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Wound Care Management

R.Senthil Kumar, Assistant Professor (SRG), KCT,Coimbatore-49.

A wound is defined as a break in the epithelial integrity of the tissues. This disruption can be deeper and involve subepithelial tissues including dermis, fascia and muscle. A wound is caused by physical trauma where the skin is torn, cut or punctured (an open wound), or where a blunt force trauma causes a contusion (a closed wound).

Surgical wound

Nature of

Epithelilising wound


granulating wound

Black nacrotic wound Infected wound

Types of wound
Wounds can be classified in many ways, by acute or chronic, by cause (e.g., pressure, trauma, venous leg ulcer, diabetic foot ulcer), by the depth of tissue involvement, or other characteristics such as closure (primary or secondary intention).

Acute wound
An acute wound is defined as a recent wound that has yet to progress through the sequential stages of wound healing. An acute wound is acquired as a result of an incision or trauma and heals in a timely and orderly manner. Surgically created wounds include all incisions, excisions, and wounds that are surgically debrided. Surgical wounds include all skin lesions that occur as a result of trauma (e.g. burns, falls), as a result of an underlying condition (e.g. leg ulcers), or as a combination of both.

Chronic wounds
Wounds that fail to heal in an anticipated time frame and orderly fashion and often recur are considered chronic. Venous leg ulcers, pressure ulcers and diabetic foot ulcers are some examples of chronic wounds.

Open and closed wounds

Open wounds: examples include incision or incised wounds, laceration, abrasions, punctured wounds and penetrating wounds. Closed wounds: examples haematoma and crush injuries. include contusions,

Bacterial level vs. Wound state

Bacteria on the surface

Bacteria attach tio tissue and colonize

Bacteria invade healthy tissues and overhelm immune response

Mechanism of wound healing

The aim of wound healing is homeostasis and restoration of tissue integrity. It is a well-orchestrated and complex process which is triggered by tissue injury and ends by regeneration or repair.

Mechanism of wound healing

1.Healing by primary intention Wound edges are approximated with sutures, staples or adhesive within hours of its creation with no defect. This enables closure to occur quickly with minimal tissue needed to repair the defect and minimal scarring. 2. Healing by secondary intention The wound is left open and no formal closure is done. Healing occurs by epithelialisation and contraction, e.g. healing associated with a large and/or deep wound in which the tissue edges cannot be approximated.

Mechanism of wound healing

Mechanism of wound healing

3. Delayed primary/tertiary healing Wound closure is delayed for several days; this is usually employed for infected wounds. Irrespective of the cause, wounds heal in a very similar fashion.

It is a dynamic and interactive process that involves a variety of blood and parenchymal cells, extracellular matrices and soluble mediators.
During this process, wound healing passes through four phases of haemostasis, infl ammation, proliferation and remodelling.

Mechanism of wound healing

4. Haemostasis The first step in the process (immediate up to 24 h) of inflammation is haemostasis, which is characterized by vasoconstriction and coagulation. It starts soon after injury and is usually completed within the first few hours. Injury to the tissues causes disruption of blood vessels and lymphatic exposing the platelets to fibrin and collagen. This activates the platelets and complement cascade. Platelets also interact with the injured tissue, causing the release of thrombin, which converts soluble, circulating fibrinogen to fibrin, which in turn traps, and activates platelets and forms the physical entity of the hemostatic plug.







Phases of Wound Healing

Scar Tissue

Phases of Wound Healing

I. Inflammatory Phase A) Immediate to 2-5 days B) Hemostasis Vasoconstriction Platelet aggregation Thromboplastin makes clot C) Inflammation Vasodilation

II. Proliferative Phase A) 2 days to 3 weeks

B) Granulation
Fibroblasts lay bed of collagen Fills defect and produces new capillaries C) Contraction Wound edges pull together to reduce defect D) Epithelialization Crosses moist surface Cell travel from point of origin in all directions


III. Remodeling Phase A) 3 weeks to 2 years B) New collagen forms which increases tensile strength to wounds C) Scar tissue is only 80 percent as strong as original tissue

Inflammatory Phase
The stage of inflammation starts soon after haemostasis (immediate up to 25 days) and is usually completed within the first 48 to 72 h but it may last as long as 5 to 7 days. The initial vasoconstriction is followed by vasodilatation and increased vascular permeability in response to histamine and other vasoactive mediators.

Role of neutrophils The net result of this change in vascular permeability is an influx of polymorphonuclear cells (PMN) and monocytes in the injured area in a protein-rich fluid. Neutrophils phagocytise debris and bacteria, they also kill bacteria by releasing caustic proteolytic enzymes and free radicals in a process called respiratory burst.

