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CompendiumWounds and Wound Management

PAUL HARTMANN AGP.O. Box 1420D-89504 HeidenheimGermany

PAUL HARTMANN AGUnit P2 ParklandsHeywood Distribution ParkPilsworth RoadHeywood, Lancs OL10 2TTUnited Kingdom

PAUL HARTMANNAsia-Pacifi c Ltd.16/F Unit 1608Kerry Cargo Centre55 Wing Kei RoadKwai Chung NT

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The HARTMANN medical edition series of publications deals with current subjects from the areas of medicine and nursing. They em-phasise not only basic knowledge, but also present specialist and interdisciplinary developments. The information goes beyond the products and is particularly important.

At a time of rapidly evolving scien-tifi c knowledge, information must above all be up to date. With this in mind, this series of books aims to be a source of advice not only for experienced workers. Those who are approaching new areas of medicine and nursing for the fi rst time are shown modern treatment methods and are given useful tips.

CompendiumWounds and Wound Management

Table of contents

Published by PAUL HARTMANN AG D-89522 Heidenheim http://www.hartmann.info

Conception, design, editing and production by CMC Medical Information D-89522 Heidenheim

Scientifi c advisers: Prof. Dr. med. Pavel Brychta Prof. Dr. med. Günther Germann Dr. med. Andreas Gericke Prof. Dr. med. Walter O. Seiler Dr. med. Jörg Tautenhahn Prof. Dr. med. Helmut Winter

Translated from the German edition ISBN 978-3-929870-60-2

Printed on chlorine-free paper

Table of contents [2.3]

Foreword 5

The skin and wounds– Functions and structure of the skin– Wounds and wound types

6 7

27

The processes of wound healing– The phases of wound healing– Quantitative classifi cation of wound healing– Infl uences on wound healing– Disorders of wound healing– Wound infection

34 35 50 54 61 65

Principles of treatment of acute wounds– The acute traumatic wound– Complex traumatic defects– Thermal injuries/burns– Incisions/surgical wounds– Epithelial wounds

80 81 85 88 94 94

Principles of treatment of chronic wounds– The venous leg ulcer– The arterial leg ulcer– The diabetic ulcer– The decubitus ulcer– The chronic post-traumatic wound– Chronic radiation damage– Wounds in tumour patients

96 105 110 116 126 130 132 134

Wound dressing– Functions and requirements– Dry wound treatment– Moist wound treatment– The dressing change

136 137 144 148 177

Glossary and indexBibliography and Pictures sources

194 199

Foreword [4.5]

Foreword

Wound healing is a natural phenomenon. In the physiologi-cal situation, nature follows a uniform pattern which, be-ginning with blood coagulation, then cleanses the wound of damaged tissue, foreign bodies and bacteria in catabolic processes. The process ends with production of new tissue to fi ll the defect which changes in time into scar tissue.

By no means is everything known about the physiology of wound healing, and this can result in many problems, espe-cially in the case of abnormal wound healing. Nevertheless, therapeutic measures can be deduced from current knowl-edge which support the body‘s own efforts to restore the continuity of the skin covering.

An attempt has been made in this compendium to repre-sent the basic features of the complex subjects of wounds and wound healing. The structure and functions of the skin are described, followed by the processes of wound healing, infl uences on wound healing and possible disturbances arising from them, principles of treatment of acute and chronic wounds and treatment with dressings as an impor-tant localised therapeutic measure. A later chapter focuses on modern hydro-active wound dressings giving a detailed description of their characteristics and uses. These expand the range of therapeutic options especially in the treatment of chronic wounds when they are used in the appropriate phase.

Wound treatment concerns all the practical disciplines of medicine and nursing. The present compendium is aimed at providing doctors and nursing staff with information and further education in this multifaceted subject.

The skin and wounds [6.7]

The skin and wounds

The healing of skin wounds is based on the skin‘s capacity for epithelial regeneration and the repair of the skin connective tissue. Regeneration means that the injured skin heals without scarring and is possible when only the uppermost skin layer is damaged. Repair, on the other hand, involves the formation of replacement tissue in order to close a skin defect. This is always the case if an injury involves the deeper skin layers. The basis for our understanding of current knowledge of wound healing is, fi rstly, adequate basic knowledge about the skin, the organ where this takes place.

Functions of the skinWith an area of between 1.6 and 2 m2 in an adult and a weight of up to 1/6 of the body weight, the skin is the largest human organ. It constitutes the outer boundary layer between the human body and its environment and functions at this exposed site both as a barrier against the outside world and simultaneously as an interface between the outside world and the internal organs. It also has a large number of tasks to fulfi l that are essential to life, which is why its undamaged state is so important to the individual‘s health. ▪ When the surface is intact, the skin prevents the loss of

body fl uids and offers protection against the invasion of microorganisms into the body‘s interior.

▪ Its mechanical resistance to pressure, impacts and blows is astonishingly high, which is why it is able to protect the internal organs against damage.

▪ To a certain extent, the skin is able to protect against the harmful effects of chemicals and ultraviolet light.

▪ It plays a decisive role in heat regulation – by expansion and contraction of the blood vessels and by perspiration – and so contributes to maintaining the vitally essential body temperature of 37 °C.

▪ As a sensory organ, the skin enables the perception of mechanical stimuli such as pressure, touch and vibration, as well as temperature and pain. Many character-forming sensations are obtained only through the skin, and the human development process could not take place at all without it.

Finally, of particular importance is the fact that the skin is capable of regeneration and repair, which means nothing other than that in the event of its being interrupted or damaged, it can heal itself and restore its own continuity.


blood vessels of the dermis. If the skin bleeds due, for ex-ample, to an abrasion, then this means that the capillaries of the dermis have been opened.

The epidermis bears the main brunt of the protective func-tions of the skin, including defence against ultraviolet rays. Wound healing is therefore seen as complete only once a new fully-functioning epithelium, which is able once more to protect the body against the outside, has formed.

The dominant cell type in the epidermis is the keratinocyte, which earns that name from its ability to synthesize kera-tins. Keratins are insoluble structural proteins which are highly resistant to extremes of temperature and pH and to enzymatic degradation. They are divided essentially into hard and soft keratins: hard keratins form hair and nails, whilst soft keratins are a main component of the horny cells of the outer epidermal layers.

Cross-section through the epider-mis at the fi ngertip, clearly show-ing the fi ve different cell layers: 1) Basal layer –

stratum basale (also called stratum germi nativum)

2) Prickle cell layer – stratum spinosum

3) Granular layer – stratum granulosum

4) Lucent layer – stratum lucidum

5) Horny layer – stratum corneum

1

2

3

4

5

The structure of the skin Like any other organ, the skin has a specifi c fi ne structure in order to be able to perform its many tasks. For this reason, it is formed in layers having different tissue types: From outside in, three layers of tissue can be distinguished: the outer layer (epidermis), the dermis (also called the corium) and the subcutis. Epidermis and dermis together constitute the cutis, i.e. the skin in the strict sense. The skin also in-cludes the skin appendages, such as hair, nails and various glands.

The epidermis The epidermis represents a keratinising stratifi ed epithelium composed of fi ve differentiated cell layers, which is perfect-ly equipped for protective functions, given its stability and imperviousness. Cell division, which is a precondition for growth and regeneration, takes place in the two deepest cell layers. From there, cells push their way to the surface with complete keratinisation occurring in the course of this migration. The uppermost horny layer is shed in a con-tinu ous fl aking process. Under physiological conditions, renewal of the epidermis from cell division to shedding of the keratinised cells takes about 30 days. The epidermis is avascular and receives its nutrients by diffusion from the

The skin consists of the avascular epidermis (1) and the dermis (2), a highly vascularised and innervated connective tissue. This is attached to the subcutis (3) which consists of loose connective tissue contain-ing adipose tissue. The thickness of the skin varies from 1 – 4 mm depending on the demands made on it in the different areas of the body; it is thickest on the palms of the hands and the soles of the feet.

1

2

3


The basal layer runs in a wavy form along the plug-like pro-jections (papillae) of the dermis. Between the basal layer and the dermis is the avascular basal membrane. It sepa-rates the two skin layers but at the same time it serves to anchor the basal cells and controls the transport of proteins.

Stratum spinosum – prickle cell layer (2) The prickle cell layer contains up to six layers of irregularly shaped cells which synthesise keratin peptides and still have slight mitotic activity. They are connected to one an other by cell bridges (desmosomes) which give the cells their “prickly” appearance. Fluid is stored between the desmosomes.

Stratum granulosum – granular cell layer (3) Gradual keratinisation begins in the granular cell layer. Depending on the thickness of the horny layer, it comprises one to three layers of fl at cells which contain large gran-ules of keratohyalin. The granules contain, beside others, a precursor protein which is believed to be involved in the formation of keratin fi bres in the intercellular space.

Apart from the keratinocytes, the epidermis has other cells known as migratory cells, these are cells that are distrib-uted through the tissues without any fi rm connection to similar cells and undertake particular functions of the epi-dermis. Important cell types: ▪ Melanocytes produce the brown/black skin colouring

agent melanin, which they release in the form of mela-nosomes to the keratinocytes. These store the pigment, which then appears as a visible coloration of the skin. This is intended to protect the keratinocytes against dam-age by UV light while they undergo cell division. The more UV light that falls on the skin, the stronger is the melanosome formation, leading ultimately to tanning of the skin. The quantity and distribution of the melanin are also responsible for differences in skin and hair colour.

▪ Merkel‘s cells, also known as Merkel‘s tactile cells, are fl attened, broadened nerve endings which function as slowly-adapting pressure receptors, i.e. they perceive longer-lasting contact. They therefore appear plentifully in the palm skin of the hands and the soles of the feet.

▪ Langerhans cells play an important role in the immune functions of the skin. They recognise a foreign antigen, absorb and process it, before performing interactions with the immunocompetent T-lymphocyte cells.

Stratum basale – basal layer (1) The basal layer is the deepest cell layer of the epidermis. It consists of cylindrical keratinocytes which are capable of cell division (mitosis), ensuring continuous regeneration of the epidermis. Cell division is subject to control by nu-merous substances such as growth factors, hormones and vitamins. The so-called chalones, in particular, appear to play an important part in keeping the regeneration process constant by their inhibitory effect on the obviously unlim-ited mitotic potential of basal cells. When there is a loss of epidermis, which is associated with a fall in the chalone level, there is rapid regeneration due to “disinhibition” of mitotic activity in the basal cells.

Section through the epidermis: At the top, the stratum corneum (brown) with its layers of corneo-cytes is visible. Adjoining this are the layers containing living cells (lilac). At bottom left, the dermis (yellow), via which the epidermis is fed, can be seen.


The dermis The dermis is attached to the basement membrane of the epidermis. It is a connective tissue rich in vessels and nerves which is subdivided histologically into two layers: the outer papillary layer (Stratum papillare) and the inner reticular layer (Stratum reticulare). The layers are distin-guished by the thickness and arrangement of their connec -t ive tissue fi bres but are not separated from one another.

Stratum papillare – Papillary layer The papillary layer is bound fi rmly to the epidermis by projections of connective tissue, the papillae. There are capillary loops in the region of the papillae which ensure nutrition of the avascular epidermis as well as free nerve endings, sensory receptors and incipient lymph vessels. The connective tissue itself consists of a framework of fi brocytes (resting form of the fi broblasts), interspersed with elastic collagen fi bres. The intercellular space is fi lled with a gel-like ground substance, the extracellular matrix, in which mobile blood and tissue cells can move.

The dermis is a connective tissue rich in vessels and nerves, which is classifi ed histologically into two layers, the papillary layer and the reticular layer.

Stratum lucidum – lucent layer (4) The lucent layer consists of non-nucleated cells in which intense enzymatic activities take place. Keratinisation is continued here which includes the breakdown of the keratohyalin granules of the granular cell layer to eleidin. Eleidin is a fat- and protein-rich acidophilic substance with strong light-diffracting properties. It appears as a homoge-nous shiny layer – and it is from this that it gets the name of stratum lucidum – and protects the epidermis from the effect of aqueous solutions.

Stratum corneum – horny layer (5) It is in this layer that the process of cornifi cation is com-pleted: The keratinocytes are fi lled with the horny material keratin and are now designated corneocytes. They lie on one another like roof tiles and are fi rmly bound to one another by keratohyalin and very fi ne fi brils (tonofi brils). The cell layer has about 15 to 20 layers of cells, the outer-most of which is lost as skin scales.

The corneal layer is involved, together with the secretions of the sweat and sebaceous glands, in forming the surface fi lm (the hydrolipid fi lm), also known as the acid protective layer. It helps to keep the colonisation of the skin with mi -croorganisms in a physiological equilibrium. If the epidermal layer is damaged by eczema or injuries, germs and harmful substances can penetrate into the skin unhindered.

The stratum lucidum protects against the ingress of aqueous solutions.

The upper skin section reveals the thickness of the corneal layer. The scanning electronmicrograph of the corneocytes shows that they are layered like roof tiles.


The fi bre proteins of the dermis The connective tissue fi bres of the dermis consist of the structural protein collagen which is an extremely resistant biological material accounting for 60 – 80 % of the dry weight of the tissue. The name “collagen” is derived from the fact that these proteins swell when being boiled and yield a glue, “colla” in Greek. Of the four biochemically dis-tinguishable collagen types occurring in the human body, the main one found in the dermis is the fi bre-forming type I collagen.

The production of collagen fi bres takes place in an intracel-lular stage and an extracellular stage, beginning with the fi broblasts. First, fi broblasts release intracellularly a triple helix of procollagen into the extracellular space. This triple helix is made up from two thirds of the characteristic amino acids of collagen (glycine, proline, hydroxyproline) and from one third of other amino acids. In the extracellular space, further enzymatic modifi cations take place by which the still soluble procollagen is changed into insoluble collagen fi brils, fi nally being assembled into collagen fi bres.

The fi broblasts represent the most important secreting cells for forming skin connective tissue (nucleus blue, cellular skeleton orange).

Stratum reticulare – Reticular layer The reticular layer consists of interwoven strong bundles of collagen fi bres between which elastic fi bre meshes are stored. This structure gives the skin its elasticity so that it can adapt to movements and volume fl uctuations of the organism. It is also capable of absorbing and giving off water in a dynamic process.

The collagen fi bres run in all directions but are oriented mainly obliquely to the epidermis or parallel to the surface of the body. The skin‘s natural crease lines, which run in the direction of the least skin elasticity and perpendicular to the skin tension lines, are called Langer‘s skin crease lines. Incisions should follow their course where possible. Skin incisions along these lines do not gape and give virtually invisible scars while incisions running across them leave markedly wider scars.

Cellular components of the dermis The predominant cell type in the skin connective tissue is the fi brocyte which in its activated form is designated as a fi broblast and provides a range of substances for producing new tissue: Fibroblasts synthesize and secrete precursors of collagen, elastin and proteoglycans which mature outside the cells into collagen and elastin fi bres and, in non-fi brous form, form the gel-like ground substance of the extracellular matrix.

In the dermis there are also found mast cells, the granules of which contain heparin and histamine, macrophages, which derive from the blood monocytes, and lymphocytes. The cells participate in the non-specifi c and specifi c defence mechanisms of the body (phagocytosis, humoral and cell-mediated immunity). In addition, they secrete biochemically active substances which have communicating and regula-tory functions and thus are essential for the progress of the repair processes.

The course of the Langer‘s skin crease lines should be borne in mind where possible for incisions to obtain cosmetically inconspic-uous scars.


Schematic diagram of the fl ow of information: cell – extracellular matrix

Another fi bre protein of the dermis is fl exible elastin which is also synthesized and secreted by the fi broblasts. Elastin is a spiral polypeptide chain with highly elastic properties from which a two-dimensional framework similar to a tram-poline net is produced outside the cell. This structure allows reversible stretching of the skin so that overstretching and tearing is largely avoided.

Non-fi bre ground substance of the dermis The space between the fi bres of the skin connective tissue is fi lled with amorphous ground substance, salts and wa-ter. An important constituent of the ground substance are proteoglycans. These are compounds of polysaccharides and proteins with a high proportion of carbohydrates which were formerly known as mucopoly-saccharides.

Electron microscopic appearance of skin connective tissue with col-lagen bundles and elastic fi bres. The substances required for the formation of the fi bre proteins are provided by the fi broblasts. They synthesize precursors of collagen and elastin which are released into the extracellular space and mature through various enzymatic processes into collagen and elastin fi bres.

Growthfactors/

cytokines

Cell growth/proliferation

Hormones/vitamins Cell shape

Cell to cellcontact

State ofdifferentiation

Cell-matrix-bonds

Biochemical products/

extracellular matrix

Proteoglycans are very hydrophilic and can bind a large volume of water so that a sticky gel-like substance is form-ed. They are not purely structural proteins but also appear to have an infl uence on cell migration, cell adhesion and cell differentiation.

Furthermore, the ground substance also contains a range of other glycoproteins with a lower proportion of carbo-hydrate such as thrombospondine, laminine/nidogen com-plex, k-laminine and tissue fi bronectin. These have a similar multiplicity of function as the proteoglycans. Fibronectin, for instance, is an adhesive protein which binds cells to collagen and thus also plays an important part in wound healing.

Extracellular matrix In tissue, the cells are usually closely bound to the sub-stances they secrete themselves. To achieve this, the macro-molecules of the extracellular substances form complex three-dimensional networks which are called the extracellu-lar matrix (ECM). Such a matrix can be found in every body tissue, where the structure and composition have tissue-specifi c differences and depend on the type of matrix-producing cells and the function of that tissue.


They are accordingly found in greatest density on the fi nger-tips. The Kraus end bulbs are important in the perception of cold, the Ruffi ni corpuscles in the subcutaneous tissue function as warmth receptors. Free nerve cells close to the skin‘s surface transmit pain sensations. The Vater Pacini corpuscles of the subcutis react to mechanical deformation and vibration.

The skin appendages The appendages of the skin include hair and nails in addi-tion to sebaceous, sweat and scent glands.

Hairs are fl exible and at the same time strong thread-like structures made of the horny substance keratin. They dev-elop from inward projections of the epidermis and the hair shaft, which is at an angle to the skin surface, extends deep into the dermis. Their growth follows an endogenous cycle which is specifi c for every hair root. Therefore no syn-chronous growth between neighbouring hairs takes place. Hair roots cannot be regenerated so scar tissue always remains hairless. However, epithelialisation can take place from the remaining epithelium of a damaged hair shaft.

Finger- and toenails are translucent keratin plates which grow outwards from the nail root to the free edge. Growth is about three millimetres a month and is closely associated with many organ functions. Thus the condition of the nails can often give important diagnostic clues.

Although all the functions of the ECM are not yet known, it is assumed that it serves not only as a fi ller substance be-tween individual cells, tissues and organs but also fulfi ls a variety of tasks in the transmission of information between the cells embedded in it.

The subcutaneous tissue The subcutaneous tissue is the deepest layer of the body‘s outer covering. This layer consists of loose connective tis-sue and is not sharply demarcated from the dermis. In its depths, it is bound to muscle fasciae or periosteum. Apart from a few sites in the body, fat can be deposited in the entire subcutaneous tissue which has insulating, storage and modelling functions.

Sensory receptors in the skin and subcutaneous tissue The skin is innervated by different types of free nerve endings and stimulus-receiving receptors which enable it to function as a sensory organ. The Merkel cells in the epi-dermis can perceive prolonged touch. Along the papillary bodies of the dermis are aligned the Meissner corpuscles which serve as touch receptors for very fi ne pressure.

A large number of nerve receptors makes the skin a sensory organ that is essential to life. Some examples of this: 1) Meissner‘s corpuscles 2) Free nerve endings 3) Vater Pacini corpuscles

Electronmicrographs of hairs (above). The illustration below shows hair roots with clearly recognisable epithelial cells. In the event of injuries, re-epithelialisa-tion can take place from the resid-ual epithelial cells. The hair roots themselves cannot be regenerated so scars always remain hairless.

1 2 3


The blood supply of the skin The stepwise distribution of vessels in the skin corresponds to the layered surface structure of this organ. Numerous vessels arise form the arteries lying under the subcutane-ous tissue, which form a cutaneous plexus between the subcutaneous tissue and dermis. Wherever the skin is more mobile, the vessels take a pronounced tortuous course. Individual arterioles run outwards perpendicular from the deep cutaneous plexus and branch at the foot of the pa-pillary layer into the subpapillary plexus. Very fi ne looplike capillaries extend from there into the papillae of the dermis and thus ensure perfusion of the avascular epidermis.

The papillary layer is supplied copiously with vessels while the reticular layer is relatively avascular. Removal of me-tabolic products is effected via the corresponding venous networks and partly also via the lymphatic system.

Sebaceous glands open into the hair funnels of the hair follicles so that their presence is associated with hair folli-cles with few exceptions. The sebum, a mixture of fats, cells and free acids, lubricates skin and hair and protects them from drying out. Control of sebum production is a complex process which has not yet been investigated in every detail.

Sweat glands also arise from cells of the epidermis, which then sprout into the depths of the dermis so that the actual gland is in the corium. The excretory ducts open in the pores on the skin‘s surface. Sweat is an acid secretion con-sisting, besides others, of water, salts, volatile fatty acids, urea and ammonia. Sweat covers the skin surface with a protective acid coating. Sweat secretion serves mainly for temperature regulation.

Scent glands, in contrast to the sweat glands, produce alka-line secretions. Scent glands are found mainly in the axillae, around the nipples and in the genital area. They commence their secretory activity with the onset of puberty.

Electronmicrographs of a sebace-ous gland (left) and a sweat pore (right). Apart from the hairless skin on the soles of the feet and the palm of the hands, sebaceous glands are found at all sites on the body and are particularly numer-ous on the face and scalp. Here there can be up to 900 sebaceous glands per square centimetre. The human body also has a plentiful covering of sweat glands, totalling about 2.5 million.

Blood vessels of the skin (electron-micrographs)

Schematic diagram of the blood supply in the skin. From the cutaneous plexus between sub-cutaneous tissue and dermis (1), individual arterioles (2) run per-pendicular to the surface and branch at the foot of the papillary layer into the subpapillary plexus (3) which supplies the epidermis.

1

2

3


Blood plasma Plasma is a yellowish clear liquid consisting of water (90 %), proteins (7 – 8 %), electrolytes and nutrients (2 – 3 %). Of the proteins, about 60 % are albumins and 40 % globulins. A constituent of plasma which is important in wound healing is fi brinogen (factor I), which is essential for blood coagulation. Plasma which no longer contains any clotting factors is called serum.

Red blood cells (erythrocytes) About 95 % of blood cells are red cells: non-nucleated disc-shaped cells with a central concavity, containing high concentrations of the red blood pigment haemoglobin. Their main function is the transport of oxygen and carbon dioxide which are bound reversibly with haemoglobin. The gas exchange itself is favoured by the hollows in the sides of the cells due to an increase in the surface area of the small blood cells. This shape also facilitates deformation of the cells when passing through the smallest capillaries. The erythrocytes are formed in the red bone marrow. Their life-span is about 120 days after which they are broken down, mainly in the spleen.

The constituents of the blood The blood, also called the liquid organ of the body, serves as a transport medium for respiratory gases, nutrients, pro-ducts of metabolism etc. Moreover, the cells of the immune system circulate in the blood in addition to the constituents of the coagulation system which contribute in the event of injured blood vessels to rapid sealing of the leaking sites. The soluble (plasma) and cellular components (red and white cells, platelets) of the blood can be separated by centrifugation.

The shape of the red blood cells with their central concavity favours the exchange of oxygen and carbon dioxide and facilitates passage through the capillaries.

Composition Function

Blood plasma Water (90 %)ElectrolytesCations: Anions:magnesium chloridepotassium bicarbonatecalcium phosphatesodium sulphateOrganic constituents Proteins (7-8 %) albumins, globulins

fi brinogen (factor I) lipids glucose

maintenance and regulation of water and electrolyte balance

maintenance of oncoticpressure, protein reserve, transport proteinsblood coagulation

Platelets blood coagulation

White cells granulocytesmonocyteslymphocytes

immune system

Red cells carriers of the red blood pigment haemoglobin

transport of the respiratory gazes:oxygen and carbon dioxide


stimuli, the leucocytes can migrate from blood vessels into the surrounding area, the site of infl ammation.

Granulocytes represent 60 – 70 % of all leucocytes. They are classifi ed according to the staining characteristics of their granules into eosinophilic (stainable with acid eosin stains) basophilic (stainable with basic stains) or neutrophilic (neu-tral staining) granulocytes. The neutrophils are the largest group, accounting for about 70 % of the granulocytes. They play a major part in wound cleansing and defence against infection. Their nuclei contain a range of proteolytic enzymes which enable them to dissolve detritus (injured or denatured cell and tissue substance) and to phagocytose bacteria.

Monocytes are the largest blood cells. In the region of an injury, they leave the circulation and migrate into the injured area. There, they mature into tissue macrophages which take care of the removal of devitalised tissue by phagocytosis (elimination of large particles) or pinocytosis (elimination of dissolved material). The processes of phago-cytosis and the other functions of the macrophages which have a key role in wound healing are described in detail in the chapter on “The processes of wound healing” from page 34.

Lymphocytes are globular cells with a round or oval nucleus which are capable of migration. They represent the main functioning agents of specifi c immunity. B lymphocytes are responsible for humoral immunity (antibodies) and T lymphocytes for cellular immunity (phagocytosis).

White blood cells (leucocytes) In contrast to the erythrocytes, the white blood cells have a nucleus. They are not a single cell type but are classifi ed into granulocytes, monocytes and lymphocytes according to their shape or the shape of their nucleus, their function, staining characteristics of the cytoplasmic granules and their site of formation.

Granulocytes and monocytes arise from bone marrow stem cells. Precursor cells of lymphocytes also arise in the bone marrow but later multiply in lymphatic organs such as the spleen and lymph nodes. Only about 5 % of the total lymphocytes in the body circulate in the blood, while the majority are stored in organs and tissues or are loosely associated with vessel walls.

Leucocytes serve for non-specifi c or specifi c defence and play a crucial part in the removal of bacteria and detritus (damaged or denatured cell and tissue substance). Their capacity for amoeba-like movement which varies according to the cell type is a precondition for them to be able to carry out their functions. When activated by chemotactic

Subtraction-stained representation of a white blood cell migrating through the endothelium of a blood vessel. Because of their capacity for movement, the leu-cocytes can migrate to the “scene of the action” and, for instance, reach an injured skin area where they can act as defence cells.

lymphocytes granulocytes monocytes

neutrophils eosinophils basophils

Classifi cation of white blood cells (leucocytes)


Wounds and wound types

A wound signifi es a break in the continuity of tissues cover-ing the body which is usually associated with a loss of substance. Deeper injuries which involve the muscle tissue, the skeletal system or internal organs are defi ned as com-plicated wounds. Wounds are distinguished into different types depending on their cause, depth and extent of the defect: ▪ mechanical or traumatic wounds ▪ thermal and chemical wounds ▪ ulcer wounds

Mechanical/traumatic wounds Mechanical wounds occur as a result of a variety of forces, including the planned surgical wound.

The type of trauma and the extent of damage are in turn used for further classifi cation for prognosis and for treat-ment. In particular, the aetiology of the wound permits assessment as clean, dirty and/or as infected. This assess-ment is of fundamental importance for subsequent wound management.

Closed wounds are characterised by injury of tissue, bones, blood vessels and nerves lying under the skin without separation of the skin taking place. Examples are closed head injuries with brain contusion, closed fractures or sprains and dislocations. Visible effects of the trauma are mainly soft tissue swelling, haematoma, and pain.

Platelets (thrombocytes) Platelets are round non-nucleated discs which are produced by fragmentation of cytoplasm from giant cells of the bone marrow (megacaryocytes). They are the smallest cellular elements of the blood. Their most important function is haemostasis. They take part in the initiation of coagulation and thrombus formation. Accordingly, their numerous gra-nules contain important blood coagulation factors (platelet factors). The coagulation processes are also described in the chapter on “The processes of wound healing” from page 34.

Non-nucleated platelets in cross section: their numerous granules can be seen clearly, containing several coagulation factors. Platelets take part in the initiation of coagulation and thrombus formation.


Superfi cial or epithelial wounds affect only the avascular epidermis. Since the epidermis is capable of regeneration, the wounds heal without scarring. The skin surface later looks no different from normal. The abrasion is an epithelial wound. Split skin graft donor sites and Reverdin graft sites should be regarded as superfi cial wounds.

Perforating wounds occurs when the division of the skin affects the epidermis and dermis and sometimes the sub-cutaneous tissue. Examples of perforating wounds, which are also designated penetrating wounds include cuts and stab wounds, tearing, bursting and contused wounds, bites and gunshot wounds. Depending on the type of trauma, muscle tissue and internal organs may also be involved so that the boundaries between a perforating wound and a complicated wound are often fl uid. The condition of the wound and tendency to heal differ considerably depending on the aetiology.

Complicated wounds such as extensive soft tissue trauma, open fractures, severe crushing with degloving, amputations and avulsion injuries can be the result of perforating and blunt force. In addition they may also be due to thermal or thermomechanical injuries. In the case of such complex patterns of injury there is also a major problem with further secondary damages. This may be due to vessel injuries with resulting ischaemia, reperfusion phenomena or compart-ment syndromes. Infections or inadequate primary care can also be further causes.

1) Haematoma in closed fracture 2) Abrasion or superfi cial (epithelial) wound 3) Split skin graft donor site which is classifi ed as a superfi cial wound 4) Perforating wound (incised) wound as planned surgical wound 5) Crushing wound to thumb 6) Complicated wound; fracture with signifi cant soft tissue damage 7) Complex open lower leg fracture after traffi c accident with severe soft tissue damage8) Crushing wound with extensive tissue destruction

1 2

3 4

5 6

7 8


Thermal and chemical woundsThermal and chemical wounds arise from the effects of heat and cold, tissue damaging rays, acids or alkalis. The skin damage depends on the severity of the impact (duration, intensity, extent). Classifi cation of burn and cold injuries into three or four degrees of severity, respectively, aids in prognostic assessment and therapeutic planning.

