Contact Hours: 2
This online independent study activity is credited for 2 contact hours at completion.
Course Purpose
The purpose of this course is to provide a brief overview of the types and stages of wounds, their causes, and possible treatment options.
Overview:
Wound healing is a natural physiological reaction to tissue injury. It is a complex, dynamic process supported by a myriad of cellular events that must be tightly coordinated to efficiently repair damaged tissue. Derangement in wound-linked cellular behaviors, as occurs with diabetes and aging, can lead to healing impairment and the formation of chronic, non-healing wounds. The effective management of wounds is complex, and to maximize outcomes for patients, it is recommended that those involved in their care and treatment have the appropriate knowledge and skills to adequately treat wounds.
Course Objectives:
Upon completion of this course, the learner will be able to:
- Review the stages of wound healing
- Identify symptoms of wound infection
- Relate causes of wounds to the various wound types
- Describe available treatment options for wounds
- Differentiate between the various wound types
Policy Statement
This activity has been planned and implemented in accordance with the policies of FastCEForLess.com.
Disclosures
The planning committee of Fast CE For Less, Inc and its authors have no disclosures. There is no commercial support.
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To access Wounds: Stages of Healing, purchase this course or a Full Access Pass.
If you already have an account, please sign in here.
| Von Willebrand Factor | A blood disorder in which the blood does not clot properly. |
| Subendothelial Matrix | A complex of many materials, most important related to coagulation being collagen and von Willebrand factor. |
| Thrombin | A proteolytic enzyme that is formed from prothrombin and facilitates the clotting of blood |
| Inflammation | A localized physical condition in which part of the body becomes reddened, swollen, hot, and often painful, especially as a reaction to injury or infection. |
| Hemostasis | The stopping of a flow of blood. |
| Chemotaxis | Orientation or movement of an organism or cell in relation to chemical agents. |
| Thrombocytes | Also called platelets, are cell fragments which circulate within the blood with a life span of about 10 days. |
| Fibroblasts | A type of cell that contributes to the formation of connective tissues. |
| Angiogenesis | The growth of blood vessels from the existing vasculature. |
| Glycosaminoglycan | A type of long, unbranched polysaccharide molecule. |
| Angiogenesis | The growth of blood vessels from preexisting blood vessels. |
| Neovascularization | The development of new blood vessels, especially in tissues where circulation has been impaired by trauma or disease. |
| Wound | An injury to living tissue caused by a cut, blow, or other impact, typically one in which the skin is cut or broken. |
| Chronic Wound | A wound that fails to progress through a normal, orderly, and timely sequence of repair. |
| Proliferation | Rapid reproduction of a cell. |
| Dermal Remodeling | A series of skin treatments to restore skin health |
| Ulcer | An open sore on an external or internal surface of the body, caused by a break in the skin or mucous membrane that fails to heal. |
| Debridement | The removal of damaged tissue or foreign objects from a wound. |
| Growth Factors | A substance, such as a vitamin or hormone which is required for the stimulation of growth in living cells. |
A wound disrupts the normal structure and function of the skin and soft tissue architecture.1 It can be described as damage or injury to the living tissue due to multiple agents.2 There are different types of wounds caused by different agents, and wounds can vary in severity.2 For instance, an acute wound demonstrates normal physiology, and healing is anticipated to progress through the expected stages of wound healing, whereas a chronic wound is broadly defined as one that is physiologically impaired.1
To ensure proper healing through the expected stages, the wound base should be well vascularized, free of devitalized tissue, clear of infection, and moist.2 Moreover, providing care for chronic wounds involves a team of multiple professionals, including nurses.3 Thus, nurses must be well-versed in chronic wound care and management.
This course will cover the different types and stages of wounds and the effective treatment strategies available.
Wounds are classified into several types depending on the healing time and the management required by healthcare professionals.9 Depending on the cause, site, and depth, a wound can be acute or chronic.9 Below is a comparison of the different types of wounds.
