medicaledition

PAUL HARTMANN AG
P.O. Box 1420
The HARTMANN medical edition
series of publications deals with Compendium
D-89504 Heidenheim
current subjects from the areas of
medicine and nursing. They em-
Wounds and Wound Management
Germany phasise not only basic knowledge,
but also present specialist and
PAUL HARTMANN AG interdisciplinary developments.
The information goes beyond
Unit P2 Parklands the products and is particularly
Heywood Distribution Park important.
Pilsworth Road
Heywood, Lancs OL10 2TT At a time of rapidly evolving scien-

HARTMANN medicaledition – Compendium Wounds and Wound Management

tific knowledge, information must
United Kingdom above all be up to date. With this
in mind, this series of books aims
PAUL HARTMANN to be a source of advice not only
Asia-Pacific Ltd. for experienced workers. Those
who are approaching new areas of
16/F Unit 1608 medicine and nursing for the first
Kerry Cargo Centre time are shown modern treatment
55 Wing Kei Road methods and are given useful tips.
Kwai Chung NT
Compendium
Wounds and Wound Management
 Table of contents
Published by
PAUL HARTMANN AG Foreword 5
D-89522 Heidenheim
The skin and wounds 6
http://www.hartmann.info
– Functions and structure of the skin 7
Conception, design, – Wounds and wound types 27
editing and production by
CMC Medical Information The processes of wound healing 34
D-89522 Heidenheim – The phases of wound healing 35
– Quantitative classification of wound healing 50
Scientific advisers:
– Influences on wound healing 54
Prof. Dr. med. Pavel Brychta
Prof. Dr. med. Günther Germann – Disorders of wound healing 61
Dr. med. Andreas Gericke – Wound infection 65
Prof. Dr. med. Walter O. Seiler
Dr. med. Jörg Tautenhahn Principles of treatment of acute wounds 80
Prof. Dr. med. Helmut Winter – The acute traumatic wound 81
– Complex traumatic defects 85
Translated from the German
– Thermal injuries/burns 88
edition ISBN 978-3-929870-60-2
– Incisions/surgical wounds 94
Printed on chlorine-free paper – Epithelial wounds 94
Principles of treatment of chronic wounds 96
– The venous leg ulcer 105
– The arterial leg ulcer 110
– The diabetic ulcer 116
– The decubitus ulcer 126
– The chronic post-traumatic wound 130
– Chronic radiation damage 132
– Wounds in tumour patients 134
Wound dressing 136
– Functions and requirements 137
– Dry wound treatment 144
– Moist wound treatment 148
– The dressing change 177
Glossary and index 194
Bibliography and Pictures sources 199

Table of contents [2.3]

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 fill 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,
influences 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.

Foreword [4.5]
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, firstly, adequate basic knowledge about the skin, the organ
where this takes place.
Functions of the skin
With 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 fulfil 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 fluids 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.
The skin and wounds [6.7]
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.
Cross-section through the epider-
mis at the fingertip, clearly show-
1 ing the five different cell layers:
1) Basal layer –
5
stratum basale (also called
stratum germinativum)
2 2) Prickle cell layer –
stratum spinosum
4 3) Granular layer –
3 stratum granulosum
4) Lucent layer –
stratum lucidum
2 5) Horny layer –
3 stratum corneum
1

The structure of the skin
Like any other organ, the skin has a specific fine 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 stratified epithelium
composed of five 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-
tinuous flaking 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
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.
The skin and wounds [8.9]
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 firm 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
flattened, 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 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
another 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 flat 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 fibres in the intercellular space.
The skin and wounds [10.11]

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.
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 cornification is com-
pleted: The keratinocytes are filled with the horny material
keratin and are now designated corneocytes. They lie on
one another like roof tiles and are firmly bound to one
another by keratohyalin and very fine fibrils (tonofibrils).
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
film (the hydrolipid film), 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 dermis is a connective tissue
rich in vessels and nerves, which
is classified histologically into two
layers, the papillary layer and the
reticular layer.
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-
tive tissue fibres but are not separated from one another.
Stratum papillare – Papillary layer
The papillary layer is bound firmly 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 fibrocytes
(resting form of the fibroblasts), interspersed with elastic
collagen fibres. The intercellular space is filled with a gel-
like ground substance, the extracellular matrix, in which
mobile blood and tissue cells can move.
The skin and wounds [12.13]

The course of the Langer‘s skin
crease lines should be borne in
mind where possible for incisions
to obtain cosmetically inconspic-
uous scars.
Stratum reticulare – Reticular layer
The reticular layer consists of interwoven strong bundles
of collagen fibres between which elastic fibre meshes are
stored. This structure gives the skin its elasticity so that it
can adapt to movements and volume fluctuations of the
organism. It is also capable of absorbing and giving off
water in a dynamic process.
The collagen fibres 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 fibrocyte which in its activated form is designated as a
fibroblast 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 fibres and, in non-fibrous
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-specific and specific 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 fibroblasts represent the most
important secreting cells for
forming skin connective tissue
(nucleus blue, cellular skeleton
orange).
The fibre proteins of the dermis
The connective tissue fibres 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 fibre-forming
type I collagen.
The production of collagen fibres takes place in an intracel-
lular stage and an extracellular stage, beginning with the
fibroblasts. First, fibroblasts 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 modifications take place by which the
still soluble procollagen is changed into insoluble collagen
fibrils, finally being assembled into collagen fibres.
The skin and wounds [14.15]
Electron microscopic appearance
of skin connective tissue with col-
lagen bundles and elastic fibres.
The substances required for the
formation of the fibre proteins are
provided by the fibroblasts. They
synthesize precursors of collagen
and elastin which are released
into the extracellular space and
mature through various enzymatic
processes into collagen and elastin
fibres.
Another fibre protein of the dermis is flexible elastin which
is also synthesized and secreted by the fibroblasts. 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-fibre ground substance of the dermis
The space between the fibres of the skin connective tissue
is filled 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.
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 influence 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 fibronectin. 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-
specific differences and depend on the type of matrix-
producing cells and the function of that tissue.
Schematic diagram of the flow of
Growth
factors/ Cell growth/ information: cell – extracellular
cytokines proliferation
matrix
Hormones/
Cell shape
vitamins

Cell to cell State of

contact differentiation

Biochemical
Cell-matrix- products/
bonds extracellular
matrix

The skin and wounds [16.17]


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
1 2
Although all the functions of the ECM are not yet known,
it is assumed that it serves not only as a filler substance be-
tween individual cells, tissues and organs but also fulfils 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 fine pressure.
3
They are accordingly found in greatest density on the finger-
tips. The Kraus end bulbs are important in the perception
of cold, the Ruffini 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 flexible 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 specific 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.
Electronmicrographs of hairs
Finger- and toenails are translucent keratin plates which (above). The illustration below
shows hair roots with clearly
grow outwards from the nail root to the free edge. Growth recognisable epithelial cells. In the
is about three millimetres a month and is closely associated event of injuries, re-epithelialisa-
with many organ functions. Thus the condition of the nails tion can take place from the resid-
can often give important diagnostic clues. ual epithelial cells. The hair roots
themselves cannot be regenerated
so scars always remain hairless.
The skin and wounds [18.19]
Electronmicrographs of a sebace- The blood supply of the skin
ous gland (left) and a sweat pore The stepwise distribution of vessels in the skin corresponds
(right). Apart from the hairless
skin on the soles of the feet and to the layered surface structure of this organ. Numerous
the palm of the hands, sebaceous vessels arise form the arteries lying under the subcutane-
glands are found at all sites on the ous tissue, which form a cutaneous plexus between the
body and are particularly numer- subcutaneous tissue and dermis. Wherever the skin is more
ous on the face and scalp. Here
there can be up to 900 sebaceous mobile, the vessels take a pronounced tortuous course.
glands per square centimetre. The Individual arterioles run outwards perpendicular from the
human body also has a plentiful deep cutaneous plexus and branch at the foot of the pa- Blood vessels of the skin (electron-
covering of sweat glands, totalling pillary layer into the subpapillary plexus. Very fine looplike micrographs)
about 2.5 million.
capillaries extend from there into the papillae of the dermis
Sebaceous glands open into the hair funnels of the hair and thus ensure perfusion of the avascular epidermis.
follicles so that their presence is associated with hair folli-
cles with few exceptions. The sebum, a mixture of fats, cells The papillary layer is supplied copiously with vessels while
and free acids, lubricates skin and hair and protects them the reticular layer is relatively avascular. Removal of me-
from drying out. Control of sebum production is a complex tabolic products is effected via the corresponding venous
process which has not yet been investigated in every detail. networks and partly also via the lymphatic system.

Sweat glands also arise from cells of the epidermis, which Schematic diagram of the blood
then sprout into the depths of the dermis so that the actual supply in the skin. From the
cutaneous plexus between sub-
gland is in the corium. The excretory ducts open in the
cutaneous tissue and dermis (1),
pores on the skin‘s surface. Sweat is an acid secretion con- 3 individual arterioles (2) run per-
sisting, besides others, of water, salts, volatile fatty acids, pendicular to the surface and
urea and ammonia. Sweat covers the skin surface with a branch at the foot of the papillary
layer into the subpapillary plexus
protective acid coating. Sweat secretion serves mainly for
2 (3) which supplies the epidermis.
temperature regulation.
1
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.