Biology of Wound Healing

The activated platelet releases cytokines and growth factors including thromboxane A-2 and serotonin which are important inflammatory mediators and also cause vasoconstriction.
The clot also serves to concentrate the elaborated cytokines and growth factors including platelet-derived growth factor (PDGF) and transforming growth factor (TGF) 1. Coagulation leads to hemostasis, which initiates healing by leaving behind messengers that bring on an inflammatory process.

Deficiency of clotting factors (Factor VII. IX, XII) leads to impaired wound healing

Phases of wound repair


Inflammatory Phase
Fibroblast proliferation Endothelial cell proliferation


Extracellular matrix production

Recruitment of macrophages

Macrophages start appearing in the wound two days after the injury and dominate the wound cell population over the next few days. Beside resident macrophages, the majority of macrophages at the wound site are recruited from the blood. Monocytes extravasate from the blood vessel, become activated and differentiate into mature tissue macrophages. Macrophages are crucial to wound healing and perform a number of functions. They act as antigen-presenting cells and remove debris and dead cells by phagocytosis. Perhaps their more important role in the process of healing is synthesis of numerous potent growth factors, such as TGF-, TGF-, basic fibroblast growth factor (bFGF), platelet-derived growth factor, and vascular endothelial growth factor, which promote cell proliferation and the synthesis of extracellular matrix molecules by resident skin cells.

Role of inflammatory mediators

Inflammatory mediators play a central and major role in the process of wound healing. They include a collection of soluble factors present either in plasma in an inactive form or released by damaged and nearby cells and leukocytes in an attempt to control the damage and initiate healing.

Mechanisms of inflammatory resolution

Inflammation performs several important functions. It clears the wound of infectious organism and debris, and brings about a change in the micro-environment of the wound to set the stage for proliferation.


Proliferative Phase
(Fibroblastic Phase)

Proliferative Phase
This phase starts around the second or third day after injury and continues for up to 3 or 4 weeks. This is marked by the appearance of fibroblasts in the wound and overlaps with the inflammatory phase.

Granulation tissue formation

Fibroblasts start to appear in the wound from the third to fourth day and their numbers peak between the seventh and fourteenth days. They migrate from the wound margins using the fibrin-based provisional matrix created during the inflammatory phase of healing. Under the influence of bFGF, TGF-, and PDGF secreted by macrophages they proliferate and synthesise glycosaminoglycans and proteoglycans, elastins and fibronectin, the building blocks of the new extracellular matrix of granulation tissue, and collagen.

As the number of macrophages diminishes, fibroblasts themselves begin to secrete bFGF, TGF-, and PDGF. They also begin producing keratinocyte growth factor and insulin like growth factor I. After secretion of collagen molecules, they are organized in the form of collagen fibres which are then cross-linked into bundles. Collagen gives the wound its tensile strength and, in addition, cells involved in inflammation, angiogenesis, and connective tissue construction attach to, grow and differentiate on the collagen matrix laid down by fibroblasts. Collagen deposition increases the tensile strength of the wound.

Angiogenesis accompanies the fibroplasia phase and is essential to scar formation. Cells, when adequately perfused, stop producing angiogenic factors, and migration and proliferation of endothelial cells is reduced

The initial event in epithelialisation is migration of undamaged epithelial cells from the wound margins.

Keratinocytes at the wound edges are stimulated by EGF and TGF- produced by activated platelets and macrophages, they proliferate and begin their migration across the wound bed within 12 to 24 h after injury.
The process of migration continues until the migrating cells from opposing sides of the wound touch each other.

Epithelial cells exhibit contact inhibition migrate across bed until single layer formed

Cells along margin divide to reform mature, multilayered epithelium

About a week after the injury, the fibroblast differentiates into myofibroblasts, pulls the edges of the wound together and the wound begins to contract. Contraction peaks at 5 to 15 days post wounding an continues even after the wound is completely re-epithelialised. Contraction reduces the size of the wound and, thus, reduces the amount of Extracellular Matrix (ECM) needed to fill the wound.

Maturation and Remodeling Phase

Maturing and Remodelling Phase

Maturation and remodelling of the collagen into an organized and well mannered network is the final stage of the healing process (from day 8 upto 2 years). On the other hand, excessive collagen synthesis can lead to the formation of a hypertrophic scar or keloid. The maturation phase can last for two years or longer, depending on the size of the wound and whether it was initially closed or left open. This phase is characterized by the removal of type III collagen and its replacement by mature type I collagen.

Remodelling phase
Remodelling is regulated by fibroblasts through the synthesis of ECM components and MMPs that control cell differentiation. All of these changes produce a cell-deficient environment with excessive connective tissue. Blood vessels that are no longer required die by apoptosis and the remainder acquire a basement membrane and become relatively impermeable.

