Skin and wound healing

The skin

The skin is the body’s largest organ (15% of its weight) forming a flexible membrane which covers its entire surface. The skin provides the body with protection via its contact with the external environment resisting mechanical, thermal and chemical aggression to a certain extent. The skin also performs, or contributes to, a broad variety of functions such as metabolic, neurological, immunological and temperature regulation.

Anatomy

The skin is composed of three main layers:

anatomy-wound

Epidermis

The outermost layer of the skin, the epidermis forms the body’s external barrier, providing the functions of protection and waterproofing. The thickness of the layer varies depending on the area of the body concerned. On average it is 0.5mm thick but can be as much as 5 mm thick on the soles of the feet.

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epidermisThe epidermis is composed of:  

  • stratum corneum or horny layer
  • stratum germinativum
  • basal layer (basement membrane)

At the basement membrane is a layer of skin cells that is responsible for constantly renewing the epidermal cells. This layer contains just one row of undifferentiated columnar stem cells that divide very frequently. Half the cells differentiate and move to the next layer to begin the maturation process while the other half stays in the basal layer to maintain it.

As cells move into the higher layers of the epidermis, they flatten and begin to produce keratin (keratinocytes) and eventually die.

The cells of the stratum corneum layer are known as corneocytes, they have completely flattened out and are composed mainly of keratin which provides strength to the layer.

Dermis

The dermis is the living layer of the skin and is highly vascularised. Highly vascularised, its role is as supporting connective tissue. It is rich in fibres that make the skin elastic and strong.

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dermisIn this living layer there are:

  • Blood and lymph vessels: ensure the movement of the nutrition and oxygen needed by living cells, removal of waste and migration of antibodies.
  • Hair follicles: produce the hairs that protect the skin surface.
  • Sweat and sebaceous glands: sweat glands help remove waste but also are essential for temperature regulation. Sebaceous glands produce sebum that lubricates and softens the skin.
  • Collagen and elastin fibres: provide respectively, the strength of the skin and its movement.
  • Fibroblasts: these cells produce and secrete procollagen and elastic fibres to form the skin’s structure.
  • Nerves: enable the sensory role of the skin, reacting to heat, cold and pain etc.
  • Macrophages: phagocytic white blood cells that form part of the innate immune system, form part of the body’s primary defence to infection.

Extracellular Matrix (ECM):

Serves many functions, including providing support, segregating tissues from one another and regulating intercellular communication.

Subcutaneous tissue

This is a sliding layer of fat cells, performing transition and storage functions for water and fat. It is in close contact with the underlying layers of muscle.

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subcutaneous-tissue

This subcutaneous connective tissue also houses larger blood vessels and nerves. It is important for temperature regulation of the skin itself and the body. The thickness of this layer varies throughout the body and from person to person.

The epidermis and dermis are clearly separated but are firmly anchored together by the basement membrane that consists of dermal papillae, however there is no clear definition between the dermis and the subcutaneous tissue.

Types of wounds

A wound interrupts skin continuity and integrity. It may be the result of trauma, either minor or severe, or of a pathological/chronic process. The healing prognosis can be very different depending on the depth and mechanism of the lesions.

Acute wounds:

Acute wounds can be defined as wounds of sudden onset and of short duration. They include surgical wounds and traumatic wounds that may include:

Traumatic wounds

Types of acute trauma involve a variety of wounds depending on the cause.

These wounds can incur massive skin loss or they can on the other hand, have little effect.

Examples of traumatic wounds are skin tears, fingertip injuries, abrasions, lacerations, blisters, gunshot wounds, stabbing and nail avulsions.

Acute wounds generally heal without complication however some acute wounds will fail to heal and become chronic. Many factors can affect the healing process; infection, irritation, and poor technique of surgical closure, suture irritation or the general condition of the patient.

Chronic wounds:

A chronic wound is one that does not heal in the expected time frame (~21 days to a month). An almost permanently inflammatory environment established in the lesion does not allow healing to follow the normal staged procedure.