Table 5: Types of Wounds
| Type | Description |
| Open wounds | Wounds with exposed underlying tissue/ organs and open to the outside environment, for example, penetrating wounds.9 Sub-classification of open wounds: Lacerations Punctures Abrasions Avulsion Perforations |
| Closed wounds | Wounds that occur without a loss of superficial surface covering the wound. Infection of such wounds is rare; if it isn’t extensive, treatment is not required.2 Examples include contusions, seromas, and blisters. |
| Internal wounds | Internal wounds can be due to impaired circulation, nervous system functions, neuropathy or medical illness, or decreased supply of blood, oxygen, or other nutrients.9 |
| External wounds | External wounds can be due to an outside force or trauma caused by penetrating objects or non-penetrating trauma.9 |
| Acute | An acute wound is defined as a recent wound that has yet to progress through the sequential stages of wound healing.10 |
| Chronic | Wounds that have not progressed through the normal healing process and are open for more than a month are classified as chronic wounds. Patients suffering from diabetes and obesity are at a high risk of developing chronic wounds.8 |
The Center for Disease Control has also classified wounds based on the contamination statuses to ensure cleanliness and conditions of the wounds and offer appropriate treatment.11
Table 6: Types of Wounds Based on Contamination 2,11
| Class | Wound type | Description |
| Class I | Clean | They are uninfected, no inflammation is present, and are primarily closed. Minimal risk of infection (1-2% infection rate). No need to use antibiotics except in immunosuppressed patients or patients having a prosthetic heart valve. |
| Class II | Clean-Contaminated | Class 2 wounds enter the respiratory, alimentary, genital, or urinary tracts under controlled conditions. Low risk of infection (<10% infection rate). Prophylactic treatment with antibiotics is required. |
| Class III | Contaminated | Fresh, open wounds can result from insult to sterile techniques or leakage from the gastrointestinal tract into the wound. High rate of infection (15-20% infection rate). Therapeutic antibiotics aimed at treatment and not prophylaxes are given. |
| Class IV | Infected | Typically results from improperly cared for traumatic wounds. Demonstrate devitalized tissue, most commonly resulting from microorganisms present in perforated viscera or the operative field. Very high risk of infection (>40% infection rate). |
Wound healing is a natural physiological reaction to tissue injury.16 It is a complex, dynamic process supported by a myriad of cellular events that must be tightly coordinated to efficiently repair damaged tissue.17 Derangement in wound-linked cellular behaviors, as occurs with diabetes and aging, can lead to healing impairment and the formation of chronic, non-healing wounds.17
Chronic wounds are a significant socioeconomic burden due to their high prevalence and recurrence.17 Thus, there is an urgent requirement for an improved biological and clinical understanding of the mechanisms that underpin wound repair.17
The skin acts as a primary defense barrier, preventing desiccation and mechanical, chemical, thermal, and photic damage to internal structures.17 The skin also has efficient mechanisms to close breaches to its barrier in a process collectively known as the wound healing response.17
Overall, the wound healing process is classically simplified into four main phases: hemostasis, inflammation, proliferation, and dermal remodeling.17
Hemostasis
When an injury occurs, the initial phase is always an outpouring of lymphatic fluid and blood. It is during this process that adequate hemostasis is achieved.16 Both the extrinsic and intrinsic coagulation pathways are activated and play a role in stopping blood loss.16 Platelets, principal contributors to hemostasis and coagulation, are activated when they encounter the vascular subendothelial matrix.17 Platelet receptors (glycoprotein VI) interact with extracellular matrix (ECM) proteins (fibronectin, collagen, and von Willebrand factor), promoting adherence to the blood vessel wall.17
Thrombin subsequently triggers platelet activation, inducing a conformational change and release of alpha and dense granules containing bioactive molecules, which reinforce coagulation. An insoluble clot (eschar) of fibrin, fibronectin, vitronectin, and thrombospondin forms, primarily plugging the wound and preventing bleeding.17
Once a sufficient clot has formed, the coagulation process is switched off, preventing excessive thrombosis.17
Inflammation
