A chronic wound is a wound that does not heal in a series of regular stages and in an estimated amount of time as most wounds do; Injuries that do not heal in three months are often considered chronic. Chronic wounds seem to be retained in one or more wound healing phases. For example, chronic wounds are often in the inflammatory stage for too long. To overcome that stage and boost the healing process, a number of factors need to be addressed such as bacterial load, necrotic tissue, and moisture balance from all wounds. In acute wounds, there is an appropriate balance between the production and degradation of molecules such as collagen; in chronic wounds, this balance is lost and degradation plays an overly large role.
Chronic wounds will never heal or it may take years to do so. These injuries cause severe emotional and physical stressors and create significant financial burdens in the patient and throughout the health system.
Acute and chronic wounds are at opposite ends of the spectrum of wound healing types that develop to heal at different rates.
Video Chronic wound
Signs and symptoms
Chronic wound patients often report pain as dominant in their lives. It is recommended that health care providers handle the pain associated with chronic wounds as one of the top priorities in chronic wound management (together with addressing the cause). Six of ten venous ulcer patients experience pain with their ulcers, and similar trends are observed for other chronic wounds.
Persistent pain (at night, at rest, and with activity) is a major problem for patients with chronic ulcers. Frustration of ineffective analgesics and care plans that they can not adhere to are also identified.
Maps Chronic wound
Cause
In addition to poor circulation, neuropathy, and difficulty moving, factors that contribute to chronic wounds include systemic disease, age, and recurrent trauma. Comorbid diseases that may contribute to the formation of chronic wounds include vasculitis (inflammation of the blood vessels), immune suppression, pyoderma gangrenosum, and the disease that causes ischemia. Immune suppression can be caused by long-term medical illness or drugs, such as steroids. Emotional stress can also negatively affect wound healing, perhaps by increasing blood pressure and cortisol levels, which decreases immunity.
What appears to be chronic injuries may also be malignancy; for example, cancer tissue can grow until blood can not reach cells and tissues become ulcers. Cancer, especially squamous cell carcinoma, can also be formed as a result of chronic wounds, possibly because of recurrent tissue damage that stimulates rapid cell proliferation.
Another factor that can cause chronic wounds is old age. The skin of older people is more easily damaged, and older cells do not proliferate rapidly and may not have adequate response to stress in terms of increased stress-related protein regulation. In older cells, stress response genes are expressed when cells are not stressed, but by then, the expression of these proteins is not regulated by as much on younger cells.
The comorbid factors that can cause ischemia are very likely to contribute to chronic wounds. These factors include chronic fibrosis, edema, sickle cell disease, and peripheral artery disease such as by atherosclerosis.
Recurrent physical trauma plays a role in the formation of chronic wounds by continuing to initiate a cascade of inflammation. Trauma can occur by accident, for example when the leg is repeatedly hit by a wheelchair, or may be due to deliberate action. Heroin users who lose venous access may use 'skin popping', or inject drugs subcutaneously, which is very damaging to the tissues and often leads to chronic ulcers. Children who repeatedly see wounds that do not heal are sometimes found to be victims of parents with Munchausen syndrome by proxies, a disease in which the offender can repeatedly pose a danger to the child to receive attention.
The periwound skin damage caused by excessive amounts of exudate and other body fluids can perpetuate the status of chronic wounds that do not heal. Maseration, excoriation, dry skin (brittle), hyperkeratosis, callus and eczema are often a problem that disrupts the integrity of the periwound skin. They can create a gateway for infection and cause damage to the wound edges preventing wound closure.
Pathophysiology
Chronic wounds may affect only the epidermis and dermis, or they can affect the tissues down to the fascia. They can be formed initially by the same things that cause acute ones, such as surgery or traumatic accidents, or they can be formed as a result of systemic, vascular, immune, or nerve insufficiency, or comorbidities such as neoplasias or metabolic disorders. The reason why the wound becomes chronic is the body's ability to deal with the damage is met by factors such as recurrent trauma, advanced pressure, ischemia, or disease.