The four grades of burns are: ▪ First degree:

functional damage to the epidermal layer (stratum corneum) manifested as erythema

▪ Superfi cial second degree:destruction of the epidermis down to the basal layer with formation of blisters

▪ Deep second degree:deep dermal burn affecting the epidermis and nearly the entire thickness of the dermis

▪ Third degree:necrosis with complete irreversible destruction of epidermis, dermis and often some of the subcutaneous tissue (full thickness burn)

▪ Fourth degree:carbonifi cation involving muscles, tendons and bones. The classifi cation fourth-degree is not normally used nowadays.

The degree of severity of thermal injury relates solely to the depth of the injury. However, an equally important criterion for prognosis and treatment is the area extent of the burn. Therefore, particularly in emergency situations, this is normally estimated using the “rule of nines” according to Wallace, and expressed as a percentage. Also possible is an estimate of the area by comparing it with the palm of the hands area of the burned person, which represents approximately 1 % of the body surface area. A more precise area assessment can then be made using tables in which

the special features of children‘s body dimensions are also taken into account.

Cold injuries are also classifi ed into four degrees of severity according to what proportion of skin is destroyed: Grade I = erythema, Grade II = blister formation, Grade III = necrosis and Grade IV = formation of thrombus and vessel oblitera-tion.

Injuries due to acids or alkalis should be classifi ed accord-ing to their pattern of damage as burn wounds (“chemical burn”). They are classifi ed and treated as burn wounds after neutralisation of the causative acid or alkali.

1) Third-degree burn with necroses of the epidermis, dermis and por-tions of the subcutis 2) Third and fourth-degree burns 3) Freezing 4) Alkali burn (“chemical burn”)

9 %

9 %9 %

18 %18 %

1 %

18 %

Wallace‘s rule of nines to measure the surface area of a burn

1 2

3 4


Ulcer wounds

A further group of wounds presenting particular healing problems is the ulcera, commonly known as ulcers. In con-trast to acute wounds, they usually occur as a result of local disorders of nutrition in the skin, caused by venous, arterial or neuropathic vascular damage or prolonged local pressure or radiation. However, an ulcer can also be a symptom of a systemic disease, e.g. as a result of certain tumours, infec-tious skin diseases or haematologic disorders. Accord ing to the severity of the trophic disorder, the damage can affect all skin layers and extend as far as bone.

Ulcer wounds usually require more than 8 weeks for healing and are therefore classifi ed by defi nition as chronic wounds. The most important chronic wound conditions are described under this classifi cation from page 96.

1) Decubitus ulcer on heel with closed cap of necrosis 2) Sacral decubitus ulcer with necrosis and wound pockets 3) Venous leg ulcer which has involved the entire lower leg, a so-called gaiter ulcer 4) Leg ulcer, caused by a basal cell carcinoma 5) Diabetic ulcer (mal perforans) 6) Radiation ulcer

1 2

3 4

5 6

The phases of wound healing Irrespective of the type of wound and the extent of tissue loss, the healing of every wound takes place in phases which overlap in time and cannot be separated from one another. The division into phases refers to the fundamental morphological alterations in the course of the repair process without refl ecting the actual complexity of the process. The usual division is into three or four wound healing phases; the system of three basic phases will be used for the follow-ing descriptions:▪ infl ammatory or exudative phase for blood clotting and

wound cleansing ▪ proliferative phase for production of granulation tissue ▪ differentiation phase for maturing, scar formation and

epithelialisation

In clinical practice, the three phases of wound healing are also, for short, called the cleansing, granulating and epithelialising phases.

Schematic representation of the temporal course of the wound healing phases:

The processes of wound healing

The regeneration of epithelium and, in particular, the demanding repair of skin connective tissue, are biologically and chronologically well organised cooperative efforts in-volving a variety of blood, immune system and tissue cells. These drive the healing process forward step-by-step in a variety of wound-healing phases.

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21

infl ammatory/exudative phase

proliferative phase

differentiation and remodelling phase

The processes of wound healing [34.35]

Sequence of physiological wound healing. In the ideal case, the tissue missing from a wound is replaced by functional scar tissue by various interdependent pro-cesses such as blood coagulation, infl ammation and breakdown of devitalised tissue, new vessel for-mation, formation of granulation tissue, epithelialisation and matu-ration. The chronologically correct appearance of the participating cells is essential for the wound healing cascade to take place in a regular fashion. If there is a dis-order of only one of these partial steps, the entire wound healing process can be infl uenced.

The infl ammatory/exudative phaseThe infl ammatory/exudative phase begins at the moment of injury and lasts about three days under physiological condi-tions. The fi rst vascular and cell reactions lead to haemos-tasis and are complete after about 10 minutes.

Vasodilatation and increased capillary permeability result in an increase in the exudation of plasma into the intersti-tium. This promotes the migration of leucocytes into the wound area, especially neutrophilic granulocytes and ma-crophages. It is their job to defend against infection and to cleanse the wound by phagocytosis. At the same time, they release biochemically active mediator substances, by means of which cells which are important for the next stage are activated and stimulated. The macrophages play a key role in that process. Their presence in adequate numbers is cru-cial to the progress of wound healing.

Haemostasis The fi rst goal of the repair process is to stop bleeding. Vasoactive substances are released from the injured cells, producing narrowing of vessels (vasoconstriction) to avoid blood loss until the vessel can be fi rst sealed by platelet aggregation. The platelets circulating in the plasma adhere to the damaged vessels at the site of injury and form a plug which fi rst seals the vessels provisionally.

The complex process of platelet aggregation activates the coagulation system in order to seal the site of injury per-manently. The coagulation cascade takes place in steps in which about 30 different factors participate. This leads to the formation of an insoluble fi brin mesh from fi brinogen. A clot is produced which seals the wound and protects against further bacterial contamination and fl uid loss.

PlateletsCoagulation factors

neutrophilicgranulocytes

Formation of a fibrin clot– as wound seal

– matrix for collagen incorporation

Release of growth factors, stimulating influx of inflammatory cells

immune defence / phagocytosis

macrophages

Release of growth factors andcytokines, stimulation ...

vascular endothelialcells

mast cells,lymphocytes

angiogenesiscollagensynthesis ephithelialisation

Filling of defectby granulation tissue

Contraction, scar formation, epithelialisation, maturation

Diffe

ren-

tiatio

nPr

olife

ratio

nIn

flam

mat

ion

and

clea

nsin

gCo

agul

atio

n

fibroblasts keratinocytes


In order not to endanger the whole organism by spreading thrombotic processes, platelet aggregation and the coagu-lation processes must remain restricted to the site of injury. In fl owing blood, the coagulation process is therefore countered constantly by substances of the fi brinolytic (clot-dissolving) system.

Infl ammatory reactions Infl ammation represents the complex defence reaction of the organism against the effects of a variety of noxious agents either mechanical, physical, chemical or bacterial origin. The goal is to eliminate or inactivate the noxious agent, cleanse the tissue and provide conditions for the subsequent proliferative processes.

Infl ammatory reactions are thus present in every wound, even a closed wound with an intact skin surface. However, they are increased in the case of open skin wounds, which are always contaminated by bacteria.

Infl ammation is characterised by the four classical symptoms of infection, which are: erythema (rubor), warmth (calor), swelling (tumor) and pain (dolor). The arterioles which constrict briefl y at the start of the injury subsequently dilate due to vasoactive substances such as histamine, serotonin and kinin. This leads to increased perfusion within the wound area and therefore an increase in the local metabo-lism required to eliminate the noxious sources. The process is apparent clinically as erythema and warmth.

The vasodilatation at the same time leads to an increase in vascular permeability with increased exudation of plasma into the interstitium. The fi rst phase of exudation takes place about 10 minutes after the injury has occurred, and a second phase occurs one to two hours later. Oedema, which is apparent as swelling, develops due to the slowed circulation and also to the localised acidosis in the wound area. Today, it is assumed that the local acidosis increases catabolic processes and that the toxic breakdown products of tissue and bacteria are diluted by the increase in tissue fl uid.

Pain develops not only as a result of exposed nerve endings and swelling but also due to a number of infl ammatory mediators such as bradykinin. Severe pain can result in a limitation of function (functio laesa).

Blood clot consisting of platelets, red blood cells and fi brin strands

Infl amed wounds with the clearly visible symptom of reddening; above, a burn wound; below, an operation scar following a vascular operation.


Phagocytosis and immune response About 2 – 4 hours after the injury, as part of the infl amma-tory reaction, inward migration of leucocytes commences. These are now called phagocytes and are capable of phago-cytos ing debris, foreign material and micro-organisms.

In the initial infl ammatory phase, neutrophilic granulocytes predominate, secreting various infl ammation-promoting messenger substances, the so-called cytokines into the wound. These cells also phagocytose bacteria and release proteolytic enzymes (proteases) which remove damaged and devitalised constituents of the extracellular matrix. This signifi es the fi rst cleansing of the wound.

About 24 hours later, monocytes migrate into the wound area in the train of the granulocytes. These then differen-tiate into macrophages and continue the phagocytosis. They also intervene crucially in the process by secreting cytokines and growth factors.

Macrophages during the phagocy-tosis of E. coli bacteria

Leucocyte migration continues for a period of about 3 days until the wound is “clean” and the infl ammatory phase is approaching its end. However, if infection occurs, the leucocyte migration persists and phagocytosis is increased. This leads to a prolongation of the infl ammatory phase and thus to a delay in wound healing.

The detritus-laden phagocytes and dissolved tissue form pus. The killing of bacterial material inside the phagocytes can only take place with the assistance of oxygen which is why an adequate oxygen supply in the wound area is of paramount importance for the immune response.

The dominant role of macrophages It is now believed that wound healing is not possible with-out functioning macrophages. The majority of the macro-phages have their origin in haematogenous monocytes whose differentiation and activation to macrophages take place in the wound area. Attracted by the chemotactic stimulus of bacterial toxins and further activation by neu-trophilic granulocytes, the cells migrate in dense rows from the circulating blood into the wound. During their phago-cytic activity, which represents the highest degree of activa-tion of the cells, the macrophages are not limited only to a direct attack on micro-organisms but they also assist in pre-sentation of antigen to the lymphocytes. Antigens captured and partially constructed by macrophages are presented to the lymphocytes in a recognisable form.

Furthermore, macrophages secrete infl ammation-promoting cytokines (interleukin-I, IL-II and tumour necrosis factor �, TNF-�) as well as various growth factors (BFGF = basis fi broblast growth factor, EGF = epidermal growth factor,

Course of phagocytosis: After opsonisation of the foreign body, the phagocyte moves delib-erately to the foreign body (1) and adhesion occurs (2). In the next stage, the phagocyte encloses the foreign body with pseudo-podia (3). By further merging of the pseudo podia (4), a vacuole (phagosome) is produced which merges with lysosomes to form phagolyso somes (5) in which “digestion” of the foreign body can then take place (6).

1 2 3

4 5 6


PDGF = platelet-derived growth factor and TGF-� and -� = transforming growth factor � and �). These growth factors are polypeptides which infl uence the cells involved in wound healing. They attract cells and promote their infl ux into the wound area (chemotaxis), subsequently stimulating the cells to proliferate.

The proliferative phase During the second phase of wound healing, cell proliferation predominates aimed at new vessel formation and fi lling of the defect by granulation tissue. The phase begins on approximately the 4th day after trauma, but the conditions for tissue growth were created in the infl ammatory exuda-tive phase: Fibroblasts from the surrounding tissue migrate into the clot and fi brin mesh formed during coagulation, using it as a provisional matrix for incorporation of collagen. The released cytokines and growth factors stimulate and regulate the migration and proliferation of the cells respon-sible for the formation of new tissue and blood vessels.

New blood vessel formation and vascularisation Without new vessels which will ensure an adequate supply of blood, oxygen and nutrients to the wound area, wound healing can not proceed. New vessel formation starts from intact blood vessels at the edge of the wound.

Through stimulation by growth factors, the cells of the epithelial layer lining the vessel walls (here called endothe-lium), are capable of breaking down their basement mem-brane, mobilising and migrating to the surrounding wound area and into the blood clot. By means of further cell divi-sion, they create a tube-shaped structure which continues to divide at its budlike end. The individual vascular buds grow towards one another and combine into capillary loops which again continue to branch until they encounter a lar-ger vessel into which they can empty. However, circulating endothelial stem cells were recently discovered in the blood which may call into question the current teaching.

A well-perfused wound is extremely rich in vessels. The permeability of newly formed capillaries is also higher than that of other capillaries which takes account of the increas-ed metabolism in the wound. However, the new capillaries are not very resistant to mechanical stresses which is why the wound area has to be protected against trauma. With the maturing of the granulation tissue to scar tissue, the vessels regress.

The model of angiogenesis: break-down of the basement membrane of intact blood vessels by various substances, with resulting release of endothelial cells, formation of vascular buds by cell division (1), which develop further into capillary loops (2).

The role of macrophages in wound healing


2

1

wounding

blood coagulation platelets

inflammation

debridement, immune response angiogenesis

collagen breakdown collagen synthesis wound contraction

macrophages – lymphocytes, granulocytesepithelial cells fibroblasts

proteoglycan synthesisremodelling

wound closure

Granulation tissue Depending on the time of new vessel formation, fi lling of the defect with new tissue begins on about the 4th day after the occurrence of the wound. So-called granulation tissue develops, the formation of which is initiated primarily by the fi broblasts. They produce collagen which matures into fi bres outside the cells and gives the tissue its strength. They also produce proteoglycans which form the gel-like ground substance of the extracellular space.

Fibroblasts The spindle-shaped fi broblasts are not transported into the wound with the blood circulation but migrate mainly from the local tissue which has been injured. They are attracted by chemotaxis. Amino acids serve as substrates, supplied by the breakdown of the blood clot by the macrophages. At the same time, the fi broblasts utilise the fi brin mesh derived from the blood clot as a matrix for the ingrowth of collagen.

The close relationship between fi broblasts and the fi brin mesh led in the past to the assumption that the fi brin is changed into collagen. In fact, however, the fi brin mesh is broken down as incorporation of collagen progresses and the sealed vessels are recanalised. This process, controlled by the enzyme plasmin, is called fi brinolysis.

Fibroblasts thus migrate into the wound area when amino acids from the dissolved blood clots are available and ne-crotic tissue has been cleared away. However, if haemato-mas, necrotic tissue, foreign bodies or bacteria are present, both the growth of new blood vessels and fi broblast migra-tion are delayed. The extent of the granulation formation corresponds directly with the extent of the blood coagula-tion and the infl ammatory process and the body‘s own wound cleansing process with the help of phagocytosis.

Even if fi broblasts are regarded as a “uniform cell type”, it is especially important for wound healing that they differ in function and reaction. Fibroblasts of various ages are found in a wound, differing both in their secretory activity and also in their reaction to growth factors. In the course of wound healing, some of the fi broblasts change into myo-fi broblasts in order to produce contraction of the wound.

Features of granulation tissue Granulation tissue may be called a temporary primitive unit of tissue or an organ which “fi nally” closes the wound and serves as a “bed” for the ensuing epithelialisation. After fulfi lling its tasks, it is gradually changed into scar tissue.

The name granulation was introduced by Theodor Billroth in 1865 and is derived from the fact that the developing tissue exhibits a surface of bright red, glassy-transparent granules. A vascular branch corresponds to each of these granules with numerous fi ne capillary loops as they develop due to the new vessel formation. The new tissue is depo-sited beside the loops. When there is good granulation, the granules increase in size with time and also increase in number so that fi nally a salmon red moist shiny surface is formed. Such granulation indicates good healing. Sta g-nating healing pro-cesses are present if the granulation is covered with sloughy deposits, looks pale and spongy or has a bluish tint.

Electronmicrograph of a fi broblast which, as the most important cell type of the skin connective tissue, is responsible for the synthesis and secretion of collagen, elastin and proteoglycans.

The structure of the granulation tissue is an important indicator in assessing the healing tendency and the quality of wound healing. The above illustration shows spongy granulation tissue where wound healing is inadequate; the fresh red granulation (below), on the other hand, is a sign of a good healing process.


The differentiation and remodelling phaseMaturing of the collagen fi bres begins between about the 6th and 10th days. As the wound contracts, the granulation tissue contains less water and fewer vessels, becomes continuously stronger and organises into scar tissue. Epi-thelialisation then concludes wound healing. This process consists of the formation of new epidermal cells by mitosis and cell migration, mainly from the edge of the wound.

Wound contraction Wound contraction brings the undestroyed tissue sub-stances closer so that the area of “incomplete repair” is kept as small as possible and wounds close spontaneously. Wound contraction is aided by mobility of the skin.

Contrary to the earlier belief, that wound contraction takes place by shrinkage of the collagen fi bres, it is now known that this shrinkage plays a subordinate role. It is rather the fi broblasts of the granulation tissue which are responsible for the contraction. After these fi broblasts have completed their secretory activity, they change partly into fi brocytes (the resting form of fi broblasts) and partly into myofi bro-blasts. The myofi broblast resembles the cells of smooth muscle and like them contains the contractile muscle protein actomyosin. The myofi broblasts contract pulling

the collagen fi bres taut at the same time. This makes the scar tissue shrink and pulls the skin tissue together at the wound margin.

Epithelialisation Epithelialisation of the wound marks the conclusion of healing with the processes of epithelialisation being closely linked to the formation of wound granulation. Granulation tissue sends chemotactic signals for the migration of mar-ginal epithelia on the one hand, while, on the other hand, the epithelial cells require a moist sliding surface for their migration.

Re-epithelialisation is also a complex process which is based on an increased rate of mitosis in the basal layer of the epidermis and the migration of new epithelial cells from the wound edge.

Mitosis and migration The metabolically active cells of the basal layer which are capable of the wound healing reaction obviously have an unlimited potential for mitosis which is normally held in check by tissue-specifi c inhibitory substances, the so-called chalones, but which becomes fully active in the event of injury. Thus, if the extracellular chalone level falls greatly after an injury of the epidermis, as a result of the loss of numerous chalone-producing cells in the wound area, there is a correspondingly high mitotic activity in the cells of the basal layer. This initiates the cell multiplication required to cover the defect.

Wound closure by clearly visible contraction and epithelialisation (left), epithelial margins still fragile (right)


Cell migration also has its special features. Where as during physiological maturing of the epidermis, the cells migrate from the basal layer to the skin surface, the reparative cell replacement takes place by advancement of the cells in a linear direction towards the opposite wound edge. Epithe-lialisation from the wound edge starts with the break in continuity of the epidermis. The separated epithelial cells creep towards one another by active amoeboid movements, which are reminiscent of the ability of single-celled orga-nisms, thus attempting to close the gap. These amoeboid movements however can occur only in slitlike superfi cial wounds. In all other injuries of the skin, the migration of the epithelia at the wound edge is linked to the fi lling of the tissue defect by granulation tissue. Epithelial cells do not descend into hollows or wound craters but require a smooth moist creeping surface.

Migration of the marginal epidermis cells does not take place uniformly or inexorably but probably takes place intermittently, depending on the structure of the wound granulation in each case. The fi rst outgrowth of the margi-nal epithelium is followed by a phase of thickening of the initially single-layered epithelial cover by a heaping up of the cells. In addition, the epithelial layers are soon several layers thick and are stronger and denser.

Features of re-epithelialisation Only superfi cial abrasions of the skin heal according to the pattern of physiological regeneration, and the regenerated tissue is accordingly complete and uniform. All other skin wounds replace the lost tissue, as described already, by cell migration from the edge of the wound and from preserved skin appendages. The result of this re-epithelialisation does not represent a complete skin replacement but a thin sub-stitute tissue which is poor in blood vessels and which lacks important constituents of the epidermis such as glands and pigment cells, and adequate innervation.

Schematic diagram of re-epitheli-alisation by cell division and cell migration. The epithelial cells creep towards one another on the slippery surface of the granulation tissue. When the defect is closed, the epithelial cells become heaped up so that the epithelial cover becomes stronger.


Mitosis

Contact inhibition

Direction ofmigration

Migrating cells

Mitosis

Quantitative classifi cation of wound healing

Since the time of Galen (A.D. 129 – 199), wound healing has been classifi ed into healing by primary intention and by secondary intention. The word “intention” in Galen‘s understanding does not refer to the physiological nature of the healing processes but to the intention of the physi-cian to achieve primary wound healing with wound edges close together and with few gaping wound edges. The classifi cation thus is above all of quantitative signifi cance (more replacement tissue has to be produced in the case of secondary healing) and is important in prognosis. In order to take into account the therapeutic problems which result from the extent and type of the tissue destruction, a further classifi cation is made today into primary delayed healing, regenerative healing and chronic wounds.

Primary wound healing (per primam intentionem)The conditions for wound healing are more favourable the less tissue has been damaged. The prospects of healing are best in the case of a smooth, closely apposed wound sur-faces of an incised wound with negligible loss of substance and without inclusion of foreign bodies in a well-perfused area of the body. Primary wound healing occurs in such cases if there is no wound infection.

Healing by primary intention usually occurs after surgi-cal incisions or accidental wounds made by sharp-edged objects. With a respective type of less tissue destruction by other mechanisms (e.g. tearing or bursting wounds), surgical debridement may create the conditions for primary healing.

Wounds capable of primary healing are closed with sutures, staples or wound closure strips. During blood coagulation, fi brin ensures temporary loose adhesion of the wound sur-faces while the phase of infl ammation and exudation takes place almost unnoticed. The repair processes supervene, characterised by the migration of fi broblasts, the formation of ground substance and incorporation of collagen fi bres. Numerous newly sprouting capillaries feed the young connective tissue and restore the connection with the cir-culation. Both wound surfaces are fi rmly united after about 8 days. However, the wound only attains its fi nal tensile strength in the course of several weeks. The result of the primary healing is a narrow linear scar which is initially red

Primary wound healing of non-infected, closely apposed wound surfaces

Delayed primary healing when the wound is at risk of infection

Secondary wound healing with fi lling of the defect by granulation tissue which changes to scar tissue in the course of healing

Regenerative or epithelial healing of injuries affecting only the epidermis


due to the large number of capillaries. Later it becomes lighter in colour as the number of vessels is reduced. Finally, the scar is whiter than the surrounding normal skin.

Delayed primary healingDelayed primary healing occurs when an infection is an-ticipated. In this case the wound should not be closed with sutures or wound closure strips. To observe for the development of infection, the wound is loosely packed and held open. If no infection occurs, the wound can be sutured approximately between the 4th and 7th days. It then heals by primary intention. If an infection becomes apparent, the wound is classifi ed as healing secondarily and receives treatment as for an open wound.

Secondary wound healing (per secundam intentionem) Secondary wound healing always occurs when tissue gaps have to be fi lled or when a purulent infection prevents direct union of the wound edges. The wound edges are now no longer closely apposed but gape. To close the wound, granulation tissue must be formed (as already described). The energy requirement of the organism is therefore greater than in the case of primary healing and likewise the forma-tion of the granulation tissue is more subject to endogenous and exogenous infl uences.

Regenerative healing Regeneration is defi ned as the replacement of destroyed cells or tissues by others of equal value and is only possible for cells which retain their capacity for mitosis. These in -c lude the basal layer of the epidermis. If only the epidermis is damaged by an injury, e.g. in a skin abrasion wound, it heals without a scar. The healing processes correspond to the wound healing phase of re-epithelialisation.

Chronic wound processes The chronic wound is one undergoing secondary healing which has to be closed by formation of tissue. If this pro-cess requires more than eight weeks, the wound is clas-sifi ed as chronic. The change from an acute to a chronic wound can occur in each of the wound healing phases. However, the majority of chronic wounds develop from progressive tissue destruction because of vascular disease from various causes such as disturbed blood circulation of arterial or venous origin, diabetes mellitus, local pressure injuries, radiation damage or tumours.

Examples of the different types of wound healing: 1) Primary wound healing, in the case of closely apposed wound edges, which is normally possible with surgically produced wounds. 2) Regenerative or epithelial heal-ing, whereby the healed tissue hardly differs from the original condition. 3) Secondary healing with tissue formation – here after dehiscence of a thoracic wound. A secondary suture is made following appropri-ate wound conditioning. 4) Chronic healing process in the case of a sacral decubitus ulcer which, with the requisite formation of granulation tissue, corresponds to secondary wound healing.

1 2

3 4


Nutritional status Wound healing is impaired if the nutrients and nutrient components required for the increased wound metabolism (proteins and calories, vitamins and minerals) are not avail-able in suffi cient quantities. If, for example, not enough protein is provided, protein synthesis is interrupted and with it, the proliferation of granulation tissue cells, and of other cells of the immune defence system. A protein defi ciency therefore impairs all the processes of wound healing, without exception.

Diseases, particularly infections and chronic ulcers, switch the metabolism via cytokine production to a catabolic state, which in turn leads to malnutrition. The body then has a shortage of nutrients available for energy production and good wound healing.

All vitamins, by their properties as coenzymes, positively infl uence wound healing and the defi ciency of only a single vitamin may delay healing. Vitamins of the B complex, for example, participate in collagen synthesis and stimulate antibody formation and infection defence. Vitamin A also participates in collagen synthesis and cross-linking. Anti-oxidants such as vitamins E and C capture the free radicals that are toxic and therefore harmful to the epithelial cells. Furthermore, vitamin C plays a key role in the formation of collagen, as well as being signifi cant for the formation of the intercellular substance, the basal membranes of vessels, complement factors, and gamma globulins.

Of the minerals, it is above all zinc and iron defi ciencies that cause disruptions. Zinc is a central component of the so-called metalloenzymes and has signifi cant biological

Infl uences on wound healing

The ability of the human organism to heal wounds is sub-ject to great individual variation. How quickly and how well a wound heals depends on the general bodily constitution of the affected organism, on the aetiology of the wound and on the resulting specifi c circumstances.

Systemic infl uences General infl uencing factors depend on the individual physi-cal status of the person affected. Their relevance for the course of healing is very variable and some “infl uences” are themselves the cause of the wound.

Patient age Clinical research suggests that physiological aging delays wound healing through the general reduction in cell activ-ities which can lead to a loss of quality in wound healing. However actual disorders of wound healing result mainly from the effects of age-related co-morbidity such as poor immune status or defi cient nutrition. Ulcer wounds as a result of metabolic disease, vascular disease and tumour in-evitably also occur more frequently. Then a correspondingly poor healing tendency can be expected.

60

50

40

30

20

10

020 40 60 80 100

Years

Days

Healing of a 20 cm² wound according to the person‘s age


effects in the organism, which also extend to wound heal-ing. Iron defi ciency leads to anaemia and therefore hinders oxygen transport to the wound area.

Malnutrition, possibly leading to cachectic conditions, can often be observed in severely ill, multimorbid and elderly persons. It can be caused by diseases such as tumours, infectious diseases, organ disorders and severe pain. Nutri-tional causes such as inadequate intake of nutrition or disorders of absorption often play a major part.

Immune status The processes of the immune response play an important role during wound healing. Accordingly, impairment or defi ciencies of the immune system cause increased sus-ceptibility to disorders of wound healing and infection. Acquired immune defi ciencies can result from operative trauma, parasitic, bacterial or viral infections and also occur after periods of malnutrition, extensive burns, injury with ionising radiation, entero- or nephropathies and cytostatic immunodepressant treatment.

Underlying diseases Diseases with an inhibitory effect on wound healing are again mainly those which impair the immune status of the affected organism such as tumours, autoimmune diseases and infections. Delayed or abnormal healing can be antici-pated also in the case of connective tissue diseases (e.g. rheumatoid disease), metabolic disease (e.g. diabetes melli-tus) and vascular diseases (e.g. peripheral vascular disease, venous insuffi ciency). Diabetes mellitus and arterial/venous vascular disease, in particular, are themselves the cause of ulceration.

Important systemic and local infl uences on wound healing

Postoperative complications Numerous postoperative complications have a direct effect on wound healing: thrombosis and thromboembolism, possibly due to the increased fi brinolytic activity, postoper-ative pneumonia, postoperative peritonitis, postoperative ileus and postoperative uraemia. The “intoxication” with degradation products before they are excreted in the urine apparently has an inhibitory effect on the course of healing.

Affects of acute trauma/shock Trauma associated with blood loss or major fl uid loss, such as in severe burns, causes a large number of mediator-induced reactions which can lead to a disorder of the micro-circulation. Subsequent tissue hypoxia, increased capillary permeability and clinically detectable abnormal perfusion develop as symptoms of shock. The resulting imbalance between oxygen requirement and supply and the delay in removal of products of metabolism particularly affects the initial phase of wound healing and the immune response.

General (systemic) Local

▪ Age▪ Nutritional status▪ Immune status▪ Underlying illnesses▪ Postoperative complications▪ Acute traumas▪ Medications▪ Psychosocial situation

▪ Extent of injury (size, depth, etc.)

▪ Condition of wound bed (pus, necrosis, etc.)

▪ Condition of wound edges(smooth, jagged)

▪ Bacterial colonisation, contamination, infection

▪ Site of wound▪ Age of wound▪ Quality of wound management▪ Surgical conditions and

circumstances


Medications Different drugs have a direct negative effect on wound healing, especially immune suppressant, cytostatic, anti-infl ammatory (mainly glucocorticoids) and anticoagulant agents. Depending on the inhibitory effect of the various drugs on coagulation, infl ammatory processes and prolif-eration, formation of granulation and scar are particularly affected so that the wound‘s resistance to tearing can be expected to be reduced. However, the effects on the repair mechanism of the tissue depend on the dosage, the time of administration and the duration of therapy.

Patient‘s psychosocial situation Wound healing, especially healing of chronic wounds of metabolic origin such as diabetic ulcers, require a large degree of collaboration of the patient. The individual‘s psychosocial situation, however, can create a wide variety of different starting conditions with regard to the patient‘s willingness and motivation for cooperating in the treatment. Above all, the number of elderly patients with chronic wounds who also suffer from dementia is constantly increas-ing, so that adequate compliance is no longer assured with these individuals. Self-harming tendencies also have to be taken into account.

Moreover, alcohol and nicotine abuse as well as illegal drugs may also have negative effects on wound healing. Apart from the vascular injury component of drug abuse (arteriosclerosis, severe perfusion abnormalities) this group of patients is often in poor general condition with reduced immune responses and a poor nutritional status.

Local infl uencesThe condition of the wound and the quality of the wound management are other important infl uences on wound healing.