The inflammatory phase begins with hemostasis and chemotaxis. Both the white cells and thrombocytes speed up the inflammatory process by releasing more mediators and cytokines.16 Besides the platelet-derived growth factor, other factors promote collagen degradation, the transformation of fibroblasts, the growth of new vessels, and re-epithelialization.16
The processes occur at the same time but in a synchronized fashion.16 For instance, platelets release mediators like serotonin and histamine, increasing cellular permeability. The platelet-derived growth factor attracts fibroblasts and enhances the division and multiplication of fibroblasts along with the transforming growth factor. The fibroblasts, in turn, synthesize collagen.16
Inflammatory cells, such as neutrophils, monocytes, and endothelial cells, adhere to a fibrin scaffold formed by platelet activation. The neutrophils enable the phagocytosis of cellular debris and bacteria, allowing for decontamination of the wound.16
Proliferation
The proliferation or granulation phase does not occur at a discrete time but is ongoing all the time in the background.16 It is characterized by extensive activation of keratinocytes, fibroblasts, macrophages, and endothelial cells to orchestrate wound closure, matrix deposition, and angiogenesis.17 The process is as follows:16
- By days 5 through 7, the fibroblasts have started to lay down new collagen and glycosaminoglycans. These proteoglycans form the core of the wound and help stabilize the wound.
- Then, re-epithelialization starts to occur with the migration of cells from the wound periphery and adjacent edges.
- Next, neovascularization occurs through both angiogenesis, forming new blood vessels from existing vessels, and vasculogenesis.
- Once collagen fibers have been laid down on the fibrin framework, the wound starts to mature. The wound also begins to contract and is facilitated by the continued deposition of fibroblasts and myofibroblasts.
Dermal Remodeling
Remodeling of the extracellular matrix spans the entire injury response, beginning with the initial deposition of a fibrin clot, and ending several months later with the formation of a mature, type I collagen-rich scar.17 Thus, it starts at around week 3 and can last up to 12 months.16 In this phase, the excess collagen degrades, and wound contraction also peaks around week 3. Wound contraction occurs much more in secondary healing than in primary healing.16 The maximal strength of the wound occurs after about 11 to 14 weeks. The ultimate resulting scar will never have 100% of the original strength of the wound.16
An improper repair process can cause severe damage like the loss of skin and initiation of infection, with consequent harm to the neighboring and deep tissues.18
The most common and inevitable prevention to wound healing is infection, mostly in the cases of chronic wounds.18 Although bacteria are a common part of the intact skin microbiota and wounds, a critical threshold of existing bacteria and biofilm formation may impede wound healing.18
Due to these circumstances, regardless of recent progress in the management of wounds, bacterial and fungal infections are still considered one of the most collective and painful states which lead to significant mortality and morbidity.18
Some prevailing microbial strains that occur in patients with infected wounds include S. aureus, methicillin-resistant, S. aureus (MRSA), and Pseudomonas aeruginosa.18
How Wound Infection Occurs
As soon as the skin is impaired, typical microorganisms of the normal skin flora and exogenous bacteria and fungi can soon access underlying tissues, which offers a humid, warm, and nutrient-rich environment for their development.18 However, when the healing is delayed, the normal microbiota of the wound changes and more aggressive microbial types are hosted. Therefore, an open wound can be a favorable place for microbial proliferation and colonization.18
An infection at a wound site starts with contamination and continues with (acute) colonization and wound infection.18 Neither contamination nor colonization of a wound initiates an immune response, but with the invasion of healthy tissues by microorganisms, a cascade of local and systemic host reactions is created, for instance, purulent expulsion, spreading erythema, or symptomatic cellulitis.18 An infected wound can lead to other symptoms, such as:19
- Aches and pains
- Fever and chills
- Nausea and vomiting
- Red streaks on the skin around the wound
- Unpleasant odor
- Warm skin around the wound
- Yellow or green discharge
Wounds can be internal or external, acute or chronic, and are caused by different agents.4 Wounds of internal origin mainly result from impaired circulation, neuropathy, or medical illness. Wounds of external origin may be caused by an outside force or trauma that causes open or closed wounds.4 Belownis a summary of the causes of internal and external wounds.