The skin and wounds [20.21]

 The constituents of the blood Blood plasma
The blood, also called the liquid organ of the body, serves Plasma is a yellowish clear liquid consisting of water
as a transport medium for respiratory gases, nutrients, pro- (90 %), proteins (7 – 8 %), electrolytes and nutrients
ducts of metabolism etc. Moreover, the cells of the immune (2 – 3 %). Of the proteins, about 60 % are albumins and
system circulate in the blood in addition to the constituents 40 % globulins. A constituent of plasma which is important
of the coagulation system which contribute in the event of in wound healing is fibrinogen (factor I), which is essential
injured blood vessels to rapid sealing of the leaking sites. for blood coagulation. Plasma which no longer contains
The soluble (plasma) and cellular components (red and any clotting factors is called serum.
white cells, platelets) of the blood can be separated by
centrifugation. Red blood cells (erythrocytes)
About 95 % of blood cells are red cells: non-nucleated
disc-shaped cells with a central concavity, containing high
Composition Function
concentrations of the red blood pigment haemoglobin.
Blood plasma Water (90 %) Their main function is the transport of oxygen and carbon
Electrolytes
Cations: Anions: maintenance and dioxide which are bound reversibly with haemoglobin. The
magnesium chloride regulation of water gas exchange itself is favoured by the hollows in the sides
potassium bicarbonate and electrolyte balance of the cells due to an increase in the surface area of the
calcium phosphate small blood cells. This shape also facilitates deformation of
sodium sulphate
Organic constituents the cells when passing through the smallest capillaries. The
Proteins (7-8 %) maintenance of oncotic erythrocytes are formed in the red bone marrow. Their life-
albumins, globulins pressure, protein reserve, span is about 120 days after which they are broken down,
transport proteins mainly in the spleen.
fibrinogen (factor I) blood coagulation
lipids
glucose The shape of the red blood cells
with their central concavity favours
Platelets blood coagulation the exchange of oxygen and
carbon dioxide and facilitates
White cells granulocytes immune system
passage through the capillaries.
monocytes
lymphocytes

Red cells carriers of the red blood transport of the respiratory gazes:
pigment haemoglobin oxygen and carbon dioxide

The skin and wounds [22.23]


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.
Classification of white blood cells
(leucocytes)
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 classified
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-specific or specific 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
lymphocytes granulocytes monocytes
neutrophils eosinophils basophils
stimuli, the leucocytes can migrate from blood vessels into
the surrounding area, the site of inflammation.
Granulocytes represent 60 – 70 % of all leucocytes. They are
classified 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 specific immunity. B lymphocytes
are responsible for humoral immunity (antibodies) and
T lymphocytes for cellular immunity (phagocytosis).
The skin and wounds [24.25]
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.
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.
Wounds and wound types
A wound signifies 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 defined 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 classification 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.
The skin and wounds [26.27]
Superficial or epithelial wounds affect only the avascular 1) Haematoma in closed fracture
2) Abrasion or superficial
epidermis. Since the epidermis is capable of regeneration,
(epithelial) wound
the wounds heal without scarring. The skin surface later 3) Split skin graft donor site which
looks no different from normal. The abrasion is an epithelial is classified as a superficial wound
wound. Split skin graft donor sites and Reverdin graft sites 4) Perforating wound (incised)
wound as planned surgical wound
should be regarded as superficial wounds.
5) Crushing wound to thumb
6) Complicated wound; fracture
Perforating wounds occurs when the division of the skin 1 2 with significant soft tissue damage
affects the epidermis and dermis and sometimes the sub- 7) Complex open lower leg fracture
after traffic accident with severe
cutaneous tissue. Examples of perforating wounds, which
soft tissue damage
are also designated penetrating wounds include cuts and 8) Crushing wound with extensive
stab wounds, tearing, bursting and contused wounds, bites tissue destruction
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 fluid. The condition of the
wound and tendency to heal differ considerably depending 3 4
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
5 6
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.

7 8

The skin and wounds [28.29]

 Thermal and chemical wounds 1) Third-degree burn with necroses
Thermal and chemical wounds arise from the effects of heat of the epidermis, dermis and por-
tions of the subcutis
and cold, tissue damaging rays, acids or alkalis. The skin 2) Third and fourth-degree burns
damage depends on the severity of the impact (duration, 3) Freezing
intensity, extent). Classification of burn and cold injuries 4) Alkali burn (“chemical burn”)
into three or four degrees of severity, respectively, aids in
prognostic assessment and therapeutic planning.
1 2
The four grades of burns are:
▪ First degree:
functional damage to the epidermal layer (stratum
corneum) manifested as erythema
▪ Superficial second degree:
destruction of the epidermis down to the basal layer
with formation of blisters
▪ Deep second degree:
3 4
deep dermal burn affecting the epidermis and nearly
the entire thickness of the dermis
▪ Third degree:
the special features of children‘s body dimensions are also
necrosis with complete irreversible destruction of
taken into account.
epidermis, dermis and often some of the subcutaneous
tissue (full thickness burn)
Cold injuries are also classified into four degrees of severity
▪ Fourth degree:
according to what proportion of skin is destroyed: Grade I =
9% carbonification involving muscles, tendons and bones.
erythema, Grade II = blister formation, Grade III = necrosis
The classification fourth-degree is not normally used
and Grade IV = formation of thrombus and vessel oblitera-
nowadays.
9% 18 % 9% tion.

The degree of severity of thermal injury relates solely to the

1% Injuries due to acids or alkalis should be classified accord-
depth of the injury. However, an equally important criterion
ing to their pattern of damage as burn wounds (“chemical
for prognosis and treatment is the area extent of the burn.
18 % 18 % burn”). They are classified and treated as burn wounds after
Therefore, particularly in emergency situations, this is
neutralisation of the causative acid or alkali.
normally estimated using the “rule of nines” according to
Wallace‘s rule of nines to measure
the surface area of a burn 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 skin and wounds [30.31]

Ulcer wounds 1) Decubitus ulcer on heel with
A further group of wounds presenting particular healing closed cap of necrosis
2) Sacral decubitus ulcer with
problems is the ulcera, commonly known as ulcers. In con- necrosis and wound pockets
trast to acute wounds, they usually occur as a result of local 3) Venous leg ulcer which has
disorders of nutrition in the skin, caused by venous, arterial involved the entire lower leg, a
or neuropathic vascular damage or prolonged local pressure so-called gaiter ulcer
4) Leg ulcer, caused by a basal cell
or radiation. However, an ulcer can also be a symptom of a carcinoma
systemic disease, e.g. as a result of certain tumours, infec- 1 2 5) Diabetic ulcer (mal perforans)
tious skin diseases or haematologic disorders. According to 6) Radiation ulcer
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 classified by definition as chronic wounds.
The most important chronic wound conditions are described
under this classification from page 96.
3 4

5 6

The skin and wounds [32.33]


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.
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 reflecting 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:
▪ inflammatory 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:
inflammatory/exudative phase
proliferative phase
differentiation and remodelling phase
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21
The processes of wound healing [34.35]
The inflammatory/exudative phase Platelets Sequence of physiological wound
Coagulation factors healing. In the ideal case, the
The inflammatory/exudative phase begins at the moment of

Coagulation
tissue missing from a wound is
injury and lasts about three days under physiological condi- Formation of a fibrin clot replaced by functional scar tissue
tions. The first vascular and cell reactions lead to haemos- – as wound seal
– matrix for collagen incorporation by various interdependent pro-
tasis and are complete after about 10 minutes. cesses such as blood coagulation,
Release of growth factors, inflammation and breakdown of
stimulating influx of inflammatory cells devitalised tissue, new vessel for-
Vasodilatation and increased capillary permeability result mation, formation of granulation
in an increase in the exudation of plasma into the intersti-

Inflammation and
tissue, epithelialisation and matu-
mast cells, neutrophilic macrophages

cleansing
tium. This promotes the migration of leucocytes into the lymphocytes granulocytes
ration. The chronologically correct
wound area, especially neutrophilic granulocytes and ma- appearance of the participating
cells is essential for the wound
crophages. It is their job to defend against infection and to healing cascade to take place in
cleanse the wound by phagocytosis. At the same time, they a regular fashion. If there is a dis-
release biochemically active mediator substances, by means immune defence / phagocytosis order of only one of these partial
of which cells which are important for the next stage are steps, the entire wound healing
Release of growth factors and process can be influenced.
activated and stimulated. The macrophages play a key role cytokines, stimulation ...
in that process. Their presence in adequate numbers is cru-
cial to the progress of wound healing. fibroblasts vascular endothelial keratinocytes
cells

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

Differen-
tiation
Contraction, scar formation, epithelialisation, maturation

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 fibrin mesh from fibrinogen.
A clot is produced which seals the wound and protects
against further bacterial contamination and fluid loss.

The processes of wound healing [36.37]