Condition of wound A range of factors must be considered when assessing the condition of the wound and the resulting consequences for wound healing:▪ aetiology/extent of injury (size, depth, involvement of

deeper structures such as fascia, muscle, tendons, cartilage, bone)

▪ condition of wound edges (smooth, irregular, jagged, undermined, with pockets)

▪ condition of the base of the wound (proportion of necrotic tissue, composition of the necrotic tissue: closed black necrosis, crust, sloughy tissue, dirty, presence of foreign body, clean)

▪ composition of exudate (bloody, serosanguinous, purulent, dried out)

▪ extent of bacterial colonisation/signs of infection (see also chapter on “Wound infection”)

▪ site of wound (in well or poorly perfused region) ▪ age of wound (acute trauma, time elapsed from injury to

fi rst aid/treatment, chronic wound conditions)

In the case of surgical wounds, the local infl uences include type of operation, site of operation, duration and type of operative preparation, and the quality of hygiene manage-ment in the operating theatre, operative techniques and duration of the operation.

Two methods for determining the size and volume of a wound: With a wound of large area (above), lay a transparent foil over it and mark the wound outline with a felt-tipped pen and calculate the area. The size and volume of a wound may be determined by measuring the fl uid-holding capacity (below), in that the wound is covered with foil and sterile fl uid injected into it. The quantity of fl uid in ml. or cc. represents the wound volume.


Quality of wound treatment The quality of wound management has a signifi cant infl u-ence on wound healing. Depending on the type and cause of the wound, wound management requires a variety of therapeutic measures. These include surgical procedures to treat acute trauma and complex causal therapies to control chronic wound conditions or correct dressing treatment. Good wound management involves many medical disci -p lin es and frequently the success in wound treatment is only possible with interdisciplinary collaboration.

The principles of wound treatment in acute (from page 80) and chronic (from page 96) wounds are described in the corresponding chapters.

Disorders of wound healing

Disorders of wound healing occur in different manifesta-tions and to a varying extent due to the effects of one or more of the infl uences described above. The more severe disorders arise from stagnating wound cleansing, poor quality or delayed formation of granulation tissue, absence of re-epithelialisation along with typical post-operative complications (seromas, haematomas, wound dehiscence and hypertrophic scar formation) and wound infections.

Seromas Seromas are hollow spaces in the wound area in which blood, serum or lymph collects. They occur due to irritation in the wound area, e.g. caused by foreign bodies, coagula-tion necroses by excessive use of electrocoagulation or mass ligatures, but also in the case of tension in the wound while having tight sutures, or subclinical infection. Transudates during protein defi ciency, generalised illnesses or impaired lymph fl ow are further causes.

Smaller seromas can be aspirated with a syringe, but a formal wound revision is necessary for larger ones. The wound is opened at the sutures and explored. Persistent lymph channels should be coagulated with diathermy. A Redivac drain is inserted and should only be removed when the skin has attached fi rmly to the underlying tissue. One complication can be that the primarily sterile seromas become infected due to the stagnant fl uids which favour bacterial growth. Those seromas must then be treated as abscesses.


Wound dehiscence (rupture) Wound dehiscence is a disorder of wound healing in which parts of the wound surfaces do not adhere and become bound by connective tissue despite apposing sutures. Examples of predisposing factors include: sutures causing ischaemia, sutures removed too soon, malnutrition, factor XIII defi ciency, obesity, consuming neoplasms, postopera-tive coughing or diabetes mellitus. In addition, treatment with cytostatics, corticoids or antibiotics also increase the risk of rupture.

Postoperative wound dehiscence after laparotomy can be complete (affecting all layers), incomplete (intact peri-toneum) or occult (skin suture still closed). The symptoms are a serosanguinous wound secretion commencing on the 3rd day, increase in wound pain, gastric atony, paralytic ileus or evisceration (bowel protruding through the wound). The dehiscence is treated by operation, if necessary insert-ing a plastic mesh. The prognosis is good when treated promptly and mortality is less than 10 %.

Hypertrophic scar formation Some people tend to form excessive scar tissue, the causes of which may be disorders of collagen formation and cross-linking. Hypertrophic scars develop soon after operation, usually remain limited to the wound and demonstrate a spontaneous tendency to regress.

The wound site also plays a part in the formation of hyper-trophic scars with regard to the skin‘s creases. If an incision runs vertical in the direction of Langer‘s lines, hypertrophic scarring can be anticipated. These circumstances gain particular signifi cance in regions of the body where tensile forces act in the longitudinal direction of the scar because of strong muscle activity. The result is then not only a cos-metic failure. The scar crossing a joint restricts the range of motion with increasing scar contracture.

Wound haematomas Wound haematomas form in the wound crevice as a result of inadequate haemostasis of the vessels opening into the wound region. Postoperative rise in blood pressure and re-perfusion of collapsed vessels are other causes. They often occur when coagulation is impaired due to anticoagulant therapy or in the event of pathological defi ciencies in the coagulation system.

The clinical signs of a secondary haemorrhage are increas-ed respiratory and pulse rate, fall in blood pressure, local swelling. A blood count and coagulation screen should be performed with monitoring of vital signs. For small haematomas, the application of ice and aspiration may be suffi cient to limit them. Larger haematomas must be eva-cuated as potential foci of infection. The revision is usually undertaken in the region of the previous skin incision. All coagulum must be removed. After irrigation with Ringer‘s solu tion, a Redivac drain is inserted and the wound is closed.

Soft tissue necrosis Soft tissue necrosis occurs when the supply of nutrients to the wound edges or soft tissues is reduced or interrupted by the injury or congestion of the supplying vessels, e.g. by inadequate type of incision, severe trauma of the skin or incorrect suture technique. As a rule, it can be recognised only in regions close to the skin wound and it should be observed for demarcation.

In the early days of wound healing, it is apparent as pale or cyanotic areas of skin which gradually become brown in colour. Skin necrosis must be kept dry and should not be removed prematurely as it functions as a sterile dressing. It is removed only after spontaneous demarcation. Moist necrosis, on the other hand, must be removed immediately because of the risk of deep retention of pus.

Necrosis of wound edge in the area of suture of an amputation stump

Extensive wound haematoma

Hypertrophic scar formation after burn

Complete rupture with muscle necrosis after a bypass operation in the knee (above), rupture after large bowel resection (below)


When burns have healed in this manner, an attempt is made to prevent scar hypertrophy by compression with custom-made elastic clothing (pressure garments).

Keloids Distinguishing keloids from hypertrophic scars is diffi cult initially. There are also scar growths which are rich in fi bres and which tend to recur even after subsequent excision. Their structure, which consists of thick glassy or hyaline cords of collagen embedded in a mucilaginous matrix, is crucial in distinguishing them from hypertrophic scarring. Even the smallest incisions can cause sizeable keloids which develop independent of muscle movement and rarely over joints. In contrast to hypertrophic scars, keloids often exceed the wound edges in their development and do not demonstrate any tendency to regress. Surgical correction often aggravates the situation.

Wound infection

Wound infection is the most serious disorder of wound healing. It is caused by a variety of micro-organisms which invade the wound and multiply, producing harmful toxic substances. The infection is usually limited locally, and leads through destruction of tissue to disturbances of wound healing which vary in severity. However, every wound infection can also extend systemically to become life-threatening sepsis.

Signs of infection The signs of wound infection described by the Roman scientist Aulus Cornelius Celsus (1st century AD) such as rubor (erythema), tumor (swelling), calor (warmth), and dolor (pain), still serve as an aid to its recognition. They are an expression of the defensive struggle of the immune system against the invading micro-organisms. General signs and symptoms include fever, rigor, leucocytosis and lymph-adenopathy and leucocytosis. Fever, in particular, requires careful elucidation.

The earlier the diagnosis of infection is made, the better is the prospect of getting it under control in good time. How-ever, recognising the onset of infections is associated with diffi culties because unequivocal symptoms are still absent.The continuation of a local state of irritation, febrile tem-peratures, persisting leucocytosis and increasing wound pain are signs and symptoms which must be taken seriously.

Keloid with typical collagen cords

Aulus Cornelius Celsus, who lived in the fi rst century AD is consider-ed, despite uncertainty about his precise dates, to be the author of the most important medical works of the ancient world.


Predisposing factors The occurrence of infection is a complex process infl uenced by many predisposing factors. Of critical importance for the initiation of an infection are fi rstly the type, the pathogen-icity, virulence and the number of micro-organisms involved. The micro-organisms then fi nd a certain environment in the wound which more or less meets their living conditions. This explains why age, genesis and the condition of the wound (degree of contamination, extent of destroyed tissue and degree of perfusion), are other important predisposing factors. How quickly and effective the local defence mecha-nisms can form, depends on the wound condition.

This, in turn, is dependent on the general immune status of the involved organism. An already weakened immune sys-tem, reduced general condition, certain metabolic diseases, malignant tumours, advanced age, and malnutrition also have negative effects on the immune response. This means that penetrating micro-organisms fi nd further favourable growth conditions.

PathogensThe causative agents of wound infections can be viruses, fungi and bacteria, with bacteria being implicated in the vast majority.

Bacteria are unicellular micro-organisms, whose cell interior is moderately differentiated. It consists of a “nucleus equi-valent” containing genetic material as well as of cytoplasm containing ribosomes, various enzymes and plasmids (carriers of resistance genes). The outer cell wall can be found covered with a capsule of varying composition which can protect the bacteria against desiccation or against phagocytic cells.

Many bacteria form poisonous substances or toxins. The basis for toxin formation can be both exotoxin from the cytoplasm and endotoxin from the cell wall. The exotoxin is produced continually by the bacteria from the interior of the cell, e.g. in the case of gas gangrene organisms. Endotoxin is liberated only when the cell breaks up with destruction of the cell wall.

Bacteria are classifi ed as obligate aerobic bacteria if they require oxygen to live, and as anaerobes if they need an oxygen-free environment. They are facultative aerobes or anaerobes if they can exist in both milieus. Differentiation of bacteria is by certain staining methods, for instance Gram‘s stain to distinguish them as gram-positive and gram-negative bacteria.

Structure and characteristics of gram-positive and gram-negative bacteria

flagellapili

cell wall cyto-plasm

cell membrane

outermembrane

plasmid

capsule

gram-positive gram-negative

periplasmic gap

nucleus equivalent

ribosomes


Pathogenicity Bacteria only merit consideration as pathogens of infectious disease or of wound infections if they possess a disease-inducing potential (pathogenic).

Bacteria may already be highly pathogenic when they in-vade the wound. The human organism then has no time to activate the body‘s own defence mechanisms. Such infec-tions are life-threatening. An example is tetanus caused by Clostridium tetani.

Other pathogenic strains are facultative, i. e. partially pathogenic. These are often bacteria from the physiological colonisation of the human organism which have left their natural location, penetrated into the wound and unleashed their pathogenic potential in the altered environment. This is the case, for example, when Escherichia coli from the bowel fl ora gets into the wound. In the case of Staphylo-coccus aureus, likewise an important causative agent of wound infections, the human carrier rate is about 30 %, with the main reservoir being the nose.

Another group of bacteria is classifi ed as non-pathogenic. However, in the predisposed patient, with reduced immune defences, this can lead to opportunistic infections and wound infection. An example is Staphylococcus epidermidis which is normally found as an innocuous bacterium on the skin.

Virulence The pathogenicity, or the potential of bacteria for causing illness, should be seen in close association with their viru-lence (infective force) which ultimately determines the degree of pathogenicity. Virulence is an acquired alterable characteristic: avirulent or slightly virulent bacteria can change genetically under the pressure of environmental infl uences and can become extremely virulent. This problem is particularly present in hospitals. Here new genotypes have developed due to the concentrated use of antibacterial therapy which are more virulent and more resistant to chemotherapeutic agents and disinfectants than, for ex-ample, the same type of bacteria in a domestic setting.

Dose of pathogen – manifest wound infection Every wound, even so-called aseptic surgical wounds, are colonised by bacteria. The mere presence of bacteria in the wound, however, does not mean the same as a wound infection, but is designated as contamination. The body‘s defence mechanisms are often capable of removing bacte-rial colonisation so that infection does not occur at all. It is only when the bacteria penetrate deeper into the wound, multiply there, damage the tissue by their toxins and pro-duce infl ammatory reactions that infection can be said to be present.

Electronmicrographs of bacteria with differing pathogenicity: 1) Clostridium tetani, gram-positive, cause of tetanus, highly pathogenic 2) Escherichia coli, gram-negative, at early stage of division, faculta-tive pathogen 3) Staphylococcus aureus, gram-positive, complete bacterium with a bacterium dissolved by effect of antibiotic in right upper corner, facultative pathogen 4) Staphylococcus epidermidis, gram-positive, during division; non-pathogenic

1 2

3 4


Multiplication of bacteria is always by division. Apart from highly virulent bacteria, the reproductive activity of bacteria begins a few hours after adapting to the new nutritional situation. This incubation time is generally eight to ten hours. After that the bacterial count increases rapidly.

Condition of wound and susceptibility to infectionThe fresh wound is highly susceptible to infection. With increasing organisation of the defence mechanisms, the risk of infection diminishes so that a wound with well vascular-i sed granulation tissue can already counter the pathogens with considerable resistance. Older chronic wounds also appear to have a lower susceptibility to infection. However, as long as the wound is not protected by a closed epithe-lium, the risk of infection persists.

The cells and substances important in local defence and antibody production and the oxygen required for phago-cytosis depend on suffi cient circulation. If perfusion in the wound area is reduced or absent, the risk of infection increases considerably.

Necrotic tissue has no perfusion and represents an ideal breeding ground for bacteria. All traumatic wounds with crushing, tearing and loculation of tissue are thus particu-larly at risk of infection. In the treatment of such wounds, infection should be assumed from the outset in order to create a “clean” wound situation in good time by compre-hensive wound excision. If there are areas of closed necro-sis (typical of decubitus ulcers) it should be borne in mind that there may be a purulent infection beneath the necrosis which can spread into deeper tissue layers.

Moreover, stagnant secretions loaded with bacteria, such as in deep and gaping wounds, are also dangerous. It may occur a so-called moist chamber where this negative effect may be reinforced by an unsuitable dressing with inadequate absorbency and moisture permeability.

Logically, the number of invading bacteria, the pathogenic dose, is of critical importance. The more bacteria invade, the greater the probability that a infection will occur. Measurements of standardised samples have shown that 104 pyogenic Streptococci/mm3 or 105 – 106 Staphylococcus aureus/mm3 have to be present to produce a wound infec-tion. Depending on the clinical condition, a bacterial count of 105/mm3 tissue is the approximate guiding principle for an infection requiring treatment.

When taking a wound swab, correct technique is crucial for a reliable result. The swabs should be taken from the depths of the wound and from the wound edges as the pathogens are concentrated at these sites.

4 hours4096 bacteria



The speed of division (generation time) in a favourable environment and at the optimum temperature is about 20 to 30 minutes for many bacteria. The diagram shows the theoretical multiplication of a single bacterium with a generation time of 20 minutes after 4, 8 and 10 hours.


Foreign bodies, such as suture material, plastic parts or im-plants may cause a local reduction of the body‘s defences. They may cause a marked ischaemia and a risk of infection. The site of the wound is also of signifi cance with respect to the risk of infection as the individual body regions have both a variable perfusion and a variable level of bacterial colonisation.

Finally, the aetiology of the wound plays a major role in the risk of infection. In the case of surgical incisions, the risk of infection is always dependent on the type of operation with its specifi c hygienic risks (aseptic and partially aseptic procedures, surgery in a primarily contaminated and in a primarily septic wound area). Other risks emanate from operative preparation and performance and from post-operative wound care. Important factors confi rmed by various studies include: ▪ duration of pre-operative stay on the ward, because

with each day the patient´s colonisation by nosocomial organisms increases

▪ preoperative antibiotic regime ▪ preoperative shaving of the operative fi eld ▪ hygiene status and quality of hygiene management in

the operating theatre ▪ operative techniques, degree of tissue trauma (faulty

incision, diathermy, suturing and ligating technique) ▪ duration of operation (the number of pathogens increas-

es, exposed tissues are jeopardised more because of drying, circulatory disturbance, reactive oedema etc.)

▪ wound drains and their postoperative care

All wounds due to external force, such as stabbing, crushing and impalement wounds, should generally be considered as being infected, as organisms always get into the wound along with the object causing the injury. The same applies to bite wounds as very virulent micro-organisms are trans-mitted with animal and human saliva.

Types of infectionThe different types of pathogens produce specifi c tissue re-actions which characterise the clinical signs and symptoms of the infection.

Pyogenic infection The causes of pyogenic, or pus-producing infections are above all the pygenic agents such as gram-positive staphy-lococci and streptococci as well as gram-negative pseudo-monas and Escherichia coli. An experienced clinician can deduce the main type of pathogen from the appearance and smell of the exudate. Nevertheless, a culture swab with antibiotic sensitivity should not be omitted as the basis for adequate antibiotic treatment. ▪ Staphylococci: creamy yellow odourless pus ▪ Streptococci: runny yellow-grey pus ▪ Pseudomonas: blue-green sweet-smelling pus ▪ Escherichia coli: brownish faeculent-smelling pus

Putrid infection Putrid infection or putrid faeculent tissue gangrene deve l ops from mixed infections with Escherichia coli and the putre-factive organisms Proteus vulgaris and Streptococcus putrides. The putrefactive organisms destroy the tissue and foul-smelling gases form during the breakdown of the protein structures. The clinical appearance is of gangrenous infl ammation with gas phlegmon in the surrounding tissue.

The blue-green sweetish-smelling pus is typical of a pyogenic pseudomonas infection


Emergency treatment with an antibiotic effective against both aerobes and anaerobes must be started without wait-ing for bacteriological diagnosis.

Gas gangrene The gas gangrene pathogens Clostridium perfringens, Clostridium novyi and Clostridium septicum which occur in soil and street dust are obligate anaerobes and fi nd ideal growth conditions in gaping, necrotic and poorly perfused wounds. They rapidly give off tissue-dissolving and gas-pro-ducing exo- and endotoxins which quickly lead to general intoxication of the organism. Genuine gas gangrene (as opposed to gas phlegmon in putrid infections) occurs rarely and is usually fatal.

Tetanus The aetiological agent is Clostridium tetani, also an obligate anaerobe occurring in soil and street dust. Once again, gaping, contaminated and poorly perfused wounds are particularly at risk, but every tiny injury of the skin can be the site of entry. The nerve toxins released by the bacteria migrate along the nerve tracks to the spinal cord and cause severe spasms which spread in a craniocaudal direction. Tetanus immunisation offers protection against tetanus which has without immunisation a fatal outcome in about 50 %. If immunisation is uncertain in the event of an injury, the patient is considered non-immune and receives active and passive immunisation protection.

Rabies Rabies, caused by rhabdovirus, is transmitted with the saliva in a bite from an infected animal. The virus enters the bite wound and ascends along the nerves to the central nervous system. Total paresis and death occur. When the condition is established, every therapy fails so that treat-ment must be given as soon as rabies is suspected (abnormal behaviour in the biting animal).

Erysipelas Erysipelas is a relatively common bacterial disease, usually caused by �-haemolytic streptococci. It starts acutely with fever, rigor, swelling, erythema, and tenderness of the affected skin. Favoured sites are the lower leg and face. The diagnosis can be made easily from the typically sharp demarcation between healthy areas of skin and the fi ery erythema. Tiny erosions of the skin or mucous membrane are suffi cient as an entry portal; outfl ow obstructions in the lymphatic and venous system favour its occurrence. A rare form causing severe illness is necrotising erysipelas with symptoms of shock.

Prevention and treatment of wound infections The prevention of a wound infection means the greatest possible prevention of bacterial colonisation, while treat-ment concentrates on a corresponding reduction of the existing bacterial colonisation or on elimination of the in-vading bacteria. The measures which serve for prophylaxis and treatment should not be seen in isolation but as an overall concept, and require a disciplined approach by all involved in wound care.

Gas gangrene with soft tissue necrosis which has already turned black; typically, there is crepitus on palpation.

Erysipelas of the lower leg with typical sharp demarcation from the healthy areas of skin (above); advanced, already necrotising erysipelas, also of the lower leg (below).


An overriding measure is strict observance of asepsis. It is an essential requirement for preoperative preparation, intra- and postoperative activity and for the open wound treatment in all acute and chronic wound conditions.

Even wounds which are already clinically infected should be treated exclusively under aseptic conditions. Apart from the fact that further secondary infections must be prevented, such wounds represent a reservoir of extremely virulent organisms, spread of which can be prevented only by com-prehensive asepsis.

Other measures to prevent and treat wound infections are in turn dependent on the condition of the wound and require an adequate procedure:

In the case of infected wounds which have had primary closure, rapid drainage of secretions should be obtained by opening the suture and using suitable wound drains. In all wounds healing secondarily such as traumatic or chronic ulcerative wounds, extensive surgical debridement is to the fore: necrotic and devitalised tissue must be removed generously, wound loculations opened up, sloughy deposits, foreign bodies and infected areas excised. At the same time, tissue per fusion is ensured with oxygen delivery which is essential for the body‘s local defences.

If surgical debridement is not possible because of certain circumstances, physical wound cleansing with moist dressing treatment and possibly the topical application of enzymatic preparations is indicated.

Antiseptics According to the general defi nition, the prophylactic/thera-peutic aims of antisepsis consist in killing or deactivating microorganisms, or preventing them from multiplying by using locally acting chemical substances designated anti-septics or antiinfectives. Since wound antiseptics have a more or less cytotoxic potential, the most suitable wound antiseptic needs to be chosen in each treatment case. The following basic requirements should be met by the prepa-ration: ▪ reliable germ-killing (microbicidal) or inactivating effect

against a wide spectrum of microorganisms ▪ no protein-related faults, i.e. no loss of effectiveness of

the antiseptic when affected by proteins (since during open wound treatment, the antiseptic is always in contact with proteins, e.g. in the blood and wound secretions, particular attention should be paid to this point)

▪ rapid onset of effect ▪ no development of microbial resistance or gaps in

effectiveness ▪ no pain caused ▪ greatest possible cell and tissue tolerance and toxi-

cological safety ▪ simple use and storage

Infective agents are present every-where, even if they are not visible to the naked eye. The illustrations show an apparently clean needle tip (1). The magnifi cations (2) and (3), however, reveal heavy bacterial colonisation (yellow).

1 2 3


A reduced-risk application of antiseptics in open wound areas therefore always presupposes that the user is thorough ly informed about the particular properties of the selected substance and, in particular, about its effects on the immunologically active cells.

In general, the principle applies that treatment with anti-septics should be carried out as briefl y as possible. Anti-septic application should be stopped as soon as the clinical signs of infection cease (e.g. when secretion and swelling subside). The progress of treatment should be assessed daily and possibly checked with microbiological diagnostic methods.

Above all in the case of chronic wounds, it is not infrequent-ly observed in clinical practice that antiseptic treatment may be continued for weeks or months without problems and without regard to any treatment success. Whereas during the infection stage, the disruption of sensitive wound heal ing processes by relatively cytotoxic antiseptics can be disregarded, since they are already severely disrupted by bacteria, long-term use carries the potential for signifi -cant damage. The undesirable effects of these substances signifi cantly worsen the poor healing tendency of chronic wounds, and can trigger contact allergies. Added to this is the fact that long-term use of antiseptics is often regarded as a suffi cient and safe wound treatment method, so that nothing is done to diagnose and treat the actual causes of the poor wound healing.

Antibiotics Treatment with local antibiotics is a controversial subject and is generally regarded today as obsolete. The reasons for this lie in their selection of resistant germs, sensitisation of the patient and the consequent loss of a potential anti-biotic for systemic treatment, as well as the danger of super-infection with fungi. Contrasted with this, the systemic administration of antibiotics for local progressive infections (phlegmons, lymphangitis, etc.), deep infections (emphyse-ma, osteomyelitis, etc.) and generalised infections (sepsis) is absolutely necessary. When choosing an anti biotic, the pathogen spectrum needs to be taken into account in accordance with the germ identifi cation and resistance testing. In the event of a dramatically developing infection process, an empirical initial treatment should be begun, and broad-spectrum antibiotics have proved valuable for this. The treatment is then assessed following performance of an antibiogram and a resistogram and adjusted accord-ingly if required.

Left: Escherichia coli, resistant to two antibiotics (no halo).

Right: Staphylococcus aureus dur-ing destruction by an antibiotic: destruction of the outer cell wall with release of intercellular mate-rial into the surroundings.


The goal of every wound treatment is to assist the organism to achieve as soon as possible functional regeneration or repair of the injured tissue. Fundamental measures include: ▪ evaluation of the wound with regard to aetiology, site,

age and condition along with any concomitant injuries and underlying illnesses

▪ elimination of bacterial colonisation and factors favour-ing it by means of thorough debridement

▪ wound closure by primary or secondary suture or by skin or fl ap transplantation

The degree and extent of the individual measures differ according to the wound fi ndings and the healing that can be expected. The principles and techniques of wound treat-ment in the case of acute traumatic wounds are summaris-ed in brief below. However, it must be borne in mind that a rigid treatment plan is ruled out by the variety of individual patient circumstances. Ultimately, the skill of the person treating the patient is of fateful signifi cance for the patient.

The acute traumatic woundRelated to the mechanism and the circumstances of the accident, traumatic injuries cause a wide spectrum of damages. They range from the incised wound to complex defects with involvement of tendons, muscles, nerves, vessels, bones or internal organs. Apart from trivial injuries, treatment is classifi ed for practical reasons as provisional or defi nitive wound treatment.

The treatment of acute traumatic wounds was probably the earliest medical activity. Pioneering successes were achieved towards the end of the 19th century when, with the dis-coveries of antisepsis and asepsis and the development of anaesthetic techniques, the restricting factors of surgery were cleared away. Today, the surgical treatment of trau-matic wounds has reached a high level. Particularly helpful are the possibilities of plastic surgery, which offer survival and acceptable wound healing results to some severely injured people.

Acute wounds [80.81]

Principles of treatment of acute wounds

Provisional wound treatment includes: ▪ fi rst aid measures for haemostasis ▪ application of an emergency dressing to protect against

infection and for transport ▪ if necessary, immobilisation of the injured body parts and

limbs

However, in the case of severe injuries accompanied by shock, immediate initiation of shock therapy and stabilisa-tion of the vital parameters, always takes precedence over provisional wound care.

Defi nitive treatment or primary care follows basic surgical principles. With the exception of superfi cial skin defects, all other wounds are explored surgically with adequate anal-gesia and under aseptic conditions. Inspection of the outer wounds suffi ces only in very rare cases. Further radiological or neurological investigations may be necessary to confi rm suspected foreign bodies in the depths of the wound, frac-tures or nerve an head injuries.

Prompt debridement has the aim of rendering a wound low in bacteria and well perfused. Tissue with impaired perfusion such as obvious necrosis and crushed soft tissues is excised in order to obtain a smooth and clean wound, thus removing the breeding ground for wound infections. Nerves, tendons and muscles should be protected and pre-served as far as possible. Injured vessels should be treated immediately by vascular surgical techniques.

Particular care is warranted in the case of deep and gaping wounds. Foreign bodies such as particles of dirt, fragments of cloth or glass splinters may be detected by soft tissue X-rays only with diffi culty but must not remain in the wound because of the associated high risk of infection. Superfi cial

Management of traumatic wounds

epithelial wounds are cleaned by irrigation. Finger and facial injuries are not excised provided the wound edges have not been crushed.

In general, debridement of the wound is a demanding sur-gical operation and requires meticulous care on the part of the surgeon, based on solid anatomical knowledge.

The decision on wound closure depends on the extent and the result of the debridement. Primary wound closure by

Provisional wound treatment

� treatment of shock, where necessary� haemostasis� emergency dressing� immobilisation� transport to hospital

Defi nitive wound treatment

Lower leg fracture (above), severe fi nger trauma due to injury on a conveyor belt (below).

� operative wound exploration� debridement� decision on wound closure

Wound closure

primary / primary delayed

secondary / open

dressing to protect wound

moist dressings to condition the wound

later closure by secondary suture,spontaneous epithelialisation,skin graft, plastic surgical procedure


suture, staples or wound closure strips is possible if the wound edges can be approximated without tension and if it can be ensured that the wound is suffi ciently clean.

A wound must never be closed under tension as every forced wound closure endangers wound healing because the sutures cause ischaemia resulting in a disturbance of tissue perfusion leading to necroses and infections. In case of doubt, the wound should be left open for secondary wound healing.

To ensure low levels of micro-organisms when primary wound closure is attempted, apart from correct debride-ment, the following conditions must be met: ▪ the wound must not be older than 6 – 8 hours and ▪ it must not be due to causes which from the start involve

a high probability of primary infection

This includes all bite wounds, including human bites, tear-ing and scratch wounds from animals, stab and shooting injuries. In addition, it includes injuries in persons who have come in contact with infectious material such as human or animal pus or excrement.

Knowledge of the mode of injury and accompanying circumstances are thus of crucial importance for assessing the risk of infection and the procedure to be adopted.

Postponed primary care is often considered in the case of wounds which are unsuitable for primary closure. The wound is debrided but is then kept open for observation with sterile moist dressings or by packing for a few days. If no signs of infection appear, the wound can be closed by suture, usually between the 4th and 7th days. The sutures for wound closure are usually inserted during the initial treatment but left untight.

The question of wound closure in the case of wounds which are healing secondarily with their varying degrees of tissue destruction is much more complex. Simple skin defects with or without exposed muscle can usually be closed by secondary suture after operative revision, adequate debri-dement and conditioning of the wound with skin substitute materials or can be covered by split skin grafts. If there are complex defects, reconstruction of the soft tissues using plastic surgical procedures is essential.

Complex traumatic defectsIn complex defects, several functionally important struc-tures of the limb are injured. This may occur in various combinations. In the case of compound fractures, muscle tears and zones of contusion are often found in addition to nerve, tendon or vascular injuries. The involved structures are exposed and cannot be managed adequately and defi -nitively with simple skin grafting.

Bite injuries from animals (at left, a dog bite wound) or gunshot wounds (right) have to be classi-fi ed as infected from the start and treated accordingly.