Table 1: Causes of Internal Wounds4
| Cause | Description |
| Impaired circulation | Can be caused by either ischemia or stasis. Ischemia results from reduced blood supply caused by the narrowing or blockage of blood vessels. Stasis is caused by immobilization for long periods or failure of the regulating valves in the veins, which leads to blood pooling and failing to flow normally to the heart. |
| Medical illness | Chronic medical illnesses like hypertension, hyperlipidemia, atherosclerosis, AIDS, diabetes, etc., can lead to immune system impairment, diminished circulation, and damaged organs. |
| Neuropathy | Neuropathy refers to nerve damage that leads to loss of sensation in the affected area. Wounds usually develop in patients with prolonged uncontrolled diabetes mellitus, where high blood sugars, derivative proteins, and metabolites accumulate and damage the nervous system, and the patient is unaware of the wounds or trauma. |
Table 2: Causes of External Wounds4
| Causes | Description |
| Contusions | Contusions are common sports-related injuries or bruises in active patients. It is caused by a direct blow to the body, which can damage the outer surface or the inner tissue, depending on the force and severity. |
| Crush injuries | Any external force that crushes a body part between two surfaces. It can either be a minor bruise or complete damage to the affected area. |
| Hematomas | Hematomas usually present as a painful, spongy rubbery lump-like lesion. Includes any injury that damages the small blood vessels and capillaries, resulting in blood collecting and pooling in a limited space. |
| Lacerations | Tear-like wounds with irregularly torn edges that are usually deeper than abrasions and cause more pain and bleeding. Caused by trauma or contact with an object. |
| Abrasions | Classified as shallow irregular wounds of the upper skin layers due to brushing against either a rough surface or a smooth surface at high speed. |
| Punctures | Small, rounded wounds that result from objects with thin pointed tips, such as needles, nails, or teeth. |
| Incisions | Likely the result of a surgical procedure or skin cut with a sharp object such as a scalpel or knife. Incisions are mostly linear in shape with smooth, even edges. Could cause serious damage if major blood vessels or vital organs are involved. |
Table 3: General Causes of Wounds
| Cause | Description |
| Mechanical agents | Any external mechanical force that causes injury to the tissue. When a mechanical force acts on tissue and causes injury with the wound remaining closed, it is said to be a contusion; when a mechanical force causes an open wound, then such an injury is called a laceration. |
| Chemical agents | Corrosive or poisonous liquids and gases that damage the tissues. Examples include snake bites, hydrochloric acid (HCL), sodium hydroxide, etc. |
| Radiant agents | Radiant agents like X-rays, atomic energy, heat, high voltage electricity, and intense cold can lead to tissue necrosis. |
| Biological agents | Biological agents or pathogenic microorganisms invade already existing wounds and cause extensive tissue damage. They use toxins to dissolve tissue and cause hypersensitive reactions. |
When discussing the causes of wounds, it is best to discuss chronic wounds separately. A chronic wound fails to progress through a normal, orderly, and timely sequence of repair, or in which the repair process fails to restore anatomic and functional integrity after three months.5 Some chronic wounds can take decades to heal, thus contributing to secondary conditions such as depression, ultimately leading to isolation and family distress.5
Note that all wounds have the potential to become chronic wounds.5 They are classified into four categories, each with its own typical location, depth, and appearance: arterial, diabetic, pressure, and venous ulcers.5
Table 4: Types of Chronic Wounds
| Wound type | Description |
| Venous ulcer | Venous leg ulcer is a chronic sore that develops inside the leg, above the ankle, and takes around 2 weeks to heal.6 It develops after a minor injury, where persistently high pressure in the veins of the legs has damaged the skin.6 |