Blood clot consisting of platelets,
red blood cells and fibrin strands
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 flowing blood, the coagulation process is therefore
countered constantly by substances of the fibrinolytic (clot-
dissolving) system.
Inflammatory reactions
Inflammation 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.
Inflammatory 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.
Inflammation is characterised by the four classical symptoms
of infection, which are: erythema (rubor), warmth (calor),
swelling (tumor) and pain (dolor). The arterioles which
constrict briefly 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 first phase of exudation takes
place about 10 minutes after the injury has occurred, and
a second phase occurs one to two hours later. Oedema, Inflamed wounds with the clearly
which is apparent as swelling, develops due to the slowed visible symptom of reddening;
above, a burn wound; below,
circulation and also to the localised acidosis in the wound an operation scar following a
area. Today, it is assumed that the local acidosis increases vascular operation.
catabolic processes and that the toxic breakdown products
of tissue and bacteria are diluted by the increase in tissue
fluid.
Pain develops not only as a result of exposed nerve endings
and swelling but also due to a number of inflammatory
mediators such as bradykinin. Severe pain can result in a
limitation of function (functio laesa).
The processes of wound healing [38.39]
 Phagocytosis and immune response
About 2 – 4 hours after the injury, as part of the inflamma-
tory reaction, inward migration of leucocytes commences.
These are now called phagocytes and are capable of phago-
cytosing debris, foreign material and micro-organisms.
In the initial inflammatory phase, neutrophilic granulocytes
predominate, secreting various inflammation-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
signifies the first 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.
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- 1 2 3 and partially constructed by macrophages are presented to
podia (3). By further merging of
the pseudopodia (4), a vacuole
(phagosome) is produced which
merges with lysosomes to form
phagolysosomes (5) in which
“digestion” of the foreign body 4 5 6 TNF-) as well as various growth factors (BFGF = basis
can then take place (6).
Leucocyte migration continues for a period of about 3 days
until the wound is “clean” and the inflammatory phase
is approaching its end. However, if infection occurs, the
leucocyte migration persists and phagocytosis is increased.
This leads to a prolongation of the inflammatory 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- Macrophages during the phagocy-
tosis of E. coli bacteria
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
the lymphocytes in a recognisable form.
Furthermore, macrophages secrete inflammation-promoting
cytokines (interleukin-I, IL-II and tumour necrosis factor ,
fibroblast growth factor, EGF = epidermal growth factor,
The processes of wound healing [40.41]
 wounding New blood vessel formation and vascularisation
Without new vessels which will ensure an adequate supply
blood coagulation platelets of blood, oxygen and nutrients to the wound area, wound
inflammation
healing can not proceed. New vessel formation starts from
intact blood vessels at the edge of the wound.
epithelial cells macrophages – lymphocytes, granulocytes fibroblasts
Through stimulation by growth factors, the cells of the
debridement, immune response angiogenesis
epithelial layer lining the vessel walls (here called endothe-
collagen breakdown collagen synthesis wound contraction lium), are capable of breaking down their basement mem-
brane, mobilising and migrating to the surrounding wound
remodelling proteoglycan synthesis
area and into the blood clot. By means of further cell divi-
wound closure sion, they create a tube-shaped structure which continues
1
to divide at its budlike end. The individual vascular buds
grow towards one another and combine into capillary loops
The role of macrophages in wound PDGF = platelet-derived growth factor and TGF- and - = which again continue to branch until they encounter a lar-
healing
transforming growth factor  and ). These growth factors ger vessel into which they can empty. However, circulating
are polypeptides which influence the cells involved in endothelial stem cells were recently discovered in the blood
wound healing. They attract cells and promote their influx which may call into question the current teaching.
into the wound area (chemotaxis), subsequently stimulating
the cells to proliferate. A well-perfused wound is extremely rich in vessels. The 2
permeability of newly formed capillaries is also higher than
The proliferative phase that of other capillaries which takes account of the increas- The model of angiogenesis: break-
ed metabolism in the wound. However, the new capillaries down of the basement membrane
During the second phase of wound healing, cell proliferation
of intact blood vessels by various
predominates aimed at new vessel formation and filling are not very resistant to mechanical stresses which is why substances, with resulting release
of the defect by granulation tissue. The phase begins on the wound area has to be protected against trauma. With of endothelial cells, formation of
approximately the 4th day after trauma, but the conditions the maturing of the granulation tissue to scar tissue, the vascular buds by cell division (1),
vessels regress. which develop further into
for tissue growth were created in the inflammatory exuda-
capillary loops (2).
tive phase: Fibroblasts from the surrounding tissue migrate
into the clot and fibrin 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.

The processes of wound healing [42.43]


Electronmicrograph of a fibroblast
which, as the most important cell
type of the skin connective tissue,
is responsible for the synthesis
and secretion of collagen, elastin
and proteoglycans.
Granulation tissue
Depending on the time of new vessel formation, filling 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 fibroblasts. They produce collagen which matures
into fibres 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 fibroblasts 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 fibroblasts utilise the fibrin mesh
derived from the blood clot as a matrix for the ingrowth of
collagen.
The close relationship between fibroblasts and the fibrin
mesh led in the past to the assumption that the fibrin is
changed into collagen. In fact, however, the fibrin mesh is
broken down as incorporation of collagen progresses and
the sealed vessels are recanalised. This process, controlled
by the enzyme plasmin, is called fibrinolysis.
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 fibroblast migra-
tion are delayed. The extent of the granulation formation
corresponds directly with the extent of the blood coagula-
tion and the inflammatory process and the body‘s own
wound cleansing process with the help of phagocytosis.
Even if fibroblasts 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 fibroblasts change into myo-
fibroblasts 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 “finally” closes the wound and
serves as a “bed” for the ensuing epithelialisation. After
fulfilling 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 fine capillary loops as they develop The structure of the granulation
tissue is an important indicator
due to the new vessel formation. The new tissue is depo-
in assessing the healing tendency
sited beside the loops. When there is good granulation,
and the quality of wound healing.
the granules increase in size with time and also increase The above illustration shows
in number so that finally a salmon red moist shiny surface spongy granulation tissue where
is formed. Such granulation indicates good healing. Stag- wound healing is inadequate; the
fresh red granulation (below), on
nating healing pro-cesses are present if the granulation is
the other hand, is a sign of a good
covered with sloughy deposits, looks pale and spongy or healing process.
has a bluish tint.
The processes of wound healing [44.45]
 The differentiation and remodelling phase
Maturing of the collagen fibres 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 fibres, it is now known
that this shrinkage plays a subordinate role. It is rather the
fibroblasts of the granulation tissue which are responsible
for the contraction. After these fibroblasts have completed
their secretory activity, they change partly into fibrocytes
(the resting form of fibroblasts) and partly into myofibro-
blasts. The myofibroblast resembles the cells of smooth
muscle and like them contains the contractile muscle
protein actomyosin. The myofibroblasts contract pulling
Wound closure by clearly visible
contraction and epithelialisation
(left), epithelial margins still fragile
(right)
the collagen fibres 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-specific 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.
The processes of wound healing [46.47]
 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 superficial
wounds. In all other injuries of the skin, the migration of
the epithelia at the wound edge is linked to the filling of
the tissue defect by granulation tissue. Epithelial cells do
not descend into hollows or wound craters but require a
smooth moist creeping surface.
Schematic diagram of re-epitheli-
Mitosis Migrating cells
alisation by cell division and cell
migration. The epithelial cells Direction of
creep towards one another on the migration
slippery surface of the granulation
tissue. When the defect is closed,
the epithelial cells become heaped
up so that the epithelial cover
becomes stronger.
Contact inhibition
Mitosis
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 first 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 superficial 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.
The processes of wound healing [48.49]
Quantitative classification of Wounds capable of primary healing are closed with sutures,
staples or wound closure strips. During blood coagulation,
wound healing fibrin ensures temporary loose adhesion of the wound sur-
faces while the phase of inflammation and exudation takes
place almost unnoticed. The repair processes supervene,
Since the time of Galen (A.D. 129 – 199), wound healing
characterised by the migration of fibroblasts, the formation
has been classified into healing by primary intention and
of ground substance and incorporation of collagen fibres.
by secondary intention. The word “intention” in Galen‘s
Numerous newly sprouting capillaries feed the young
understanding does not refer to the physiological nature
connective tissue and restore the connection with the cir-
of the healing processes but to the intention of the physi-
culation. Both wound surfaces are firmly united after about
cian to achieve primary wound healing with wound edges
8 days. However, the wound only attains its final tensile
close together and with few gaping wound edges. The
strength in the course of several weeks. The result of the
classification thus is above all of quantitative significance
primary healing is a narrow linear scar which is initially red
(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
Primary wound healing of non-
from the extent and type of the tissue destruction, a further infected, closely apposed wound
classification is made today into primary delayed healing, surfaces
regenerative healing and chronic wounds.

Primary wound healing (per primam intentionem)

Delayed primary healing when the
The conditions for wound healing are more favourable the wound is at risk of infection
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
Secondary wound healing with
area of the body. Primary wound healing occurs in such
filling of the defect by granulation
cases if there is no wound infection. tissue which changes to scar
tissue in the course of healing
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 Regenerative or epithelial healing
of injuries affecting only the
by other mechanisms (e.g. tearing or bursting wounds), epidermis
surgical debridement may create the conditions for primary
healing.

The processes of wound healing [50.51]

 due to the large number of capillaries. Later it becomes Secondary wound healing (per secundam
lighter in colour as the number of vessels is reduced. intentionem)
Finally, the scar is whiter than the surrounding normal skin. Secondary wound healing always occurs when tissue gaps
have to be filled or when a purulent infection prevents
Delayed primary healing direct union of the wound edges. The wound edges are now
Delayed primary healing occurs when an infection is an- no longer closely apposed but gape. To close the wound,
ticipated. In this case the wound should not be closed granulation tissue must be formed (as already described).
with sutures or wound closure strips. To observe for the The energy requirement of the organism is therefore greater
development of infection, the wound is loosely packed and than in the case of primary healing and likewise the forma-
held open. If no infection occurs, the wound can be sutured tion of the granulation tissue is more subject to endogenous
approximately between the 4th and 7th days. It then heals and exogenous influences.
by primary intention. If an infection becomes apparent,
the wound is classified as healing secondarily and receives Regenerative healing
treatment as for an open wound. Regeneration is defined 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-
Examples of the different types of clude the basal layer of the epidermis. If only the epidermis
wound healing: is damaged by an injury, e.g. in a skin abrasion wound, it
1) Primary wound healing, in the
case of closely apposed wound heals without a scar. The healing processes correspond to
edges, which is normally possible the wound healing phase of re-epithelialisation.
with surgically produced wounds.
2) Regenerative or epithelial heal- Chronic wound processes
ing, whereby the healed tissue
hardly differs from the original 1 2
The chronic wound is one undergoing secondary healing
condition. which has to be closed by formation of tissue. If this pro-
3) Secondary healing with tissue cess requires more than eight weeks, the wound is clas-
formation – here after dehiscence sified as chronic. The change from an acute to a chronic
of a thoracic wound. A secondary
suture is made following appropri- wound can occur in each of the wound healing phases.
ate wound conditioning. However, the majority of chronic wounds develop from
4) Chronic healing process in progressive tissue destruction because of vascular disease
the case of a sacral decubitus from various causes such as disturbed blood circulation of
ulcer which, with the requisite
formation of granulation tissue, arterial or venous origin, diabetes mellitus, local pressure
3 4
corresponds to secondary wound injuries, radiation damage or tumours.
healing.