Later in the course of such an injury after inadequate pri-mary treatment, a soft tissue or bone infection can occur which then complicates the local situation. The emphasis is then on treatment of the infection by means of stable soft tissue cover. Reconstruction of defective structures under such conditions has to be carried out secondarily, as the risk of infection is too great for the reconstructed structure if done primarily.

The same basic principles of treatment apply to all stages of soft tissue injury. Securing and stabilising the vital parame-ters are followed by evaluation of the patient, in interdisci-plinary collaboration whenever possible. During the primary operative exploration, the fracture is stabilised, the wound is debrided and where possible all damaged structures are reconstructed.

If defi nitive debridement is possible during the initial man-agement, the wound can receive its fi nal primary covering. If there are doubts about the vitality of the remaining tissue, defi nitive optimum closure can be attempted within 5 – 7 days following a planned “second look”.

The guiding principle of treatment must be to offer the pa tient the “optimum” solution. This means that the pro-cedure at the correct stage to reconstruct the soft tissues is guided by the size and nature of the defect, the local situa-tion, the patient‘s overall condition, and also the medical and social profi le of the patient. The wound should receive its defi nitive treatment as soon as possible. In the case of complex defects, where immediate reconstruction is not possible, an interim soft tissue cover is required.

Covering of defect by plastic surgical procedure: 1) Complex defect on the dorsum of the hand after a motorcycle accident with loss of all soft tissues and extensor tendons of the middle fi ngers. 2) A tendo-fasciocutaneous fl ap is raised from the dorsum of the foot. 3) Function after 8 weeks. 4) Acceptable defect at donor site.

Treatment of a traumatic fi nger injury: 1) Partial amputation of 2nd to 5th fi ngers on admission. 2) Subsequent completion of amputation with two free skin fl aps. Revision was necessary because of increasing necrosis of the ring fi nger. 3) Findings after 8 weeks. 4) Good functional result.

Principles of treatment of complex defects ▪ Stabilisation of the patient ▪ Interdisciplinary evaluation of

the patient ▪ Operative exploration of soft

tissue and bone situation ▪ Fracture treatment ▪ Radical debridement ▪ Primary reconstruction of injured

structures ▪ Possible second look ▪ Defi nitive differentiated cover/

closure within 5 – 7 days

1 2

3 4

1 2

3 4


Thermal injuries/burnsDepending on the intensity and type of the thermal medi-um acting on the skin, a burn wound of varying severity is produced. Its appearance ranges from superfi cial erythema to total skin necrosis. Extensive severe burns are among the worst injuries which a human being can sustain.

At the accident site a decision is made, based on fi ndings, as to whether treatment should be undertaken on an out-patient or an inpatient basis. For superfi cial fi rst-degree burns and second-degree burns of type a, covering less than 10 % of the body surface area or third-degree burns over less than 0.5 % of the body surface area and located on the trunk, upper arm or thigh, outpatient treatment is recommended. For deep second-degree of type b or third-degree burns, covering more than 10 % of the body surface area, the patient is admitted to the nearest hospital regard-less of the location of the burns. A decision must then be made whether transfer of the patient to a centre for burned persons is necessary.

During emergency treatment, cooling of burn wounds as soon as possible with tap water for approximately 30 min-ut es is a priority measure. However, care should be taken with babies and young children to avoid hypothermia. Cooling can lessen pain and reduce or avoid “afterburning”, which is caused by energy storage for almost an hour in the well heat-insulated skin. This heat, together with con-tinuing intravascular coagulation in the injured skin, lead to further tissue damage, so that a primarily superfi cial burn can turn into a deep burn.

In the case of a fi rst-degree burn, which is characterised as damage to the uppermost epidermal layer and manifests itself as erythema, healing takes place spontaneously in a few days without scar formation.

A second-degree burn of type a, involves the entire epi-dermis and is extremely painful. Vesiculation, caused by plasma escaping from the injured capillaries, occurs after a delay of between 12 and 24 hours after burns. Since in the papillary cones and in the intact skin appendages, enough vital cells are still present for rapid re-epithelisa-tion, spontaneous healing without scar formation generally occurs within about 14 days. Of great importance is sterile treatment of the wound by disinfection and covering with suitable wound dressings (e.g. ointment dressings, such as Atrauman, or cooling hydrogel dressings, such as Hydrosorb). Large area injuries of this degree of severity, e.g. scalding in children, can induce a shock reaction.

The severity of burns is classifi ed into three degrees for prognosis and treatment, with second degree further subdivided into grades IIa and IIb. The classifi cation refers to the depth of the injury, i.e. which parts of the skin are burnt.

grade I

Epidermis

Subcutis

Muscles, tendonsand fascia

Burn grade

Dermis/corium

grade IIa grade IIb grade III


In second-degree burns of type b, the epidermis, almost the entire depth of the dermis and, to a large extent, the skin appendages are destroyed. In such cases, spontaneous healing takes several weeks and frequently leaves a hyper-trophic scar. Often, despite all efforts, the injury deepens to become a third-degree wound. In general, second-degree, type b wounds resemble third-degree burns in their clinical appearance, so that treatment by necrosis removal and subsequent covering of the defect (with the patient‘s own skin or a skin replacement) is also similar to that for third-degree wounds.

In third-degree burns, the epidermis, dermis – and often partially the subcutis also – are irreversibly destroyed (full thickness burn). Spontaneous healing with very slight extension of the wound edges is possible only with scar tissue. Otherwise, the coagulation necrosis of the skin causes massive contractions. The patient does not feel any more pain and the nails and hair fall out. Treatment of such burn wounds is purely surgical.

On principle there is a high infection and sepsis risk with all open burn wounds. Wound infections represent the commonest cause of death in burned persons. A badly burned person is exposed to additional risk of burn shock and consequent sickness. Careful observation of the clinical appearance, informed decisions on individual treatment steps and adequate intensive care are therefore of decisive importance to the survival of the patient.

Wound conditioning of deep burns The aim is the creation of a vital wound base into which a variety of skin transplants or skin replacement materials can become incorporated for defi nitive or temporary wound closure. A variety of techniques are available for removing necroses, depending on the depth and extent of the burn.

With the so-called granulation method, in a phased process (about every 3 or 4 days), the eschar is thinned on the surface with a knife or removed with hard brushes. Between debridements, the burn wounds are protected against infection usually by antimicrobial (ointment) dressings. This “closed treatment” also prevents drying out of the wound surfaces, so that the danger of secondary necrosis is reduc ed.

In the case of third-degree circumferential burns on the neck, trunk and extremities, relieving incisions (escharo-tomy) in the eschar are necessary. Otherwise, the conta-minated, necrotic skin coupled with the excessive oedema formation lead, during the course of the burn disease, to suffocation symptoms and to disturbed blood circulation and compression of the neurovascular bundles.

A further technique for removing necrotic skin tissue is tangential excision. This comprises area removal of destroy-ed skin with a dermatome, layer by layer until a bleeding, vital wound surface is reached, onto which the split-skin graft can grow. A disadvantage of this method is the poorly controlled capillary bleeding and the diffi culty of fi nding exactly the right excision depth at the transition to the healthy tissue. Following the excision, wound closing is immediately carried out with patient‘s own skin transplan-tation.

Treatment of burn wounds ▪ Degree I

Spontaneous healing in a few days

▪ Degree IIa Spontaneous healing within about 14 days

▪ Degree IIb Partly conservative, partly surgical depending on clinical appearance

▪ Degree III Surgical with necrosectomy and skin grafting

Grade IIb: Deep dermal burn of the epidermis and almost the entire dermis with the skin appendages. The wound base is red or whitish at the more deeply burned skin areas. There is always an acute risk of increasing the thickness to that of a third degree burn.

Degree III: Necrosis of epidermis, dermis and parts of the subcutaneous tissue (left); the skin is brownish, black, leathery and insensitive to pain, hairs and nails fall out. Circum-ferential burns on the trunk with relieving incisions to facilitate breathing (right).


Using the technique of total or deep epifascial excision, however, the destroyed skin is radically removed down to the healthy muscle fascia. Bleeding can be controlled better than in the case of tangential excision and healing of the grafts is generally good, since a healthy wound base is reliably produced by the deep excision. The cosmetic result cannot be regarded as optimum, however. This method is indicated, above all, for life-threatening third-degree burns whereby survival is a higher consideration than function and aesthetic result.

Less well-known is necrosectomy with 40 % benzoic acid in white vaseline (salicylic acid was used in the past) for bloodless removal of necrosis, e.g. in elderly patients, in the case of burns on the dorsum of the hand and wherever sub-cutaneous structures are directly beneath the skin surface.

Temporary coverage of burns After removal of necrotic skin tissue by the various excision methods, the wound surface is usually immediately trans-planted. In cases where the wound cannot be grafted or there are not enough donor sites because of the extent of the burns, the wound still has to be covered temporarily. Biological wound covering materials are used, the most suit-able of which is an allograft of human skin. This is either fresh skin or preserved cadaver skin. Apart from its massive stimulatory effect on wound healing, allografts stem the loss of secretions and protein, reduce pain and contribute markedly to microbial reduction.

A further option for temporary coverage is xenotransplan-tation with porcine skin. While the allografts heal for about 14 days, the xenografts have to be removed after 3 – 4 days. The xenografts have the basic effect as human skin replace-ment even if not to the same extent. Not least for cost reasons, synthetic wound dressings such as Syspur-derm are often used for temporary cover. The use of allo- or xenografts is primarily limited to cases of critical burns.

Methods of autografting Split skin is taken initially for autografting using a special knife or dermatome. If there are enough donor areas, it can be left in this form for grafting. Usually, however, because of a lack of donor sites, the skin has to be processed into a mesh graft with a mesh dermatome. For both aesthetic and functional reasons, use of mesh transplants is contra-indicat ed on the face, neck and hands.

The mesh transplant is laid on the well-prepared wound, fi xed with sutures and staples and covered by a slightly compressing, non-adhering and absorbent dressing. Depending on the secretion, the dressing is changed at intervals of a few days, about every 2 – 5 days.

Autografting split skin graft: remov-al of donor skin (left); coverage of well-prepared wound surface with the mesh graft and fi xation with staples (right).

Deep epifascial excision with radical removal of destroyed skin and fatty tissue down to the fascia.


Abrasions are cleaned mechanically, and haemostasis of the exsudate with warm moist compresses may be required. A dressing is then applied which protects against infection but, if selected correctly, can also promote the process of epithelialisation. The dressing has to keep the wound moist and supple and must not dry out or adhere. Drying results in formation of a scab which delays healing. If the dressing adheres, newly formed epithelial cells are removed when the dressing is changed and the change of dressing is painful. Suitable dressings for treating epithelial wounds are ointment dressings such as Atrauman, absorbent dress-ings with a non adhering gel coating such as Comprigel or hydrocolloid and hydrogel dressings such as Hydrocoll and Hydrosorb.

Split skin and Reverdin donor sites are like skin abrasion wounds and are treated accordingly. Removal is followed by haemostasis and the wound surface is dressed with a moist dressing in the operating theatre.

With critical burns affecting 80 % of body surface, thelack of donor sites is dramatic. A solution for this situationcould be the method of culturing keratinocytes in vitro, bymeans of which up to 1 – 2 m2 of autologous epithelium can be grown from 2 – 4 cm2 of the burn patient‘s skin. To do this, the keratinocytes are isolated from the piece of the patient‘s skin using certain processes and brought to divis ion in a nutrient medium until a layer of cells capable of being grafted has formed.

Incisions/surgical woundsSurgical wounds usually involve negligible tissue loss and are predestined for rapid healing by primary intention, if there are no wound infections or other disorders of wound healing. According to the circumstances of operation, wound drains are inserted to remove serous secretions and blood in order to avoid seromas and haematomas.

The surgical wound is covered with an absorbent and air-permeable dressing pad which has the function of ab-sorbing any secondary bleeding and protecting the wound against secondary infection and mechanical irritation.

Epithelial wounds Epithelial wounds or superfi cial wounds affect only the avascular epidermis. They re-epithelialise spontaneously and heal without scarring because replacement tissue does not have to be produced. However, because the fi ne capil-laries lying directly under the germinal layer are also open-ed, superfi cial wounds can bleed and secrete a great deal and therefore tend to adhere to the dressing. The wounds are also often quite painful because many nerve endings are exposed. Epithelial wounds are produced by accidental skin abrasions or by split skin removal.

Epithelial wounds affecting only the avascular epidermis heal with-out scarring.

Moist wound treatment is of crucial importance for a cosmetic result of wound healing of epithe-lial wounds: 1) Primary aseptic wound after re-moval of split skin from the thigh. 2) Application of Hydrosorb plus* on the split skin donor site. 3) Re-epithelialisation is complete on the 5th day. 4) Condition 5 months after the start of treatment, the donor area has regenerated almost complete ly. *Hydrosorb plus is also avail able as Hydrosorb comfort with a trans-parent continuous adhesive edge.

1 2

3 4

Incisions closed with sutures are predestined to heal rapidly by primary intention provided there are no wound infections or other disorder of wound healing.


By defi nition, a wound healing secondarily which shows no tendency to heal after 8 weeks, despite correct local and causal treatment, is designated as chronic. Chronic wounds can develop at any time from an acute wound, because of an undetected persisting infection or inadequate primary management. In the majority of cases, however, chronic wounds represent the fi nal stage of progressive tissue de struction, produced by venous, arterial or metabolic vascular disorders, pressure injuries, radiation damage or tumours.

As might be expected from the causes, it is mainly elderly people who are affected by chronic wounds and the altera -tion in the age structure of the population with an increas-ed proportion of elderly persons will lead to a further marked increase in chronic wounds. In order to meet this requirement, it is urgently necessary, on the one hand, to enhance the prophylactic efforts and, on the other hand, to introduce a scientifi cally based and effective wound management with corresponding quality controls.

General principles of therapyAlthough the appearance of chronic ulcers is very hetero-geneous, the pathophysiological mechanisms leading to chronicity are very similar. All underlying vessel damage, even if of different origin, results ultimately in disorders of nutrition of the skin tissue, with increasing hypoxia and ischaemia which then results in cell death (necrosis).

This situation is the worst conceivable starting point for wound healing which, as with acute wounds, takes place in the three known phases of cleansing, granulation formation and epithelisation.

Principles of treatment of chronic wounds

The treatment of chronic wounds of varying genesis places the greatest demands on therapeutic management. After all, by no means all the processes that can adequately explain faulty cell mechanisms are known. It is, however, increasingly possible, based on the actual knowledge about physiological wound healing mechanisms to inter-vene actively and correctively even in disrupted healing processes.

Examples of chronic wounds: mixed ulcer due to chronic venous insuffi ciency and peripheral ar-terial occlusive disease (above), venous ulcer as a result of post-thrombotic syndrome (below).

Chronic wounds [96.97]

Examples of chronic wounds: trophic ulcer in diabetes mellitus (above), decubitus ulcer due to effect of pressure (below).

The repair work of the cells has to be started in a skin area which is extremely metabolically damaged, so that from the start it cannot be guaranteed that the “right cells do the right thing at the right time”. However, regular wound heal-ing is only possible if the involved cells appear in proper chronological order.

During chronic wound healing, the continuing tissue dam-age maintains the infl ux into the wound area of infl ammato-ry cells such as neutrophilic granulocytes and macrophages. These in turn secrete infl ammation-promoting cytokines which synergistically increase the production of certain proteases (matrix-metalloproteases, MMP), while the rate of synthesis of the MMP inhibitor (tissue inhibitor of me-talloprotease, TIMP) is reduced. Because of the increased activity of the MMPs, extracellular matrix is broken down, and cell migration and laying down of connective tissue are disturbed.

Moreover, growth factors including their receptors are degraded on the target cells, so that the wound healing cascade cannot be continued because the mediators for the corresponding stimulation are missing. The infl amma-tion persists. At the same time, toxic breakdown products from the tissue and also bacteria infi ltrate the surrounding wound area, causing further tissue destruction and sustain-ing the chronicity of the wound.

According to this hypothesis, the wound healing cascade can only be restored when the vicious circle of persisting infl ammation with its increased protease activity is interrupt-ed. Two interdependent conditions appear to be essential for this: ▪ The blood supply and microcirculation in the affected

area of skin must be normalised, in order to put an end to the defective nutritional situation which has led to the

tissue destruction. In practice, this means treatment of the cause, i.e. the causes of the ulcer must be diagnosed exactly and treated adequately.

▪ By thorough cleansing of the wound bed, the chronic wound should be converted into the condition of an acute wound. This gives an opportunity of starting the processes required for healing in the physiologically correct cellular and temporal sequence which can then take place in an orderly fashion.

The possibilities for causal therapy such as vein surgery, compression therapy, recanalisation of lumen narrowing by dilation techniques, optimal diabetic control and relief of pressure will be listed when describing the most important types of ulcers.

Local therapeutic methods

Wound cleansing The treatment of choice to clean the wound bed is surgical or sharp debridement. It means excising of necrotic tissue exactly at the border with healthy tissue using a surgical instrument such as a scalpel, scissors, sharp curette or laser. This method is classifi ed as selective, since healthy tissue is not damaged when it is carried out properly, or – if required for prophylactic reasons – is excised only in minimal quantities.

The advantages of surgical debridement lie, among other things, in its life-saving speed when combating severe infections. It also saves time during wound treatment. Through surgical debridement, all the factors that hinder local wound healing, such as necroses, coatings, foreign bodies, germs, etc., are thoroughly cleared from the wound. It is particularly indicated in ulcers with thick, adherent, necrotic deposits and is necessary when there is advanced cellulitis or sepsis.


Surgical debridement is a task for the doctor in both the inpatient and outpatient setting. Depending on the wound situation, a decision should be made on an individual basis as to whether the necrosis should be removed in a single procedure by operation under general anaesthetic or if a removal step by step in several treatment sections should take place. In the case of clinically apparent infection, a single-stage procedure is advisable, in order to remove the nutrient medium as quickly as possible from the infection.

Should surgical debridement not be possible due to specifi c situations (patient refusal, multimorbidity and poor general condition, Marcumar or heparin treatment, fever, metabolic disturbances, etc.), moist wound treatment in order to soften necroses and, if necessary, enzymatic debridement with proteolytically active substances offer an alternative. Both methods may be indicated in addition to the surgical debridement to loosen thin superfi cial layers of necrosis, which are impossible or diffi cult to remove by mechanical excision.

A range of hydroactive wound dressings are available for wound cleansing using moist wound treatment, which are effective and can be used without problems. They absorb bacteria-laden exudate, by providing moisture they pro-mote the loosening of coatings and overall they create a physiological cell-preserving microclimate that effectively promotes the body‘s own autolytic cleansing mechanism.

Sharp debridement is best per-formed in the operating theatre, especially when extensive debri-dement is required or it is not yet clear how deeply it must extend.

Algorithm of treatment of chronic wounds

for exact clarifi cation of the cause of ulcer including differential diagnostic measures

if possible by surgical debridement, otherwise wound cleansing by means of moist wound treatment, possibly enzymatic also

� by contraction and spontaneous epithelialisation � closure by split skin grafting� by plastic surgical procedures (myocutaneous fl ap)

History and baseline diagnosis

Causal therapy

to restore or compensate the circulatory situation as much as possible in the diseased area of skin

Measures according to the causes, e.g. � vein surgery� compression therapy� angiosurgical dilation techniques � optimum diabetic control� relief of pressure

Wound diagnoses/assessment

Wound bed treatment/cleansing

Wound conditioning/promotion of granulation

Wound closure

with the use of moist wound treatment


It should be pointed out explicitly that disorders can arise because of the cytotoxicity and other side effects of sub-stances used for wound treatment. Antiseptics, antibiotic-containing ointments, dyes, stain solutions, metal-contain-ing pastes, etc., all have a more or less marked potential for wound-healing impairment. When such substances are used for short periods, it may be assumed that local damage is slight, whereas with long-term use on chronic skin ulcers, the situation is different. Healing may be signifi cantly de-lay ed or impaired by their undesirable effects, quite apart from the fact that the various substances may be trigger of contact allergies and the development of resistance.

Wound conditioning (wound bed preparation) If direct surgical closure of the defect, e.g. by various fl ap procedures is not possible following surgical debridement, the wound has to be conditioned. That means all treatment measures which are suited to promote granulation tissue until the defect has fi lled up almost to the level of the skin. In the case of successful conditioning there is a fresh and clean granulating surface which represents the basic pre-condition for subsequent spontaneous epithelialisation or coverage by a skin graft.

The most important measure for promoting granulation growth is keeping the wound bed permanently moist by treating it with hydroactive wound dressings. This prevents the cells from dying by drying out and creates a micro-climate in which the necessary proliferative cell activities can take place.

Moist wound treatment is also regarded as selective, since only devitalised tissue is softened and cleared. Healthy tissue is not traumatised. The method is safe, free from side-effects, and simple to carry out in all the treatment domains, for example also during wound treatment at home. It must always be considered, however, that this type of wound cleansing requires more time than surgical debridement. The mode of action of the individual wound dressings is described in detail in the section headed “The wound dressing”.

In the case of very diffi cult infectious wounds, additional continuous irrigation with Ringer‘s solution through an in situ catheter has a good cleansing effect. If necessary, irrigation just at every change of dressing can be suffi cient.

With the initial debridement, however, the process of cleans-ing and treating the wound bed in the case of chronic wounds is usually not complete, as the improvement in the nutritional state of the tissue cannot be improved promptly. Depending on the development of further necrosis or the formation of fi brin deposits, fi ne debridement, careful freshening of the wound edges or removal of the fi brin deposits may become necessary just as bacterially conta-minated and excessive exudate still has to be removed from the wound. Correctly performed moist wound treatment is once again an adequate means for this.

An attempt is often made precisely in the treatment of chronic wounds to curtail the cleansing and healing process by scientifi cally unproven use of a wide variety of measures.

Conditioning of the wound takes place by means of a moist dressing treatment. The examples show conditioning with the calcium alginate compress Sorbalgon, which is packed in dry and then changes into a moist gel when it absorbs secretions.

Necroses removal and refreshing of the wound edge with a scalpel in the case of a decubitus


The venous leg ulcer Vein abnormalities and vein disorders are among the com-monest disorders of health and well-being and about 70 % of leg ulcers are caused due to vein disorders. Many ulcer patients have suffered for decades because of inadequate and frustrating attempts at therapy.

The venous leg ulcer refl ects the worst metabolic disturb-ance of the skin and subcutaneous tissue due to chronic venous insuffi ciency. If the venous return of blood to the heart is disturbed (venous insuffi ciency), less blood is trans-ported out of the involved venous segments and the venous pressure does not fall suffi ciently (venous hypertension). This overstretching of the veins acts as a backward decom-pensation back to the capillaries of the fi nal circulation. The low pressure values required for a regular metabolism can not raise, and the circulation in the vessels is slowed or even at a standstill. Metabolism, particularly in the skin and subcutaneous tissue, is impaired. In the long term, the lym-phatic system is also affected by this, since it is only able to compensate in the early stages of an impaired drainage situation for fl uid build-up in the intercellular spaces (inter-stitial fl uid) by increased lymph fl ow.

The earliest identifi able result of the disturbance in venous return is oedema, which in turn results in further rises in pressure and deposition of fl uid, thus increasing the meta-bolic disturbances. Perivascular fi brosis and degenerative and infl ammatory processes occur with trophic skin chan-ges. Through further obliterative infl ammatory processes in the venules and arterioles, a leg ulcer fi nally develops fi rst in areas with poor venous haemodynamics (ankle area), as the now visible sign of decompensated venous hyperten-sion an the metabolic disorder.

Wound closure Epithelialisation concludes wound healing. However, chronic ulcers usually epithelialise poorly. As Seiler et al. demonstrated in 1989 for decubitus ulcers, epithelial cells at the immediate edge of the ulcer demonstrate a greatly limited migration. The rate of outgrowth was only 2 – 7 %, while the rate of outgrowth of healthy skin in controls was about 80 %.

The current standard in the treatment of the epithelialising wound surface is a moist and atraumatic wound therapy. Every drying and every injury of epithelial cells during dressing changes result in the destruction of cells and thus a further reduction of this already scanty cell population, delaying the wound healing.

If the tendency to spontaneous epithelialisation is poor, especially with large wound surfaces, wound closure with a split skin graft or Reverdin graft should be considered. Another possibility is grafting of autologous keratinocytes cultured in vitro. However, a prerequisite for all procedures is an adequately conditioned, well-perfused and infection-free wound base. To prepare the base for grafting or when there is no tendency to heal despite correct therapy, local application of growth factors can sometimes be worth-while.Transplantation of autologous

keratinocytes cultured in a suitable nutrient solution seems to have a variety of stimulating effects in the treatment of chronic wounds.

Post-thrombotic vascular and fl ow situation: the deep vein is scarred and recanalised after the throm-bosis (1). Blow out by dilated communicating veins (2), resulting in development of secondary varicosities (3).

Lymphatic ankle oedema

1

2

3


The severity, site and duration of the disorder in venous return and the degree and duration of the load on the leg vein system determine the various clinical symptoms which gradually and continually increase. They are summarised under the concept of chronic venous insuffi ciency (CVI) and usually classifi ed into three degrees of severity:▪ CVI grade I is characterised by venous fl are around the

ankles and above the arch of the foot. There is also ankle oedema.

▪ Grade II is expressed by hyper- and depigmentation of the skin, oedema of the lower leg and dermatoliposcle-rosis extending to white atrophy (also called capillaritis alba).

▪ Grade III is manifested as a fl orid or healed venous leg ulcer. It occurs mainly in the area of the ankle but can also occur at other sites on the lower leg.

CVI can result both from primary varicose veins when the dilated lumen and valve insuffi ciency of the superfi cial leg veins extend to the perforating veins and subfascial veins, and can also be the sequela of a postthrombotic syndrome with decompensated subfascial veins. It also represents the sequela of a postthrombotic syndrome (PTS), which usually occurs as a secondary consequence of a deep leg vein thrombosis. PTS is the commonest cause of a leg ulcer (ulcus cruris postthromboticum), whereby the anatomical location of the fl ow impediment is a decisive factor for the clinical prognosis. In the case of primary varicose veins when the valve apparatus of the perforating veins is still functioning, ulcerations can nearly always be attributed to injuries, blunt trauma or rupture of a varix. Its prognosis is accordingly more favourable.

Diagnosis of a venous leg ulcer (ulcus cruris venosum) includes reliable anamnesis, clinical and laboratory exami-nation with recording of the venous and arterial status as well as differential diagnostic measures to exclude factors of non-venous origin.

Ulcus cruris venosum (venous leg ulcer) is a chronic wound which heals poorly or not at all and which, because of its cause, cannot be induced to heal by local treatment alone. The venous hypertension causing the ulcer must effectively be rectifi ed in order to improve the nutritional situation in the damaged skin area. An ulceration can only heal when the oedema has ceased and the venous outfl ow in the leg has again reached a compensated condition (Hach).

These therapeutic aims may be essentially achieved by compression treatment and possibly by invasive treatment methods. In modern phlebology, sclerosing therapy and operation offer mutually complementary invasive methods.

1) Marked dermatoliposclerosis in CVI grade II, which can be attribut-ed to increasing fi brosis of the skin and subcutaneous tissue. 2) White atrophy with white atrophic skin changes. 3) Florid venous leg ulcer in grade III. 4) “Gaiter ulcer” involving the entire lower leg. 1 2

3 4


Which method is used depends fi nally on the anatomical location of the disorder in venous return and the extent of chronic venous incompetence.

Local ulcer therapy is based on proper wound treatment which is appropriately geared to the individual healing phases. During treatment, wherever possible, all factors that have a generally impairing effect on wound healing, such as infections, the infl uence of concomitant diseases, the side-effects of other treatments and negative psycho-social factors, must be removed.

Proper wound treatment includes, phase-adapted, thorough cleansing and conditioning of the wound and promotionof epithelisation. If the patient‘s medical condition allows, the most complete possible removal of necrotic tissue and inadequately perfused tissue by means of surgical debride-ment should be attempted. If surgical debridement is not practicable, cleansing should be carried out with moist wound treatment, which is continued in order to condition the wound bed until complete epithelisation has been achieved. Continuous compression treatment to improve the haemodynamic situation is also important.

Uncertainties in the treatment often arise with regard to prevention and treatment of infection. Bacterial colonisa-tion of the ulcer may usually be assum, though the conta-mination leads – particularly in the case of purely venous ulcers – rarely to a clinically manifest infection. The gener-ally observed low infection susceptibility of older chronic wounds also appears to apply to venous leg ulcer (ulcus cruris venosum). Prophylactic disinfection of the ulcer or topically used antibiotic therapy may therefore generally be considered as not useful, especially with regard to the potential for inhibiting wound healing of many of these substances as well as the high risk of sensitisation. In the case of severe infections and markedly increased C-RP

� clinical examination� diagnostic investigations� differential diagnosis (arterial ulcers, venousarterial mixed

ulcers, diabetic ulcers, exogenous infectious ulcers, ulcers due to blood disorders, neoplastic ulcers)

Diagnosis

Treatment

Compression therapy

Invasive therapy

Local ulcer therapy

Treatment algorithm in venous leg ulcer

� compression stocking to preserve the result of therapy� avoidance of risk factors with as much movement as possible

and elevation of the legs, weight reduction if indicated� possibly drug support by anti-oedema medications

� prolonged bandaging with zinc adhesive dressings� changes of dressing with elastic bandages� general: the patient should move as much as

possible with the bandage

Aftercare

� to compensate the CVI: sclerosing therapy, phlebosurgery

� to treat the ulcer: possibly paratibial fasciotomy or endoscopic ligation of perforating veins

� surgical debridement� physical cleansing by moist dressing treatment� continuation of the moist dressing treatment during

the production of granulation tissue until spon-taneous epithelialisation or skin grafting

A range of hydroactive wound dressings are available for trouble-free moist wound treatment. The example shows treatment of an extensive venous ulcer with TenderWet, which brings about rapid cleansing of wounds with its “absorbing and rinsing” effect.


(C-reactive protein; indicator of infl ammation) and with problem ulcers, on the other hand, systemic antibiotic therapy can be necessary.

With treatment-resistant ulceration, a vascular reconstruc-tion may be required. Procedures with good success rates have proved to be the paratibial fasciotomy and the endo-scopic ligation of perforating veins, in particular.