| Diabetic ulcer | It is a complication of diabetes mellitus, which leads to increased overall morbidity in patients.7 There are three types of diabetic foot ulcer described, namely neuropathic, neuro-ischemic, and ischamic.7 |
| Pressure ulcer | Pressure, or pressure in combination with shear and/or friction, promotes the development of localized ulcers called pressure ulcers (PUs).8 The incidence of PU increases with age and is promoted by a lack of skin perfusion, moisture, and nutrition.8 |
| Arterial ulcer | Arterial ulcers are typically located on the distal extremities and may be deep, with tendon or bone exposed.5 |
Wound healing has been under the aegis of basic nursing practices, such as wound covering management, therapeutic nutrition, mobility, and psychosocial support.8 Thus, nurses play a critical role in treating and managing acute and chronic wounds.8
Initially, all chronic wounds should be treated according to the TIME principle: tissue debridement (in all cases except arterial ulcers), infection control, moisture balance, and wound edges.5 After these general measures are addressed, the ulcer must be correctly diagnosed and classified so that appropriate care can be provided.5 The aim of wound management is to prevent complications by converting contaminated wounds into clean wounds.2
Wound Debridement
Debridement, the removal of damaged tissue from a wound, is the first line of care for chronic wounds.5 Debridement is also useful for wounds that have devitalized tissue, contamination, or residual suture material.1 The procedure includes irrigating the wound with normal saline or clean water with a soapy antiseptic to remove ingrained pieces.2
Bleeding from the surface of the wound commonly occurs during debridement.1 Bleeding can impair the ability to visualize tissue in need of debridement. If bleeding occurs after a dressing is removed, the bleeding should be stopped before starting debridement.1
There are several different types of debridement: surgical, autolytic, enzymatic, and biologic.5
Table 7: Types of Debridement
| Type | Characteristics |
| Surgical | Sharp excisional debridement uses a scalpel or other sharp instruments (e.g., scissors or curette) to remove devitalized tissue and accumulated debris (biofilm).1 Most appropriate choice for removing large areas of necrotic tissue and where there is any evidence of infection.1 |
| Autolytic | Autolytic debridement is the lysis, or breakdown, of damaged tissue at a wound site by the body’s natural defense system by enzymes that digest specific components of body tissues or cells, e.g., proteins, fibrin, and collagen.12 |
| Enzymatic | Enzymatic debridement involves applying exogenous enzymatic agents to the wound.1 Good option for patients that require debridement but are not surgical candidates.1 |
| Biologic | An additional method of wound debridement that uses the larvae of the Australian sheep blowfly (Lucilia [Phaenicia] cuprina) or green bottle fly (Lucilia [Phaenicia] sericata, Medical Maggots.1 Maggot therapy reduces the duration of antibiotic therapy in some patients.1 |
Wound Packing
Wound packing is considered basic standard care.1 It is associated with significant dead space or undermining and is important to reduce physiological dead space, absorb exudate/seroma collection, and reduce the potential for infection.1 Undermined wounds are those that have large soft-tissue defects and may have an area of dead space between the surface of intact, healthy skin and the wound base.1
Moreover, packing can also be an effective temporary dressing technique between planned serial debridements.1 A traditional gauze dressing is often used to pack wounds to aid in continuing debridement of devitalized tissue from the wound bed. The gauze is moistened with normal saline or sterile water, placed into the wound, and covered with dry layers of gauze. As the moistened gauze dries, it adheres to surface tissues, which are then removed when the dressing is changed.1
Moisture Control
Moisture control is also an essential part of wound care, as moist wounds have the potential to heal quicker and have less risk of infection.5 In addition to faster wound healing, wounds treated with occlusive dressings are associated with less prominent scar formation.1