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The chronic wound environment is characterised by an imbalance between the degradation of damaged tissue by proteases Matrix Metallo-Proteinases (MMPs) and growth factors which would stimulate fibroblasts to generate new tissue. The detrimental role of MMP hyper-production has been widely demonstrated in many different types of chronic wound and their neutralisation can speed up wound healing and prevent chronicity. 

Patients with chronic wounds are under severe emotional and physical stress and a significant financial burden is put on patients and the whole healthcare system.

Infected wounds

Any open wound is susceptible to infection which occurs when there is a host response to bacteria in the wound. Infection delays wound healing and if not readily controlled can spread both locally and systemically leading to serious complications.

Infection

Infection is due to several factors:

  • Large numbers of microorganisms present >105/g of tissue
  • Bacterial virulence factors
  • Reduction in the patient’s immune defence mechanism

Infection may remain localised to the wound itself or the whole body may be involved “systemic” infection

Local or systemic clinical symptoms include:

Local inflammation :  systemic symptoms: fever, etc.
Heat : 
inflammatory response
Odour : 
healing halted
Pain : 
wounds that are worsening deterioration of the wound
Pus : 
bone contact

Among the microorganisms likely to cause infection are the bacteria:

  • Staphylococcus aureus
  • Streptococcus  pyogens
  • Enterococcus faecalis
  • Enterobacteriaceae e.g. E. coli
  • Pseudomonas aeruginosa

Wounds may occasionally be infected by yeast e.g. Candida albicans rather than bacteria.

Complications of infection

Untreated, an infection can eventually lead to the exposure of underlying anatomical structures such as ligaments or bones. In diabetic foot ulcers, it is essential to ensure that the infection has not spread to the bone and consequently an X-ray or MRI scan will be necessary.

Systemic symptoms include fever, fatigue, regional lymphangitis and abnormal laboratory findings (Sedimentation Rate and C-reactive protein). In patients at high risk e.g. elderly, immunocompromised, diabetes, smoker, obese, resulting systemic infections can have high morbidity and mortality.

Infection will always require the use of local or general (atopic or systemic) antibacterial treatments.

Local infection or critical colonisation (with local signs such as pus, redness, increased exudate or odor) must be differentiated from infection with regional signs (cellulitis) or systemic signs (ie fever.)

To learn more about infection, click here.

 

These advices or recommendations do not replace expert opinion based on a full diagnosis.

Basis of wound healing

Wound healing, or wound repair, is the body’s natural process of regenerating dermal and epidermal tissue. When a wound occurs, a set of complex biochemical events take place in a closely orchestrated cascade, to ensure that the damage is repaired.

The healing process

The healing process can be divided into 3 phases, there is a degree of overlap between the different phases as shown in the table.

The three main phases of a normal healing

Haemostasis
Inflammation
Reconstruction
Granulation
Epithelisation
Remodelling
Time before initiation of
the phase
Appearance
of the wound
Immediate to a few minutes A few hours to a few days About 1 week (reorganisation of the extracellular matrix
Duration A few hours to 2/3 days 1 to 3 weeks A few month to a few years
Key cells Platelets
Neutrophils then macrophages +++
Fibroblasts +++
Keratinocytes
Macrophages
Fibroblasts
Effects
  •  Formation of a temporary extracellular ECM
  • Secretion and activation of mediators
  • Recruitement of inflammatory cells, fibroblasts and endothelial cells

Formation of granulation tissue:

  • Cell proliferation : fibroblasts, endothelial cells
  • Synthesis of a new ECM
  • Angiogenesis

Re-epitelialisation:

  • Transformation of fibroblasts into myofibroblasts
  • Migration of epithelial cells from edges
  • Restoration of the barrier function of the epidermis by keratocytes
  •  Progressive reorganisation of the matrix under the influence of myofibroblasts
  • Modifications of the % of different types of collagen: collagen I, collagen III
  • Apoptosis of myrofibroblasts
  • Synthesis of a stronger extracellular matrix by fibroblasts

 

Inflammatory phase

inflamatory-phaseThe inflammatory phase begins immediately and, in acute wounds lasts from a few hours to a few days. In chronic wounds this process can last longer.

