Managing Symptoms & Overall Patient Condition

When treating a wound the underlying cause is most important to manage and then tissue types at the wound bed are to be given next importance. The associated symptoms which include infection, exudate, pain and odour etc need to be effectively managed due to the negative effect they can have on the wound healing process as well as the patient’s quality of life.

Symptom management is critical to ensure patient comfort and positive treatment outcomes. This section aims to explore the importance of each symptom and its importance to wound healing.

Odour

Infected wounds and wounds which are necrotic / sloughy can often become malodorous and hence the cause, the infection or the necrotic tissue must be treated to control or remove the odour. Odours are a common feature of many chronic wounds; especially leg ulcers and fungating wounds and some acute wounds; dehisced surgical wounds and contaminated traumatic wounds. Aversion to malodour is deeply ingrained in human behaviour. It may lead to social isolation and depression. An odour assessment may be completed to help guide the healthcare professional to the appropriate treatment regime.

Pain

Wound pain is complex and patient specific.  Pain is shaped by an individual’s emotions and significantly impacts on quality of life. Pain associated with wound care may be as a result of exposed structures in the wound, such as nerve endings or underlying pathophysiology, such as ischaemic vascular pain. Wound infection can lead to pain due to the vasodilatation and increased exudate and pressure on the tissues. Pain also can be attributable to the peri-wound area if it becomes excoriated by wound exudate. Pain can also be associated to the endotoxins released on the wound as body response to wound and it’s healing process.

Selection of the correct dressing regime coupled with appropriate levels of analgesia is critical. Traditional dressings and antiseptics can cause trauma and pain and stinging to the wound bed on application / removal and whilst in situ as they are either abrasive or can adhere and dry out sticking to the wound bed.

Hydrofera is a dressing which can take care of the pain in these patients by removing the endotoxins from the wound bed and cause no trauma while being removed . The Soft PVA foam removes all the exudates from the wound bed and provides comfortable moist wound healing.

Exudate

Maintenance of a moist wound healing environment is widely accepted as the ‘ideal’ environment for wounds to heal. Wound fluid or ‘exudate’ in the right amount can bathe the wound with nutrients and actively cleanse the wound’s surface. The amount of exudate which is produced is individual to the wound however always tends to rise during the inflammatory phase and if infection is present. A delicate balance to keep the correct amount of fluid at the wound interface needs to be achieved. This can be done by the use of modern dressing materials which either lock the exudate within the body of the dressing or allow the safe passage of exudate through the dressing by means of its MVTR (moisture vapour transmission rate).

Excessive wound fluid can inhibit wound healing and can lead to maceration of the peri-wound skin, further breakdown, and excoriation and skin sensitivities if inappropriately managed as it can be corrosive in nature.

Infection

Wound Infection is caused by multiplying pathogenic bacteria which cause a reaction in the patient. Infection can be systemic, causing the patient to become ill or local, only affecting the wound bed and surrounding tissues. At assessment the health care professional should observe for the clinical signs of infection: pain, heat, erythema, cellulitus, oedema, pyrexia, malodour, delayed healing, wound breakdown, fragile granulation tissue, excessive exudate and the presence of pus. Patients who are immune compromised cannot display these signs as they do not host a traditional immune response and therefore need to be monitored very closely and carefully. Wounds which are necrotic / sloughy need to have this tissue removed as it can act as a focal point for bacteria and the peri-wound protected as the exudate levels can be high. The species of bacteria present in the wound bed needs to be confirmed as this will lead to accurate treatment. Typical bacteria found in wounds include: staphylococcus aureus and pseudomonas aureginosa. Certain bacteria are associated with distinctive malodours.

Systemic wound infection may be treated with antibiotics; local wound infection may be managed with antimicrobial dressings or topical antiseptics. Any dressing selected should be considered for its viral / bacterial properties to minimise cross infection. Dressings should be changed more frequently and the wound closely monitored during this time.

Moist Wound Healing

The principle of moist wound healing challenges the normal physiological process of wound repair; ‘dry healing’ seen by the formation of a scab. It is recognised that in moist occlusive / semi-occlusive environments, epithelialisation occurs at twice the rate when compared to a dry one. Moist wound healing can be achieved with advanced wound care dressings; a wet environment can be detrimental as this can lead to maceration and tissue breakdown.

Moist wound healing is not suitable for all wounds.  Necrotic digits due to ischaemia and / or neuropathy should be kept dry or monitored very closely (daily often). These patients experience problems fighting infection. Modern wound dressings can be used but the wound needs to be monitored closely to identify for early signs of clinical infection and to prevent maceration.

Maintaining a moist wound environment facilities the wound-healing process. The beneficial effects of a moist versus a dry wound environment include: prevention of tissue dehydration and cell death, accelerated angiogenesis, increased breakdown of dead tissue and fibrin, i.e., pericapillary fibrin cuffs, and potentiating the interaction of growth factors with their target cells. In addition, pain is significantly reduced when wounds are covered with an occlusive dressing. Concerns that moisture in wounds would increase the risk of clinical infection over traditional therapies are unfounded.

Deterrents to wound healing

Acute wounds generally proceed through an orderly and timely reparative process that results in a durable restoration of anatomic and functional integrity. However, various physiologic and mechanical factors may impair the healing response, resulting in a chronic wound that fails to proceed through the usual stepwise progression. Local infection, hypoxia, trauma, foreign bodies, or systemic problems such as diabetes mellitus, malnutrition, immunodeficiency, or medications are most frequently responsible.