Although much progress has been made in recent chronic wound studies, progress in their healing studies has lagged behind expectations. This is partly because animal studies are difficult because animals do not get chronic wounds, because they usually have loose skins that contract rapidly, and they are usually not old enough or have contagious diseases such as neuropathy or a crippling chronic disease. Nonetheless, current researchers now understand some of the major factors that cause chronic wounds, among them are ischemia, reperfusion injury, and bacterial colonization.
Ischemia
Ischemia is an important factor in the formation and persistence of injury, especially when it occurs repeatedly (as usual) or when combined with the patient's old age. Ischemia causes the tissues to become inflamed and the cells to release factors that attract neutrophils such as interleukin, chemokines, leukotrienes, and complementary factors.
While they fight pathogens, neutrophils also release cytokines and inflammatory enzymes that damage cells. One of their important jobs is producing Reactive Oxygen Species (ROS) to kill bacteria, which they use an enzyme called myeloperoxidase. Enzymes and ROS are produced by neutrophils and other leukocyte damage cells and prevent cell proliferation and wound closure by destroying DNA, lipids, proteins, extracellular matrix (ECM), and cytokines that accelerate healing. Neutrophils remain in chronic wounds longer than they do in acute wounds, and contribute to the fact that chronic wounds have higher levels of inflammatory cytokines and ROS. Because the wound fluid from the chronic wound has excess proteases and ROS, the fluid itself can inhibit healing by inhibiting cell growth and break down growth and protein factors in ECM. The healing response of this disorder is considered uncoordinated. However, a dissolved mediator of the immune system (growth factor), cell-based therapy and therapeutic chemicals can propagate coordinated healing.
It has been suggested that the three fundamental factors underlying the pathogenesis of chronic wounds are cellular and systemic changes of aging, recurrent attacks of ischemic-reperfusion injury, and bacterial colonization with the resulting inflammatory host response.
Colonization of bacteria
Because more oxygen in the wound environment allows white blood cells to produce ROS to kill bacteria, patients with inadequate tissue oxygenation, such as those suffering from hypothermia during surgery, are at high risk for infection. The host immune response to the presence of bacteria prolongs inflammation, delayed healing, and tissue damage. Infection can cause not only chronic injuries but also gangrene, loss of infected limbs, and patient death. More recently, the interaction between bacterial colonization and the increase in reactive oxygen species leading to the formation and production of biofilms has been shown to produce chronic wounds.
Like ischemia, bacterial colonization and tissue damage infections by causing more neutrophils to enter the wound site. In patients with chronic wounds, bacteria with resistance to antibiotics may have time to develop. In addition, patients carrying drug-resistant bacterial strains such as methicillin-resistant Staphylococcus aureus (MRSA) have more chronic injuries.
Growth factor and proteolytic enzyme
Chronic wounds are also different in the makeup of acute wounds because of their proteolytic enzyme levels such as elastase. and metalloproteinase matrices (MMPs) are higher, while their growth factor concentrations such as growth factor derived from Platelet and Keratinocyte Growth Factors are lower.
Because growth factors (GFs) are important in timely wound healing, inadequate GF levels may be an important factor in the formation of chronic wounds. In chronic wounds, the formation and release of growth factors can be prevented, factors can be sequestered and unable to perform their metabolic role, or are degraded excessively by cellular or bacterial proteases.
Chronic injuries such as diabetic ulcers and veins are also caused by fibroblast failure to produce adequate ECM proteins and by keratinocytes for wound epithelialization. The expression of the fibroblast gene differs in chronic wounds rather than acute wounds.
Although all injuries require certain levels of elastase and protease for proper healing, too high a concentration is damaging. Leukocytes in the wound area release elastase, which increases inflammation, destroys tissue, proteoglycans, and collagen, and impairs growth factors, fibronectin, and protease inhibiting factors. Elastase activity is increased by human serum albumin, which is the most abundant protein found in chronic wounds. However, chronic wounds with inadequate albumin are highly unlikely to be cured, so adjusting for possible future injury rates of proteins may prove useful in chronic wound healing.