A clot formed after the rupture of blood vessels covers the wound and forms a temporary extracellular matrix – composed of fibrin and fibronectin – which seals the wound and minimises blood loss and helps to guide cell migration. Platelets secrete and activate mediators to recruit inflammatory cells (polynuclear neutrophils and macrophages), fibroblasts and endothelial cells. Bleeding is controlled at the end of the inflammatory phase, and the wound bed is cleaned through phagocytosis.

Proliferation (granulation) phase

proliferation-phaseThe granulation phase can begin quickly with the proliferation of endothelial cells and fibroblasts leading to the formation of new blood vessels (angiogenesis) and the synthesis of a new extracellular matrix (ECM). As the new ECM is re-modelled, the existing matrix is degraded by a number of proteases, enzymes known as Matrix Metallo-proteinases (MMPs), the MMPs help with autolytic debridement (cleansing) of the wound and cell migration. Their levels increase within the wound after injury and decrease when inflammation subsides. In excess however, MMPs can be detrimental to wound healing.

Fibroblasts then acquire the morphology and biochemical characteristics of smooth muscle cells to become myofibroblasts.

 Myofibroblasts are responsible for synthesis of the extracellular matrix and contribute to reorganisation of the ECM as the wound contracts. Re-epithelialisation occurs to close the wound with the migration of epithelial cells starting from the edges of the wound and skin appendages. Differentiation of keratinocytes then helps to restore the barrier function of the epidermis.

Remodelling phase

remodelling-phaseThe final remodelling phase will last for several months and result in the final scar. This phase begins early, during the formation of the granulation tissue, with progressive reorganisation of the matrix under the influence of myofibroblasts. These cells contract their microfilament bundles which adhere to the extracellular matrix, causing compaction of the collagen network and contraction of the wound. New components are then secreted to increase the density of and stabilise the matrix. There is a change in the proportion the different types of collagen present: type I collagen increases while type III collagen decreases (from 30% to 10%). The cell density of myofibroblasts is reduced by apoptosis to leave room for fibroblasts which will strengthen the extracellular matrix, giving better resistance to mechanical forces.

Wound care

Wound care protocols will be specific to the local community or hospital. However before care starts the healthcare professional must ensure that the diagnostic process and evaluation is complete and that the origin of the wound has been found.

Healing in a moist environment

Moist wound healing is 30% faster than wound healing in a dry environment.

Natural healing takes place in a moist wound environment. Cellular and molecular elements migrate and develop more effectively under these conditions. This was first demonstrated in 1962 by Winter, who showed that healing under a synthetic semi-occlusive dressing was faster than when a wound was left open to the air.

Bacteriology of wounds

Because the surface of normal skin harbours bacteria (natural colonisation) bacteria are inevitably present in wounds.

The difference between colonisation and infection depends on the number and types of bacteria present and the body’s response to these bacteria.

The presence of large quantities of bacteria hinders the natural healing process leading to delayed wound healing.

Unlike infection, bacterial colonisation is perfectly normal does not require any specific therapeutic procedure.

Colonisation

Colonisation is the presence of bacteria within a wound without this leading to an inflammatory response.

Most colonisation of acute wounds is by bacteria such as streptococci and staphylococci which are already present on normal healthy skin (commensal organisms).

The bacterial population in chronic wounds is much more varied, including commensal skin bacteria such as Staphylococcus (S. aureus, coagulase-negative staphylococci), Corynebacteria and α-haemolytic streptococci. Following multiplication of microorganisms within the wound and adherence to epithelial cells, an equilibrium is set up between the patient and their microbial flora. The microorganisms remain at the surface of the wound and can form a biofilm.

Biofilm

Biofilms are complex microbial communities containing bacteria and fungi. The microorganisms synthesise and secrete a protective matrix that attaches the biofilm firmly to a living (e.g. wound) or non-living surface. Biofilms are dynamic heterogeneous communities that are continuously changing. They may consist of a single bacterial or fungal species, or may be contain multiple diverse species.

