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Pressure Ulceration and the Use of Active Leptospermum Honey for Debridement and Healing
The National Pressure Ulcer Advisory Panel1 (NPUAP) defines a pressure ulcer (PU) as “a localized injury to the skin and/or underlying tissue, usually over a bony prominence, that results from pressure (including pressure associated with shear)”; the Panel adds, “the significance of contributing and confounding factors that influence pressure ulcer formation have not been fully determined.”
PUs are a significant healthcare problem. Prevalence in acute care ranges from 1.4% to 36.4% and costs of care are estimated to range from $2.2 to $3.6 billion annually in the US.2 Although prevention is espoused, experts at a recent NPUAP consensus conference concurred the development of pressure ulcers may be unavoidable in certain situations3 — unavoidability meaning that the ulcer developed despite evaluation of the individual’s clinical condition and PU risk factors and implementation of a plan for recognized prevention measures that are consistent with the needs and goals for the patient. For example, in critical care hemodynamic instability may preclude turning or repositioning, leading to eventual pressure ulceration.3
Once a PU develops, a plan of care to address the multiple needs for the patient and the wound is developed. If the PU does not demonstrate progress toward healing in 2 weeks, or if the PU deteriorates, the plan of care should be adjusted immediately.4 Partial-thickness, Stage II pressure ulcers generally heal faster than full-thickness ulcers; healing has been reported to be twice as long for full-thickness wounds of the same etiology. Stage III and Stage IV full-thickness pressure ulcers have been reported to take the longest time to heal. A recent investigation,5 using validated protocols of care that generally avoided gauze dressings, revealed 36% of 373 full-thickness pressure ulcers had an average time to healing of 62 days (SD = 54) as opposed to 31 days (SD = 41) (P <.001) for partial-thickness ulcers. The study also showed that wounds that worsened from partial-thickness to full-thickness take longer to heal, increasing the economic burden associated with wound care and exposing the patient to increased risks of infection and pain, negatively affecting quality of life.
It is imperative to prepare the wound bed by removing barriers to healing such as necrotic or devitalized tissue and bacteria and to optimize the healing environment. A growing body of evidence supports the use of active Leptospermum honey (ALH) for use in chronic nonhealing wounds. ALH dressings have debriding and antimicrobial effects. The dressings have recently been added in the NPUAP Pressure Ulcer Prevention and Treatment Clinical Practice Guideline,4 which cites evidence for honey-impregnated dressings for wound bed preparation and treatment and for use as a topical antimicrobial agent.
Debridement. ALH’s mechanism of action for debriding includes autolysis and osmosis. The dressing provides a moist environment, aiding the body’s own process of autolysis6; the high sugar content of ALH promotes movement of fluid from an area of greater concentration to an area of lower concentration, drawing lymph fluid to the surface of the wound, resulting in a pooling, or osmotic effect, that bathes the wound.7 Additionally, circulating plasminogen in the lymph fluid is likely converted to the enzyme plasmin, which disturbs the adherent bonds tethering necrotic tissue to the wound bed.8
Antimicrobial. ALH’s florally derived antibacterial activity9 has demonstrated the ability to inhibit the growth of multiple organisms including methicillin-resistant Staphylococcus aureus, vancomycin-resistant Enterococcus, Pseudomonas aeruginosa, and beta-hemolytic Streptococci.10
Case Study
A 56-year-old woman with a history of cirrhosis of the liver, acute pancreatitis, congestive heart failure, malnutrition, and hepatic encephalopathy developed abdominal compartment syndrome with hypotension resulting in tissue ischemia and a sacral PU. The patient reported constant extreme pain (10 out of 10 on a visual analog scale) at the pressure ulcer location. Fentanyl patches, IV hydromorphone, topical lidocaine, and complete offloading were used for pain management. Despite optimal treatment (pressure redistribution, turning and positioning, and nutritional support), the wound developed a thick eschar. The patient was not a candidate for surgical debridement; therefore, collagenase ointment was applied daily to promote enzymatic debridement. After 3 weeks, little progress toward debridement and no healing were noted. The wound measured 8.0 cm x 10.0 cm x 1.0 cm, with a moderate amount of serosanguinous exudate, periwound erythema, and adherent loose necrotic slough tissue in the wound base.
On April 10, 2009, ALH paste was initiated and covered with an absorbent calcium alginate dressing daily (see Figure 1). Minimal sharp debridement was performed as needed to remove loosened necrotic slough tissue. By June 16, 2009, the wound was fully debrided and exhibited reduced exudate and erythema. The wound measurements decreased to 6.0 cm x 8.0 cm x 1.0 cm and healthy granulation tissue was evident with a small amount of exposed fascia (see Figure 2). The patient’s pain scores gradually improved, allowing for gradual reduction and eventual discontinuation of pain relief medication. By August 10, 2009, the wound was completely closed with only a small scab remaining (see Figure 3).
ALH dressings demonstrated the ability to promote autolytic debridement of adherent slough tissue and reinitiate healing for this patient with multiple comorbidities and pressure ulceration. In this author’s facility, ALH dressings have become the treatment of choice when pressure ulcer healing has stalled or when debridement of devitalized tissue is needed and the patient is not a candidate for surgical debridement.