The processes of wound healing [52.53]

 Influences 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 specific circumstances.
Systemic influences
General influencing factors depend on the individual physi-
cal status of the person affected. Their relevance for the
course of healing is very variable and some “influences”
are themselves the cause of the wound.
60 Years Patient age
50 Clinical research suggests that physiological aging delays
40 wound healing through the general reduction in cell activ-
30 ities which can lead to a loss of quality in wound healing.
20 However actual disorders of wound healing result mainly
10 from the effects of age-related co-morbidity such as poor
Days immune status or deficient nutrition. Ulcer wounds as a
0 antibody formation and infection defence. Vitamin A also
20 40 60 80 100
result of metabolic disease, vascular disease and tumour in-
Healing of a 20 cm² wound evitably also occur more frequently. Then a correspondingly
according to the person‘s poor healing tendency can be expected.
age
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 sufficient 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
deficiency 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
influence wound healing and the deficiency of only a single
vitamin may delay healing. Vitamins of the B complex, for
example, participate in collagen synthesis and stimulate
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 significant 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 deficiencies
that cause disruptions. Zinc is a central component of the
so-called metalloenzymes and has significant biological
The processes of wound healing [54.55]
effects in the organism, which also extend to wound heal- General (systemic) Local
Important systemic and local
ing. Iron deficiency leads to anaemia and therefore hinders influences on wound healing

oxygen transport to the wound area. ▪ Age ▪ Extent of injury

▪ Nutritional status (size, depth, etc.)
▪ Immune status ▪ Condition of wound bed
Malnutrition, possibly leading to cachectic conditions, can ▪ Underlying illnesses (pus, necrosis, etc.)
often be observed in severely ill, multimorbid and elderly ▪ Postoperative complications ▪ Condition of wound edges
persons. It can be caused by diseases such as tumours, ▪ Acute traumas (smooth, jagged)
▪ Medications ▪ Bacterial colonisation,
infectious diseases, organ disorders and severe pain. Nutri- ▪ Psychosocial situation contamination, infection
tional causes such as inadequate intake of nutrition or ▪ Site of wound
disorders of absorption often play a major part. ▪ Age of wound
▪ Quality of wound management
▪ Surgical conditions and
Immune status circumstances
The processes of the immune response play an important
role during wound healing. Accordingly, impairment or
deficiencies of the immune system cause increased sus- Postoperative complications
ceptibility to disorders of wound healing and infection. Numerous postoperative complications have a direct effect
Acquired immune deficiencies can result from operative on wound healing: thrombosis and thromboembolism,
trauma, parasitic, bacterial or viral infections and also occur possibly due to the increased fibrinolytic activity, postoper-
after periods of malnutrition, extensive burns, injury with ative pneumonia, postoperative peritonitis, postoperative
ionising radiation, entero- or nephropathies and cytostatic ileus and postoperative uraemia. The “intoxication” with
immunodepressant treatment. degradation products before they are excreted in the urine
apparently has an inhibitory effect on the course of healing.
Underlying diseases
Diseases with an inhibitory effect on wound healing are Affects of acute trauma/shock
again mainly those which impair the immune status of the Trauma associated with blood loss or major fluid loss, such
affected organism such as tumours, autoimmune diseases as in severe burns, causes a large number of mediator-
and infections. Delayed or abnormal healing can be antici- induced reactions which can lead to a disorder of the micro-
pated also in the case of connective tissue diseases (e.g. circulation. Subsequent tissue hypoxia, increased capillary
rheumatoid disease), metabolic disease (e.g. diabetes melli- permeability and clinically detectable abnormal perfusion
tus) and vascular diseases (e.g. peripheral vascular disease, develop as symptoms of shock. The resulting imbalance
venous insufficiency). Diabetes mellitus and arterial/venous between oxygen requirement and supply and the delay in
vascular disease, in particular, are themselves the cause of removal of products of metabolism particularly affects the
ulceration. initial phase of wound healing and the immune response.

The processes of wound healing [56.57]

Medications
Different drugs have a direct negative effect on wound
healing, especially immune suppressant, cytostatic, anti-
inflammatory (mainly glucocorticoids) and anticoagulant
agents. Depending on the inhibitory effect of the various
drugs on coagulation, inflammatory 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 influences
The condition of the wound and the quality of the wound
management are other important influences 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”) Two methods for determining the
▪ site of wound (in well or poorly perfused region) size and volume of a wound: With
a wound of large area (above), lay
▪ age of wound (acute trauma, time elapsed from injury to a transparent foil over it and mark
first aid/treatment, chronic wound conditions) the wound outline with a felt-
tipped pen and calculate the area.
In the case of surgical wounds, the local influences include The size and volume of a wound
may be determined by measuring
type of operation, site of operation, duration and type of the fluid-holding capacity (below),
operative preparation, and the quality of hygiene manage- in that the wound is covered with
ment in the operating theatre, operative techniques and foil and sterile fluid injected into
duration of the operation. it. The quantity of fluid in ml. or
cc. represents the wound volume.
The processes of wound healing [58.59]
Quality of wound treatment
The quality of wound management has a significant influ-
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-
plines 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 influences 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 deficiency, generalised illnesses or impaired
lymph flow 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 firmly to the underlying tissue.
One complication can be that the primarily sterile seromas
become infected due to the stagnant fluids which favour
bacterial growth. Those seromas must then be treated as
abscesses.
The processes of wound healing [60.61]

Extensive wound haematoma
Necrosis of wound edge in the
area of suture of an amputation
stump
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 deficiencies 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
sufficient 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
solution, 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.
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 deficiency, 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). Complete rupture with muscle
The dehiscence is treated by operation, if necessary insert- necrosis after a bypass operation
in the knee (above), rupture after
ing a plastic mesh. The prognosis is good when treated large bowel resection (below)
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 Hypertrophic scar formation after
runs vertical in the direction of Langer‘s lines, hypertrophic burn
scarring can be anticipated. These circumstances gain
particular significance 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.
The processes of wound healing [62.63]

Keloid with typical collagen cords
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 difficult
initially. There are also scar growths which are rich in fibres
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
difficulties 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.
Aulus Cornelius Celsus, who lived
in the first 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.

The processes of wound healing [64.65]

Predisposing factors
The occurrence of infection is a complex process influenced
by many predisposing factors. Of critical importance for the
initiation of an infection are firstly the type, the pathogen-
icity, virulence and the number of micro-organisms involved.
The micro-organisms then find 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 find further favourable
growth conditions.
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 classified 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.

Pathogens
The causative agents of wound infections can be viruses, gram-positive gram-negative Structure and characteristics of
fungi and bacteria, with bacteria being implicated in the gram-positive and gram-negative
bacteria
vast majority. nucleus equivalent capsule

Bacteria are unicellular micro-organisms, whose cell interior

plasmid
is moderately differentiated. It consists of a “nucleus equi-
valent” containing genetic material as well as of cytoplasm
containing ribosomes, various enzymes and plasmids ribosomes
outer
(carriers of resistance genes). The outer cell wall can be membrane
found covered with a capsule of varying composition which
pili periplasmic gap
can protect the bacteria against desiccation or against flagella
cell wall cyto- cell membrane
phagocytic cells. plasm

The processes of wound healing [66.67]

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 1 2
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
3 4
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 flora 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 classified 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
influences 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 inflammatory reactions that infection can be said to
be present.
The processes of wound healing [68.69]
 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.
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.
4 hours 8 hours 10 hours
4096 bacteria 16777216 bacteria 1073741824 bacteria
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.
Condition of wound and susceptibility to infection
The 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-
ised 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 sufficient 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.
The processes of wound healing [70.71]
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 significance 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 specific 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 confirmed 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 field
▪ 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 infection
The different types of pathogens produce specific 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
The blue-green sweetish-smelling
adequate antibiotic treatment. pus is typical of a pyogenic
▪ Staphylococci: creamy yellow odourless pus pseudomonas infection
▪ 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 develops
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
inflammation with gas phlegmon in the surrounding tissue.
The processes of wound healing [72.73]

Gas gangrene with soft tissue
necrosis which has already turned
black; typically, there is crepitus on
palpation.
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 find 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 fiery
erythema. Tiny erosions of the skin or mucous membrane
are sufficient as an entry portal; outflow 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 Erysipelas of the lower leg with
existing bacterial colonisation or on elimination of the in- typical sharp demarcation from
the healthy areas of skin (above);
vading bacteria. The measures which serve for prophylaxis advanced, already necrotising
and treatment should not be seen in isolation but as an erysipelas, also of the lower leg
overall concept, and require a disciplined approach by all (below).
involved in wound care.
The processes of wound healing [74.75]
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 perfusion 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 definition, 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 magnifications (2) and
(3), however, reveal heavy bacterial
colonisation (yellow).
1 2 3
The processes of wound healing [76.77]
A reduced-risk application of antiseptics in open wound
areas therefore always presupposes that the user is
thoroughly 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 briefly 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
healing 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
significantly 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 sufficient and safe wound treatment method, so that
nothing is done to diagnose and treat the actual causes of
the poor wound healing.
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.
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 antibiotic, the
pathogen spectrum needs to be taken into account in
accordance with the germ identification 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.
The processes of wound healing [78.79]
Principles of treatment of acute wounds
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.
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 flap transplantation
The degree and extent of the individual measures differ
according to the wound findings 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 significance for the patient.
The acute traumatic wound
Related 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 classified for practical reasons as provisional or
definitive wound treatment.
Acute wounds [80.81]
 Provisional wound treatment includes: Provisional wound treatment Management of traumatic
wounds
▪ first aid measures for haemostasis
 treatment of shock, where necessary
▪ application of an emergency dressing to protect against  haemostasis
infection and for transport  emergency dressing
▪ if necessary, immobilisation of the injured body parts and  immobilisation
limbs  transport to hospital