The arterial leg ulcer The cause of the arterial leg ulcer is predominantly arteri-osclerosis obliterans of the large and medium vessels with resulting tissue ischaemia. Sketched in outline, it originates from a lesion of the intima of the vessel wall, which pro-duces platelet aggregation at the damaged site in reaction and in turn results in increased proliferation and migration of smooth muscle cells from the media into the intima of the vessel wall. The muscle cells produce large quantities of fi bre proteins (collagen and elastin) and proteoglycans (important constituents of the extracellular matrix), which change into the so-called atherosclerotic plaques by accu-mulation of lipids. These plaques then lead to stenosis or

complete closure of the affected vessel, while the extent of the resulting underperfusion depends on the degree of stenosis and on the available collateral circulation.

Circulatory disorders of the legs can result both from oblit-erative processes of the aorta itself and also of the periph-eral arteries. Depending on the site of the obstruction, the site of obliteration is classifi ed according to Ratshow, as aortic bifurcation type, pelvic type, femoral type and periph-eral leg type with combinations of these being possible.

Arteriosclerosis as such is not purely a disease of old age. While there is a rapid increase in severity between the ages of 45 and 60, there is a signifi cant range of contributory risk factors implicated in the occurrence of the illness. Apart from constitutional disposition, hypertension, diabetes mellitus, hypothyroidism, nephrosis, abnormalities of lipid metabolism, thrombophilia, respiratory insuffi ciency, a faulty life style with a diet high in fats and calories, over-weight, stress and above all smoking are important risk factors.

Atherosclerotic plaques (grey deposits) in an arterial wall

Typical of arteriosclerosis is the formation of plaques at particular foci. These arise after damage to the vessel inner wall when blood fat and calcium compounds which are transported in the blood-stream, become deposited at the site of damage.


Men suffer from obliterative arteriosclerosis about 5 times more often than women, though the sex differences level off in older age groups.

Furthermore, it is of importance for the occurrence of the illness that a conjunction of several risk factors causes the risk of the disease to rise nearly exponentially when a single risk factor such as diabetes mellitus can multiply the prob-ability of developing arterial obstruction of the lower limbs. It is thus a very complex disorder that demands treatment of all the factors which have a negative infl uence.

Sites of predilection for arteriosclerotic ulcers on the foot are the distal phalanges of the toes and nails, the nail bed and the heads of the 1st and 2nd metatarsals. They often arise due to pressure of the shoe on bony prominences and are apparent as haemorrhages which appear dark blue to black. Another frequent cause of ulcers are lesions from incorrect pedicure or trivial injuries of the toes.

Necrosis due to severe circulatory disorders are situated mostly on the lateral foot edge, the heel, in the interdigital space and on the extensor sides of the lower leg. In the differential diagnosis of the venous ulcer, there is pain in the area of the ulcer. In diabetics, the ulcer is also distin-guished as an angiopathic or a neuropathic form (see from page 117). The degree of wound severity can be divided into six grades according to the classifi cation formulated by Knighton for chronic wounds into stage I to VI.

In the initial stages, prompt recognition facilitates therapy and improves the prognosis, while a detailed history should pay attention to the typical features of claudication pain. The clinical staging of occlusive arterial disease is modifi ed after Fontaine: ▪ Stage I: asymptomatic, possibly slight fatigability ▪ Stage IIa: onset of pain after walking 200 m ▪ Stage IIb: walking distance less than 200 m ▪ Stage III: rest pain ▪ Stage IV: continuous pain, necrosis, ulcer, gangrene.

After making the diagnosis and localising the site of oblit-eration, a plan of treatment must be drawn up, taking into account the various pathogenetic factors where possible. It contains: ▪ elimination of risk factors ▪ treatment of concomitant illnesses (e.g. achieving normal

blood sugar levels in diabetes mellitus) ▪ measures to restore or improve the circulation by vascular

surgery, angiology and interventional radiology ▪ local wound treatment

Examples of arterial ulcers: 1) Toe necrosis 2) Necrosis on the lateral border of the foot and region of calcaneus and Achilles tendon 3) Complete gangrene of the lower leg 4) Mixed leg ulcer of the lower leg 1 2

3 4


In the hierarchy of treatment measures, reconstructive arte-rial procedures and angioplasty are the most important methods of treating the primary cause of the arterial leg ul-cer. The choice of the surgical procedure should be guided by the location and extent of the arterial occlusion as well as by the general condition of the patient. Apart from revas-cularisation, drugs may be considered to improve perfusion, which can infl uence in particular the hyperproliferative cell processes and the fl ow characteristics of the blood, e.g. prostaglandin E1.

During local wound treatment, the basic risk must be borne in mind that the tiniest injuries in a patient with occlusive disease, ignored or trivialised at fi rst, can extend rapidly within a few days.

A further central problem is the high risk of infection of arterial ulcers. Accordingly, surgical debridement serves for rapid treatment of infection. Necrotic areas must be remov-ed, loculations opened up widely, sloughy deposits remov-ed and infected areas excised. Free fl ow of secretions is ensured by drainage (osteomyelitis suction/irrigation drain).

Examples of treatment: 1) Occlusive arterial disease of femoral-lower leg type stage IV, condition after surgical debride-ment, posterior tibial saphenous vein bypass. 2) Diabetic gangrene with occlu-sive arterial disease of femoral-lower leg type stage IV, condition after incision and drainage. 3) Dry gangrene in the area of the 4th and 5th rays, of the lateral edge of the foot, in the calcaneus and in the dorsal area of the foot. 4) 4 months later following remov-al of necroses and amputation of the 4th and 5th rays.

� determine severity of peripheral arterial disease and site of obstruction

� evaluation of concomitant illnesses/risk factors (hypertension, diabetes mellitus, abnormalities of lipid metabolism, smoking, overweight etc.)

Diagnosis

Treatment

Causal therapy

Local ulcer treatment

Treatment algorithm in arterial leg ulcer

� train patients, reinforce their own responsibility� orthopaedic shoes with appropriate distribution of pressure� inspect feet daily for changes (callosities, fi ssures, fungal

infections of the nails) � do not use any cutting implements for foot care, foot baths

at body heat only, do not go barefoot, use no outside heat sources to promote perfusion (hot water bottles, heated pads) but only body warmth (socks, fl eece boots)

� removal of risk factors (avoid smoking, alcohol consumption)

� treatment of concomitant illnesses (reduce high blood pressure, obtain normal blood sugar etc.)

� measure to restore or improve the circulation (angioplasty/vascularsurgery; medical procedures, leg lowering, vessel training)

Aftercare

� surgical debridement� treatment of infection (systemic antibiotic therapy)� moist dressing treatment for further wound

cleansing, conditioning and epithelialisation� if amputation is indicated: – heal infection as much as possible – convert wet to dry gangrene – attempt maximum possible revascularisation

1 2

3 4


After surgical debridement, wound cleaning and condition-ing are continued using moist wound treatment. Antiseptic dressings may be indicated until the infection subsides.

If amputation is necessary, this should be performed if possible after resolution of the concomitant infection, after conversion of a wet gangrene into a dry gangrene and achievement of maximum revascularisation in the necrotic border zone.

The diabetic ulcerDiabetes mellitus is a chronic disruption of the carbohydrate metabolism and has reached almost epidemic proportions worldwide. In Germany currently, some 300,000 people suffer from type I diabetes and about 4 or 5 million are affected by type II diabetes. Since type II diabetes is partial-ly age-dependent, increasing numbers of diabetics can be expected, purely due to changing age patterns.

Among the complications of diabetes, diabetic foot syn-drome (DFS) takes a prominent position. According to epide-miological surveys, it may be assumed that approximately 15 % of diabetes mellitus patients suffer from foot lesions of differing severity and characteristics during the course of their disease, and these all too often end in amputation.

The basic precondition for the occurrence of diabetic foot lesions is the presence of diabetic (poly)neuropathy and/or peripheral arterial disturbed blood circulation. Although the statistical surveys differ somewhat, the following distribu-tion can be taken to apply: in about 45 % of cases, diabetic neuropathy is the cause, whilst in a further 45 %, the aetiol-ogy is a mixture of neuropathy and disturbed blood circula-tion and, in 10 % of cases, isolated peripheral disturbed blood circulation alone.

Occurrence of a neuropathic lesion Diabetic neuropathy, characterised as increasing sacchari-fi cation of the nerve cells and progressive damage to the nervous tissue affects autonomous, sensory and motor fi bres equally. Clinically, these types of damage lead, alone or together, to the characteristic changes in the foot of a diabetic person:

Neuropathic foot Angiopathic-ischaemic foot

Anamnesis Diabetes mellitus for many years, possibly additional alcohol con-sumption, further delayed damage from diabetes

Diabetes mellitus for many years, possibly lipid metabolism disrup-tion, heart diseases, nicotine abuse and arterial hypertension

Clinical presentation

Skin colour/temperature rosy, warm pale to livid (position-dependent), cool

Sweating/secretion disturbed; dry, cracked skin atrophic skin, loss of skinappendages (hair loss)

Sensibility reduction or loss of perception of vibration, pain, pressure, tempera-ture, touch; refl exes impaired

unaffected, sensation present

Pain pain at rest or at night present, claudicatio intermittens; pain symptoms

Foot pulse palpable not palpable

Hyperkeratosis frequently at sites exposed to pressure

relatively minor

Bone deformation frequently changed bone structure, early osteolysis

rarely

Predisposed sites of lesions foot sole, in particular in region of metatarsophalangeal joints

acral necroses


▪ Damage to the autonomous fi bres causes a reduction in sweat secretion with atrophic dry warm skin.

▪ Sensory function impairment brings about reduced pain and temperature sensations or loss of pain sensations.

▪ Reduction in motor neural activity leads to atrophy of the foot internal musculature with static changes and defec-tive regulation of the foot motor function.

This produces the conditions for development of a neuro-pathic ulcer, whereby callus formation on the foot sole is a possible indicator of impending ulceration. The reason for this is that enhanced cornifi ed skin formation (hyperkera-tosis) leading to formation of a callus results as a reaction to the effect of increased pressure on the foot sole (with the preferred localisation being the metatarsophalangeal joints). The callus then conducts the pressure forces into deeper tissue layers lying beneath the skin.

At the same time, due to increased pressure and shearing forces, detachment of the cutis and subcutis occur in the hyperkeratotically changed skin, with formation of fi ssures, haemorrhages and haematomas, which later become colonised by bacteria. As a result, a central, infected tissue defect, “mal perforant du pied” (Malum perforans pedis) develops.

Ulcer formation can also be triggered by other traumas. Among these is the unphysiological pressure loading due to ill-fi tting footwear, also pressure points due to in-growing toenails, minor injuries, such as, from cutting, sharp devices used for foot care or thermal trauma, e.g. from excessively hot footbaths.

Excessive pressure and shear forces due to changed static forces in the foot and changed motor function...

lead to hyperkeratosis and callus formation,...

cracks, haemorrhage, haematoma and bacteria colonisation,...

and fi nally to an infected defect, known as a “mal perforant”

Added to this is the diffi culty that the processes of ulcer development are often barely noticed by the person affect-ed, since pain perception is impaired. This therefore often brings about a risky temporal delay since, with the diabetic patient‘s generally weakened infection defence, the initially localised infection can rapidly spread in depth and jeopard-ise the main anatomical structures (tendons, muscles) and bones (bacterial osteitis). Infl ammation of the bones can even lead to the total collapse of the foot skeleton. The consequence is that Charcot‘s foot, or deep infl ammation of the foot tissues (pedal phlegmon) arises, which endangers the blood circulation to the toes, so that fi nally, diabetic gangrene threatens to develop.

The formation of a “mal perforant”


The fi rst signs of neuropathic disruptions in the legs are dry skin, burning and tingling sensations and pains at rest, particularly at night. However, there is hardly any pain sensation from injuries.

Occurrence of an angiopathic-ischaemic lesion Reduced blood circulation in the tissue due to micro- or macroangiopathy is a serious risk factor for the develop-ment of a diabetic foot ulceration and impairs the healing of existing ulcerations.

The macroangiopathy of the diabetic person, which has no independent existence either from the histological or from the histochemical standpoint, can be characterised as an advanced, particularly severe type of arteriosclerosis. This sclerosing of the arteries ages an individual by 10 to 15 years relative to a person of healthy metabolism, with the result that diabetic person suffer cardiac infarctions, strokes and occlusions in the legs earlier and more often than per-sons of healthy metabolism.

Microangiopathies are diseases of the terminal vessels and are grouped together as microcirculation disruptions. They involve, in particular, vessel wall restructuring, blood fl ow properties and conditions, and metabolic processes at the interstitium and in the peripheral portions of the lymphatic system. The aetiology is still unclear, although the meta-bolic theory remains at the forefront of pathogenic observa-tions.

The preferred sites for ischaemic diabetic ulcer are similar to those for arterial ulcer: the end phalanges of the toes and the nails, the nail beds and the heads of metatarsals I and II. Necroses resulting from the most severe blood circulation insuffi ciency are usually located on the lateral foot edge, the heel, in the interdigital spaces, and on the extensor sides of the lower leg. Not uncommonly, traumatic events, such as pressure points from shoes, improperly

Degree 2: deep ulcer reaching to joint capsule, tendons or bones

Degree 0: no lesion, possibly deformation of foot or cellulites

Degree 1: superfi cial ulceration

Degree 3: deep ulcer with abscess formation, osteomyelitis and infec-tion of joint capsule

Degree 4: limited necrosis in forefoot or heel region

Degree 5: necrosis of entire foot

Stage 1: necrosis of epidermis (pressure point)

Stage 4: infection no longer restricted to a region spreading from a malum perforans

Stages of a malum performans, according to Arlt

Stage 3: malum perforans with bone and/or joint involvement

Stage 2: malum perforans extend ing subcutaneously as far as the bones or joints, but without lesions in these

In order to plan treatment and assess the prognosis, a precise description and classifi cation of the various lesion types is indis-pensable. This also serves to en-sure clear communication between the different individuals involved in the necessarily multidisciplinary treatment. A variety of classifi ca-tions are available for describing the lesions, of which the so-called Wagner classifi cation is the most widespread classifi cation of dia-betic foot lesions throughout the world. With its six stages (0 to 5), it has the advantage that is simple to use in clinical practice.


performed pedicures and other minor injuries of the toes also contribute to the development of ulcers.

Before ulcera tions ever develop, inspection can reveal trophically disturb ed nails, mycoses, reddening, marbling and loss of hair, which illustrates how regular inspections can contribute to prevention.

The principles of treatment The aim of treatment for diabetic foot syndrome is primarily a reduction in amputations, preserving function in the ex-tremities and maintaining the quality of life of the diabetic patient. Treatment is an interdisciplinary task and success is only possible with broadly spread measures. The special-ists involved are internal medicine specialists, vascular surgeons, orthopaedic specialists, neurologists and derma-tologists.

A basic measure in the treatment of all diabetic lesions is optimal adjustment of the diabetes (normoglycaemia), which is also the best treatment for the neuropathy. Further conservative treatment is focused on improving the central haemodynamics (treatment of cardiac insuffi ciency or ven-tilation disruption, blood pressure regulation), the haemor-heology and vasodynamic (blood fl ow/conditions) as well as the anticoagulation.

A primary and central problem in the treatment of diabetic ulceration is the extraordinarily high risk of infection. Only very few angiopathic lesions show no sign of surrounding infection. Mixed forms of neuropathic and angiopathic foot and purely neuropathic ulcers, however, can generally be assumed to be infected. The opportunities for spreading of an infection in the foot are particularly favourable, due to the differentiated connective tissue apparatus, so that con-sistent systemic antibiotic treatment is always worthwhile.

exact verifi cation:� of underlying cause (according to symptoms of neuropathy

and angiopathy, mixed ulcer)� of the immediate trigger of the lesion (injury, infection, etc.)� of the metabolic situation of the diabetes� of the infl ammatory parameters

Diagnosis

Treatment

Causal treatment


Treatment algorithm for neuro pathic ulcer

Treatment algorithm for angio-pathic ulcer corresponds to that for Ulcus cruris arteriosum (arterial leg ulcer)

� train patients, reinforce their own responsibility� orthopaedic shoes with appropriate distribution of pressure� inspect feet daily for changes (callosities, rhagades, fungal

infections of the nails)� do not use any cutting implements for foot care, foot baths

at body heat only, do not go barefoot

� optimum adjustment of diabetes

Aftercare

� treatment of infection (systemic antibiotic therapy)� absolute relief of pressure on ulcer until healed

(walking aids, wheelchair, bed rest)� adequate surgical debridement� moist dressing treatment for further wound

cleansing, conditioning and epithelialisation


Diabetic ulcers of neuropathic genesis under conservative treatment

The following therapeutic principles may be formulated for the local treatment of the neuropathic ulcer: ▪ absolute removal of pressure on the lesion (walking aids,

wheelchair, bed rest) ▪ correct wound treatment with adequate debridement

and moist dressing treatment until there is complete wound closure by strong epithelium

▪ treatment with suitable orthopaedic footwear ▪ specialised aftercare, training of the patient and preven-

tion of recurrence

Despite all diffi culties, a neuropathic lesion always implies a prospect of wound healing, so that, where possible, after surgical debridement, a conservative procedure is primarily indicated for conditioning of the wound area. The most frequent local surgical measure for correcting pressure points that hinder wound healing is resection of the meta-tarsal head.

The angiopathic gangrene in the presence of arterial occlu-sive disease requires a different approach, which depends essentially on the vascular status and on the result of re-vascularisation. In contrast to the neuropathic foot lesion, amputation are not easily avoided.

The methods for treating the wound ground, in principle, are surgical removal of necrosis, border zone amputation with extensive secondary wound healing as well as ampu-tations through the classical amputation lines with primary wound closure. Determination of the treatment measures in each case requires clinical experience. The decision should be made after careful consideration and should not be hasty. The supreme goal of treatment is preservation of the extremities.

If surgical removal of necrosis is suffi cient, this should be regarded as the method of choice. Even if secondary heal-ing can possibly take months, the result obtained in this manner is still the best. With good prophylaxis against infections, the patient can put pressure on the foot – in contrast to the neuropathic foot – in the case that the wound is free of necrosis. The so-called vascular training favours revascularisation and wound healing.

Border zone amputations are always required when bony parts of the foot lie within the necrotic area. Yet the point of time for amputation should only be determined if an extensive demarcation of the fi ndings is clear. Demarcation denotes the clearly visible border between black (dead) and healthy tissue. Operations in infl amed tissue often result in secondary necrosis due to wound oedema when blood circulation is reduced. When determing the amputation line, the subsequent possibilities for prosthetic or special shoe provision should be kept in mind.


The Decubital ulcer A decubitus is defi ned as damage to the skin as a result of continuous local pressure. Its occurrence can be sketched out schematically as follows: when sitting or lying, the human body exerts pressure on its contact surface, which in turn exerts a counterpressure on the skin area of contact. The size of the counterpressure depends on the hardness of the contact surface, although normally it is above the physiological arterial capillary pressure of ca. 25 – 35 mm Hg.

In the short term, the skin itself can tolerate the applica-tion of relatively high pressures. However, if the pressure is maintained, due to compression of the capillaries con-veying the blood in the affected skin area, blood circulation insuffi ciency and oxygen shortage (hypoxia) come about. The body reacts to this nascent damage in the form of a warning pressure pain. In a healthy person capable of movement, this is the trigger to relieve the compressed skin areas by a positional change.

If a person is not able to perceive this pressure pain due, for example, to complete immobility from unconsciousness or narcosis, or due to relative immobility as a consequence of severe pain, fever, dementia, age-related weakness, etc., then the compression of the skin area is sustained. The blood circulation insuffi ciency worsens and leads to a build-up of toxic metabolic products in the tissues and increased capillary permeability, vascular dilatation, cellular infi ltra-tion and oedema.

Assuming the affected skin area is completely relieved of the pressure, the cells are still able to regenerate at this time, since the infl ammatory reactions favour the removal of toxic metabolic products. However, if the pressure is

sustained, as a consequence of the further increased ischaemia and hypoxia, irreversible skin cell death with necroses and ulceration formation take place.

The time for which the skin tissue can survive under ischaemic application of pressure without damage is about two hours. However, this tolerance range is subject to great variations from one patient to the next. It is infl uenced by the severity of the applied pressure, and the general con-dition of the skin. A young, elastic skin is more resistant to pressure than the thinner aged skin. Furthermore, any disease associated with acute or chronic hypoxic conditions of the skin cells, or external damage to the skin is signifi -cant.

Epidermis

Subcutis

Muscles,Tendons,Bones

Stage I

Stage II

Stage III

Stage IV

Dermis

�

Classifi cation of decubital ulcer: Stage I: Sharply defi ned reddening of intact skin, which does not blanch on pressure. As a guide: overheating of the skin, hardening or oedema. Stage II: Partial skin loss of the epidermis up to the dermis. This is a superfi cial ulcer which appears clinically as an abrasion, blister or fl at crater. Stage III: Damage to all skin layers (epidermis, dermis, subcutis) which can extend to fascia, although these are not yet involved. The ulcer appears as a deep, open ulcer with or without undermining the surrounding tissue. Stage IV: Skin loss over the entire thickness of the skin with exten-sive tissue necroses and damage to muscles, tendons and bones. Even undermining and pocket forma tions occur often. In stage III and IV risk through septic com-plica tions! (according to “National Pressure Ulcer Advisory Panel”, 1989)

��

�


Pressure / pressure rest time

local blood circulation insufficiency

oxygen shortage / build-up of toxic

metabolic products

increase of capillary permeability,vascular dilatation, cellular

infiltration, oedema formation

vesiculation

total ischaemia, irreversible death

of skin cells

Ulcer / necrosis

Decubital ulcers can in principle develop in any sites of the body. However, the greatest risk occurs when the pressure on the body, and the counterpressure from the surface be-low, act on a skin area lying over a bony prominence which is not cushioned by subcutaneous fat tissue. Therefore the classical sites are: the sacral region, heels, ischia, greater trochanters and lateral malleoli. About 95 % of all decubi-tal ulcers occur at these sites.

Apart from perpendicular application of pressure on a skin area, a risk also exists from shearing forces. The term shearing implies tangential displacement of the skin layers over one another, by means of which blood vessels are also narrowed and compressed. It is above all the region of the buttocks that is subject to tangential shearing forces, for instance when the patient is pulled into a new position instead of being lifted, or if he slips when sitting up in bed, due to insuffi cient support for the feet.

The treatment of the decubitus is based on three therapeu-tic principles: The supreme requirement of every decubitus treatment is restoration of the blood supply of the damaged skin area by a complete relief of the pressure. Without relieving the pressure, healing is not possible and all other measures may fail. Therefore the relief of pressure must be maintained throughout the entire period of treatment. Every pressure, even if only for a few minutes, causes fresh damage and leads to relapses in the healing process.

Local wound treatment includes thorough debridement, surgical if possible, as well as continuing wound cleansing with hydroactive wound dressings. This is followed by conditioning of the wound with formation of granulation tissue as well as eventual epithelialisation by moist wound treatment.


� improve general condition� improve nutritional status� pain control� establish and, as far as possible, eliminate local

and general elements disrupting wound healing

� localisation of ulcer, degree of severity, general condition of wound

� evaluation of patient status, compliance

Initial assessment of overall situation

Treatment

Causal treatment


Treatment algorithm in decubital ulcer

monitoring and continuation of therapy according to treatment plan

careful scrutiny of measures (especially if relief of pressure is suffi cient)

� complete pressure relief to restore blood supply throughout the treatment period for the ulcer until healed

Ulcer healing?

� adequate surgical debridement� treatment of infection if required � moist dressing treatment for further wound

cleansing, conditioning and epithelialisation� plastic surgical procedure if required

yes

no

Adjuvant treatments

As the case may be the long lasting and stressing healing times can be reduced by plastic surgical covering of the decubitus. But even in this case previous wound condi-tioning is recommended to ensure the surgical result and avoid recurrences.

As the third therapeutic principle, adjuvant therapies are indicated to improve the patient‘s general condition and the nutritional status as well as the pain control. Cachexia with conditions of protein defi ciency, which inhibit wound healing, is often observed in elderly patients so that ade-quate nutritional intake and a suffi cient supply of vitamins and minerals must be ensured.

The chronic post-traumatic wound The chronic post-traumatic wound occurs as a result of inadequate primary treatment of an injury or due to com-plications during primary management which were not rectifi ed in the immediately following phase of treatment. Typical causes of post-traumatic wounds taking a chronic course are soft tissue contusions, degloving injuries, skin necrosis, osteitis, infected implants, joint arthroplasty infections, joint infections or deep soft tissue infections. Frequently, this development can be attributed to an initial underestimation of the soft tissue injury underlying the ini-tial trauma. Among primary injuries, the compound fracture is particularly diffi cult. Contamination can cause soft tissue and bone infections which often prove to be severe.

The unstable scar, such as that found in areas subject to mechanical stress after wounds have undergone secondary healing or after split skin grafting occupies a special posi-tion. With this type of scar, the integrity of the skin is not broken, but ulceration easily occurs with a corresponding risk of infection, so that treatment of the soft tissues is required in this situation also.

The goal of all measures to treat a chronic post-traumatic wound is stable soft tissue cover. Debridement and the removal of all areas of necrosis and foci of infection in turn represent the fi rst step. It can sometimes be impossible to take into consideration functional structures such as tendons, fascia and even nerves and vessels. A soft tissue situation must be created in which it is possible to cover the defect without a risk of persisting necrosis and thus persistence and spread of infection.

Planning of later reconstructive procedures must be includ-ed during the debridement operation. A decision must be made early as to whether both soft tissue and bone defects can be closed in a single session or whether individual re-construction steps should be postponed, to be performed later when the soft tissues have healed.

Unstable scar in the popliteal fossa after burn as a special form of chronic post-traumatic wound (above) and its treatment by microsurgical scapula fl aps (below)

Overview of causes, causal treat-ments and treatment of other chronic skin ulcers


Post-traumatic ulcers Radiation damage Tumour wounds

Cause inadequate primary therapy, e.g. of soft tissue contusions; complications of wound healing which were not dealt with immediately, such as necrosis, infections, unstable scars etc.

ionising radiation, some-times in association with other risk factors such as trauma, chemical factors infections etc.

benign, malignant or semimalignant cell growth

Causaltherapy

removal of focus of infection where necessary and anti-microbial treatment

adequate tumour therapy and/or therapy of concomi-tant risk factors as needed

tumour therapy as needed

Treatment cleansing as early as pos-sible by radical debridement and plastic reconstructive procedure

cleansing as early as pos-sible by radical debridement and plastic reconstructive procedure

if radical therapy is possible, the wound caused by the tumour is converted into a surgical wound and treated as such

Overall, the time factor should not be overlooked in plan-ning. Bones and tendons exposed after debridement can become infected secondarily or can dry out. As a rule, defi nitive wound closure can be undertaken two days after the fi rst debridement during a planned second look. Plastic reconstructive methods are required for soft tissue cover, ranging from simple split skin graft to free microsurgical fl ap transfer. Skin grafts always need a clean granulating surface with covered functional structures and no mechani-cally stressed regions.

Chronic radiation damage Treatments with ionising radiation lead to inevitable dam-age to the skin and the underlying tissue. Even though this damage does not have to be visible macroscopically, the fi rst sign of the chronic sequelae of radiation is telangiecta-sia, which can be interpreted as re-generation of destroyed capillaries.

The skin and subcutaneous tissue are not as well perfused after exposure to radiation and undergo secondary atrophy. The skin becomes thinner and is bound fi rmly to the un-derlying structures due to the loss of the subcutaneous fat. In addition, there is general tissue fi brosis and direct cell damage with chromosomal changes. Local lymphoedema, increasing hyalinisation at the expense of elastic fi bres and thrombosis in the arterioles and venules lead ultimately to local disturbances of nutrition and thus to a poorly healing ulcer. These ulcers, in the worst case, may undergo malig-nant transformation after a latency of 4 to 40 years.

If an initially stable area of irradiated skin suddenly becomes unstable, recurrence of the primary tumour or a malignant neoplasm due to the radiation can be the reason. Skin metastases occur preferentially in irradiated areas of skin. Other causes for such a development are trauma such as injections, biopsies, insect bites or chemical factors such a topical therapy, local long-term irritation or occupational exposure to hazardous chemicals. Skin infections, osteomy-elitis and non-infectious skin diseases, such as varicose vein disease and varicose dermatitis can also produce chronic injury, as can internal illnesses such as diabetes mellitus or arteriosclerosis.

A 64-year-old patient developed a squamous cell carcinoma after ir-radiation of a haemangioma in his youth, which led to amputation of the arm. 1) Preoperative appearance 2) and 3) In order to obtain a stump capable of taking a prosthesis, a pedicled latissimus dorsi fl ap was wrapped around the upper arm... 4) ...and a stress-stable amputa-tion stump was obtained.

1 2

3 4


The indications for surgical treatment consist of the resec-tion of local recurrences, resection of an unstable scar or resection of the radiation-damaged skin to relieve pain, facilitate nursing and improve the patient‘s quality of life.

The surgical treatment of the consequences of radiation fi rstly requires radical debridement with histological exa-mination of the resected tissue, the resection edges and depth. This can also require resection of bone, including ribs, sternum or the entire chest wall. Without such debri-dement, osteoradionecrosis in particular cannot be treated. As direct wound closure should usually not be attempted and cover with a split skin graft is also often insuffi cient, well-vascularised skin (muscle) fl aps should be considered to cover the often large defects.

It must be noted that many radiation injuries are often treat-ed conservatively and therefore undergo surgical treatment too late. Experience has shown and it should be borne more in mind that ulcers in irradiated areas as a rule do not heal with conservative treatment and that chronic ulcers in this situation can all too easily become the site of seconda-ry malignancies. Quite apart from the fact that the patient‘s suffering can be cut short, early surgical treatment in many cases obviate the need for complex reconstructions.

Wounds in tumour patients The growth of benign or malignant tumours under or in the skin leads to destruction of tissue continuity. Ongoing over months and years these growths may lead to open ulcera-tion.

