony prominences, compressing tissue between external force and bone.

Etiology of Pressure Ulcers

  • Increased pressure exceeds intracapillary pressure, leading to tissue ischemia (no blood flow, tissue death).
  • Compression of lymphatic channels results in increased waste and acidosis, causing further cellular death.
  • Fibrin deposits in capillaries contribute to the cycle of pressure, ischemia, and necrosis.
  • Damage is related to pressure and time.
  • The effect depends on the force per unit area: increased pressure for longer periods causes more tissue damage.
  • There is an inverse relationship between pressure and duration.
  • No optimal duration for pressure relief has been identified due to variance in tissue types and individual differences.
  • General guidelines:
    • In bed: Patients should be moved every two hours to relieve pressure.
    • In sitting: Weight shifting or pressure-relieving techniques should be performed every 15 minutes.
    • High-risk, dependent patients may require repositioning every hour.

Risk Factors for Pressure Ulcers

  • Internal factors include critical illness, low cardiac output, and low blood pressure.
  • External factors include hard bed surfaces and moisture (e.g., incontinence).
  • Medications can also affect the risk.

Staging System for Pressure Ulcers

  • The National Pressure Ulcer Advisory Panel has developed a naming system for pressure sores.
  • The staging system is not used for prognosis.
  • The stage is not changed once categorized, even as it heals. A healing stage 4 remains a stage 4.
Stage 1
  • Involves the epidermis only (superficial).
  • Characterized by non-blanchable redness: the area remains red even when pressure is applied.
  • Skin color may differ from surrounding tissue.
  • May be painful, warmer, cooler, firmer, or softer than surrounding tissues.
  • Intervention: Relieve pressure to allow healing.
Stage 2
  • Involves the epidermis and dermis (partial thickness).
  • Shallow, open ulcer without bruising or slough (necrotic tissue).
Stage 3
  • Full-thickness tissue loss extending through the epidermis and dermis.
  • May see fat, but no bone, tendon, or muscle is visible.
  • Depth varies by location and fat amount.
  • Slough may be present.
Stage 4
  • Deepest observable pressure ulcer: the base of the wound is visible.
  • Full-thickness loss with exposed bone, tendon, or muscle.
  • Depth depends on location and tissue amount.
  • Necrosis is typically present.
  • Undermining, sinus tracts, or tunnels may be present.
  • Osteomyelitis (bone infection) or osteitis (bone inflammation) is possible, requiring close coordination with the medical team.
Unstageable
  • Full-thickness tissue loss, but the depth cannot be determined due to eschar (hard, dry, dead tissue) and/or slough covering the wound.
  • Once cleaned, the stage can be reassessed.
  • Stable eschar should not be removed.
Suspected Deep Tissue Injury
  • Skin is intact, but the extent of damage is unknown.
  • Purple or maroon discoloration, may be a blood-filled blister.
  • May be painful, firm, mushy, boggy, warmer, or cooler.
  • Monitor for evolution or improvement.

Risk Assessment

  • Screening tools are used to assess risk, not for prognosis.
  • Facility-dependent.
  • The Braden scale is recommended as the most common and reliable scale. Other scales include the Norton risk assessment scale and a Gosnell scale.

Medical and Surgical Interventions

  • Medical interventions:
    • Radiology to assess damage extent.
    • Antibiotic therapy for osteomyelitis, cellulitis, or sepsis.
    • Nutritional supplements.
    • Management of comorbidities.
  • Surgical interventions:
    • Surgical debridement (stage 3 or 4 ulcers) to remove necrotic tissue.
    • Musculocutaneous flap: Damaged muscle tissue is removed and replaced with surrounding muscle tissue to close the wound (typically stage 4).

Diabetic Ulcers (Neuropathic Ulcers)

  • Slow-healing ulcers affecting individuals with diabetes, decreased sensation, and an arterial component.
  • Diabetic ulcers are a type of arterial ulcer occurring in diabetic patients, typically on the feet.
  • Approximately 11.6% of the U.S. population has diabetes, and 25% of that population has or has had a diabetic ulcer.

Risk Factors

  • Vascular disease: Diabetes is a leading risk factor for coronary artery disease, cerebral vascular accidents, and peripheral vascular disease.
  • Neuropathy: The most common complication of diabetes mellitus, affecting sensory, motor, and autonomic systems.
    • Motor neuropathy: Can lead to paralysis of intrinsic muscles, problems managing pressure and shearing, and decreased stability.
    • Hallux valgus (bunion) and claw toe can lead to pressure on the dorsum of the toes and plantar surface of the metatarsal heads.
    • Autonomic nervous system involvement: Can decrease sweat, increase callus formation, and possibly decrease blood flow.
  • Mechanical stress: Greater pressure on the forefoot than the rearfoot. In such cases, special shoes may be needed.
  • Abnormal foot function: Decreased range of motion, Charcot foot deformity.
  • Charcot foot: Loss of intrinsics leads to arch reduction and foot drop.
  • Footwear: Protect the foot to prevent shear force and accommodate deformities. Consider diabetic shoes or foot orthotics.
  • Immune response and healing: Diabetes impacts circulation and tissue growth. Immunity issues will result in reduction to white blood cells.
  • Vision: Long-term diabetes can cause visual issues, such as damage to the retina.
  • Increased risk of trauma and decreased foot care: Decreased sensation can lead to unnoticed wounds or worsening existing ulcers.

Location

  • Neuropathic ulcers can occur anywhere on the foot.
  • Feet are the most problematic due to reduced blood supply and loss of protective sensation.
  • Common locations:
    • Plantar aspect of the metatarsal heads.
    • Metatarsal heads of the toes.
  • These are usually due to bony changes, intrinsic muscle atrophy, loss of protective sensation with weight-bearing pressure, and decreased blood flow.

Periwound

  • Dry, cracked skin.
  • Redness.
  • Callous buildup.
  • Infection.
  • Possibility of gangrene.
  • Decreased body temperature.

PT Tests and Measures

  • Vascular assessment: Pulses, capillary refill test, Ruber of dependency, Doppler test.
  • Sensory integrity: Monofilament testing (Sims Weinstein monofilament).
  • Wagner grading scale: A standardized test, not covered in this course.

Medical and Surgical Intervention

  • Pharmacology: Managing diabetes, neuropathic pain, and comorbidities.
  • Surgical intervention:
    • Wound debridement.
    • Antimicrobial beads can be implanted into the wound
    • Correction of foot deformity (Charcot foot).
    • Amputation.