Definitive wound treatment

Lower leg fracture (above), severe
finger trauma due to injury on a
conveyor belt (below).
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.
Definitive treatment or primary care follows basic surgical
principles. With the exception of superficial skin defects, all
other wounds are explored surgically with adequate anal-
gesia and under aseptic conditions. Inspection of the outer
wounds suffices only in very rare cases. Further radiological
or neurological investigations may be necessary to confirm
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 difficulty but must not remain in the wound
because of the associated high risk of infection. Superficial
 operative wound exploration
 debridement
 decision on wound closure
Wound closure
primary / primary delayed
dressing to protect wound
secondary / open
moist dressings to condition the wound
later closure by secondary suture,
spontaneous epithelialisation,
skin graft, plastic surgical procedure
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

Acute wounds [82.83]

 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 sufficiently 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.
Bite injuries from animals (at left,
a dog bite wound) or gunshot
wounds (right) have to be classi-
fied as infected from the start and
treated accordingly.
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 defects
In 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.
Acute wounds [84.85]
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 fingers.
2) A tendo-fasciocutaneous flap
1 2
is raised from the dorsum of the
foot.
3) Function after 8 weeks.
4) Acceptable defect at donor site.
3 4
Treatment of a traumatic finger
injury:
1) Partial amputation of 2nd to
5th fingers on admission.
2) Subsequent completion of
amputation with two free skin
flaps. Revision was necessary
because of increasing necrosis
1 2
of the ring finger.
3) Findings after 8 weeks.
4) Good functional result.
3 4
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.
Principles of treatment of
The same basic principles of treatment apply to all stages of
complex defects
soft tissue injury. Securing and stabilising the vital parame-
▪ Stabilisation of the patient
ters are followed by evaluation of the patient, in interdisci- ▪ Interdisciplinary evaluation of
plinary collaboration whenever possible. During the primary the patient
operative exploration, the fracture is stabilised, the wound ▪ Operative exploration of soft
tissue and bone situation
is debrided and where possible all damaged structures are
▪ Fracture treatment
reconstructed. ▪ Radical debridement
▪ Primary reconstruction of injured
structures
If definitive debridement is possible during the initial man-
▪ Possible second look
agement, the wound can receive its final primary covering.
▪ Definitive differentiated cover/
If there are doubts about the vitality of the remaining closure within 5 – 7 days
tissue, definitive optimum closure can be attempted within
5 – 7 days following a planned “second look”.
The guiding principle of treatment must be to offer the
patient 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 profile of the patient. The wound should receive
its definitive treatment as soon as possible. In the case of
complex defects, where immediate reconstruction is not
possible, an interim soft tissue cover is required.
Acute wounds [86.87]
 Thermal injuries/burns
Depending 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 superficial 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 findings,
as to whether treatment should be undertaken on an out-
patient or an inpatient basis. For superficial first-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.
The severity of burns is classified
into three degrees for prognosis Epidermis
and treatment, with second degree
further subdivided into grades IIa
and IIb. The classification refers to Dermis/
the depth of the injury, i.e. which corium
parts of the skin are burnt.
During emergency treatment, cooling of burn wounds as
soon as possible with tap water for approximately 30 min-
utes 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 superficial
burn can turn into a deep burn.
In the case of a first-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.

Subcutis

Muscles, tendons
and fascia

grade I grade IIa grade IIb grade III Burn grade

Acute wounds [88.89]


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.
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 definitive or temporary wound
closure. A variety of techniques are available for removing
necroses, depending on the depth and extent of the 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).
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. Treatment of burn wounds
▪ Degree I
This “closed treatment” also prevents drying out of the
Spontaneous healing in a
wound surfaces, so that the danger of secondary necrosis few days
is reduced. ▪ Degree IIa
Spontaneous healing within
In the case of third-degree circumferential burns on the about 14 days
▪ Degree IIb
neck, trunk and extremities, relieving incisions (escharo- Partly conservative, partly
tomy) in the eschar are necessary. Otherwise, the conta- surgical depending on clinical
minated, necrotic skin coupled with the excessive oedema appearance
formation lead, during the course of the burn disease, to ▪ Degree III
Surgical with necrosectomy and
suffocation symptoms and to disturbed blood circulation skin grafting
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 difficulty of finding
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.
Acute wounds [90.91]

Deep epifascial excision with
radical removal of destroyed
skin and fatty tissue down to
the fascia.
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-
indicated on the face, neck and hands.
The mesh transplant is laid on the well-prepared wound,
fixed 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 fixation with
staples (right).
Acute wounds [92.93]

Incisions closed with sutures are
predestined to heal rapidly by
primary intention provided there
are no wound infections or other
disorder of wound healing.
Epithelial wounds affecting only
the avascular epidermis heal with-
out scarring.
With critical burns affecting 80 % of body surface, the
lack of donor sites is dramatic. A solution for this situation
could be the method of culturing keratinocytes in vitro, by
means 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
division in a nutrient medium until a layer of cells capable
of being grafted has formed.
Incisions/surgical wounds
Surgical 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 superficial 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 fine capil-
laries lying directly under the germinal layer are also open-
ed, superficial 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.
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.
1 2 3) Re-epithelialisation is complete
on the 5th day.
4) Condition 5 months after the
start of treatment, the donor area
has regenerated almost completely.
*Hydrosorb plus is also available
as Hydrosorb comfort with a trans-
parent continuous adhesive edge.
3 4
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.
Acute wounds [94.95]
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.
By definition, 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 final stage of progressive tissue
destruction, 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 Examples of chronic wounds:
requirement, it is urgently necessary, on the one hand, to mixed ulcer due to chronic venous
insufficiency and peripheral ar-
enhance the prophylactic efforts and, on the other hand, terial occlusive disease (above),
to introduce a scientifically based and effective wound venous ulcer as a result of post-
management with corresponding quality controls. thrombotic syndrome (below).
General principles of therapy
Although 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.
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 influx into the wound area of inflammato-
ry cells such as neutrophilic granulocytes and macrophages.
These in turn secrete inflammation-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 inflamma-
tion persists. At the same time, toxic breakdown products
from the tissue and also bacteria infiltrate 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
inflammation 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 classified 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.
Chronic wounds [98.99]

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.
Surgical debridement is a task for the doctor in both the History and baseline diagnosis Algorithm of treatment
inpatient and outpatient setting. Depending on the wound of chronic wounds
for exact clarification of the cause of ulcer including differential
situation, a decision should be made on an individual basis diagnostic measures
as to whether the necrosis should be removed in a single
procedure by operation under general anaesthetic or if a Causal therapy
removal step by step in several treatment sections should
to restore or compensate the circulatory situation as much
take place. In the case of clinically apparent infection, a as possible in the diseased area of skin
single-stage procedure is advisable, in order to remove the
Measures according to the causes, e.g.
nutrient medium as quickly as possible from the infection.  vein surgery
 compression therapy
Should surgical debridement not be possible due to specific  angiosurgical dilation techniques
 optimum diabetic control
situations (patient refusal, multimorbidity and poor general
 relief of pressure
condition, Marcumar or heparin treatment, fever, metabolic
disturbances, etc.), moist wound treatment in order to Wound diagnoses/assessment
soften necroses and, if necessary, enzymatic debridement
with proteolytically active substances offer an alternative.
Wound bed treatment/cleansing
Both methods may be indicated in addition to the surgical
debridement to loosen thin superficial layers of necrosis, if possible by surgical debridement, otherwise wound
which are impossible or difficult to remove by mechanical cleansing by means of moist wound treatment,
possibly enzymatic also
excision.
Wound conditioning/promotion of
A range of hydroactive wound dressings are available for granulation
wound cleansing using moist wound treatment, which are
with the use of moist wound treatment
effective and can be used without problems. They absorb
bacteria-laden exudate, by providing moisture they pro-
Wound closure
mote the loosening of coatings and overall they create a
physiological cell-preserving microclimate that effectively  by contraction and spontaneous epithelialisation
promotes the body‘s own autolytic cleansing mechanism.  closure by split skin grafting
 by plastic surgical procedures (myocutaneous flap)
Chronic wounds [100.101]

Necroses removal and refreshing
of the wound edge with a scalpel
in the case of a decubitus
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 difficult 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 sufficient.
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 fibrin deposits, fine debridement, careful
freshening of the wound edges or removal of the fibrin
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 scientifically unproven use of a wide variety of measures.
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 significantly de-
layed 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 flap
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 filled 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. Conditioning of the wound takes
place by means of a moist dressing
treatment. The examples show
The most important measure for promoting granulation conditioning with the calcium
growth is keeping the wound bed permanently moist by alginate compress Sorbalgon,
treating it with hydroactive wound dressings. This prevents which is packed in dry and then
the cells from dying by drying out and creates a micro- changes into a moist gel when
it absorbs secretions.
climate in which the necessary proliferative cell activities
can take place.
Chronic wounds [102.103]

Transplantation of autologous
keratinocytes cultured in a suitable
nutrient solution seems to have a
variety of stimulating effects in the
treatment of chronic wounds.
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.
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 1
and frustrating attempts at therapy.
The venous leg ulcer reflects the worst metabolic disturb-
2
ance of the skin and subcutaneous tissue due to chronic
venous insufficiency. If the venous return of blood to the 3
heart is disturbed (venous insufficiency), less blood is trans-
ported out of the involved venous segments and the venous
pressure does not fall sufficiently (venous hypertension).
This overstretching of the veins acts as a backward decom- Post-thrombotic vascular and flow
pensation back to the capillaries of the final circulation. situation: the deep vein is scarred
and recanalised after the throm-
The low pressure values required for a regular metabolism bosis (1). Blow out by dilated
can not raise, and the circulation in the vessels is slowed or communicating veins (2), resulting
even at a standstill. Metabolism, particularly in the skin and in development of secondary
subcutaneous tissue, is impaired. In the long term, the lym- varicosities (3).
phatic system is also affected by this, since it is only able
to compensate in the early stages of an impaired drainage
situation for fluid build-up in the intercellular spaces (inter-
stitial fluid) by increased lymph flow.
The earliest identifiable result of the disturbance in venous
return is oedema, which in turn results in further rises in
pressure and deposition of fluid, thus increasing the meta-
bolic disturbances. Perivascular fibrosis and degenerative
and inflammatory processes occur with trophic skin chan-
ges. Through further obliterative inflammatory processes in
the venules and arterioles, a leg ulcer finally develops first
in areas with poor venous haemodynamics (ankle area), as
the now visible sign of decompensated venous hyperten- Lymphatic ankle oedema
sion an the metabolic disorder.
Chronic wounds [104.105]
 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 insufficiency (CVI) and
usually classified into three degrees of severity:
▪ CVI grade I is characterised by venous flare 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 florid 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.
1) Marked dermatoliposclerosis in
CVI grade II, which can be attribut-
ed to increasing fibrosis 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
CVI can result both from primary varicose veins when the
dilated lumen and valve insufficiency of the superficial 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 flow 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 rectified 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 outflow 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.
Chronic wounds [106.107]