Excess matrix metalloproteinase, released by leukocytes, can also cause wounds to become chronic. MMP breaks down ECM molecules, growth factors, and protease inhibitors, and thus increases degradation while reducing construction, throwing a fine compromise between unbalanced production and degradation.
Diagnosis
Infection
If chronic injuries become more painful, this is a good indication that he is infected. The lack of pain however does not mean that it is not infected. Other determination methods are less effective.
Classification
Most chronic wounds can be classified into three categories: venous ulcers, diabetes, and pressure ulcers. A small number of wounds that do not fall into this category may be due to causes such as radiation poisoning or ischemia.
Venous and arterial ulcers
Venous ulcers, which usually occur in the legs, cause about 70% to 90% of chronic wounds and mostly affect the elderly. They are thought to be due to venous hypertension caused by improper valve functioning in the blood vessels to prevent blood from flowing backwards. Ischemia results from dysfunction and, combined with reperfusion injury, causes tissue damage that leads to injury.
diabetic ulcers
Another major cause of chronic wounds, diabetes, increases in prevalence. Diabetics have a 15% higher risk for amputation than the general population due to chronic ulcers. Diabetes causes neuropathy, which inhibits nociception and pain perception. Thus the patient may initially not see any small cuts on the legs and feet, and therefore fails to prevent infection or recurrent injuries. Furthermore, diabetes causes immune compromise and damage to small blood vessels, preventing adequate tissue oxygenation, which can lead to chronic wounds. Pressure also plays a role in the formation of diabetic ulcers.
Pressure ulcers
Other types of chronic wounds are pressure ulcers, which usually occur in people with conditions such as paralysis that inhibit the movement of body parts that normally experience stresses such as the heel, shoulder blades, and the sacrum. The pressure ulcers are caused by ischemia that occurs when the pressure on the tissue is greater than the pressure in the capillaries, and thus limits blood flow to the area. Muscle tissue, which requires more oxygen and nutrients than the skin, shows the worst effects of prolonged stress. As with other chronic ulcers, reperfusion injuries damage tissues.
Treatment
Although treatments for different types of chronic wounds differ slightly, appropriate treatments seek to address the problem of chronic wound root, including ischemia, bacterial load, and protease imbalance. The periwound skin problems should be assessed and their reduction included in the proposed treatment plan. Various methods exist to correct this problem, including the use of antibiotics and antibacterials, debridement, irrigation, vacuum-assisted closure, heating, oxygenation, wound healing wounds (term pioneered by George D. Winter), eliminating mechanical stress, and adding to cells or other. ingredients to remove or improve the healing factor level.
The challenge of any treatment is to tackle as many of the adverse factors as possible, so that each receives the same attention and does not continue to deter healing during the treatment.
Preventing and treating infections
To reduce the amount of bacteria in the wound, the therapist may use topical antibiotics, which kill the bacteria and can also help by keeping the environment moist, which is important to accelerate the healing of chronic wounds. Some researchers have experimented with the use of tea tree oil, an antibacterial agent that also has anti-inflammatory effects. Disinfectants are contraindicated because they damage tissue and delay wound contractions. Furthermore, they become ineffective by organic matter in wounds such as blood and exudates and are thus useless in open wounds.
A greater amount of exudate and necrotic tissue in the wound increases the likelihood of infection by serving as a medium for bacterial growth away from the host defense. As the bacteria develop in dead tissue, the wound is often surgically removed to remove the tissue that has been destroyed. Debridement and wound fluid drainage are a very important part of the treatment for diabetic ulcers, which can create amputation needs if the infection goes out of control. The removal of mechanical bacteria and devitalized tissue is also the idea behind wound irrigation, which is achieved by using pulsed lavage.