If the stage, extent and site of the tumour allow, a radical operation is attempted as the surest way to treat the tumour. This means that the lesions caused by the tumour are con-verted into surgical wounds and can be treated and closed accordingly. Depending on the extent of the tumour surgery, closure of the defect can be required after conditioning of the wound. If only palliative treatment of the tumour is possible at the terminal stage, this also applies equally to wound treatment. Dressings in this situation serve primari-ly to relieve pain, stem unpleasant odours and keep the wound in a tolerable condition as long as possible.

Large defect on the back following excision in accordance with lymph fl ow continuity of a malignant melanoma (left); ulcerated breast carcinoma (right)


As always, wound coverings have the task of protecting the wound against the ingress of external noxious infl uences. Furthermore, the most up-to-date wound dressings can be used individually and in targeted manner for wound heal-ing, because of their differentiated physical effects. Latest experience in wound treatment, in conjunction with special wound dressing materials have led particularly, to an in-creased extent, to staged wound treatment being practiced, and this stimulates cellular activity in the individual stages for qualitatively better wound healing.

Functions of the dressing Until the wound has healed and the skin defect is closed, the dressing takes over important functions of the intact skin in the interim. It offers: ▪ protection against mechanical infl uences (dirt, impacts,

chafi ng), against contamination and chemical irritation ▪ protection against secondary infections ▪ protection against drying and loss of body fl uids

(electrolyte losses) ▪ protection against loss of heat

Apart from comprehensive wound protection, the wound dressing can also infl uence the healing process actively by cleansing the wound, creating a microclimate which pro-motes wound healing and maintaining rest for the wound.

Functions in the cleansing phase In every wound, an exudate fi rst collects in a variable amount which is full of dead cells, fragments of tissue, dirt and bacteria. If large quantities of exudate remain in the wound, the progress of healing is hindered both mechanically and biologically, and the risk of infection grows. Excessive exudate must therefore be absorbed by the dressing. In this way, bacteria, harmful metabolic products, devitalised tissue, dirt and foreign bodies are removed from the wound at the same time and do not have to be eliminated by the body‘s own phagocytosis. The dressing supports and

Picture from the inside of an Attic bowl of the potter Sosias, c. 500 BC: Achilles bandaging Patroclos

The wound dressing

Since ancient times, humans have bound their wounds and thus instinctively taken the right measures; arresting of bleeding and wound protection have been the main tasks of dressings for thousands of years. And they are still today. But thanks to the biochemical and morphological relationships of wound healing that have come to light over the last few decades, it has been possible to develop wound dressings that serve therapeutic purposes to a high degree. Thus the modern wound dressing has become an indispensable component of local wound treatment, in particular for treating chronic wounds.

The wound dressing [136.137]

Functions of the dressing: 1) In the cleansing phase, the dressing absorbs excessive con-taminated secretions and supports the body‘s own cleansing mecha-nisms 2) In the granulation phase, the dressing promotes tissue forma-tion by means of a moist environ-ment 3) In the epithelialisation phase, the dressing speeds up cell migra-tion and cell division

speeds up the cleaning of the wound and helps to prevent infection by the pathogenic micro-organisms present. At the same time, it protects the wound against further con-tamination.

Functions in the granulation phase Apart from a functioning microcirculation, a balanced moist wound environment is another important requirement for the formation of granulation tissue. The progress of healing is disturbed both by drying of the wound and by excessive secretion.

Appropriate regulation of wound moisture is only possible by means of the dressing; it absorbs excessive secre tions, prevents drying of the wound and delivers adequate amounts of moisture to it as needed. Naturally, the wound dressings employed must have specifi c physical character-istics if they are to fulfi l these functions. The principles of action of the individual dressing materials are explained from page 148 on.

Protection of the granulation tissues against every kind of further trauma is also important in this phase. Due to the protein-rich secretions and the large number of fi ne hair-like capillaries, it has an extraordinary tendency to adhere. That is the reason why the wound dressing must be atrau-matic, which means it must not stick to the wound. Other-wise the granulation tissue is damaged by cell stripping at every dressing change so that it regresses at least partially to the infl ammatory phase. Furthermore, the dressing also

has the function of ensuring secure protection against infection, even though the risk of infection decreases in proportion to the formation of healthy granulation tissue.

Functions in the epithelialisation phase Mature granulation and a moist sliding surface are the requirements for fi nal epithelialisation. The dressing, there-fore, must continue to keep the wound moist in balanced fashion. If excessive secretions remain in the wound, the epithelial cells swim upwards. If the wound is too dry, scab forms which impairs re-epithelialisation because the epithe-lial cells have to creep under the scab. Hydroactive atrau-matic wound dressings are needed in this phase to protect the wound surface from drying and protect the epithelial cells from cell stripping during dressing changes.

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Requirements of wound dressings To what extent the individual wound dressing can fulfi l the specifi c functions depends on the characteristics of the material employed. Never the less a few basic demands can be made of wound dressings.

Absorbency and absorptive capacityThe defi ned absorbency of a wound dressing is one of its most important characteristics so that it can cleanse the wound by absorbing excessive exudate. In order to prevent recontamination, the exudate should be absorbed into the capillaries, i.e. into the material structure of the dressing, and should be held there.

Textile materials such as woven gauze, non-woven mate-rials, combined dressing pads of non-woven material with pulp fi lling or foam dressings have a high spontaneous ab-sorptive capacity. However, this can also lead to excessive stimulation of the fl ow of secretion by the suction action and the risk of oedema is increased. Moreover, absorption of the exudate by textile materials is mainly intercapillary, that is, between the fi bres, so that secure inclusion of bacteria with protection against recontamination is not guaranteed.

Interactive wound dressings for moist wound treatment such as calcium alginate dressings, dressings with superab-sorbent material in the absorbent pad and hydrocolloid or hydrogel dressings, have a material structure which allows intracapillary absorption of secretions which thus retain the bacteria-laden secretion. The degree of their absorptive capacity is determined by the nature of the material. For instance, calcium alginate dressings have a higher spon-taneous absorption than hydrogel dressings, but the latter can absorb secretion over a prolonged period.

Gas permeability Another important function of wound dressings is to allow gas exchange of oxygen and carbon dioxide and the giving off of water vapour. It is assumed that continuous gas exchange has effects on the concentration of oxygen and the pH in the wound and thus infl uences cellular processes. In particular, epithelialisation of the wound is promoted by the availability of oxygen which dissolves in the wound secretions and is utilised directly by the epidermal cells. The permeability of wound dressings for water vapour contrib -ut es to provision of a balanced moist wound environment.

The degree of gas and water vapour permeability of a wound dressing depends on the material used. It is higher in the case of textile and textile-like materials such as gauze, non-woven materials or calcium alginate dressings than in the case of synthetic materials like hydrogels or hydrocol-loids with their occlusive characteristics. The latter permit gas exchange to a certain extent which is actually increased as saturation with absorbed wound secretions and the associat ed stretching of the material structures increase. They are described as semipermeable.

The gas and water vapour permeability of a wound dressing is regarded in clinical practice as an important criterion of its suitability for use in the case of infected wounds. Wound dressings made of textile and textile-like materials with higher permeability are considered more suitable than semipermeable systems such as hydrogels or hydrocolloids which continue to be contra-indicated in the case of clini-cally apparent infections as a precaution.


This contra-indication is based on experience with the earlier occlusive dressings which were usually airtight so that there was a danger of the formation of moist chambers and a high risk of infection especially with regard to anaerobe infections. Modern semi-permeable wound dressings, how -ever, are so constructed that this potential risk is minimised. They absorb infected secretions so that dangerous pooling of secretions leading to a moist chamber does not even occur, and the bacteria are enclosed securely in the material structure. In addition, the gas exchange which is possible to a certain degree contributes to the balanced moisture level.

Atraumatic wound treatment A disadvantage of textile absorbent dressing materials such as gauze or non-woven dressings is their marked tendency to stick to the secreting wound surface when the absorbed secretion dries into the dressing and becomes rigidly bound to it. This leads to the underlying newly formed tissue being torn off along with the dried secretions when the dressing is changed.

In order to avoid this disorder of wound healing, wound dressings must have wound-friendly or atraumatic charac-teristics. They must not adhere even after prolonged use on secreting wounds so that further damage is prevented

Gauze dressing materials adhere to the wound (left); during dress-ing changes, newly formed tissue is pulled off also. This disturbance of wound healing can be avoided by the use of atraumatic wound dressings such as calcium alginate dressings (right).

when the dressing is changed. At the same time, the atraumatic characteristics of a wound dressing allow a less painful change of dressing.

With textile absorbent dressings, atraumatic characteristics are achieved with water-repellent impregnation such as ointments (ointment dressings) or coating with gels. More-over, the risk of adhesion can be counter-acted by the use of a layer of hydrophobic fi bres adjacent to the wound. All hydroactive wound dressings are also wound-friendly as they do not adhere to the wound surface because of their specifi c material structure despite their absorbency.

Safety in use Wound dressings must be inert mechanically and biochemi-cally. Mechanical irritation is due especially to movement of the dressing and occurs mainly in the case of dressings with a textile basis. They must not become wrinkled or be too thin or loosely-woven as two-dimensional movements on the wound lead to stimulation of secretion.

The biochemical inertness refers to the possible potential for a wound dressing to have a cell-damaging (cytotoxic) and sensitising effect; the traditional wound dressings of textile materials and the new synthetic materials are affect-ed equally by these problems. In order to exclude interfe-rence, wound dressings must also be neutral in behaviour towards other substances which are used for local wound treatment.

Sterile, ready-to-use and individu-ally packed wound dressings facilitate wound care under sterile conditions.


Safety in use also means that a wound dressing is easy to use, is packed ready to use and clearly labled. Naturally, all wound dressings must be sterilisable or be available already sterilised and ready to use.

Methods of wound treatmentDepending on its conditions, wounds are treated “dry” or “moist”. Moist wound treatment is further distinguished into moist wound treatment with permeable, that is, air- and water vapour-permeable dressings and occlusive moist wound treatment with semipermeable dressings.

Dry wound treatment The use of dry wound dressings is today limited to the following indications: ▪ treatment of wounds as part of fi rst aid ▪ treatment of primarily healing wounds closed with

su tures to absorb oozing blood, to protect against secondary infection and as a cushioning protection against mechanical irritation

A special indication for dry dressing treatment is represent-ed by the interim covering of burn wounds or conditioning of soft tissue defects with synthetic skin substitutes.

Finally, ointment dressings, which are used to keep wound surfaces supple, are neither dry nor moist. As they them-selves have no absorbency because of the ointment im-pregnation, they have to be combined with absorbent dry wound dressings to absorb secretions.


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1) Zetuvit - combined absorbent dressing pad with good padding effect.2) Zetuvit Plus - combined absorb-ent dressing pad with superab-sorbent polymer (SAP) for the treatment of very severely exuding wounds. [144.145]

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Wound dressing pads Apart from classical gauze dressings (ES gauze swabs) or gauze-like non-woven materials (Medicomp), combined wound dressings are used for dry wound treatment. These are constructed in layers from different materials and thus demonstrate good absorbency. Exudate is not only distrib-uted over the area but is drawn away from the wound and held in the depths of the absorbent core. They are perme-able to air and water vapour, soft and drapable and have a good padding effect to protect the wound. Examples of dif-ferent kinds of absorbent dressing pads are Zetuvit, Zetuvit Plus and Cosmopor steril.

Zetuvit derives its wound-friendly characteristics from its non-adherent non-woven cover and can also absorb large quantities of secretion because of its core of highly ab-sorbent cellulose fl uff. Zetuvit is therefore suitable for the treatment of acute highly secreting fl at wounds and for the treatment of primarily healing wounds.

Zetuvit Plus is a combined absorbent dressing pad espe-cially for the treatment of very severely exuding wounds. Four layers of different materials provide Zetuvit Plus with its excellent performance characteristics: The absorbent core consisting of soft cellulose fl uffs is blended with liquid-absorbent polymers (superabsorbent polymer (SAP)) (1). Due to this Zetuvit Plus absorbs more than double the vol-ume of conventional absorbent dressing pads. The exudate is trapped in the absorbent core, so that Zetuvit Plus can also be applied under pressure, e.g. beneath a compression bandage.

However, the inclusion of excessive exudate also contri-butes to reducing the risk of infection as germ-laden ex-udate is kept away from the wound and the risk of reinfec-tion is reduced. In addition the soft quality of the absorbent core provides a good padding effect whereby the wound is well protected from harmful mechanical infl uences such as pressure or impact. The particularly highly absorbent core is completely covered with thin non-woven fabric (2) which evenly distributes the fl uid and/or the exudate to the absorb-ent core. A hydrophobic but air-permeable special non-woven (3) on the side of the absorbent core facing away from the wound counteracts moisture penetration of the dressing. The special non-woven is dyed green so that Zetuvit Plus can be correctly applied. The green side is always the side facing away from the wound (See photo-graph on page 145). The outer covering of Zetuvit Plus comprising a two-layer non-woven (4) has the following functions: The hydrophobic outer surface of the non-woven reduces the tendency of adhesion to the wound which also provides for a more pleasant dressing change. The hydro-philic cellulose fi bres of the inner surface of the non-woven, however, have a high capillary activity and pass exudate quickly in the absorbent core. As a result accumulation of exudate on the wound is prevented.

Cosmopor steril is a self-adhesive wound dressing made of a soft non-woven fabric as support material and with a wound dressing pad made of 100 % absorbent cotton wool. As a reliable protection against adhesion to the wound Cosmopor steril has a hydrophobic microgrid layer as wound-facing layer which additionally pass wound ex-udate or exudate quickly to the absorbent pad above. Due to a hypoallergenic polyacrylate adhesive, the self-adhesive area is particularly tolerable to the skin. Cosmopor steril allows problem-free treatment of surgical wounds but also of minor injuries, e.g. in fi rst aid treatment.

Ointment dressings Ointment dressings such as Atrauman consist of a thin soft open-weave tulle of hydrophobic polyester fi bres impregnat-ed with a non-medicated ointment. Both the hydrophobic polyester tulle and the ointment impregnation counteract adhesion to the wound so that very gentle dressing change is possible with Atrauman. The ointment allows Atrauman to keep both wound surface and wound edges supple, pro-tects the wound from drying and prevents scar contracture. The ointment itself is gas-permeable and permeable to secretions. This ensures adequate air access to the wound as well as rapid removal of excessive secretions. An ab-sorbent dressing should be applied on top of Atrauman to absorb the secretions.

Ointment dressings are used for atraumatic wound treat-ment in all phases of wound healing, e.g. for abrasions, burns, scalds, and to cover skin graft donor and recipient sites.

For the treatment of infected wounds or wounds in dan-ger of infection the silver-containing ointment dressing Atrauman Ag with antimicrobial effect is indicated. It consists of wide-meshed hydrophobic lattice tulle made of polyamide which fi bres are coated with elemental silver and additionally impregnated with an ointment mass. The silver ions are chemically fi rmly bonded to the carrier material resulting in good tissue tolerability with only slight cytoto-xicity. The good tissue tolerability has been substantiated in tests with the human keratinocyte cell line HaCaT. The antimicrobial activity spectrum is extraordinarily broad and includes both gram-positive and gram-negative strains of bacteria. The ointment impregnation keeps the wound mar-gins soft and supple. Atrauman Ag can even be combined with hydroactive wound and foam dressings without loss of effect.


Cosmopor steril, self-adhesive wound dressing with hydropho-bic microgrid layer as protection against adhesion.

The ointment dressing Atrauman keeps the wound margins and surfaces supple and prevents ad-hesion to the wound.

The silver-containing ointment dressing Atrauman Ag with a wide antimicrobial effect is indicated in infected wounds or in wounds in danger of infection.

Moist wound treatment Moist wound treatment is regarded as the standard treat-ment for all wounds undergoing secondary healing where production of tissue is required to fi ll the defect. It has prov-en its worth especially in the treatment of chronic problem wounds. The scientifi c basis of moist treatment was laid by the work of G. D. Winter (1962, fi rst published in “Nature”). He proved that a moist and permeable wound dressing and the resulting moist wound environment led to more rapid healing than a dry wound environment exposed to the air.

Moist wound treatment has positive effects on all phases of wound healing: during the cleansing phase moist wound dressings show a good wound cleansing effect and allow physical debridement without damaging cells. Furthermore, the moist environment is able to avoid the deactivation of immunocompetent cells (Seiler).

In the granulation phase moist dressings create a physio-logical microclimate similar to a cell culture medium which promotes cell proliferation and therefore the formation of granulation tissue. According to Turner/Beatty et al. (1990), permanently moist treatment brings about a signifi cantly faster reduction in the wound area and leads to a larger quantity of granulation tissue.

In the epithelialisation phase the conditions for mitosis and migration of epithelial cells are improved under moist dressings. This generally leads to rapid epithelialisation with cosmetically more favourable results.

Generally patients cite a relieving of pain under moist wound treatment. Modern hydroactive wound dressings used for moist wound treatment do not normally adhere to the wound due to their atraumatic properties allowing thus painless and atraumatic dressing changes for the patient.

Therefore cell stripping during dressing changes, which disrupts the wound healing process, is avoided. Resting of the wound, so important to healing, is preserved.

Wound dressings for moist wound treatment A series of hydroactive wound dressings are available today for moist treatment and can be used to cover the whole bandwidth of therapeutic requirements within the frame-work of phase-adapted wound treatment.

TenderWet – wound pad dressing with super absorber TenderWet is an extremely effective wound dressing for quick cleansing, necroses detachment, germ reduction and for treating the wound ground especially of chronic and infected wounds. The basis of the high effectiveness is the unique mode of action which allows continuous “rinsing” of the wound.

TenderWet is a multilayered, pad-shaped wound dressing containing superabsorbent polyacrylate as the central component of its absorbing and rinsing core. The non-medicated super absorber is activated before use with an appropriate quantity of Ringer‘s solution which is then delivered continuously to the wound for hours. By the per-manent delivery of Ringer‘s solution necroses are softened, loosened and rinsed out (1).

Even at the same time, germ-laden wound exudate is absorbed and bound into the wound dressing pad. This exchange – Ringer‘s solution is delivered and proteins are taken up – functions because the super absorber of the wound dressing pad has a greater affi nity for the protein-containing wound exudate than for the salt-containing Ringer‘s solution (2). Thus the Ringer‘s solution is displaced from the pad.

The mode of action of TenderWet

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As soon as the wound healing-inhibiting factors have been removed, i.e. the wound is cleansed of necroses, detritus and coatings, the conditions are provided for the formation of granulation tissue: Proliferative cells are able to migrate into the wound area and new capillary growth can take place (3). The moisture and the electrolytes contained in the Ringer‘s solution such as sodium, potassium and calcium contribute to the cell proliferation.

TenderWet has no contra-indications and can also be used on infected wounds. In certain cases, there is an apparent increase in the size of the wound during the initial clean-sing with TenderWet. This means that with this method devitalised tissue which was not recognisable as such was removed.

In the case of deep wound conditions, TenderWet should be packed in loosely without pressure to ensure the direct contact needed for the fl uid exchange. The physical pro-perties of the super absorber in conjunction with the outer woven cover of the wound dressing pad give TenderWet the necessary tamponing properties. With extensive wounds, the TenderWet wound dressing pads should overlap slightly when applied.

TenderWet is available in different sizes and round and rec-tangular shapes to ensure it fi ts well to the various wounds.

For simplifi ed application, TenderWet is available in an already activated form as TenderWet active cavity and TenderWet 24 active with an integrated moisture-repellent protective layer. These “active” wound dressing pads are soaked with ready-to-use Ringer‘s solution and can be applied immediately. This means that a preparatory proce-dure can be omitted, that helps saving time. But a further advantage of already activated wound dressing pads is also that a signifi cantly greater volume of Ringer‘s solution can be introduced into the absorbent core than with manual

TenderWet has no contra-indica-tion and can be used in all wound conditions, both infected and non-infected. The rinsing effect of TenderWet is seen to best advantage during the cleansing phase and at the beginning of the granulating phase. The examples show TenderWet and TenderWet 24 used for treating venous ulcers (1 and 2), a burn wound (3) and a diabetic foot lesion (4).

The rapid and effi cient cleansing effect of TenderWet proved its value with this dehiscent medial abdominal wound in an 83-year old patient (case report M. Butcher, Plymouth, England). 5) Condition of the wound follow ing dehiscence with fi rmly adhering necrotic coatings6) Start of TenderWet treatment on 28/1 with 10x10 cm TenderWet and dressing changes every 12 hours 7) Wound condition two days after start of treatment already with marked reduction of the coatings 8) Condition of the wound on 17/2 with graftable granulation tissue; fi nal covering takes place with a split skin

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TenderWet 24 active and TenderWet active cavity are pre-activitated with Ringer‘s solution and ready-to-use



immersion. This way the wound can be kept moist over a longer period.

Furthermore, the wound dressing pads are soft and easy to mould; this is a particular distinguishing feature of Tender-Wet active cavity, with which even deeper wounds can be packed without diffi culty (=cavity). TenderWet 24 active, by contrast, should not be packed, due to its moisture-repel-lent protective layer.

Prior to its application the classic TenderWet has to be soaked with Ringer's solution. How much Ringer‘s solution is needed for activation depends on the dressing size and is indicated on the package correspondingly. For the easy activation of TenderWet as well as of TenderWet 24, Tender-Wet solution is available in ready-to-use ampoules as well. The composition of the sterile, pyrogen-free and isotonic solution is similar to that of a Ringer‘s solution.

TenderWet 24 active and TenderWet 24 have a special design feature which also contributes to prolonging the ab-sorbing and rinsing effect to around 24 hours: The wound dressing pads are fi tted with a moisture-repellent protective layer, primarily in order to prevent moisture emerging from the dressing to the outside. The dressing side with integrat-ed protective layer is marked with parallel coloured stripes, ensuring the wound dressing pad can properly be applied. As already mentioned, TenderWet 24 active and TenderWet 24 should not be packed because of this protective layer.

The following applies, in general, for all TenderWet wound dressing pads: they are not self-adhesive and must be ade-quately fi xed, for instance completely covered with elastic non-woven sheet dressings (e.g. Omnifi x) or with elastic conforming bandages (e.g. Peha-crepp, Peha-haft).

The packing of deep decubiti with gauze strips (Fig. 1) soaked with antiseptic does not always guaran-tee adequate cleansing so that as an alternative rapid and thorough debridement with the TenderWet active cavity wound dressing pad should be considered (Fig. 2 to 4, case report F. Meuleneire, Belgium). Local wound treatment must of course be consistently supported by pressure-relieving measures such as placing the pa-tient on antidecubitus mattresses or regularly repositioning.

The rapid necrosis removal and methods for treating the wound ground possible with TenderWet 24 active was also seen in the debridement of a haematoma with distinct blood clots, 78-year old female patient (Case report F. Meuleneire, Belgium).5) Debridement of the haematoma on 2/26) Condition after debridement, wound with necrotic residues7) Start of wound cleansing only with TenderWet 24 active, dress-ing change once daily8) Just 5 days after the start of treatment (7/2) the wound is al-most completely clean. The female patient was also very pleased with the rapid wound cleansing and dressing changes were problem and pain-free.

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TenderWet and TenderWet 24 must be activated before use with TenderWet solution or with Ringer‘s solution

In clinical practice, not only does Sorbalgon prove to be well suited to the cleansing of wounds, but also shows itself in the condition-ing of wounds: 85-year old patient, stage III decubitus (case report F. Lang, Leonberg, Germany). 5) Admission fi nding: there was a large necrotic plate on the os sacrum, which was removed with surgical debridement 6) and 7) Start of the treatment with Sorbalgon 10 days after the surgical debridement 8) Wound condition after 20 days of exclusive Sorbalgon treatment showing well developed granula-tion tissue – patient then discharg-ed for further care at home

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Due to its excellent packing capability, Sorbalgon is the ideal wound dressing for problema-tically sited and deep wounds, as examples 1 – 4 show. Sorbalgon ensures tissue-protecting tampo-nade, which can also be removed atraumatically and without caus-ing pain.

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Sorbalgon – tamponading calcium alginate dressings Sorbalgon is especially suited for cleansing and the formati-on of granulation in superfi cial and deep, infected and non-infected wounds. Sorbalgon can excellently be packed and thus provides effective wound cleansing and conditioning, particularly even in deep wounds.

Sorbalgon is a non-woven dressing made of high-quality calcium alginate fi bres which are packed dry into the wound (1). On contact with sodium salts, such as those found in blood and wound secretions, the fi bres swell and transform into a moist absorbent gel which fi lls the wound (2). The close adaption of Sorbalgon to the wound surface means that bacteria are absorbed deep in the wound and enclosed securely in the gel structure (3). This leads to effective reduction in bacteria and helps to avoid re-contamination (3). Wounds are cleansed rapidly so that Sorbalgon has proved valuable especially in the treatment of chronic and infected wounds.

Sorbalgon‘s gel-like consistency also acts like a moist dress-ing which prevents the wound from drying. A microclimate favourable for wound healing is produced which promotes the formation of granulation tissue and keeps the wound surfaces supple.

Because of the gel formation, Sorbalgon does not stick to the wound and dressing changes are painless. However, complete conversion of the calcium alginate fi bres to a gel needs adequate secretion. Should gaping wounds produc-ing little secretion be packed, moisten Sorbalgon with Ringer‘s solution. Any fi bres remaining in the wound can be rinsed out with Ringer‘s solution; otherwise the gel plug can be removed from the wound with forceps.

The mode of action of Sorbalgon

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The large foam pores on the wound-facing side ensure that even viscous secretions and detritus are absorbed without blocking the pores. By absorbing the wound exudate the polyurethane foam swells slightly insuring thus the contact with the wound base required for exudate removal.

The absorbed wound exudate becomes distributed laterally under the top layer. An important factor here is that Perma-Foam – due mainly to its special pore structure – has a large retention capacity for fl uids. Even if pressure is applied from outside, for example with compression bandaging, the exu-date is still held within the foam material. Added to this is the fact that PermaFoam loses its absorption capacity only slightly when under pressure from a compression bandage. For example, under a pressure of 42 mmHg, the absorption capacity is reduced by only 12 % compared with the unload-ed condition.

All these properties together bring about not only the desired rapid regulation of exudation, but also protect the wound edges against maceration, since the absorbed wound exudate no longer presses back into the wound. Furthermore, the good water vapour permeability of the top layer brings about a balanced moist microclimate in the wound, which further promotes healing.

The basis for the therapeutic effec-tiveness of PermaFoam is its spe-cial pore structure: large pores on the wound-facing side decrease steadily in size towards the top layer, which produces a strong ver-tical capillary effect. This causes exudate to be rapidly absorbed into the depth of the absorbent core, and also provides for a high level of retention for reliable bind-ing of the fl uid.


The frequency of dressing changes depends on the individ-ual wound situation. During the wound cleansing phase, a dressing change once or twice daily may be required depending on the degree of exudation. Later, as granulat-ing commences, a dressing change every two to three days may be suffi cient. Sorbalgon is offered in three dressing sizes. Particularly in cases of voluminous wounds Sorbalgon T is available as tamponing ribbons.

PermaFoam – hydroactive foam dressing The foam dressing PermaFoam is indicated for medium to heavily exuding, non-infected wounds in the cleansing phase and during the granulation phase. The basis for its therapeutic effect is its special pore structure.

PermaFoam is a combination of two differently structured foam materials, which are linked to one another by means of a special lamination. The absorbent layer of PermaFoam comprises hydrophilic polyurethane polymers, which are able to store up to nine times their own weight of fl uid in their polymer chains. The polyurethane matrix has a unique pore gradient, i.e. the large pores on the wound-facing side become ever smaller towards the top layer, which creates a large vertical capillary effect. The top layer of PermaFoam is made of a fl exible, closed-pore polyurethane foam and is semipermeable, i.e. impermeable to germs, but allows water vapour through.

This material combination and structure provides product properties with which the maceration problem that fre-quent ly occurs in chronic wounds can be limited: as a consequence of the large capillary effect, excess aggressive wound exudate is rapidly carried to beneath the top layer.

The hydrophilic foam dressing PermaFoam expands the treat-ment options for chronic wounds with its excellent physical effect

Sorbalgon is available in three dressing sizes and as tamponing ribbons.

PermaFoam is atraumatic, adhesion to the wound or growth of the tissue into the foam structure is minimised. Thanks to the high absorption capacity and very good retention, even where secretion is severe (in the absence of complications) PermaFoam can be left on the wound for several days.

PermaFoam is soft and supple and fi ts snugly to the wound shape. The foam dressing is fi xed with elastic conforming bandages (e.g. Peha-haft) or over the whole surface with elastic non-woven sheet dressing for dressing retention (e.g. Omnifi x elastic). The product version PermaFoam comfort is designed for an easy fi xation with an adhesive border. The used adhesive is gentle on the skin. PermaFoam is available in a variety of versions and sizes.

Hydrocoll – absorbent hydrocolloid dressing Hydrocoll is a self-adhesive absorbent hydrocolloid wound dressing for cleansing and conditioning non-infected wounds with moderately severely to slighty secretion.

The term “colloid” derives from Greek and means a sub-stance which is integrated in a matrix when dispersed into its smallest constituents. Accordingly, Hydrocoll consists of absorbent and capable to swelling hydrocolloids covered by a self-adhesive elastomere. A semipermeable layer func-tions as an impermeable to liquids and bacteria cover.

The hydrocolloids, included in the carrier layer, represent the main component of the mode of action of Hydrocoll. When wound secretions are absorbed, the hydrocolloids swell up and change into a gel which expands in the wound and keeps the wound moist. The gel remains ab-sorbent until the hydrocolloids are saturated. At the same time, along with the swelling process, the wound secretion, which is always laden with detritus, bacteria and their toxins, is securely bound into the gel structure.

The mode of action of Hydrocoll

PermaFoam is available in special sizes adapted to different wounds, so that optimum wound treatment can be achieved in every case.PermaFoam sacral (1) for the use in the sacral region, PermaFoam concave (2) for the use on heel and elbow, PermaFoam trache-ostomy (3) for the treatment of puncture points, PermaFoam cavity (4) for the treatment of deep wounds and PermaFoam round (5) for the treatment of smaller ulcers at problem zones.