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.
Which method is used depends finally 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 influence 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 promotion
of 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
Diagnosis Treatment algorithm in
venous leg ulcer
 clinical examination
 diagnostic investigations
 differential diagnosis (arterial ulcers, venousarterial mixed
ulcers, diabetic ulcers, exogenous infectious ulcers, ulcers
due to blood disorders, neoplastic ulcers)
Treatment
Compression therapy
 prolonged bandaging with zinc adhesive dressings
 changes of dressing with elastic bandages
 general: the patient should move as much as
possible with the bandage
Invasive therapy
 to compensate the CVI: sclerosing therapy,
phlebosurgery
 to treat the ulcer: possibly paratibial fasciotomy or
endoscopic ligation of perforating veins
Local ulcer therapy
 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
Aftercare
 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
Chronic wounds [108.109]
 (C-reactive protein; indicator of inflammation) 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 fibre 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
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.
Atherosclerotic plaques (grey
deposits) in an arterial wall
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 classified 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 significant 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 insufficiency, a
faulty life style with a diet high in fats and calories, over-
weight, stress and above all smoking are important risk
factors.
Chronic wounds [110.111]
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
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 influence.
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 classification 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 modified
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
Chronic wounds [112.113]
 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 influence in particular the hyperproliferative cell
processes and the flow 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 first, 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 flow 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- 1 2
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.
3 4
Diagnosis Treatment algorithm in
arterial leg ulcer
 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.)
Treatment
Causal therapy
 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)
Local ulcer treatment
 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
Aftercare
 train patients, reinforce their own responsibility
 orthopaedic shoes with appropriate distribution of pressure
 inspect feet daily for changes (callosities, fissures, 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, fleece boots)
Chronic wounds [114.115]
After surgical debridement, wound cleaning and condition- Neuropathic foot Angiopathic-ischaemic foot
ing are continued using moist wound treatment. Antiseptic
Anamnesis Diabetes mellitus for many years, Diabetes mellitus for many years,
dressings may be indicated until the infection subsides.
possibly additional alcohol con- possibly lipid metabolism disrup-
sumption, further delayed damage tion, heart diseases, nicotine
If amputation is necessary, this should be performed if from diabetes abuse and arterial hypertension
possible after resolution of the concomitant infection, after Clinical presentation
conversion of a wet gangrene into a dry gangrene and
Skin colour/temperature rosy, warm pale to livid (position-dependent),
achievement of maximum revascularisation in the necrotic
cool
border zone.
Sweating/secretion disturbed; dry, cracked skin atrophic skin, loss of skin
appendages (hair loss)
The diabetic ulcer
Diabetes mellitus is a chronic disruption of the carbohydrate Sensibility reduction or loss of perception of unaffected, sensation present
vibration, pain, pressure, tempera-
metabolism and has reached almost epidemic proportions
ture, touch; reflexes impaired
worldwide. In Germany currently, some 300,000 people
suffer from type I diabetes and about 4 or 5 million are Pain pain at rest or at night present, claudicatio intermittens;
pain symptoms
affected by type II diabetes. Since type II diabetes is partial-
ly age-dependent, increasing numbers of diabetics can Foot pulse palpable not palpable
be expected, purely due to changing age patterns. Hyperkeratosis frequently at sites exposed to relatively minor
pressure
Among the complications of diabetes, diabetic foot syn- Bone deformation frequently changed bone rarely
drome (DFS) takes a prominent position. According to epide- structure, early osteolysis
miological surveys, it may be assumed that approximately Predisposed sites of lesions foot sole, in particular in region of acral necroses
15 % of diabetes mellitus patients suffer from foot lesions metatarsophalangeal joints
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-
fication of the nerve cells and progressive damage to the
nervous tissue affects autonomous, sensory and motor
fibres equally. Clinically, these types of damage lead, alone
or together, to the characteristic changes in the foot of a
diabetic person:

Chronic wounds [116.117]

▪ Damage to the autonomous fibres causes a reduction in The formation of a
“mal perforant”
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.
Excessive pressure and shear forces lead to hyperkeratosis and callus
due to changed static forces in the formation,...
This produces the conditions for development of a neuro- foot and changed motor function...
pathic ulcer, whereby callus formation on the foot sole is a
possible indicator of impending ulceration. The reason for
this is that enhanced cornified 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.
cracks, haemorrhage, haematoma and finally to an infected defect,
and bacteria colonisation,... known as a “mal perforant”
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 fissures, Added to this is the difficulty that the processes of ulcer
haemorrhages and haematomas, which later become development are often barely noticed by the person affect-
colonised by bacteria. As a result, a central, infected tissue ed, since pain perception is impaired. This therefore often
defect, “mal perforant du pied” (Malum perforans pedis) brings about a risky temporal delay since, with the diabetic
develops. patient‘s generally weakened infection defence, the initially
localised infection can rapidly spread in depth and jeopard-
Ulcer formation can also be triggered by other traumas. ise the main anatomical structures (tendons, muscles) and
Among these is the unphysiological pressure loading due to bones (bacterial osteitis). Inflammation of the bones can
ill-fitting footwear, also pressure points due to in-growing even lead to the total collapse of the foot skeleton. The
toenails, minor injuries, such as, from cutting, sharp devices consequence is that Charcot‘s foot, or deep inflammation of
used for foot care or thermal trauma, e.g. from excessively the foot tissues (pedal phlegmon) arises, which endangers
hot footbaths. the blood circulation to the toes, so that finally, diabetic
gangrene threatens to develop.

Chronic wounds [118.119]

In order to plan treatment and
assess the prognosis, a precise
description and classification 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 classifica-
tions are available for describing
the lesions, of which the so-called
Wagner classification is the most
widespread classification 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.
Stages of a malum performans,
according to Arlt
Degree 0: no lesion, possibly
deformation of foot or cellulites
Degree 2: deep ulcer reaching to
joint capsule, tendons or bones
Degree 4: limited necrosis in
forefoot or heel region
Stage 1: necrosis of epidermis
(pressure point)
Stage 3: malum perforans with
bone and/or joint involvement
Degree 1: superficial ulceration
Degree 3: deep ulcer with abscess
formation, osteomyelitis and infec-
tion of joint capsule
Degree 5: necrosis of entire foot
Stage 2: malum perforans extending
subcutaneously as far as the bones
or joints, but without lesions in these
Stage 4: infection no longer restrict-
ed to a region spreading from a
malum perforans
The first 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 flow
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 insufficiency 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
Chronic wounds [120.121]
performed pedicures and other minor injuries of the toes Diagnosis Treatment algorithm for
also contribute to the development of ulcers. neuropathic ulcer
exact verification:
 of underlying cause (according to symptoms of neuropathy Treatment algorithm for angio-
Before ulcerations ever develop, inspection can reveal and angiopathy, mixed ulcer) pathic ulcer corresponds to that
trophically disturbed nails, mycoses, reddening, marbling  of the immediate trigger of the lesion (injury, infection, etc.) for Ulcus cruris arteriosum
and loss of hair, which illustrates how regular inspections  of the metabolic situation of the diabetes (arterial leg ulcer)
 of the inflammatory parameters
can contribute to prevention.
Treatment
The principles of treatment
The aim of treatment for diabetic foot syndrome is primarily Causal treatment
a reduction in amputations, preserving function in the ex-  optimum adjustment of diabetes
tremities and maintaining the quality of life of the diabetic
patient. Treatment is an interdisciplinary task and success Local ulcer treatment
is only possible with broadly spread measures. The special-
 treatment of infection (systemic antibiotic therapy)
ists involved are internal medicine specialists, vascular
 absolute relief of pressure on ulcer until healed
surgeons, orthopaedic specialists, neurologists and derma- (walking aids, wheelchair, bed rest)
tologists.  adequate surgical debridement
 moist dressing treatment for further wound
cleansing, conditioning and epithelialisation
A basic measure in the treatment of all diabetic lesions
is optimal adjustment of the diabetes (normoglycaemia),
Aftercare
which is also the best treatment for the neuropathy. Further
conservative treatment is focused on improving the central  train patients, reinforce their own responsibility
haemodynamics (treatment of cardiac insufficiency or ven-  orthopaedic shoes with appropriate distribution of pressure
 inspect feet daily for changes (callosities, rhagades, fungal
tilation disruption, blood pressure regulation), the haemor- infections of the nails)
heology and vasodynamic (blood flow/conditions) as well  do not use any cutting implements for foot care, foot baths
as the anticoagulation. at body heat only, do not go barefoot

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.