Disposing of unprotected necrotic tissue or tissue is also a goal of maggot therapy, the deliberate introduction of health-care practitioners from diseased live maggots to non-healing wounds. Maggots dissolve only the infected necrotic tissue; disinfect wounds by killing bacteria; and stimulate wound healing. Maggot therapy has been shown to accelerate the debridement of necrotic wounds and reduce the bacterial burden of the wound, leading to previous healing, reducing scarring and reducing pain. The combination and interaction of these actions make maggots a very powerful tool in the treatment of chronic wounds.
Negative wound pressure therapy (NPWT) is a treatment that increases ischemic tissue and removes the wound fluid used by bacteria. This therapy, also known as vacuum-assisted closure, reduces tissue swelling, which brings more blood and nutrients to the area, as well as the negative pressure itself. Treatment also decompresses tissue and changes cell shape, causing them to express different mRNAs and proliferate and produce ECM molecules.
Recent technological advances result in new approaches such as self-adaptive wound dressings that depend on intelligent polymer properties that are sensitive to changes in moisture levels. Dressing provides absorption or hydration as needed above any independent wound area and aids the natural process of autolithic debridement. It effectively eliminates fluid and necrotic tissue, discontinued bacterial biofilms and harmful exudate components, known to slow the healing process. Treatment also reduces bacterial load by effective evacuation and immobilization of microorganisms from the wound bed, and subsequent chemical bonding of available water is necessary for their replication. Adaptive self-dressing protects periwound skin from extrinsic factors and infections while regulating moisture balance over vulnerable skin around the wound.
Treat trauma and painful wounds
Persistent chronic pain associated with non-healing wounds is caused by tissue damage (nociceptive) or nerve (neuropathic) and is affected by chronic dressing and inflammation changes. Chronic wounds take a long time to heal and patients can suffer chronic wounds for years. Chronic wound healing can be compromised by common underlying conditions, such as venous return venous flow, peripheral vascular disease, uncontrolled edema and diabetes mellitus.
If injuries are not assessed and documented they may be ignored and/or not treated properly. It is important to remember that increased wound pain can be an indicator of wound complications requiring treatment, and therefore practitioners should constantly review the wounds and associated pain.
Optimal wound care requires holistic assessment. Documentation of patient pain experience is very important and can range from the use of patient diaries, (which the patient should encourage), to recording the pain completely by a health care professional or caregiver. Effective communication between patient and health team is essential for this holistic approach. The more health care professionals measure the pain, the more likely it is to introduce or change the practice of pain management.
There are currently several local options for the treatment of persistent pain, while managing the level of exudate present in many chronic wounds. An important feature of such local options is that they provide optimal wound healing environments, while providing constant local low-dose ibuprofen release during childhood.
If local treatment does not provide adequate pain reduction, it may be necessary for patients with chronic, chronic wounds to be prescribed additional systemic treatment for the physical components of their pain. Physicians should consult with their prescribing counterpart to refer to the WHO pain relief stairs from systemic treatment options for guidance. For each pharmacological intervention there are potential benefits and side effects to be considered by the doctor prescribed in relation to the wound care care team.
Ischemia and hypoxia
The blood vessels narrow in the tissues that become cold and widen in warm tissue, altering blood flow to the area. Thus keeping warm tissue may be necessary to fight infection and ischemia. Some health care professionals use 'radiation bandages' to keep the area warm, and care should be taken during surgery to prevent hypothermia, which increases the rate of post-operative infection.
Underlying ischaemia can also be treated by surgery by arterial revascularization, for example in diabetic ulcers, and patients with venous ulcers may undergo surgery to improve venous dysfunction.
Patients with non-candidate diabetes for surgery (and others) may also have their tissue oxygenation elevated by Hyperbaric Oxygen Therapy, or HBOT, which can provide short-term improvement in healing by increasing oxygenated blood supply to the wound. In addition to killing bacteria, higher oxygen content in tissues accelerates the production of growth factors, growth of fibroblasts, and angiogenesis. However, increased oxygen levels also mean increased ROS production. Antioxidants, molecules that can lose electrons into free radicals without them being radical, can lower oxidant levels in the body and have been used with some success in wound healing.