If a wound appears dry, moisture should be added, which can be accomplished by choosing an appropriate dressing.5 Conversely, if a wound is draining, the drainage should be controlled and kept off the wounds surrounding areas. The proper dressing should hold the moisture on the wound bed to prevent desiccation.5
Wound Dressing
A wound dressing that is correctly applied and changed frequently can significantly impact the speed of wound healing, the strength and function of the repaired skin, and the cosmetic appearance of the resulting scar.1 No single wound dressing is perfect for all wound types; thus, the selection is made on a case-by-case basis.1
General wound dressing principles for acute and chronic wounds include hydrogels for the debridement stage, low-adherent dressings that maintain moisture balance for the granulation stage, and low-adherent dressings for the epithelialization stage.1
Table 8: Wound Dressings5
| Wound Appearance | Dressing Type |
| Draining | Calcium alginate Composite Foam Collagen Hydrocolloid for mild to moderate drainage |
| Necrotic | Hydrocolloid (autolytic debridement) Honey impregnated (autolytic debridement) Maggots (biologic debridement) Collagenase (enzymatic debridement) |
| Infected/Inflamed | Silver impregnated Cadexomer iodine Polyhexamethylene biguanide |
| Nondraining/Dry | Composite Hydrogel Hydrocolloid Transparent film Collagen gel |
An ideal dressing has the following characteristics:1
- Absorbs excessive fluid
- Maintains a moist environment
- Debrides necrotic tissue
- Protects the wound from further damage
- Minimizes dressing changes
- Eliminates dead space that conforms to the wound shape
- Is transparent and allows easy monitoring
- Prevents bacterial invasion or proliferation
There are several other therapies that help improve wound healing.1 The following topical therapies are performed after appropriately addressing debridement of necrotic tissue, pressure offloading, infection, and ischemia.1
Antiseptics and Antimicrobial Agents
If a wound has already become infected, antibiotics or antiseptics should be used to kill or slow the growth of the micro‐organisms causing the infection and prevent it from getting worse or spreading.14 They also help heal the wound by reducing the population of microorganisms present in the wound.14
The five broad classes of topical antimicrobial agents currently used in chronic wounds with superficial critical colonization include Polyhexamethylene biguanide (PHMB), ionized silver, slow-release iodine, methylene blue, gentian violet, and honey.13
Iodine-Based
The role of iodine in wound care is primarily as an antimicrobial agent.15 The microbicidal activity of iodine appears to involve the inhibition of vital bacterial cellular mechanisms and structures and oxidizes nucleotides and fatty/amino acids in bacterial cell membranes.15
Cadexomer iodine (Iodosorb) is an antimicrobial that reduces bacterial load within the wound and stimulates healing by providing a moist wound environment.1 It has higher healing rates but should only be used for the short-term or until the symptoms subside.1
Silver-Based
Many clinicians use silver-based dressings to decrease heavy bacterial surface contamination.1 However, silver-containing dressings have not demonstrated significant benefits in comparison with other topical wound dressings, even though silver is toxic to bacteria.1
Honey
Honey has broad-spectrum antimicrobial activity due to its high osmolarity and high concentration of hydrogen peroxide.1 Medical-grade honey products are now available as a gel, paste, and impregnated into adhesive, alginate, and colloid dressings.1 However, sufficient evidence is unavailable to ensure that honey is suitable for all wound types. For instance, it might be beneficial for burn wounds but not for chronic venous ulcers.1
Beta Blockers
Keratinocytes have beta-adrenergic receptors, and beta blockers may influence their activity and increase the rate of maturation and migration.1
Growth Factors