All wounds are contaminated, but most successfully resist invasive infection. When the concentration exceeds 100,000 (105) organisms per gram of tissue or the immune system becomes compromised, infection frequently ensues. Cellulitis prolongs the inflammatory phase by maintaining high levels of proinflammatory cytokines and tissue proteases, which degrade granulation tissue and tissue growth factors, and by delaying collagen deposition.

Debridement (surgical, enzymatic, and/or by dressing changes) and antibiotics are the mainstays of antibiotic treatment. Debridement removes devitalized tissue, which can be a source of endotoxins that inhibit fibroblast and keratinocyte migration into the wound. Foreign bodies may also require removal, as the presence of a silk suture reduces the number of bacteria required to incite infection 10,000-fold. (For a detailed description of technique, see eMedicine article Foreign Body Removal, Wound.)

Cellular hypoxia retards wound healing through various means. Collagen fibril crosslinking requires oxygen to hydroxylate proline and lysine and fails when tissue pressure is below 40 mm Hg. The bactericidal potency of leukocyte oxidative phosphorylation also suffers in a hypoxic environment, reducing the threshold for infection. Measures to improve oxygen delivery depend on the etiology. Tobacco use, which causes vasoconstriction and increases platelet adherence, should be stopped. Angioplasty or arterial bypass grafting may be required for peripheral vascular disease. Adjunctive measures to improve systemic perfusion in cases of cardiac failure may be indicated. Hematocrit value less than 15% should be treated and euvolemia restored, as needed. Venous stasis or lymphatic insufficiency may be improved with compressive garments.

Systemic disease can dramatically prolong or interrupt wound healing. Glycosylation in diabetes mellitus impairs neutrophil and macrophage phagocytosis of bacteria, prolonging the inflammatory phase. The proliferative phase is also protracted in the same disease as erythrocytes become less pliable and less able to deliver oxygen to the wound for tissue metabolism and collagen synthesis.

Malnutrition results in diminished fibroblast proliferation, impaired neovascularization, and decreased cellular and humoral immunity. Wounds exert heightened metabolic demands, particularly within granulation tissue. Amino acids such as methionine, proline, glycine, and lysine, are essential for normal cell function and the repair of cutaneous wounds. Fatty acids are critical constituents of cell membranes and are the substrate for the eicosanoids that mediate the inflammatory process. Essential fatty acids linolenic and linoleic acid must be supplied in the diet, as the human body is incapable of de novo synthesis of these molecules.

Adequate vitamins and minerals must be available for cell metabolism, acting as cellular signals and cofactors. Vitamin C (ascorbic acid) and iron are required for the hydroxylation of lysine and proline, which crosslink and stabilize the triple helix structure of collagen; copper also plays an role in stabilizing collagen. Vitamin A (retinoic acid) plays an important role in modulating collagen production and degradation and is particularly important in epithelialization. A potent antioxidant, vitamin E (alpha tocopherol) appears to accelerate dermal and bone healing in animals, and supplementation may have a role in humans. Trace metal, particularly zinc, deficiency is also associated with poor wound healing; this should be replenished, as appropriate.

Ovid purportedly wrote, “medications sometimes heal, sometimes kill.” This is certainly true regarding wound healing. Corticosteroids blunt the processes of the entire inflammatory phase. Vitamin A (topically or 25,000 IU/d orally) mitigates the detrimental healing effects of corticosteroids, but hepatotoxicity may result from prolonged use (ie, >1 mo). Nonsteroidal antiinflammatory medications (NSAIDs) also interfere with arachidonic acid metabolism and, therefore, wound healing. Additionally, NSAIDs inhibit platelet function, one of the earliest processes in the inflammatory phase.

Emerging Trends in Wound Healing

• Hyperbaric oxygen significantly increases the oxygen saturation of plasma, raising the partial pressure available to tissues. Recent Cochrane data analysis concluded that hyperbaric therapy for diabetic foot ulcers can significantly reduce the risk of major amputation, but that for other chronic wounds, the routine application of this therapy is not currently justified.
• Adjuncts to surgical wound debridement can help remove excess fluid from the wound, hastening healing. Negative pressure wound therapy has revolutionized wound care in both civilian and military wounds. Nonmechanical topical products such as cadexomer, which absorbs up to 6 times its own weight in exudate and transudate, serve a similar purpose and have been shown to help accelerate wound closure in chronic lesions.
• Biologically-derived molecules from humans as well as other species may find more clinical applications in the future. Dirhamnolipids are a class of molecules produced by Pseudomonas species that, when applied topically, have been reported to improve healing in chronic wounds in mice and humans.Cell adhesion proteins such as amelogenin, when topically added to compression therapy, appear to promote ulcer healing in the lower extremity.
• Therapies directed at autologous cytokines and enzymes may also prove increasingly fruitful. Metalloproteinases such as ADAM 12 appear to play a regulatory role involving growth factors and are increased in chronic ulcers, leading some to speculate that therapy directed at ADAM 12 may prove useful. Other, systemic molecules, such as angiotensin II, have recently been described as acting on keratinocyte and fibroblast migration through a heparin-binding epidermal growth factor (EGF)-like growth factor, providing another potential future target for intervention.
• Perhaps most intriguing, recent developments in mesenchymal stem cell therapy have been applied to problem wounds with some success, providing injured tissue with pluripotential cells that develop into durable tissue and elaborate growth factors and cytokines. Yoshikawa et al demonstrated wound healing in previously refractory wounds with autologous marrow mesenchymal stem cells implanted in a collagen dermal substitute for human burn, pressure, and venous ulcers.Therapy with genes encoding for growth factor and/or cytokines used independently or with stem cells may also eventually prove to be useful in treating wounds resistant to more traditional approaches; Branski et al provide a lucid outline of these technologies.