All of these factors lead to the increase in tensile strength, decrease in erythema and scar tissue bulk, and the final appearance of the healed scar.

Wound Dressing Materials

Ideal Dressing
Removes exudate and toxic components Maintains high humidity at interface Allows gaseous exchange Insulates thermally Protects from secondary infection Allows removal without trauma

Occlusive, adhesive wafers Provides a moist environment For clean wound to granulate For necrotic wound- promote autolytic debridement

Superficial, partial thickness wounds Light to moderate exudate Wounds with slough or necrotic tissue

Method of Use
2 cm margin of the dried surrounding skin is needed for good adhesion

Change frequency
Usually 3- 7 days, depends on the wound condition and exudate

Derived from seaweed soft., non-woven fibres Absorb exudates up to 20 times of their weight Form a soft gel, maintain a moist environment for healing Partial to full thickness wounds Moderate to heavy exudate Cavity or sinus wound Infected wounds


Method of Use
Light exudate- soak with normal saline solution Heavy exudate- put directly

Change frequency
Usually 12 hours to 4 days, depends.

Characteristics / Functions
Alginates are soft non-woven fibers comrising galuronic and mannuronic acid, derived from seaweed. They are usually in the forms of pads, ropes or ribbons. Alginates absorb wound exudate and form a gel-like covering over the wound, maintaining a moist wound environment. Most alginates absorb many times their own weight. The dry dressing, however, is extremely lightweight.

Film Dressing
Adhesive, semi permeable membrane Allow oxygen and water vapour to cross the barrier Impermeable to fluid and bacteria Moist environment to promote granulation

Superficial wounds Light or no exudate Necrotic or sloughy wounds

Change frequency
24 or 72 hours, depends

Hydrogels are water or glycerin-based amorphous gel or sheet dressings Unable to absorb large amounts of exudate

Partial to full thickness wounds Necrotic or sloughy wounds Light to moderate exudate Burns and tissue damage by radiation

Change frequency
Usually 12 to 48 hours, depends


left: The individual macromolecules with their enclosed water molecules are attached by special cross-links to form polymer chains. middle: Uptake of secretions. right: The cross-links are expanded to generate niches for the inclusion of bacteria, secretions, and odour molecules.

Hydrofibre (Aquacel)
Soft, non-woven pad composed of hydrocolloid fibres Hydrophillic action Absorbing exudate vertically and entrapping it in the fibres It forms gel when it interacts with wound exudate Provide moist environment

Light to heavy exudate Dehisced wounds and sinuses Partial thickness burn wound

Change frequency
When saturated Infected wound- daily Non-infected wounds, not more than 7 days

Hydrocolloid Dressings are pectins, gelatins, sodium carboxymethylcellulose soft absorptive, adhesive wafers that become gel-like as they absorb and are best used on lightly to moderately draining wounds. They are waterproof and impermeable to bacteria and contaminates. Easy application. Various thicknesses available. Not recommended for infected wounds.


Hydrocolloid is applied to the wound.

Upon absorption of wound exudates the hydrocolloids present in the dressing begin to swell and transform into a gel.

When the dressing is removed, a protective gel layer remains on the wound that can then be easily rinsed away.


Calcium alginate dressing Hydrogel dressings Hydrocolloid dressing

Sorbalgon is applied in a dry state to cover or lightly pack the wound (1). Upon contact with the secretions from the wound, the fibres transform into a gel, which closely adapts to the wound surface. The lesion is thus filled and maintained in an appropriately moist condition (2). The gelatinous dressing may be removed without traumatisation as one intact gel plug.

Hydrosorb is a ready-to-use gel dressing with a high water content, that from the very beginning ensures excellent moisture supply for the injury (1). The gel is highly absorbent, so that wound exudates are retained in the gel structure. The dressing subsequently begins to swell and fills the wound area without losing its integrity (2). Hydrosorb can be removed without traumatisation as one intact dressing.

Hydrocoll is a selfadhesive elastomer enriched with hydrocolloids that are provided with a considerable swelling activity (1). Upon uptake of secretions, these hydrocolloids transform into a gel that expands into the wound and maintains a moist environment (2). During dressing removal, a protective gel layer remains on the wound that must be rinsed off.

Tulle Gras
As a wound contact layer to reduce the adherence of the dressing to granulating wounds

Minor traumatic injuries, ulcers, burns and skin grafts

Change frequency
Every 12 to 24 hours, depends

Non-adherent dressings (melolin)

Have a plastic film or other non-sticking materials on their contact surface to prevent them from adhering to the wound Plastic film can be perforated to allow the passage of exudate

Dry sutured wounds Superficial cuts Abrasions and lightly exudating lesions

Change frequency
Usually every 2 to 3 days Dry sutured wound for 7 to 10 days