Platelet-derived growth factor (PDGF), fibroblast growth factor (FGF), granulocyte-macrophage colony-stimulating factor (GM-CSF), etc., are important growth factors for wound healing.1 Platelet-derived growth factor (PDGF) promotes cellular proliferation and angiogenesis and thereby improving wound healing.1 Becaplermin is a PDGF gel that is approved for use in the United States as an adjuvant therapy for the treatment of diabetic foot ulcers and is the only pharmacological agent approved for the treatment of chronic wounds.1
Despite the obvious advantages, some healthcare professionals do not always appreciate the link between nutrition and wound healing, and the patient’s diet is often not considered until their wound becomes infected or fails to heal in a timely manner.20
In recent years, several lines of evidence have pointed out the biochemical and molecular effects of several nutrients in the wound healing process, supporting the notion that a complementary nutritional approach may be useful in wound treatment, especially for chronic non-healing wounds.21
Vitamins
Successful activation of the clotting cascade and formation of the fibrin clot during hemostasis requires calcium and vitamin K. It is required to modify some proteins used for coagulation and bone metabolism.20
Vitamin A is also important during the early inflammatory response and is required for migrating macrophages, monocytes, and fibroblasts, but too much vitamin A causes various metabolic changes in the skin, such as roughness and scaling, as well as weakening the hair.20
Vitamin E is also essential for the stability of cell walls, and deficiency can expedite the death of blood cells.20
Amino Acids
Arginine is an amino acid that is not essential in a healthy individual, but its metabolic demand increases during surgery, trauma, and in psychologically stressful circumstances, which often involve a wound.20
Moreover, glutamine, the most abundant amino acid in the blood, provides a source of glucose preferred as an energy source by white blood cells and is required for the glutathione antioxidant used in healing.20 It is crucial for stimulating the inflammatory response.20
Vitamin B Complex
Vitamin B complex supports the metabolic rate and promotes cell proliferation.20 Some dieticians have suggested providing 200% of the recommended daily amount of vitamin B complex for patients with wounds.20
Amino Acids
Amino acids are essential for the successful progression of this phase of healing.20
- Arginine aids the modulation of collagen deposition, enhances angiogenesis, and has a role in wound contraction.
- The amino acids cysteine and proline adversely affect some processes, such as neoangiogenesis (the formation of new blood vessels in tumors) and collagen synthesis.
Minerals
Zinc is involved with cell proliferation and is therefore necessary for proliferation when the wound is rebuilding itself.20 Moreover, the role of iron in preventing anemia is well understood. However, iron’s role in forming hemoglobin also means that it has a key role in optimizing tissue perfusion, which is important throughout the healing process.20
Other Considerations
- Vitamin C (ascorbic acid) is required in the synthesis of collagen and stabilizes the triple helix structure of collagen.20
- Vitamin E is used in many skin moisturizer products and is believed to have a role in reducing scar formation.20
- Arginine can aid the regulation of collagen deposition.20
- Glutamine supplements have been shown to improve wound strength and increase levels of mature collagen.20
- Zinc is a cofactor in collagen synthesis and has a role in collagen maturation.20
Lastly, the importance of water to wound healing is often overlooked. Water provides a structural component in the cytoplasm of skin cells as well as an environmental component, allowing the migration and maturation of epidermal cells.20
As soon as the skin is impaired, typical microorganisms of the normal skin flora and exogenous bacteria and fungi can soon access underlying tissues, which offers a humid, warm, and nutrient-rich environment for their development, and the formation of a wound. The presence of a wound represents a considerable burden in terms of economic cost to health organizations and impact on the patient’s quality of life, as any acute wound can become chronic.