Chronic wounds [122.123]

 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 difficulties, 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.
Diabetic ulcers of neuropathic
genesis under conservative
treatment
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 sufficient, 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 findings is clear. Demarcation
denotes the clearly visible border between black (dead) and
healthy tissue. Operations in inflamed 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.
Chronic wounds [124.125]
 The Decubital ulcer Classification of decubital ulcer:
A decubitus is defined as damage to the skin as a result of Epidermis Stage I: Sharply defined reddening
of intact skin, which does not
continuous local pressure. Its occurrence can be sketched blanch on pressure. As a guide:
Stage I


out schematically as follows: when sitting or lying, the overheating of the skin, hardening
human body exerts pressure on its contact surface, which Dermis Stage II
or oedema.


in turn exerts a counterpressure on the skin area of contact. Stage II: Partial skin loss of the
epidermis up to the dermis. This is
The size of the counterpressure depends on the hardness a superficial ulcer which appears
of the contact surface, although normally it is above the clinically as an abrasion, blister or
physiological arterial capillary pressure of ca. 25 – 35 mm Hg. Subcutis
flat crater.
Stage III Stage III: Damage to all skin layers

Pressure /
pressure rest time
local blood circulation insufficiency
oxygen shortage /

(epidermis, dermis, subcutis) which
In the short term, the skin itself can tolerate the applica- can extend to fascia, although
tion of relatively high pressures. However, if the pressure these are not yet involved. The
is maintained, due to compression of the capillaries con- Muscles, ulcer appears as a deep, open ulcer
veying the blood in the affected skin area, blood circulation Tendons, with or without undermining the
Bones surrounding tissue.
insufficiency and oxygen shortage (hypoxia) come about. Stage IV

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
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 insufficiency worsens and leads to a build-
up of toxic metabolic products in the tissues and increased
capillary permeability, vascular dilatation, cellular infiltra-
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 inflammatory reactions favour the removal
of toxic metabolic products. However, if the pressure is

Stage IV: Skin loss over the entire
thickness of the skin with exten-
sive tissue necroses and damage
sustained, as a consequence of the further increased to muscles, tendons and bones.
Even undermining and pocket for-
ischaemia and hypoxia, irreversible skin cell death with mations occur often. In stage III
necroses and ulceration formation take place. and IV risk through septic com-
plications!
The time for which the skin tissue can survive under (according to “National Pressure
Ulcer Advisory Panel”, 1989)
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 influenced 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.

Chronic wounds [126.127]

Decubital ulcers can in principle develop in any sites of the Initial assessment of overall situation Treatment algorithm in
body. However, the greatest risk occurs when the pressure decubital ulcer
 localisation of ulcer, degree of severity,
on the body, and the counterpressure from the surface be- general condition of wound
low, act on a skin area lying over a bony prominence which  evaluation of patient status, compliance
is not cushioned by subcutaneous fat tissue. Therefore the
classical sites are: the sacral region, heels, ischia, greater Treatment
trochanters and lateral malleoli. About 95 % of all decubi-
Causal treatment
tal ulcers occur at these sites.
 complete pressure relief to restore blood supply
Apart from perpendicular application of pressure on a throughout the treatment period for the ulcer
until healed
skin area, a risk also exists from shearing forces. The term
shearing implies tangential displacement of the skin layers
Local ulcer treatment
over one another, by means of which blood vessels are also
narrowed and compressed. It is above all the region of the  adequate surgical debridement
buttocks that is subject to tangential shearing forces, for  treatment of infection if required
 moist dressing treatment for further wound
instance when the patient is pulled into a new position cleansing, conditioning and epithelialisation
instead of being lifted, or if he slips when sitting up in bed,  plastic surgical procedure if required
due to insufficient support for the feet.
Adjuvant treatments
The treatment of the decubitus is based on three therapeu-
 improve general condition
tic principles: The supreme requirement of every decubitus  improve nutritional status
treatment is restoration of the blood supply of the damaged  pain control
skin area by a complete relief of the pressure. Without  establish and, as far as possible, eliminate local
and general elements disrupting wound healing
relieving the pressure, healing is not possible and all other
measures may fail. Therefore the relief of pressure must
Ulcer healing?
be maintained throughout the entire period of treatment.
Every pressure, even if only for a few minutes, causes fresh
yes monitoring and continuation of therapy
damage and leads to relapses in the healing process. according to treatment plan

Local wound treatment includes thorough debridement, no careful scrutiny of measures (especially if
surgical if possible, as well as continuing wound cleansing relief of pressure is sufficient)

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.

Chronic wounds [128.129]


Unstable scar in the popliteal
fossa after burn as a special form
of chronic post-traumatic wound
(above) and its treatment by
microsurgical scapula flaps
(below)
As the case may be the long lasting and stressing healing Post-traumatic ulcers Radiation damage Tumour wounds
times can be reduced by plastic surgical covering of the
Cause inadequate primary therapy, ionising radiation, some- benign, malignant or
decubitus. But even in this case previous wound condi-
e.g. of soft tissue contusions; times in association with semimalignant cell growth
tioning is recommended to ensure the surgical result and complications of wound other risk factors such as
avoid recurrences. healing which were not trauma, chemical factors
dealt with immediately, infections etc.
such as necrosis, infections,
As the third therapeutic principle, adjuvant therapies are
unstable scars etc.
indicated to improve the patient‘s general condition and
the nutritional status as well as the pain control. Cachexia Causal removal of focus of infection adequate tumour therapy tumour therapy as needed
therapy where necessary and anti- and/or therapy of concomi-
with conditions of protein deficiency, which inhibit wound microbial treatment tant risk factors as needed
healing, is often observed in elderly patients so that ade-
Treatment cleansing as early as pos- cleansing as early as pos- if radical therapy is possible,
quate nutritional intake and a sufficient supply of vitamins
sible by radical debridement sible by radical debridement the wound caused by the
and minerals must be ensured. and plastic reconstructive and plastic reconstructive tumour is converted into a
procedure procedure surgical wound and treated
The chronic post-traumatic wound as such
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 The goal of all measures to treat a chronic post-traumatic Overview of causes, causal treat-
rectified in the immediately following phase of treatment. wound is stable soft tissue cover. Debridement and the ments and treatment of other
chronic skin ulcers
Typical causes of post-traumatic wounds taking a chronic removal of all areas of necrosis and foci of infection in turn
course are soft tissue contusions, degloving injuries, skin represent the first step. It can sometimes be impossible
necrosis, osteitis, infected implants, joint arthroplasty to take into consideration functional structures such as
infections, joint infections or deep soft tissue infections. tendons, fascia and even nerves and vessels. A soft tissue
Frequently, this development can be attributed to an initial situation must be created in which it is possible to cover
underestimation of the soft tissue injury underlying the ini- the defect without a risk of persisting necrosis and thus
tial trauma. Among primary injuries, the compound fracture persistence and spread of infection.
is particularly difficult. Contamination can cause soft tissue
and bone infections which often prove to be severe. Planning of later reconstructive procedures must be includ-
ed during the debridement operation. A decision must be
The unstable scar, such as that found in areas subject to made early as to whether both soft tissue and bone defects
mechanical stress after wounds have undergone secondary can be closed in a single session or whether individual re-
healing or after split skin grafting occupies a special posi- construction steps should be postponed, to be performed
tion. With this type of scar, the integrity of the skin is not later when the soft tissues have healed.
broken, but ulceration easily occurs with a corresponding
risk of infection, so that treatment of the soft tissues is
required in this situation also.
Chronic wounds [130.131]
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,
definitive wound closure can be undertaken two days after
the first debridement during a planned second look. Plastic
reconstructive methods are required for soft tissue cover,
ranging from simple split skin graft to free microsurgical
flap 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
first 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 firmly to the un-
derlying structures due to the loss of the subcutaneous fat.
In addition, there is general tissue fibrosis and direct cell
damage with chromosomal changes. Local lymphoedema,
increasing hyalinisation at the expense of elastic fibres 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.
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 flap was
1 2 wrapped around the upper arm...
4) ...and a stress-stable amputa-
tion stump was obtained.
3 4
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.
Chronic wounds [132.133]
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
firstly 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 insufficient,
well-vascularised skin (muscle) flaps 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.
Large defect on the back following
excision in accordance with lymph
flow continuity of a malignant
melanoma (left); ulcerated breast
carcinoma (right)
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.
Chronic wounds [134.135]

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.
As always, wound coverings have the task of protecting the
wound against the ingress of external noxious influences.
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 Picture from the inside of an Attic
for qualitatively better wound healing. bowl of the potter Sosias, c. 500
BC: Achilles bandaging Patroclos
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 influences (dirt, impacts,
chafing), against contamination and chemical irritation
▪ protection against secondary infections
▪ protection against drying and loss of body fluids
(electrolyte losses)
▪ protection against loss of heat
Apart from comprehensive wound protection, the wound
dressing can also influence 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 first 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
The wound dressing [136.137]
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 secretions,
prevents drying of the wound and delivers adequate
amounts of moisture to it as needed. Naturally, the wound
dressings employed must have specific physical character-
istics if they are to fulfil 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 fine 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 inflammatory phase. Furthermore, the dressing also
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
1 2 3
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 final 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.
The wound dressing [138.139]
Requirements of wound dressings
To what extent the individual wound dressing can fulfil the
specific 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 capacity
The defined 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 filling or foam dressings have a high spontaneous ab-
sorptive capacity. However, this can also lead to excessive
stimulation of the flow 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 fibres, 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 influences 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-
utes 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
associated 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.
The wound dressing [140.141]
 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 fibres adjacent to the wound. All
hydroactive wound dressings are also wound-friendly as
they do not adhere to the wound surface because of their
specific 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 Sterile, ready-to-use and individu-
for a wound dressing to have a cell-damaging (cytotoxic) ally packed wound dressings
facilitate wound care under sterile
and sensitising effect; the traditional wound dressings of conditions.
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.
The wound dressing [142.143]
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 treatment
Depending 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 first aid
▪ treatment of primarily healing wounds closed with
sutures 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.
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 fluff. Zetuvit is therefore suitable for the
treatment of acute highly secreting flat wounds and for the
treatment of primarily healing wounds.
1
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 fluffs 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 2
is trapped in the absorbent core, so that Zetuvit Plus can 1) Zetuvit - combined absorbent
also be applied under pressure, e.g. beneath a compression dressing pad with good padding
bandage. effect.
2) Zetuvit Plus - combined absorb-
ent dressing pad with superab-
sorbent polymer (SAP) for the
treatment of very severely exuding
[144.145] wounds.
4
1
3
2
The wound dressing [144.145]