Low-level laser therapy has been repeatedly shown to significantly reduce the severity and severity of diabetic ulcers and other pressure ulcers.
Pressure wounds are often a result of local ischemia due to increased pressure. Increased pressure also plays a role in many diabetic foot ulcers because changes due to illness cause the foot to experience limited mobility of the joints and create pressure points on the bottom of the foot. Effective measures to treat this include a surgical procedure called gastrocnemius recession in which the calf muscle is extended to reduce the fulcrum created by this muscle and result in a decrease in plantar foot pressure.
Growth and hormone factors
Because chronic wounds become a growth factor that is not needed for tissue healing, chronic wound healing can be accelerated by replacing or stimulating these factors and by preventing the formation of excessive proteases such as the elastase that damages them.
One way to increase the concentration of growth factors in the wound is to apply the growth factor directly. This usually requires a lot of repetition and requires a large number of factors, although biomaterials are being developed that control the delivery of growth factors over time. Another way is to spread to the gel wound from the patient's own blood platelets, which then secrete growth factors such as vascular endothelial growth factor (VEGF), growth factors such as insulin 1-2 (IGF), PDGF, change-growth factor? (TGF-?), And epidermal growth factor (EGF). Other treatments include implanting cultured keratinocytes into the wound to reepithelialize it and cultivate and implant the fibroblasts into wounds. Some patients are treated with artificial skin substitutes that have fibroblasts and keratinocytes in a collagen matrix to replicate the skin and release growth factors.
In other cases, the skin of the carcass is grafted onto the wound, providing cover to prevent bacteria and prevent the buildup of granulation tissue too much, which can cause excessive scarring. Although the allograft (transplanted skin of members of the same species) is replaced by granulation tissue and is not actually inserted into the healing wound, it encourages cell proliferation and provides structures for epithelial cells to crawl across. In the most difficult chronic wounds, allografts may be malfunctioning, requiring skin grafts from elsewhere in the patient, which can cause further pain and pressure in the patient's system.
Collagen dressing is another way to provide a matrix for cellular proliferation and migration, while also keeping the wound moist and absorbing exudates. In addition Collagen has been proven chemotactic for human blood monocytes, which can enter the wound site and turn into beneficial wound healing cells.
Because protease inhibitor levels are lowered in chronic wounds, some researchers are looking for ways to heal the tissues by replacing these inhibitors in them. Leukocyte protease inhibitor proteins (SLPI), which not only inhibit proteases but also inflammation and microorganisms such as viruses, bacteria, and fungi, may prove to be effective treatments.
Research on hormones and wound healing has shown estrogen to accelerate wound healing in elderly humans and in animals that have excrete their ovaries, perhaps by preventing excessive neutrophils from entering the wound and releasing elastase. Thus the use of estrogen is a possible future for treating chronic wounds.
Epidemiology/More
Chronic injuries mostly affect people over the age of 60. The incidence is 0.78% of the population and prevalence ranges from 0.18 to 0.32%. As people age, the number of chronic injuries is expected to increase. Ulcers that heal within 12 weeks are usually classified as acute, and longer as chronic.
References
Further reading
-
Injury Practice (2nd ed.). Flagstaff, AZ: The Best Publishing Company. ISBN: 978-1-930536-38-8.
External links
- Maggot Therapy Project website at the University of California, Irvine, list of practitioners of maggot therapy
- BioTherapeutics Education and Research Foundation
- Hyde, Cheryl; Ward, Betty; Horsfall, Jan; Hours, Giselle (1999). "The experience of older women living with chronic foot ulcers". Journal of International Nursing Practice . 5 (4): 189-98. doi: 10.1046/j.1440-172x.1999.00170.x. PMID 10839029.
- Accredited and interactive wound care education is offered at no cost
- Awareness campaign website by the Australian Wound Management Association
- The Web site of the European Wound Management Association (EWMA)
Source of the article : Wikipedia
0 Comments