A biofilm can be described as bacteria embedded in a thick, slimy barrier of sugars and proteins. A typical example of a biofilm is the yellow slimy film that can be seen on the teeth if left unbrushed. The biofilm barrier protects the microorganisms from external threats. Biofilms can be found in wounds and are suspected to delay healing in some cases.

(adapted from  : http://www.woundsinternational.com/made-easys/biofilms-made-easy)

Infection

The term infection is used when the presence of micro-organisms leads to a local, regional or general inflammatory response with clinical symptoms. Infection will not only delay wound healing it and can also lead to severe systemic complications. Infection always requires treatment with antiseptic or antibiotics.

Local infection or critical colonisation (with signs such as pus, redness, increased exudate or odor) must be differentiated from infection with regional signs (cellulitis) or systemic signs (ie fever.)

To learn more about infection, click here.

Healing steps

Healing by primary intention

First-line healing concerns surgical wounds or surgically sutured traumatic wounds. The first healing phase is reconstruction of skin continuity and corresponds to the time during which the surgeon leaves the suture in place.

The sutures are removed after a period of 5 to 15 days. The duration of this period depends on the skin thickness and the tension applied to the edges.

Healing is still not complete when the sutures are removed, because an inflammation phenomenon is observed that can last for up to two months. After two or even three months, the scar will progressively reduce although it will not disappear entirely.

Healing by secondary intention or directed healing

Here the wound is left open. This method may be used when there is considerable tissue loss, the surface area is shallow but large, or where there may have been an infection or a risk of infection (bites). Debridement (desloughing) is nearly always necessary as the first step towards successful healing. Wound healing progresses by granulation, contraction and epithelialisation.

Debridement or desloughing

desloughingThe desloughing phase is the phase that occurs after wound cleaning and once bleeding has stopped.

It eliminates all foreign waste and/or necrotic tissue. Once this elimination phase is complete, tissue reconstruction can begin. In a chronic wound, the desloughing phase is often the healing phase that obstructs tissue reconstruction. The term “desloughing” covers 2 concepts:

  • natural desloughing, which is achieved thanks to our own cells. This is the cleaning process performed by the body itself thanks to our white blood cells or proteolytic enzymes produced by our white blood cells.
  • assisted desloughing is essential when the body’s own cleaning capacities are unable to cope with the quantity of tissue damage (exudate, slough).

A number of different techniques exist.

1.Autolytic desloughing

Principle

Autolytic desloughing consists in promoting the elimination of waste by softening necrotic tissue and/or absorbing exudate and slough using dressings.

Indications

It is indicated for:

  • dry necrosis: with an hydrogel
  • moist necrosis: with alginates, hydrofibres and hydrodesloughing dressings.

Each one of these dressings has its own specific action depending on the type of necrosis.

2. Enzymatic desloughing

Principle
This consists in using proteolytic enzymes to compensate for the concentration of our own enzymes.

Indications
Local adjuvant treatment of wounds, skin ulcers and pressure sores during the desloughing phase.

3. Biological desloughing

Principle
This method results from the observation that some maggots only feed on necrotic tissue. In addition, their movements on the wound are thought to mechanically stimulate healing.

Indications
This method can be used on both dry and moist necrosis.

4. Assisted desloughing by negative pressure

Principle
Assisted desloughing using negative pressure therapy is a method to eliminate exudate and organic waste using pressure lower than atmospheric pressure. This continuous or discontinuous aspiration pressure is exerted through a polyurethane foam or a pad. It is performed using an aspirating motor. The pressure can be adjusted on the basis of wound type: from 50 mm Hg for burns to up to 175 mm Hg for surgical wounds.

Indications
It is indicated in the desloughing of difficult-to-heal wounds and to speed up granulation.

5. Mechanical desloughing

Principle
This is performed using a variety of surgical instruments, such as a scalpel, tweezers, scissors or curette.