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Extensive observational studies have shown convincingly that PermaFoam is able to meet require-ments for cleansing and condition-ing of problematic wounds. Case example 1 (F. Lang, Leonberg, Germany): 83-year old female patient with decubitus in gluteal region on right and left sides with infected necrosis on the right; surgical removal of all necroses into healthy tissue. 1) Condition of decubitus after surgical debridement 2) and 3) Cleansing and condi-tioning were carried out exclusively with PermaFoam; continuous healing progress observed 4) Condition of wound after 65 days with partially stable epithelium

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Case report 2 (F. Lang, Leonberg, Germany):86-year old female patient with large abscess of the abdominal wall after dislocated PEG.5) First dressing change after PEG removal and abscess removal, wound cavity with necrotic resi-dues, severely exuding6) PermaFoam cavity is placed loosely into the abscess cavity. The soft foam material and the special pore structure allow good adaptation to the wound surfaces.7) Wound cavity ready packed with PermaFoam cavity.8) During treatment with Perma-Foam cavity granulation issue increasingly forms so that on the day of discharge the treatment is changed to Sorbalgon. 7 8

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Hydrocoll is a self-adhesive, absorb ent hydrocolloid wound dressing for cleansing and con-ditioning non-infected wounds with moderate or slight secretion. For clinically appropriate and economical application, Hydrocoll is available in a variety of shapes and presentations: 1) Hydrocoll in the standard version 2) Hydrocoll thin for already epithelised wounds 3) Hydrocoll sacral specifi cally for wound treatment in the sacral region 4) Hydrocoll concave in a form perfectly adapted to elbows and heels

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Illustrations 5 – 8 show stages in the course of wound healing of a stage II decubitus with vesicu-lation on the left heel. Wound treatment was carried out with Hydrocoll and was free from com-plications. Due to its high absorp-tion capacity, Hydrocoll could be left on the wound for several days, making treatment simple and, due to the reduced dressing change frequency, more economical (documentation Gabi Michl, Kötzting).


The adhesion of the elastomer means that Hydrocoll can be applied to the wound like a plaster. As the gel forms, the adhesion in the region of the wound disappears, so that Hydrocoll protects the wound by being fi xed only to the intact skin surrounding the wound.

The hydrocolloids used in Hydrocoll have particularly good absorbing and swelling capabilities, as well as the prop-erty that their gel structure remains compact. Hydrocoll expands as usual into the wound, but in the gel condition, it may then be removed in one piece from the wound. No gel residues remain in the wound, so that the rinsing out of gel residues with a pus-like consistency, as was previously necessary, is largely dispensed with. Dressing changes are therefore simpler and less unpleasant. In addition, reliable wound assessment is also immediately possible.

The mode of action of Hydrocoll shows its effects in all wound-healing phases. Since excessive bacteria-laden wound secretion is rapidly absorbed, by the absorption and swelling process, into the hydrocolloid portions of the dressing, rapid and good wound cleansing takes place. General investigations have shown that the microcircula -tion in the wound area is also improved with enhanced cleansing. Particularly in chronic wound conditions with a stagnating cleansing phase, the body‘s own cleansing mechanisms are reactivated. During the granulation phase, the moist environment under Hydrocoll stimulates and promotes the formation of granulation tissue. This means that with Hydrocoll, a balanced moist wound environment may be maintained without diffi culty and without the dan-ger of exudate accumulation, even over long treatment pe-riods, and drying out of the granulation tissue is reliably


prevent ed. In the epithelisation phase, the cell-friendly moist en vironment promotes mitosis and migration of the epithelial cells. In addition, unwanted eschar formation, which would impede healing, is prevented. The imperme-able to bacteria and liquid top layer acts as a reliable barrier against germs and protects the wound against dirt and moisture. Mobile patients are able to shower with the dressing in place.

Hydrocoll is available in different shapes, e.g. as “concave” for the wound treatment to elbows and heels or as “sacral” for the treatment of sacral decubitus ulcers: The rectangular standard version is also available in sizes suitable for small wounds. The “Hydrocoll thin” version is specifi cally suited to wounds that are already epithelising.

Hydrotul – hydroactive ointment dressing The development of the hydroactive ointment dressing Hydrotul combines the benefi ts of conventional ointment dressing with modern hydrocolloid technology. This opens up wide areas of application for the hydroactive ointment dressing. Hydrotul is suitable for the treatment of acute as well as chronic superfi cial wounds in the granulation and/or epithelisation phase.

1) Hydrocolloid particles keep the wound moist.

3) The honeycomb like structure of the carrier material prevents accumulation of exudate.

2) The Hydrotul ointment keeps the wound margins soft and

Treatment of a split-skin graft donor site (1) and the recipient site – an accident injury on the right knee (2) - with the hydro-active ointment dressing Hydrotul (Case report F. Lang, Leonberg, Germany). Complication-free healing process with cosmetically very acceptable healing results (3/4). The new epithelium is fi ne and uniform and forms conspi-cuously rapidly from the margin of the wound.

5 6

7 8

1 2

43

Treatment of an acute wound (Burst blister as a result of hyper-keratosis) with Hydrotul (Docu-mentation from an observational study). The condition of the wound before the start of treatment on 30/05 (5) and treatment of the wound with Hydrotul (6). The secondary dressing for absorbing wound exudate consisted of gauze swabs. First dressing change on 02/06 (7), second change on 06/06 (8), the wound was com-pletely epithelised.

The adequate mesh width of the polyamide carrier fabric of Hydrotul (3) permits the removal of the excessive wound exudate without congestion in the secondary wound dressing. As with classic ointment dressings Hydrotul can be combined with all common absorbent dressing pads. The hydroactive ointment dressing Hydrotul can also be handled without any diffi culties. It can be readily cut to size using sterile scissors to fi t the wound size and shape and won’t stick to examination gloves.

In observational studies it could also be confi rmed that in local treatment the hydroactive ointment dressing Hydrotul did not only reduce persistent wound pains, Hydrotul could be removed during the change of a dressing without any problems or pain. The dressing Hydrotul is available in the sizes 5 x 5 cm, 10 x 12 cm and 15 x 20 cm as a sterile and individually sealed version.

Hydrosorb – transparent hydrogel dressing In case of wounds of large areas, Hydrosorb is particularly suitable, for keeping granulation tissue moist as well as promoting new formation of epithelial cells. Hydrosorb is thus the optimum wound dressing for phase-adapted further treatment after wound treatment with TenderWet, Sorbalgon or PermaFoam.

In physical terms Hydrosorb is a three-dimensional network of hydrophilic and thus absorbent polymers with a high water content of 60 %. In spite of this high water content, Hydrosorb can additionally bind large quantities of fl uids due to the presence of hydrophilic groups. In doing so Hy-drosorb swells up without losing its gel structure. This pro-perty results in the specifi c benefi t of Hydrosorb in wound treatment: Right from the start Hydrosorb constitutes a fully functional moist dressing which in contrast to calcium al-ginates or hydrocolloids no longer requires wound exudate for gel conversion.


The results of various observational studies allow the con-clusion to be drawn that the hydroactive ointment dressing Hydrotul promotes the healing process, particularly in the case of acute and chronic wounds in which previous treat-ments were unsuccessful. The presence of an infection is not a contra-indication as unimpeded exudate removal is possible.

The hydrocolloid particles (1) deposited in the polyamide fab-ric is decisive for the improved wound healing-promoting effect and the atraumatic properties of Hydrotul. These ab-sorbing granules made of carboxymethyl cellulose take up the wound exudate and create a physiological moist wound environment as in conventional hydrocolloid dressings, which assist the wound-healing process in all phases. A fur-ther advantage of hydrocolloids is that Hydrotul can remain on the wound without the risk of drying out for longer than conventional ointment dressings as the wound base is kept moist by the mode of action of the hydrocolloids.

In addition, the impregnation of the polyamide carrier fabric with a non-medicated hydroactive ointment mass on trigly-ceride basis (2) is important as it prevents an adhesion of the dressing to the wound surface and increases the atrau-matic properties of the hydrocolloid component, keeps the wound margins soft and supple and prevents macerations. Also, with this triglyceride based ointment mass it was pos-sible to develop a fat component that does not leave un-pleasant ointment residues and can be broken down in the wound. In this way the condition of the wound can always be reliably assessed. This is of practical importance for the treatment of all wounds, but particularly important for burn wounds in the case of which reliable wound assessment must be possible at all times in order to detect any deterio-ration in good time. Hydrotul should be used on 3rd degree burns only when ordered by the treating physician.

The mode of action of Hydrosorb.

1

2

The adequate mesh width of the carrier fabric of Hydrotul (Photo-graph above) permits an unimped-ed exudate removal. How well Hydrotul keeps wound surfaces moist and supple without sticking is shown by the use of Hydrotul in the case of a burn wound (Photo-graph below).

A CB

Thus, with its very good biocompatibility Hydrosorb au-tomatically delivers moisture to the wound over a period of several days immediately after application (1). At the same time, Hydrosorb absorbs excessive, germ-laden exu-date which is trapped in the gel structure. Because with the absorption of exudate the cross-links of the polymer chains expand so that within these macromolecules there is room for included foreign bodies, such as germs, detritus and odour molecules from which they cannot escape. This exchange ensures the optimum moisture level for wound healing and thus accelerates the formation of granulation and epithelisation (2). The surface is impermeable to water and germs in order to safely protect against secondary in-fections.

However, it should be noted that hydrogels show a differ-ent absorption behaviour from, for example, textile mate-rials or calcium alginates. Hydrogels cannot spontaneously absorb fl uids; their fl uid absorption capability only begins after some time and increases slowly. However, hydrogels such as Hydrosorb are then able to provide long-lasting and continuous absorption capacity. Hydrosorb does not stick to the wound and can be removed even after prolonged peri-ods on the wound without the risk of wound irritation. Hydrosorb can be removed in its entirety as the gel struc-ture does not break down because of the absorbed wound exudate. No residues remain in the wound and the con-dition of the wound can be assessed safely without prior rinsing.


Superfi cial wounds, such as burns of degree 1 and 2a or chemical burns can be treated optimally with the hydrogel dressing Hydro-sorb. The slightly cooling effect is perceived as particularly pleasant and pain-relieving by the patients (Case report 1: F. Meuleneire, Belgium)1) Treatment of a chemical burn wound with the hydrogel dressing Hydrosorb2) Good wound cleansing results after only one week3) Further treatment with Hydro-sorb4) Healing result after one month

5 6

1 2

43

The hydrogel dressing Hydrosorb is ideal for a phase-adapted further treatment in the granulation and epithelisation phase.In the shown case report (F. Meu-leneire, Belgium) an ulcer due to haematoma was initially cleansed with TenderWet 24 active, then conditioned with PermaFoam and fi nally treated with Hydrosorb for moisturisation and protection against granulation and epitheli-um (5 to 8), which rapidly brought on the re-epithelisation of the wound. Within a little over two months the problematic wound had practically healed with this therapeutical concept.

7 8

A) The individual macromolecules with their integrated water mole-cules form polymer chains through special cross-links.B) Absorption of the exudate.C) The cross-links are expanded and create room for the secure inclusion of germs, exudates and odour molecules.

The transparency of Hydrosorb is one important factor for the economical use. The wound can be inspected any time through the dressing so that Hydrosorb can stay on the wound for days and dressing changes are unnecessary.

Hydrosorb is available in two versions as Hydrosorb and Hydrosorb comfort. Hydrosorb does not have a self-adhe-sive fi xing edge and is secured with a conforming bandage, adhesive tapes or with a compression bandage. Hydrosorb comfort is fi tted with a hypoallergenic adhesive fi lm for a reliable and impermeable to germs fi xation.

Hydrosorb Gel – for rehydration of dry woundsHydrosorb Gel is a clear, viscous and sterile gel, based on carboxymethyl cellulose, Ringer’s solution and glycerine that immediately delivers healing-promoting moisture to dry, deep and fi ssured wounds and wounds at risk of drying out.

The constituents of Hydrosorb Gel guarantee continuous and adequate delivery of moisture to the dry wound with subsequent therapeutic benefi ts: Fibrinous and necrotic coatings are softened and detached. To a small extent Hy-drosorb Gel can simultaneously absorb germ and detritus-laden exudate. This effectively supports endogenic, physical debridement and the physiological exudation necessary for wound healing can be restored. In the wound conditioning stage with the build-up of granulation tissue the electro-lytes, such as sodium, potassium and calcium, contained in the Ringer solution contribute to cell proliferation.

Dry wounds or wounds at risk of drying out particularly develop in long existing, chronic leg ulcers (Ulcus cruris) and decubital ulcers. In burn wounds up to degree IIb Hy-drosorb Gel has a cooling and pain-relieving effect due to its moisture. It should only be used in the case of infected wounds under medical supervision.

Hydrosorb Gel is available in practical dosing syringes with 15 g and 8 g, which ensure simple application in all wound conditions: Through the long syringe outlet Hydrosorb Gel can be administered directly and cleanly even into deep and fi ssured wounds. This reliable application is supported

by the consistency of the gel. The gel is fi rm enough not to run immediately and soft enough to adapt to the wound base.

The dosing syringe is simply to use with one hand whereby the dose of the gel can easily and precisely be set. In addi-tion, unlike tubes, where a lot of gel often tends to be left unused, the Hydrosorb Gel syringe can be effectively emp-tied. Precisely the amount required for wound treatment can be taken from the syringe. Of particular advantage is also the reverse ml scale of the syringe. This allows imme-diate determination of how much gel is still in the syringe and how much as been administered into the wound.The administered quantity of gel can be used to deter-mine the wound volume and can be entered in the wound documentation folder. After the application of Hydrosorb Gel, the wound must be covered with a suitable secondary dressing whereby almost all current wound dressings can be used.


Hydrosorb Gel serves for effi cient rehydration of dry wounds and is available in easy to use dosing syringes with 15 g and 8 g.


Wound dressings for chronic problematic wounds/wound pattern

Wound cleansing Granulation Epithelisation

Necrosis Infection Fibrin coating

superfi cial wounds

Exudate ++

� TenderWet 24 active (if needed in combination with Atrauman Ag*)

� TenderWet 24 active� Sorbalgon� Atrauman Ag*� PermaFoam (in infected wounds only under medical supervision)

intact wound site� PermaFoam comfort� PermaFoam sacral� PermaFoam concave� TenderWet 24 activepreviously damagedwound site� PermaFoam

intact wound site� PermaFoam comfort� PermaFoam sacral� PermaFoam concavepreviously damagedwound site� PermaFoam� Hydrotul*

intact wound site� Hydrocoll thin� Hydrosorb comfort� Hydrofi lm**� Hydrotul*previously damagedwound site� Hydrosorb� Hydrotul*Exudate +

� TenderWet 24 active� Atrauman Ag*

� TenderWet 24 active intact wound site� Hydrocoll� Hydrocoll sacral� Hydrocoll concavepreviously damagedwound site� Hydrosorb� Hydrotul*

deep or gaping wounds

Exudate ++

� TenderWet active cavity� Hydrosorb Gel

� TenderWet active cavity� Sorbalgon/Sorbalgon T� Atrauman Ag*� PermaFoam cavity

� TenderWet active cavity� PermaFoam cavity� Sorbalgon/Sorbalgon T

� PermaFoam cavity� Sorbalgon/Sorbalgon T

Exudate +

� TenderWet active cavity� Atrauman Ag*

� TenderWet active cavity� Hydrosorb Gel

� Hydrosorb Gel

Further products

Cosmopor steril Self-adhesive wound dressing with high absorption capacity and good cushioning effect for postoperative wound treatment as well as for sterile treatment of minor injuries.

Hydrofi lm plus Self-adhesive, waterproof, trans-parent wound dressing with good absorption and padding effect for postoperative care of slightly secreting wounds and for protec-tion against secondary infection.

Rolta Soft Very soft, skin-friendly synthetic padding bandage, which is particularly suitable as padding material under support bandages and compression dressings.

Cosmopor I.V: Medicomp Drain Peha-Slit dressing PermaFoam tracheostomy For the use with drainages and extensions

Fixation normal skin: Omnifi x elastic, Omniplast, Omnisilk, Peha-haft, Stülpa-fi x sensitive skin: Pehalast, Omnipor, Peha-crepp, Extremities: Peha-haft, Pehalast, Stülpa-fi x Joints: Lastodur straff, Stülpa-fi x, Omnifi x elastic Fingers and toes: Stülpa Fertigverband, Peha-haft Sacral region: Omnifi x elastic, Stülpa-fi x,Molipants (inco-system),

* As primary wound dressing in combination with absorbent wound dressings** For wounds with almost no exudate


Zetuvit Zetuvit Plus Cosmopor steril Atrauman Atrauman Ag

Products for dry wound treatment

Product characteristic Wound compatible absorbent dressing with non-adherent non-woven cover and absorbent core of cellulose fl uffs.

Combined absorbent dressing pad consisting of four layers of different materials: Absorbent core consisting of cellulose fl uffs, blended with super absorber, non-woven covering of the absorbent core, water-repellent special non-woven and two-layer outer non-woven.

Self-adhesive wound dressing with hydrophobic wound contact layer, absorbent pad of pure cotton wool, soft non-woven support, coated with hypoaller-genic polyacrylate adhesive.

Wound compatible ointment dressing made of hydrophobic polyester tulle, impregnated with an ointment mass that is free from active agents.

Silver-containing ointment dress-ing with antibacterial effect. The support fabric, which is coated with silver and made from hydro-phobic tulle is also impregnated with an ointment mass that is free from active agents.

Properties and use Highly absorbent, soft and con-formable, permeable to air, good cushioning effect, for treatment of acute wounds of large area with very severe secretion, good protection against contamination due to an integrated hydrophobic cellulose layer which prevents the secretions from striking through.

Extra absorbent, absorbs more than double the volume of con-ventional absorbent dressing pads, the super absorber traps exudate in the absorbent core, reduced tendency of adhesion by the hydrophobic outer surface of the non-woven, well protection against contamination by water-repellent special non-woven, for the treatment of very severely exuding wounds.

Fast transfer of secretions into the absorbent pad through the hydrophobic wound contact la-yer, non-adherent, good absorp-tion capacity and cushioning ef-fect, permeable to air and water vapour, reliable adhesive zone at the edges of the dressing, for postoperative wound treatment and for sterile treatment of minor injuries as part of fi rst aid.

Permeable to secretions and air, does not adhere to the wound, no residues in the wound because of self-emulsifying ointment mass, no sensitising effect, to keep acute and chronic wounds supple, especially in dermatology as well as in patients with sensitive skin and drug intolerances.

For treating infected wounds and those in danger of infection; broad antibacterial activity spectrum gram-positive/gram- negative, long-lasting bacteri-cidal effect, demonstrable good tissue tolerance and only slight toxicity; the ointment impregna-tion treats wound edges; apply with absorbent secondary dress-ing.

Presentations Zetuvit, sterile and non-sterile,10x10, 10x20, 13.5x25, 20x20 and 20x40 cm

Zetuvit Plus, sterile, 10x10, 10x20, 20x25 und 20x40 cm

Cosmopor steril, 7.2x5, 10x6, 15x6, 10x8, 15x8, 20x8, 20x10, 25x10 and 35x10 cm

Atrauman, sterile, 5x5 and 7.5x10 cm

Atrauman Ag, sterile, 5x5, 10x10 and 10x20 cm


TenderWet Sorbalgon PermaFoam Hydrocoll Hydrotul

Products for hydroactive wound treatment

Product characteristic Wound dressing pad with absorb ing and rinsing core of superabsorbent polyacrylate, is activated prior to use with Ringer‘s solution, which is then continuously delivered to the wound in exchange with wound secretions.

Calcium alginate dressing free from active agents and can be used to pack wounds, which transforms into a moist gel on contact with wound secretions; with the swell ing process, germs are also secure ly enclosed within the gel structure.

Hydroactive foam dressing made from foam materials of differing structure, with high vertical capillary effect and retention for reliable fl uid binding, top layer impermeable to germs.

Self-adhesive hydrocolloid wound dressing with particularly ab-sorbent and swelling-capable hydrocolloids, combined with a semipermeable top layer, imper-meable to bacteria and liquids.

Hydroactive ointment dressing with integrated hydrocolloid particles in the wide-meshed polyamide carrier tissue and non-medicated ointment impregna-tion based on triglyceride.

Properties and use Fast active wound cleansing and promotion of proliferation of tissue cells by continuous supply of Ringer‘s solution and simul-taneous absorption of bacteria-laden secretion (= absorbing and rinsing effect), for treatment of chronic, infected and non-infect-ed wounds during the cleansing phase and at the start of the granulation phase.

High absorption capacity with ef-fi cient cleansing effect, keeps the wound moist after transformation into gel, promotes formation of granulation, by means of its excellent packing characteristics it is particularly suitable for cleansing and conditioning deep and gaping, infected and non-infected wounds as well as after a surgical debridement.

Fast regulation of wound exudate, protects wound edges against maceration, particularly suitable for treatment of venous ulcers in combination with a compression treatment, for the treatment of burns up to second-degree, type a, for deep wounds or problem zones that are diffi cult to treat, the respective specifi c sizes.

Provide for good cleansing, improved microcirculation in the wound area, promotes granula-tion formation, no adhesion to the wound, in the gel condition, can be removed from the wound in one piece, particularly suitable for conditioning non-infected wounds with moderate or slight secretion.

Ensures an optimum moist wound environment for fast healing, does not stick to the wound, protects against trau- matisation during dressing changes, keeps wound margins soft and supple and prevents maceration, for the treatment of superfi cial, acute and chronic wounds in the granulation and epithelisation phase.

Presentations TenderWet 24 active, sterile, Ø 4, Ø 5.5, 4x7, 7.5x7.5, 10x10 and 7.5x20 cm; TenderWet active cavity, sterile, Ø 4, Ø 5.5, 4x7, 7.5x7.5, 10x10 and 7.5x20 cm; TenderWet 24, sterile, Ø 4, Ø 5.5, 7.5x7.5 and 10x10 cm; TenderWet, sterile, Ø 4, Ø 5.5, 7.5x7.5 and 10x10 cm

Sorbalgon, sterile, 5x5, 10x10 and 10x20 cm; Sorbalgon T ribbons, sterile, 1 g/30 cm and 2 g/30 cm

PermaFoam, sterile, Ø 6, 10x10, 10x20, 15x15, 20x20 cm; Per-maFoam comfort, sterile, 8x8, 11x11, 10x20, 15x15, 20x20 cm; PermaFoam sacral, sterile, 18x18, 22x22 cm; Perma Foam concave, sterile, 16.5x18 cm; PermaFoam cavity, sterile, 10x10 cm; PermaFoam trache-ostomy, sterile, 8x8 cm

Hydrocoll, sterile, 5x5, 7.5x7.5, 10x10, 15x15 and 20x20 cm; Hydrocoll sacral, sterile, 12x18 cm; Hydrocoll concave, sterile, 8x12 cm; Hydrocoll thin, sterile, 5x25, 7.5x7.5, 10x10 and 15x15 cm

Hydrotul, sterile, 5 x 5 cm, 10 x 12 cm und 15 x 20 cm

ostomy, sterile, 8x8 cm7.5x7.5 and 10x10 cm

Hydrosorb Hydrosorb Gel

Products for hydroactive wound treatment

Product characteristic Transparent gel dressing made of absorbent polyurethane polymers in which a large water content of 60 % is stored, combined with semipermeable, top layer imper-meable to germs and liquids.

Clear, viscous and sterile hydrogel based on carboxymethyl cellulose, Ringer’s solution and glycerine.

Properties and use Provides the wound from the beginning with moisture, enables inspection of the wound due to its transparency at any time without dressing change, (= high economic effi ciency because of longer dressing change intervals), ideal for keeping granulation and epithelium moist after therapy with TenderWet, Sorbalgon or PermaFoam.

Rehydrates wounds at risk of drying out and dry deep and fi ssured wounds; fi brinous and necrotic coatings are softened and detached; effectively sup-ports the autolytic debridement; the electrolytes contained in the Ringer‘s solution contribute to the cell proliferation; easy to use by dosing syringes.

Presentations Hydrosorb, sterile, 5x7.5, 10x10and 20x20 cm; Hydrosorb comfort, sterile, 4.5x6.5, 7.5x10, 12.5x12.5 and 21.5x24 cm

Hydrosorb Gel, sterile, dosing syringes with 15 g und 8 g

The dressing change

Depending on the type of wound being treated the dressing change is characterised by special problems. Primarily heal-ing wounds closed by suturing cause the least diffi culties. The dressing has the function of absorbing any oozing and protecting the wound against secondary infections or mechanical irritation. In contrast, the demands made on those responsible for changing the dressings of acute and chronic wounds undergoing secondary healing are higher. In this case, the wound dressing is an essential therapeutic measure which can infl uence all the phases of wound heal-ing. Accordingly, the quality of the dressing change contrib-utes to the further healing process.

Complete asepsis Every dressing change must take place under sterile condi-tions. Even wounds which are already clinically infected must be treated exclusively under aseptic conditions. Apart from the fact that secondary infections must also be prevented, such infected wounds represent a reservoir of extremely virulent germs, spread of which may only be prevented by comprehensive asepsis.

Since most wound infections are transmitted by hand, the so-called “no-touch technique” must always be used during dressing changes, so that the wound and the dressing are never touched with bare hands. This is carried out by two people in order to counter the increased risk of infection when a septic dressing is being changed.


The dressing trolley is used for transport and preparation of the necessary materials

Material requirements and planning needs All materials which come, or could come, into direct contact with the wound, or which are used in a sterile procedure, must be sterile. The sterile material needs should be estimat-ed as precisely as possible in order to avoid sending items back for resterilisation.

The material is stored in the dressing trolley which is used for transport and to prepare for the change of dressing. It has proven useful in practice to leave the dressing trolley outside the patient‘s room and assemble the materials required for the individual dressing change on a tray (or on a multifunction trolley in the case of dressing changes requiring a lot of materials). The tray must not be placed on the patient‘s bed. If necessary, it can be put on the locker extension.

The working surface is placed so that it is beside the person doing the dressing, never behind him/her. Arrangement of materials into sterile and non-sterile is such that non-sterile materials are closer to the patient, and sterile materials furthest from him. This arrangement avoids reaching over

Sterile material Non-sterile material

� Toothed and non-toothed forceps for removing dressing, debridement and cleansing

� Scissors and scalpels for debridement and for freshening wound edges

� Staple remover� Blunt cannulas and probes to explore the depth of

the wound and for irrigation� Syringes and irrigation fl uids (sterile water, normal

saline, Ringer‘s solution), a well tolerated wound disinfectant if required (Lavasept)

� Swabs and cotton wool applications for wound cleansing

� Appropriate wound dressings or packs� Disposable gloves and drapes

� Fixing materials such as adhesive tapes, dressing retention sheets, bandages, net or tubular bandages

� Dressing scissors� Disposable gloves � Containers for refuse and disinfectant � Hand disinfectants � Protective clothing such as disposable apron

and face masks, possibly also surgical caps


sterile material, for instance when discarding used dressing materials.

The sterile materials must lie on a sterile sheet. Further-more, the materials should not be prepared too early so that they are contaminated by standing open for long periods. If early preparation of materials cannot be avoided, the materials should be protected with a sterile covering.

All multi-use items (dressing tables, trays and instruments) must be easy to clean and disinfect or sterilise. A disinfec-tion container (disposal box) and a refuse container must also be available for immediate disinfection of instruments and to dispose of dressings. In the case of septic dressings, it should be remembered that these are usually very large in volume and this should be borne in mind when choosing a refuse container.

If several dressing changes are to be carried out on the ward, the non-infected wounds should be treated fi rst.

The practical performance of dressing change

Protective measures In accordance with hygiene guidelines, hygienic hand disinfection must take place prior to preparation of the materials. 3 – 5 ml of a suitable hand disinfectant from a dispenser or single bottle, are rubbed in thoroughly for at least 30 seconds. Take care that the spaces between the fi ngers are even disinfected.

A fresh (disposable) apron is put on over clean protective clothing. A face mask is required when large area wounds (e.g. burns) are being treated or when the person doing the dressing is suffering from a cold. Covering the hair with a surgical hood is indicated in the treatment of large wounds, those at high risk of infection or those already infected.

When changing dressings in AIDS and hepatitis patients or patients with treatment-resistant staphylococcus strains, the person doing the dressing must protect him/herself particularly against the risk of infection: Suitable disposable gloves, eye protection and a mouth and nose mask are required.

Preparation of the patient The patient should be informed about the imminent change of dressing and wound treatment. If pain is to be expected during the dressing change because of the condition of the wound, pain-relieving medication should be given about half an hour before the dressing change. The use of a local anaesthetic cream may be indicated for pain reduction. Take care of the exposure times recommended by the manufacturer.

The patient should be positioned so that he is lying com-fortably and the wound area is readily accessible. A good light source is particularly important. Privacy and dignity of the patient must be observed.

During the change of dressing, the room should not be entered by other persons, to prevent organisms from being stirred up. That is the reason why there should also be no draught in the patient‘s room. Cut fl owers or other obvious reservoirs of organisms should be removed from the area of the dressing change.

If wound irrigation or other more extensive wound cleans-ing has to be undertaken, the bed should be protected against contamination by disposable sheets.


Removal of the dressing Put on non-sterile disposable gloves, remove and discard the dressing carefully with a sterile forceps. If the wound dressing cannot be removed because it has stuck to the wound, it should never be pulled off. It should be moisten-ed with Ringer‘s solution until the adhesion has dissolved.

The wound dressing is examined for signs of pus and other deposits and discarded into the refuse container. The used forceps should be put in the disposal box fi lled with disin-fectant solution.

The gloves are then changed, and sterile disposable gloves are put on.

Wound inspection Assessing the condition of the wound correctly is not always easy even for the experienced. However, reliable evaluation is an important basis for choosing subsequent local therapy. The following should be assessed: ▪ wound size, wound depth, undermining etc. (Has the

wound got bigger/smaller since the last dressing change?) ▪ degree and nature of deposits and necrotic tissue

(black, leathery, scab, sloughy, purulent) ▪ nature of exudate (serous, bloody) and degree of

secretion (highly secreting, wound becoming desiccated) ▪ presence and nature of granulation (no granulation tissue

present, pale, spongy, pink, red, fi rm) ▪ extent of epithelial formation ▪ degree of bleeding tendency ▪ painfulness of the wound ▪ signs of infection (swelling, erythema, yellowish or

greenish sloughy deposits, odour)

The condition of the wound is documented in writing only after the dressing change is complete so that there is no interruption which could jeopardise the sterile chain.