All chronic wounds should be treated according to the TIME principle: tissue debridement (in all cases except arterial ulcers), infection control, moisture balance, and wound edges. Antibiotics or antiseptics should also be considered to kill or slow the growth of the micro‐organisms causing the infection. In addition to antibiotic therapy, a diet rich in vitamins and minerals should be consumed by the patient to improve wound healing. The effective management of wounds is complex, and to maximize outcomes for patients, nurses must have knowledge and skills to adequately treat wounds.22
- Samaneh Online Medilib. www.medilib.ir. https://www.medilib.ir/uptodate/show/15912
- Wounds: Types, Classification of wounds, Treatment and Wound care. Jotscroll. Published 2018. https://www.jotscroll.com/forums/11/posts/171/wounds-types-classification-of-wounds-treatment-and-wound-care.html
- Kielo E, Suhonen R, Salminen L, Stolt M. Competence areas for registered nurses and podiatrists in chronic wound care, and their role in wound care practice. Journal of Clinical Nursing. 2019;28(21-22):4021-4034. doi:10.1111/jocn.14991
- Causes of Wounds. Woundcarecenters.org. Published 2014. https://www.woundcarecenters.org/article/wound-basics/causes-of-wounds
- Bowers S, Franco E. Chronic Wounds: Evaluation and Management. American Family Physician. 2020;101(3):159-166. Accessed October 31, 2022. https://www.aafp.org/pubs/afp/issues/2020/0201/p159.html#causes-of-chronic-wounds
- NHS Choices. Overview – Venous leg ulcer. NHS. Published January 11, 2019. https://www.nhs.uk/conditions/leg-ulcer/
- Packer CF, Manna B. Diabetic Ulcer. PubMed. Published 2020. https://www.ncbi.nlm.nih.gov/books/NBK499887/
- Sen CK. Human Wounds and Its Burden: An Updated Compendium of Estimates. Advances in Wound Care. 2019;8(2):39-48. doi:10.1089/wound.2019.0946
- Different Types Of Wounds – Wound Care Surgeons. https://www.woundcaresurgeons.org. Accessed October 31, 2022. https://www.woundcaresurgeons.org/blogs/know-about-different-types-of-wounds#:~:text=Open%20wounds%20are%20the%20wounds
- Acute Wound – an overview | ScienceDirect Topics. Sciencedirect.com. Published 2014. https://www.sciencedirect.com/topics/engineering/acute-wound
- Herman TF, Bordoni B. Wound Classification. PubMed. Published 2020. https://www.ncbi.nlm.nih.gov/books/NBK554456/
- Choo J, Nixon J, Nelson A, McGinnis E. Autolytic debridement for pressure ulcers. Cochrane Database of Systematic Reviews. Published online June 17, 2019. doi:10.1002/14651858.cd011331.pub2
- Maliyar K, Mufti A, Sibbald RG. The Use of Antiseptic and Antibacterial Agents on Wounds and the Skin. Local Wound Care for Dermatologists. Published online 2020:35-52. doi:10.1007/978-3-030-28872-3_5
- Norman G, Dumville JC, Mohapatra DP, Owens GL, Crosbie EJ. Antibiotics and antiseptics for surgical wounds healing by secondary intention. Cochrane Database of Systematic Reviews. Published online March 29, 2016. doi:10.1002/14651858.cd011712.pub2
- Bigliardi PL, Alsagoff SAL, El-Kafrawi HY, Pyon JK, Wa CTC, Villa MA. Povidone iodine in wound healing: A review of current concepts and practices. International Journal of Surgery. 2017;44:260-268. doi:10.1016/j.ijsu.2017.06.073
- Wallace HA, Zito PM. Wound Healing Phases. Nih.gov. Published January 19, 2019. https://www.ncbi.nlm.nih.gov/books/NBK470443/
- Wilkinson HN, Hardman MJ. Wound healing: cellular mechanisms and pathological outcomes. Open Biology. 2020;10(9):200223. doi:10.1098/rsob.200223
- Negut I, Grumezescu V, Grumezescu A. Treatment Strategies for Infected Wounds. Molecules. 2018;23(9):2392. doi:10.3390/molecules23092392
- Infected wound: Recognition, treatment, and when to see a doctor. www.medicalnewstoday.com. https://www.medicalnewstoday.com/articles/325040#treatment
- Bishop A, Witts S, Martin T. The role of nutrition in successful wound healing. JCN. 2018;4(32).
- Barchitta M, Maugeri A, Favara G, et al. Nutrition and Wound Healing: An Overview Focusing on the Beneficial Effects of Curcumin. International Journal of Molecular Sciences. 2019;20(5):1119. doi:10.3390/ijms20051119
- Welsh L. Wound care evidence, knowledge and education amongst nurses: a semi-systematic literature review. International Wound Journal. 2017;15(1):53-61. doi:10.1111/iwj.12822
- Peate I, Stephens M. Wound Care at a Glance. John Wiley & Sons, Incorporated; 2020.
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