Management of pressure ulcers - What is new?

Pressure ulcers (PUs) are an important aspect of geriatrics and palliative care that amplifies morbidity of the chronically bed-ridden patients posing a threat to health-care economy and resources. PUs can interfere with functional recovery, may be complicated by pain and infection and can prolong hospital length of stay. Their presence may be a marker of poor overall prognosis and premature mortality. The pathogenesis and progress in the management of PUs is discussed.

Pressure ulcers (PUs) are an important aspect of geriatrics and palliative care that amplifies morbidity of the chronically bed-ridden patients posing a threat to health-care economy and resources. Skin microcirculation changes (mainly ischemia–reperfusion (I/R) injury) characterize the early stages of PU development. Lower mean arterial pressure (MAP), serum albumin level (<2.8 g/dL), urinary incontinence, lower score on Braden Scale, wound size, and exudate amount and inclusion of a nutritionist in the team are the variables found to have significant effect on PU healing.[1]

There is a dangerous myth that PU is an inevitable part of aging. It needs to be understood that the prevention of PU is quality outcome of care, with nursing care being paramountly important. Most PUs are preventable and a majority of PUs arises because of medical negligence.[2] There is a significant financial burden too related to PUs (up to £2.1 billion for the treatment of PU in the United Kingdom).[3] This emphasizes the adage that prevention is better than cure.

The National Pressure Ulcer Advisory Panel's staging system defines stage I as intact skin with nonblanchable redness of a localized area, stage II as shallow open ulcer with a red pink wound bed without slough (representing partial thickness loss of dermis), stage III as full-thickness tissue loss with visible subcutaneous fat/slough, and stage IV as full thickness loss with exposed bone, tendon, or muscles that often includes undermining/tunneling with slough/eschar.[4]

As a tertiary care setting, we have had improved outcomes mainly with preventive care such as the usage of self-inflating mattresses, periodic position changing of the patient, enriched diet, and keen supervision. We have used saline dressings, hydrocolloid, collagen protein hydrolysate supplements, dextranomer paste, untrasonic therapy, and debridement (in morbid cases) with satisfactory outcomes.

A study analyzed self-adhesive polyurethane foam and saline-soaked gauze dressing for (stage II) PUs and found that the former is more cost-effective than the latter.[5] Calcium alginate dressings have shown improved healing compared with dextranomer paste (mean wound surface area reduction per week, 2.39 cm2 vs. 0.27 cm2, respectively).[6] Significant PU healing has been reported with nanosilver hydrogel.[7]

Another study showed that patients with PU have significantly lower plasma arginine concentration compared to those without PU and replenishment with arginine resulted in significant improvement in PU area, perimeter, (depth, exudates, size, inflammation/infection, granulation, necrosis, and pocket-Rating) DESIGN-R and Pressure Ulcer Scale for Healing (PUSH) scores.[8] High-protein diets enriched with arginine, vitamin C, vitamin E, and zinc, when used with standard PU care, have shown to significantly reduce the mean PU area. A diet enriched with eicosapentaenoic acid, gamma-linolenic acid, and vitamins A, C, and E is associated with a significantly lower occurrence of new PUs in critically ill patients.

The use of autologous stem cells from bone marrow (bone marrow mononuclear cells BM-MNCs) to promote the healing of PUs in patients with spinal cord injury (SCI) was tested and in 86.36% of the patients, the PU (type IV) treated with BM-MC fully healed after a mean time of 21 days with no recurrence. It also offered a reduction in mean intrahospital stay from 85.16 (with conventional surgical treatment) to 43.06 days.[9] Bone-marrow-derived stem cells when injected/applied topically into the wound along with platelets, fibrin glue, and bone-marrow-impregnated collagen matrix have shown remarkable wound closure.

Platelet-rich plasma (PRP) treatment probably via sustained release of autologous growth factors, cytokines, and other mediators along with its favorable mononuclear cell profile has shown consistent results in the formation of granulation tissue and improved vascularity in SCI with stage IV-PU. PRP may stimulate wound healing and resolve chronic inflammation.[10]

Sustained-release adrenomedullin (AM), an endogenous vasodilator peptide, significantly improves wound healing of PU through acceleration of granulation, stimulation of proliferation, and migration of various cells including endothelial cells, fibroblasts and keratinocytes, and induction of angiogenesis and lymphangiogenesis.

In a study, the use of electric stimulation therapy (EST) along with community standard wound care (SWC) significantly decreased the percentage of wound surface area in stage III, IV, or X PUs compared to SWC alone.[11] Ultrasonic therapy used alongside standard treatment has also shown promise in healing of PU.

Prevention is the cornerstone of managing PUs. Position changes (although ideally recommended for every 15 min, 2nd hourly may suffice), head end elevation not more than 30° (to avoid lying directly on hipbones), pillow below knee to support calf and heel and in between knees and ankles to avoid contact, foam, air, gel, or water mattresses (including self-inflatable), daily skin inspections, and a maximally nutritious diet are some of the ways that can help prevent PUs.

Management of PU can be challenging to health-care providers and it certainly helps to be up-to-date on the newer advances in the field.