Indications
Mechanical desloughing is often employed in addition to the use of dressings.
It is also used for trimming blisters.

6.Surgical desloughing

Principle
Surgical desloughing is a surgical procedure.
It makes it possible to remove all necrotic tissue in the event of difficult wounds.
If the wound is infected, it can be used to eliminate all infected tissue. In general, it is used for wounds for which desloughing is impossible using a gentler method.

Indications
The indications for this method are all necroses that cannot be eliminated using easier methods.

7. Pressurised jet desloughing

Principle
This is performed using water jets of variable pressures depending on the type of system. The level of wound desloughing varies according to the pressure delivered: the wound can be cleaned at low pressure or the tissue trimmed at high pressure.

Indications
Pressurised jets are used in addition to other desloughing methods.

Granulation

granulationOnce necrotic tissue has been removed, neo-vascularisation creates buds that progressively fill the wound bed.

Granulation tissue contains fibroblasts, collagen and elastin.

Granulation normally stops when the volume of lost tissue has been replaced. However, there are occasions when too much granulation occurs. Hyper-granulation should be limited so as not to hinder the next phase, which is epithelialisation.

Epithelisation

epithelisationOnce granulation is complete and lost dermis has been replaced, terminal epithelialisation which is the last phase of the healing process can begin.

Epithelialisation will take place from skin edge to skin edge.

Marginally, the basal cells slide over the surface of the granulation buds through multiplication and generate a neo-epidermis on the surface of the healed wound.

The final scar is not the same as normal skin there are no hair, sebaceous glands, or sweat glands and sensitivity is impaired.

 

These advices or recommendations do not replace expert opinion based on a full diagnosis.

Our benchmarks

Urgo Medical has introduced the use of benchmarks to help you easily identify the best product to use at each stage of the wound healing process. To find out more, click here.

Types of wound dressing

Different medical products are available to dress the wound depending on the wound type, the level of exudate, whether infection is present and the stage of healing.

The various product families are:

Hydrogels

Hydrogels release water. They contain more than 80% water and are cohesive so that do not run and stay on the wound. They facilitate the debridement phase for dry fibrin and dry necrosis.

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hydrogelsHydrogels are gels composed of 80% water with or without CarboxyMethylCellulose.
They come in the form of a gel, sheets or impregnated pads.
They act by moistening and softening the tissues to make them easier to eliminate.

Alginates – Hydrofibres – Hydro-desloughing dressings

These are highly absorbent dressings which are indicated for the debridement of wet slough and necrosis.

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alginates-hydrofibre-hydro-desloughing-dressingsThe UrgoClean range, an innovation from URGO, is composed of hydro-desloughing fibres with a high capacity to absorb, drain and trap sloughy residues.

These new-generation hydro-desloughing fibres are composed of polyacrylate polymers surrounding an acrylic core for removal of the dressing in one piece.

Hydrocellular/foam dressings

Hydrocellular/foam dressings are absorbent, semi-permeable/impermeable polyurethane dressings indicated for the treatment of exuding wounds.

Standard hydrocolloids

Hydrocolloids are the pioneers of moist wound healing and are composed mainly of carboxymethylcellulose. They have the characteristics of absorbing, swelling and then gelling.

They are recommended for use in the granulation and epithelialisation phases (thin hydrocolloids).

Greasy gauzes and impregnated pads

These are composed of a loose mesh of cotton impregnated with a fatty substance and are used mainly in the epithelialisation phase.

Contact layers

Interfaces composed of a tight mesh of a synthetic material, coated with a special substance, recommended for use at the end of the granulation and epithelialisation phases.

Active dressings

These dressings contain active substances, for specific purposes:

  • To facilitate and stimulate wound healing
  • To provide an antibacterial action
  • To control unpleasant odours

Charcoal dressings

Charcoal dressings are odour-absorbing, deodorising the wound by absorbing bacteria and bacterial spores away from the wound.

 

These advices or recommendations do not replace expert opinion based on a full diagnosis.

Last update : December 9, 2017