Cleaning the wound and wound surroundings Simple cleaning with a sterile swab or sterile cotton wool applicator from within outwards is suffi cient for prima-rily healing aseptic wounds. Disinfection of the wound surround ings is usually not necessary.

By the latest recommendations, also infected and septic wounds are cleaned from the outside inwards, using a well tolerated disinfectant if appropriate. Depending on the condition of the wound, more extensive cleansing measures may be necessary for wounds healing secondarily:

Slough and devitalised tissue can be removed mechani-cally with scalpel, scissors or a sharp curette. Of the three instruments, the scalpel is to be preferred as removal with frequently blunt scissors or blunt curettes involves a risk of crushing and traumatising tissue.

Mechanical removal can be facilitated if the slough is softened beforehand by hydroactive wound dressings.

Adequate pain relief should be ensured for debridement. Extensive formal debridement should be performed in the operating theatre.

Disinfection of the wound area should only be undertaken where strongly indicated and, where possible, only for a short time with an antiseptic which has proven effective-ness, low cytotoxicity and causes no pain.

Removal of necrotic tissue and slough is best done with a scalpel in order to avoid tissue crushing


Irrigation with Ringer‘s solution contributes to effi cient wound cleansing. The irrigation fl uid is drawn sterile into a syringe (10 to 20 ml depending on wound depth and con-dition) and the wound is irrigated with light pressure. With deeper gaping wounds, irrigation is through a blunt probe or short catheter. The fl uid can be collected either with compresses or a kidney dish. After irrigation, the wound area is dried carefully with sterile compresses.

This can be followed by another change of gloves, e.g. in the event of contamination during the cleansing procedure.

The wound surroundings may exhibit eczematous altera-tions, especially in the case of chronic wounds. Treatment is in accordance with the principles of eczema therapy: Superinfected eczema can be treated with suitable anti-septic solutions. Caution: The antiseptics should not reach the wound. Subacute or chronic eczema requires different treatment where exclusively non-allergenic ointment bases and medications should be used.

If self-adhesive dressings are applied after this treatment, they must be suffi ciently large to adhere to non-greasy skin.

If cleansing is necessary, it is done from the inside outwards in the case of primarily healing, aseptic wounds (left) as well as in the case of septic wounds (right) in order to prevent germ migration into the wound.

Care of granulation tissue and wound edges The presence and nature of the granulation tissue is an important indicator of the quality of the repair process in secondary wound healing. The granulation tissue may be designated a “temporary organ unit” which reacts ex-tremely sensitively to exogenous infl uences and disturbing factors. It should be treated as gently as possible.

Fresh red granulation does not need cleaning and irrigation with disinfectants and no ointments for supposed promo-tion of granulation. Maintenance of an undisturbed wound is essential by using atraumatic, non-adherent wound dressings and keeping the granulation surface moist constantly to prevent it from drying out. Hydrosorb or alternatively Hydrocoll are available for this purpose. These ensure that the wound is kept moist in a simple and time-sparing manner and also provide for an atraumatic dressing change.

With sloughy, lax or stagnating granulation, the treatment measures used previously should be reevaluated. Possible causes for reduced production of granulation tissue may be reduced blood supply in the wound, pressure or inadequate wound cleansing.

Excessive granulation is usually removed with a caustic stick (silver nitrate), more or less for want of a better method.

It is not uncommon to fi nd that parts of the wound are already granulating while other parts are still at the cleans-ing phase. Particular caution is needed around the granula-tion tissue if wound disinfection is required and during mechanical cleansing.

The best way of promoting well-formed fresh red granulation tissue is to keep it moist continuously and to protect it from trauma during dressing changes


Reverdin‘s method for wound clo-sure: Epidermal fl aps are obtained with a scalpel and transplanted onto the well-conditioned wound. Further epithelisation is able to spread out from these islands of epithelium

In the case of chronic wounds with their often prolonged healing process, the wound edges tend to epithelialise and project inwards. Since no further epithelialisation can then take place from the wound edges, freshening of the edges with the scalpel or with a sharp scissors is indicated.

The sensitive skin area immediately surrounding the wound should, if necessary, be treated with a moisturising cream or a water in oil emulsion. The preparations used must not contain preservatives or perfumes. Ointment dressings such as Atrauman are also suitable for the care and protection of wound edges and the surroundings of the wound. Skin are-as which have evidence of eczematous changes are treated according to the principles of eczema therapy, as described earlier.

Treatment of epithelialising wounds Well-advanced epithelial cells, like well-developed granu-lation tissue, need no other treatment beyond being kept moist and protected from cell stripping during the dressing change. Smaller epithelialising wound surfaces can be treated with Comprigel. For more extensive wounds, espe-cially chronic wounds, Hydrosorb is particularly suitable because it provides the epithelial cells with more moisture.

If there is no spontaneous epithelialisation or the process is stagnating, which is frequently the case with chronic wounds, plastic surgical measures (e.g. skin grafting) should be considered to achieve wound closure.

Application of the new dressing The new dressing is chosen which has a mode of action meeting specifi c wound requirements (see overview wound dressing p. 170 – 176). It should be ensured that the selected dressing fi ts the wound surface well, for wound secretion can only be absorbed when there is good contact between the dressing and the wound. Deep and gaping wounds should be packed carefully with suitable dressings such as Sorbalgon to ensure absorption of infected secre-tions even deep within the wound.

In the case of deep, gaping wounds, particular care should be taken that they are not too fi rmly packed. The pressure of excessive packing impairs the microcirculation of the wound surface and particularly of the granulation tissue. White sloughy deposits and necrosis appear as a result of the compression. If the fi rm packing continues, sepsis may occur. Moreover, it should be possible to remove the packing without cell stripping and increased pain, which is ensured with Sorbalgon.

Securing the dressing Securing the dressing using adhesive tapes is usually suffi cient in the case of primarily or small secondarily healing wounds.

In the case of larger injuries, adhesion over the entire area with adhesive dressing retention sheets or conforming bandages is indicated. Dressings which are not secured fi rmly can cause irritation of the wound leading to disturb-ances and delays in wound healing.

The wound dressing must provide optimum fi t to the wound base so that wound secretion can be absorbed. Examples for use of this are TenderWet (above) to treat wounds of large area or Sorbalgon (below) to pack deep wounds.


* Warning: Since Peha-haft is a cohesive conforming bandage, it should be used with care in patients with disturbed blood circulation. Do not apply too tightly.

Possible dressing fi xations: Even dressing with the adhesive tape Omniplast which ensures secure fi xation because of its adhesive strength (left). The hypoallergenic adhesive tape Omnipor made of highly air and water vapour permea-ble non-woven support is well-suit ed for patients with hypersensitive skin (right).

The non-woven for dressing reten-tion Omnifi x elastic is easy to use. It fi ts securely and without creases even to joints and conical parts of the body by means of the transver-sely elastic support of non-woven fabric.

The highly elastic net tubular bandage Stülpa-fi x only needs to be lifted to change the wound dressing (left). The tubular band-age Stülpa is indispensable espe-cially for special fi xations, e.g. as a fi nger bandage (right).

The cohesive elastic conforming bandage Peha-haft* holds securely without end-fi xation and is par-ticularly economical to use (left). Simple securing with elastic bandages over joints, in this case with Pehalast (right).

In some wounds, it is necessary to prevent the occurrence of oedema at the wound edges by slight fl at pressure on the wound surface. Even pressure is obtained by applying elastic cohesive bandages or cotton crêpe low-stretch bandages somewhat more tightly. It is necessary to check carefully that there is no tourniquet effect. Elastic support bandages are also available to stabilize wounds after chest and abdominal operations.

A dressing retention bandage helps to protect the wound from the penetration of dirt and micro-organisms in addi-tion to the wound dressing and to cushion it against pres-sure and impacts. It also has a psychological effect. As a visible conclusion of wound treatment, it may be assessed by the patient as a professional treatment and so give him the feeling that he is being well looked after.

Concluding tasks After the dressing change, the patient is replaced in the desired or required position (for example, avoiding pressure on the wound area in the case of pressure sores, legs lower in the case of peripheral arterial occlusive disease).

The used materials are prepared for fi nal disposal or for reprocessing in accordance with the hygiene plan. Hygienic hand disinfection concludes the procedure.

Frequency of dressing change Not only an atraumatic dressing change but also the correct timing are important for an optimal healing process. The frequency of the changes of dressing depends on the con-dition of the wound and the characteristics of the wound dressing. Unnecessary changes should be avoided as every dressing change means a disturbance of the wound.


The dressing should be inspected and, if necessary, remov-ed promptly:▪ if the patient complains of pain, ▪ if pyrexia occurs, ▪ if the dressing is softened and soiled or the absorptive

capacity of the dressing is exhausted, ▪ if the dressing has come loose.

In the case of an aseptic wound undergoing primary heal-ing, a surgical wound, the dressing normally stays in place until the sutures are removed. However, the dressing should be replaced if blood oozes during the hours after the opera-tion.

On the other hand, it is more diffi cult to estimate the frequency of changes of dressing in wounds undergoing secondary healing. In the cleansing phase, depending on the degree of exudate or in the presence of an infection, a change of dressing once or twice a day may be necessary.

If the wound is clean, free from infection and bright red granulation tissue is gradually becoming visible, the frequency of dressing changes can be reduced. When hydroactive dressings such as Hydrosorb or Hydrocoll are used, they can be left on the wound for a few days. With Hydrocoll, the formation of a blister indicates that the absorption capacity is exhausted while in the case of Hydrosorb, the gel has a slight milky to cloudy appearance indicating that the dressings need to be changed. Hydro-sorb also allows problem-free observation of the wound because of its transparency. It gives the doctor and nursing staff the security of knowing that any complications can be recognised immediately.

The formation of a blister in the hydrocolloid dressing Hydrocoll indicates that the dressing needs to be changed

With increasing wound contraction and advancing epitheli-alisation, the physiological secretion of the wound dimin-ishes so that the intervals between dressing changes can become longer. Provided there are no complications of wound healing, Hydrocoll and Hydrosorb can remain on the wound for up to seven days.

Documentation of dressing changes and wound care Precise wound documentation describes all the criteria that serve both, treatment planning and prognosis estimation, as well as treatment control and the healing process. It is therefore the basis for every effective wound treatment, but should also be regarded and accepted as an indispensable instrument for securing treatment quality.

Careful recording of data is a compulsory guideline for all involved in wound treatment and care and it simplifi es consistent procedure, starting from diagnosis of the reasons for the wound, determining adequate causal treatment, i.e. estimation of the wound condition, and from this, sti-pulation of local wound treatment. The treating personnel therefore concern themselves extensively with the wound problem in question. In the case of chronic wounds, this increases the chances of the defect healing more rapidly, which may possibly spare the patient years of suffering.

Precise initial recording of fi ndings which acknowledges wound problems promotes, in particular, the urgently need-ed early interdisciplinary cooperation. If, for example, the hazardousness of a beginning diabetic ulceration is recog-nised and if coordinated treatment by diabetics specialists, angiologists, surgeons, etc., is begun early, life-threatening amputations can be avoided in many cases.


Furthermore, wound documentation allows progress, stagna tion or set-backs in the treatment to be assessed reli-ably, so that treatment measures may possibly be amended accord ingly.

The documentation also, above all, ensures an information fl ow between physicians and nursing staff. This can also prevent, for example, that contrary measures are taken from one dressing change to the next, because different people are performing the wound treatment.

And lastly, evidence of medical/nursing care which meets the prevailing standard is made by law into a self-evident obligation, so that written documentation is indispensable for safeguarding the medical or nursing care from the legal and third party liability standpoint. Oral agreements, for instance during ward hand-over or ward consultations are not suitable for providing the legally required evidence of the quality of treatment and care.

The entry of data in the documentation should be made as soon as possible following the performance of wound treatment or a dressing change. This means that the wound condition is still fresh in the memory and no important in-formation will be lost. The documentation is then always up to date during a shift. The practice sometimes followed of making entries collectively shortly before a ward hand-over should be avoided as unreliable and imprecise.

For the sake of useful documentation, an “appropriate” choice of words which precisely describes the condition of the wound is of great signifi cance. However, this frequently presents diffi culties in practice and the statements are

often relatively imprecise. In order to avoid lack of clarity, a documentation system can contain clear descriptions of the individual parameters, which then need only to be ticked off. Or the descriptions to be used are worked out in a team and stipulated as the “norm” for the documentation, which is then binding on all in the wound team.

Additional photographic documentation is also particularly well suited to recording the condition as well as the healing process of the wound clearly and precisely. Misinterpreta-tions that can arise in purely written wound descriptions are avoided. Certain legal aspects need to be paid regard to in the context of photographic documentation, mainly relating to the consent of the patient.

Here are a few tips for carrying out the documentation:▪ Basically it has to take care that photographs which record the progress of a wound are always taken under the same conditions in order that, even if the dates of the photography are different, useful comparisons can be made.▪ Digital photography has been become the standard means of imaging, allowing photographs to be produced and fi led cost-effectively. Even though cameras with over 10 million pixels are now available, for the purpose of wound documentation a model with 3 million pixels is usually suffi cient.▪ Perhaps, all pictures have to retain their evidential value even years later. Therefore it is important that the fi les are carefully administered. This includes meaningful naming of the fi les (e.g. “Surname_Forename_Date.jpg” instead of “DSC35469.jpg”), regularly backing up all fi les (e.g. on CD-ROM or DVD) and if necessary keeping print-outs produced with suitable photo printers in the patient fi les (1).

▪ With regard to the settings used it must be ensured that not only the central wound area is sharply defi ned but also the near and further way areas of the body.▪ If there is not suffi cient daylight available, a fl ash can be used for illumination if necessary, whereby it must be ensured that no refl ections occur. The use of special colour cards is also useful which in the case of differing light conditions allow the images to be corrected to “standard conditions” and can thereby be compared.▪ The selected background should be as “quiet” as possible – i.e. without any structure (2).▪ The camera should be held with its exposure plane as far as possible parallel to the subject. If the exposure plane and the subject are not parallel, the image will be dis- torted and will not show the exact size relationships (3).


1 2 3

A

Acid and alkali injuries ➞ 31

Acidophil ➞ acid-loving, stainable with acidic dyes

Acute traumatic wounds ➞ 81

Adhesive tape ➞ 178

Adhesive dressing retention sheet ➞ 178

Adiposity, adipose ➞ excessive accumulation of fatty tissue in the body, obesity

Age of patient ➞ 54

Agent ➞ medical: factor/substance causing ill

Aggregation ➞ medical: accu-mulation/amalgamation of platelets (thrombocytes) ➞ 36

Allo- ➞ other, foreign (Greek: allos = other)

Antibiotics ➞ 79

Antiphlogistics ➞ medication that counter infl ammation

Antiseptics ➞ 77

Apocrine sweat glands ➞ 20

Arterioles ➞ the smallest arterial blood vessels, splitting into capilla-ries (Latin: arteriola = little artery)

Asepsis ➞ 168

B

Basal layer ➞ 10

Basal membrane ➞ 10

Betahaemolysis, betahaemolytic ➞ complete haemolysis (dissolu-tion of erythrocytes and of freed haemoglobulin) in blood agar (culture medium) on colonisation of the culture medium with beta-streptococci and staphylococci

Blood ➞ 22

Blood coagulation ➞ 36

Blood plasma ➞ 23

Blood supply to the skin ➞ 21

Burns ➞ 30, 89

C

Cachexia, cachectic ➞ wasting away due to severe weight loss, reduction in strength as a result of an underlying disease, wasted ➞ 56, 66

Capillaries ➞ smallest blood vessels

Chemotaxis ➞ chemical stimulus which activates the movement of cells, such as leukocytes or macrophages

Chronic post-traumatic wound ➞ 130

Chronic wounds ➞ 96

Chronic wound healing ➞ 33, 53, 97

Closed wounds ➞ 27

Clostridium tetani ➞ 68

Coagulation necrosis ➞ dead tissue (necrosis) as a result of protein coagulation ➞ 90

Combined absorbent dressings ➞ 145

Complicated wounds ➞ 28

Conforming bandages ➞ 178

Contraction, contract ➞ pulling together, e.g. of muscles or granula tion tissue during reformation of scar tissue ➞ 46

Contusion, contusion zone ➞ bruising, crushing, bruising or crushing region

Corneal layer (stratum corneum) ➞ 12

Corium (dermis) ➞ 13

Cytoplasm fragmentation ➞ break-up of cellular plasma into fragments

Cytostatics ➞ medications, which delay or hinder nuclear or plasma division

D

Debridement ➞ 99

Dehiscence ➞ splitting apart of structures/tissue sections, e.g. a wound suture, by mechanical forces

Decubital ulcer, decubitus ➞ 33, 102, 126, 153, 156, 159

Degree I ➞ 30, 89

Degree IIa ➞ 30, 89

Degree IIb ➞ 30, 90

Degree III ➞ 30, 90

Delayed primary healing ➞ 52

Glossary & Index Dermatome, mesh dermatome ➞ surgical cutting instrument for removing skin fl aps for trans-plantation

Dermis (Corium) ➞ 13

Diabetic ulcer ➞ 33, 117

Differentiation stage ➞ 46

Disposing factors for wound infection ➞ 66

Disruptions of wound healing ➞ 61

Distortion ➞ sprain, closed joint injury (Latin: distorsio = twisting, sprain)

Documentation ➞ 181

Dressing change ➞ 168

Dry wound treatment ➞ 144

E

Electrocoagulation ➞ (thermo-coagulation), surgical procedure for destruction of tissue with a powerful electric current; heating of the protein also stops bleeding

Embolism ➞ sudden occlusion of an artery by a blocking particle, e.g. a thrombus

Emphysema ➞ infl ation, medical: Accumulation of air (gas) in the lungs (pulmonary emphysema) or in other tissues, e.g. the skin

Endotoxin ➞ bacterial toxin that is released on cellular breakdown with disintegration of the cell wall

Enzymatic, enzymes ➞ brought about by enzymes

Enzymatic debridement ➞ 100

Enzymes = protein molecules which, as a catalysts, accelerate biochemical reactions

Epidermis, top skin layer ➞ 8

Epithelial wounds ➞ 94, 176

Epithelisation ➞ 47

Epithelium ➞ covering tissue as the delimiting cell layer of internal and external body tissue (Latin: epithelium = uppermost cell layer, covering tissue)

Erysipelas ➞ 75

Erythrocytes (red blood corpuscles) ➞ 23

Escherichia coli ➞ 68, 79

Excision, excising ➞ cutting out or removal of part of a tissue or organ with the aid of a sharp instrument

Execution ➞ 169

Exogenous ➞ medical: exerting an infl uence on the organism from outside, entering into it, e.g. a pathogen (Latin: ex(-) = ex(-)

Exotoxin (Ectotoxin) ➞ toxin continuously discharged from the interior of bacterial cells

Exudative phase ➞ 36

F

Fasciae ➞ collagenous connec -t ive tissue sheath round skeletal muscles

Fibrinogen ➞ component of blood plasma, factor I for blood coagula-tion ➞ 23, 38

Fixation of the wound dressing ➞ 177

Fracture ➞ break, surgery: bone breakage ➞ 29

Frequency ➞ 179

Freezing ➞ 31

Functions of the skin ➞ 7

G

Galen ➞ Claudius (Clarissimus?) Galenus of Pergamon (129 – 199 AD) regarded as the most important of the historically recorded ancient physicians

Gas gangrene ➞ 74

Gas permeability ➞ 141

Gauze dressings ➞ 142, 145

Genotype ➞ total genetic information of an organism

Germ layer (basal layer, Stratum basale) ➞ 10

Gram-positive, gram-negative ➞ staining of bacteria by Gram‘s staining technique; blue = gram-positive, red = gram-negative; staining behaviour is an important criterion for bacterial classifi cation and for antibiotic therapy

Granular cell layer (Stratum granulosum) ➞ 11

Granulation tissue ➞ 44

Granulocytes ➞ 24

H

Haematoma ➞ 29, 62

Haemodynamic situation ➞ study of the physical basis of blood fl ow ➞ 105

Haemostasis ➞ 36

Glossary & Index [194.195]

Hair ➞ 19

Hyalinisation, hyaline ➞ abnormal formation of glassy, transparent substances, e.g. in the connective tissue (Latin: hyalus = glass)

Hydrocoll (hydrocolloid dressing) ➞ 157

Hydrosorb (hydrogel dressing) ➞ 160

Hydrosorb Gel ➞ 168

Hydrotul (hydroactive impreg-nated dressing ➞ 162

Hypertrophic ➞ medical: showing excessively enlarged tissue

Hypertrophic scar formation ➞ 63

I

Ileus ➞ intestinal obstruction ➞ 57, 63

Immune status ➞ 56

Immunosuppressant ➞ medica-tion for artifi cial suppression of immune reactions, e.g. on transplantation of organs or in autoimmune disease ➞ 58

Incisions/operation wounds ➞ 94

Incretory disruption ➞ disruption affecting internal secretions

Infection symptoms ➞ 65

Infection types ➞ 73

Infective agents ➞ 66

Infl ammatory reactions ➞ 38

Infl ammatory stage ➞ 36

Infl uences on wound healing ➞ 54

Interference ➞ overlay, intersecting

Interrupt ➞ stop, cease

Interstitium ➞ intermediate space between organs and tissues

Intoxication ➞ poisoning (Greek: toxicon = poison)

Ischaemising ➞ causing blood cir-culation insuffi ciency or ischaemia

K

Keloids ➞ 64

Krause‘s corpuscles ➞ 19

L

Langer‘s lines ➞ 14, 63

Leukocytes (white blood corpuscles) ➞ 24

Leukocytosis ➞ increase in the number of white blood corpuscles (more than 10,000 leukocytes per micro litre of blood) through various causes, e.g. infections, diseases of the blood-forming system etc.

Lucent layer (Stratum lucidum) ➞ 12

Luxation ➞ dislocation (Latin: luxare = dislocate)

Lymphangitis ➞ infl ammation of the lymphatic vessels

Lymphocytes ➞ 24

M

Macrophages ➞ 41

Manifestation, manifest ➞ appa-rent, clear, medical: the becoming clear of a disease by the relevant symptoms

Mechanical wounds ➞ 27

Meissner‘s corpuscles ➞ 18

Merkel‘s cells ➞ 10, 18

Migration ➞ 47

Minor injuries ➞ 81

Mitosis ➞ 47

Moist wound treatment ➞ 147

Monocytes ➞ 24

Morphologic, morphology ➞ of the form/shape; Morphology = the study of the shape of the body and the form and structure of the inter-nal organs (Greek: morphe = form)

Myofi broblasts ➞ 47

N

Nails ➞ 19

Necrosis ➞ local tissue death, dead tissue (Latin: necros = corpse)

Neoplasm ➞ new formation of tissue in the form of a swelling

Reticular layer > Stratum reticulare ➞ 14

Net tubular bandages ➞ 178

Noxious infl uences ➞ harmful-ness, disease cause (Latin: noxa = harm, cause of disease)

Nutrition ➞ 55

O

Obsolete ➞ old-fashioned, super-seded, no longer corresponding to the rules of medicine (Latin: obso-letus = worn-out, old-fashioned)

Ointment dressing ➞ 146

Operative wound examination ➞ 83

Osteomyelitis ➞ acute or chronic infl ammation of bone marrow including the bone tissue and the periosteum

P

palliative ➞ disease-reducing (Latin: palliativus = removing immediate symptoms)

Papillary layer (Stratum papillare) ➞ 13

Pathogen dose ➞ 69

Pathogenicity ➞ 68

PAOD ➞ peripheral occlusive arterial disease

Perforating wounds ➞ 28

Peritonitis ➞ infl ammation of peritoneum (Latin: peritonaeum = peritoneum)

Permeability, permeable ➞ allow-ing passage; pervious

PermaFoam (hydroactive foam dressing) ➞ 154

Per primam intentionem ➞ primary wound healing ➞ 50

Per secundam intentionem ➞ secondary wound healing ➞ 53

Persisting ➞ enduring (Latin: persistens = continuing, ongoing, permanent)

Phagocytosis ➞ 40

Phases of wound healing ➞ 35

Photographic documentation ➞ 183

Physiological ➞ relating to normal (natural) life processes, not diseased

Platelets ➞ 22, 26

Pneumonia ➞ lung infl ammation

Post(-) ➞ Latin: after Postopera-tive wound-healing impairments ➞ 61

Predisposition ➞ proneness/susceptibility to a particular disease brought about by various factors

Prickle cell layer (Stratum spinosum) ➞ 11

Primary wound healing ➞ 50

Proliferation ➞ increase of tissue due to overgrowth as a result of infl ammatory processes, e.g. in the context of wound healing following the infl ammatory stage (Latin: proliferatus = sprouting, overgrown)

Proliferative stage ➞ 42

Provisional wound treatment ➞ 82

Putrid infection ➞ 73

Pyogenic infection ➞ 73

Q

Quantitative classifi cation of wound healing ➞ 50

R

Rabies ➞ 75

Radiation lesion ➞ 33, 132

Regeneration ➞ biological: renew-al, restoration; medical: new for-mation of lost cells and tissue; the capacity for regeneration is linked to particular cell and tissue types in humans

Regenerative wound healing ➞ 53

Repair ➞ medical: replacement of body tissue by granulation or scar tissue

Requirements to wound dressings ➞ 140

Reverdin‘s graft ➞ skin transplant-ing procedure with epidermal fl aps obtained with a scalpel (named after Jacques-Louis Reverdin, 1842 – 1908) ➞ 176

Reversible ➞ able to reverse (lat. reversibilis = able to reverse)

Recurrent ➞ relapse, medical: return of a disease

Red blood corpuscles (erythrocytes) ➞ 23

Ruffi ni‘s corpuscles ➞ 19

Rupture ➞ tearing of tissue or organ, usually due to injury (Latin: ruptura = crack, burst) ➞ 63

S

Sebaceous glands ➞ 20

Secretion ➞ product of an organ or a wound (Latin: secretum = exudation)

Secondary healing ➞ wound heal-ing by formation of replacement tissue (granulation tissue) in con-trast to wound healing by wound suture = primary healing ➞ 53

Sensory receptors ➞ 18

Sepsis ➞ colloquially “blood poisoning”, reaction of the organism to an uncontrollable infection spreading throughout the whole body via the blood-stream

Seromas ➞ 61

Skin appendages ➞ 19

Skin glands ➞ 20

Sorbalgon (packable calcium alginate dressings) ➞ 152

Split-skin removal ➞ 93, 95

Glossary & Index [196.197]

Soft tissue necroses ➞ 62

Squamous epithelium ➞ upper-most top layer, made of fl attened, particularly resistant cells ➞ 8

Staphylococcus ➞ 68, 79

Stratum basale (basal layer) ➞ 10

Stratum corneum (corneal layer) ➞ 12

Stratum granulosum (granular cell layer) ➞ 11

Stratum lucidum (lucent layer) ➞ 12

Stratum papillare (papillary layer) ➞ 13

Stratum reticulare (reticular layer) ➞ 14

Stratum spinosum (prickle cell layer) ➞ 11

Subcutis ➞ 18

Superfi cial wounds ➞ 28

Sweat glands ➞ 20

T

Temporary covering of burn wounds ➞ 92

TenderWet (wound dressing pad with super absorber) ➞ 148

Tetanus ➞ 74

Thermal and chemical wounds ➞ 30, 88

Thrombocytes ➞ 26

Total paresis ➞ complete paralysis

Transudate ➞ largely cell, protein and fi brinogen-free fl uid in body cavities, e.g. a wound cavity

Traumatic injuries ➞ 27, 80, 85

Treatment of acute wounds ➞ 80

Tubular bandage ➞ 178

U

Ulcera ➞ 32

Ulcus cruris arteriosum – arterial leg ulcer ➞ 110

Ulcus cruris venosum – venous leg ulcer ➞ 105

Uraemia ➞ “Urea poisoning” as a consequence of acute or chronic renal insuffi ciency/acute renal failure (Greek: uraemia = urea poisoning of blood)

V

Vascularisation ➞ 43

Vasculogenesis ➞ 43

Vasoactive ➞ affecting vascular tone

Vater Pacini corpuscles ➞ 18

Virulence ➞ 69

W

White blood corpuscles (leukocytes) ➞ 24

Wound conditioning ➞ 103

Wound contraction ➞ 46

Wound dehiscence ➞ 63

Wound documentation ➞ 181

Wound dressings ➞ 140

Wound infection ➞ 65

Wound inspection ➞ 59, 172

Wound haematoma ➞ 62

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Ellermann, J.: Leitfaden zur Be-handlung von Dekubitalulzera, in WundForum 4/1995

Ferber, Th., Mähr, R., Straub, A.: Interaktive Naßtherapie mit Ten-derWet – drei Jahre klinische Er-fahrung bei chronischen Wunden, in WundForum 4/1995

Gericke, A.: Die Behandlung des Ulcus cruris venosum, in WundFo-rum 1/1998

Germann, G.: Prinzipien der Defektdeckung bei akuten post-traumatischen Wunden, in Wund-Forum 4/1994

Germann, G., Schmidt, J.: Die chronisch posttraumatische Wunde, in WundForum 1/1996

Gray D.: A pocket guide to clini-cal decision making in wound management, Wounds-UK Books 2005

Gray D., White R., Cooper P. and Kingsley A.: Essential wound management: an introduction for undergraduates, Wounds-UK Books 2005

Gray D., White R., Cooper P. and Kingsley A.: Wound healing: a systematic approach to advanced wound healing and management, Wounds-UK Books 2005

Howe, M., Germann, G.: Die Be-handlung von Strahlenschäden der Haut, in WundForum 4/1995

Lang, F., Lippert, H., Piatek, S., Vanscheidt, W., Winter, H.: Häu-fi ge Probleme bei der Behandlung chronischer Wunden, in WundFo-rum 1/1996

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Mast, B. A., Schultz, G. S.: Inter-aktionen von Zytokinen, Wachs-tumsfaktoren und Proteasen in akuten und chronischen Wunden, in WundForum 3/1997

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