Cosmopor steril, self-adhesive
wound dressing with hydropho-
bic microgrid layer as protection
against adhesion.
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 influences such as
pressure or impact. The particularly highly absorbent core
is completely covered with thin non-woven fabric (2) which
evenly distributes the fluid 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 fibres 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 first aid treatment.
Ointment dressings
Ointment dressings such as Atrauman consist of a thin soft
open-weave tulle of hydrophobic polyester fibres 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-
The ointment dressing Atrauman
ment in all phases of wound healing, e.g. for abrasions, keeps the wound margins and
burns, scalds, and to cover skin graft donor and recipient surfaces supple and prevents ad-
sites. hesion to the wound.
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 fibres are coated with elemental silver and
additionally impregnated with an ointment mass. The silver
ions are chemically firmly bonded to the carrier material
resulting in good tissue tolerability with only slight cytoto-
xicity. The good tissue tolerability has been substantiated The silver-containing ointment
in tests with the human keratinocyte cell line HaCaT. The dressing Atrauman Ag with a wide
antimicrobial effect is indicated in
antimicrobial activity spectrum is extraordinarily broad and
infected wounds or in wounds in
includes both gram-positive and gram-negative strains of danger of infection.
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.
The wound dressing [146.147]
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 fill the defect. It has prov-
en its worth especially in the treatment of chronic problem
wounds. The scientific basis of moist treatment was laid by
the work of G. D. Winter (1962, first 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 significantly
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.
1
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”
2
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 3
delivered continuously to the wound for hours. By the per- The mode of action of TenderWet
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 affinity 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 wound dressing [148.149]

TenderWet 24 active and
TenderWet active cavity are
pre-activitated with Ringer‘s
solution and ready-to-use
As soon as the wound healing-inhibiting factors have been TenderWet has no contra-indica-
removed, i.e. the wound is cleansed of necroses, detritus tion and can be used in all wound
conditions, both infected and
and coatings, the conditions are provided for the formation non-infected. The rinsing effect
of granulation tissue: Proliferative cells are able to migrate of TenderWet is seen to best
into the wound area and new capillary growth can take advantage during the cleansing
place (3). The moisture and the electrolytes contained in the phase and at the beginning of the
granulating phase. The examples
Ringer‘s solution such as sodium, potassium and calcium show TenderWet and TenderWet 24
contribute to the cell proliferation. 1 2 used for treating venous ulcers
(1 and 2), a burn wound (3) and a
TenderWet has no contra-indications and can also be used diabetic foot lesion (4).
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 3 4
be packed in loosely without pressure to ensure the direct
contact needed for the fluid exchange. The physical pro-
perties of the super absorber in conjunction with the outer The rapid and efficient cleansing
woven cover of the wound dressing pad give TenderWet the effect of TenderWet proved its
value with this dehiscent medial
necessary tamponing properties. With extensive wounds, abdominal wound in an 83-year
the TenderWet wound dressing pads should overlap slightly old patient (case report M. Butcher,
when applied. Plymouth, England).
5) Condition of the wound
following dehiscence with firmly
TenderWet is available in different sizes and round and rec- adhering necrotic coatings
tangular shapes to ensure it fits well to the various wounds. 5 6 6) Start of TenderWet treatment on
28/1 with 10x10 cm TenderWet
For simplified application, TenderWet is available in an and dressing changes every
12 hours
already activated form as TenderWet active cavity and 7) Wound condition two days after
TenderWet 24 active with an integrated moisture-repellent start of treatment already with
protective layer. These “active” wound dressing pads are marked reduction of the coatings
soaked with ready-to-use Ringer‘s solution and can be 8) Condition of the wound on 17/2
with graftable granulation tissue;
applied immediately. This means that a preparatory proce- final covering takes place with a
dure can be omitted, that helps saving time. But a further split skin
advantage of already activated wound dressing pads is also 7 8
that a significantly greater volume of Ringer‘s solution can
be introduced into the absorbent core than with manual
The wound dressing [150.151]
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 2/2
6) Condition after debridement,
wound with necrotic residues
7) Start of wound cleansing only
with TenderWet 24 active, dress-
ing change once daily
8) 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.
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 difficulty (=cavity). TenderWet 24 active, by
1 2 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.
3 4 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-
TenderWet and TenderWet 24
sorbing and rinsing effect to around 24 hours: The wound
must be activated before use
dressing pads are fitted with a moisture-repellent protective with TenderWet solution or with
layer, primarily in order to prevent moisture emerging from Ringer‘s solution
the dressing to the outside. The dressing side with integrat-
ed protective layer is marked with parallel coloured stripes,
5 6 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 fixed, for instance completely covered with elastic
non-woven sheet dressings (e.g. Omnifix) or with elastic
conforming bandages (e.g. Peha-crepp, Peha-haft).
7 8
The wound dressing [152.153]
 Sorbalgon – Due to its excellent packing
tamponading calcium alginate dressings capability, Sorbalgon is the ideal
wound dressing for problema-
Sorbalgon is especially suited for cleansing and the formati- tically sited and deep wounds, as
on of granulation in superficial and deep, infected and non- examples 1 – 4 show. Sorbalgon
infected wounds. Sorbalgon can excellently be packed and ensures tissue-protecting tampo-
thus provides effective wound cleansing and conditioning, nade, which can also be removed
atraumatically and without caus-
particularly even in deep wounds. ing pain.
1 2
Sorbalgon is a non-woven dressing made of high-quality
calcium alginate fibres which are packed dry into the
wound (1). On contact with sodium salts, such as those
found in blood and wound secretions, the fibres swell and
1 transform into a moist absorbent gel which fills 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- 3 4
contamination (3). Wounds are cleansed rapidly so that
Sorbalgon has proved valuable especially in the treatment
2
of chronic and infected wounds. In clinical practice, not only does
Sorbalgon prove to be well suited
to the cleansing of wounds, but
Sorbalgon‘s gel-like consistency also acts like a moist dress- also shows itself in the condition-
ing which prevents the wound from drying. A microclimate ing of wounds: 85-year old patient,
favourable for wound healing is produced which promotes stage III decubitus (case report
the formation of granulation tissue and keeps the wound F. Lang, Leonberg, Germany).
3 5) Admission finding: there was
surfaces supple. a large necrotic plate on the os
The mode of action of Sorbalgon 5 6 sacrum, which was removed with
Because of the gel formation, Sorbalgon does not stick to surgical debridement
the wound and dressing changes are painless. However, 6) and 7) Start of the treatment
with Sorbalgon 10 days after the
complete conversion of the calcium alginate fibres to a gel surgical debridement
needs adequate secretion. Should gaping wounds produc- 8) Wound condition after 20 days
ing little secretion be packed, moisten Sorbalgon with of exclusive Sorbalgon treatment
Ringer‘s solution. Any fibres remaining in the wound can showing well developed granula-
tion tissue – patient then discharg-
be rinsed out with Ringer‘s solution; otherwise the gel plug ed for further care at home
can be removed from the wound with forceps.
7 8

The wound dressing [154.155]


Sorbalgon is available in three
dressing sizes and as tamponing
ribbons.
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 sufficient. 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
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 fluids. Even if pressure is applied from
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 fluid.

The hydrophilic foam dressing
PermaFoam expands the treat-
ment options for chronic wounds
with its excellent physical effect
comprises hydrophilic polyurethane polymers, which are
able to store up to nine times their own weight of fluid 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 flexible, 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-
quently 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.
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 wound dressing [156.157]

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
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 exuding
6) 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.
PermaFoam is atraumatic, adhesion to the wound or growth 1
2
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. 5 4
3
PermaFoam is soft and supple and fits snugly to the wound PermaFoam is available in special
shape. The foam dressing is fixed with elastic conforming sizes adapted to different wounds,
1 2
so that optimum wound treatment
bandages (e.g. Peha-haft) or over the whole surface with can be achieved in every case.
elastic non-woven sheet dressing for dressing retention PermaFoam sacral (1) for the use
(e.g. Omnifix elastic). The product version PermaFoam in the sacral region, PermaFoam
comfort is designed for an easy fixation with an adhesive concave (2) for the use on heel
and elbow, PermaFoam trache-
border. The used adhesive is gentle on the skin. PermaFoam ostomy (3) for the treatment of
is available in a variety of versions and sizes. puncture points, PermaFoam
cavity (4) for the treatment of deep
Hydrocoll – absorbent hydrocolloid dressing wounds and PermaFoam round (5)
for the treatment of smaller ulcers
3 4 Hydrocoll is a self-adhesive absorbent hydrocolloid wound at problem zones.
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 mode of action of Hydrocoll
5 6
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
7 8 toxins, is securely bound into the gel structure.
The wound dressing [158.159]
The adhesion of the elastomer means that Hydrocoll can be Hydrocoll is a self-adhesive,
applied to the wound like a plaster. As the gel forms, the absorbent hydrocolloid wound
dressing for cleansing and con-
adhesion in the region of the wound disappears, so that ditioning non-infected wounds
Hydrocoll protects the wound by being fixed only to the with moderate or slight secretion.
intact skin surrounding the wound. For clinically appropriate and
economical application, Hydrocoll
is available in a variety of shapes
The hydrocolloids used in Hydrocoll have particularly good and presentations:
absorbing and swelling capabilities, as well as the prop- 1 2 1) Hydrocoll in the standard version
erty that their gel structure remains compact. Hydrocoll 2) Hydrocoll thin for already
expands as usual into the wound, but in the gel condition, epithelised wounds
3) Hydrocoll sacral specifically for
it may then be removed in one piece from the wound. No wound treatment in the sacral
gel residues remain in the wound, so that the rinsing out of region
gel residues with a pus-like consistency, as was previously 4) Hydrocoll concave in a form
necessary, is largely dispensed with. Dressing changes are perfectly adapted to elbows and
heels
therefore simpler and less unpleasant. In addition, reliable
wound assessment is also immediately possible.
3 4
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 Illustrations 5 – 8 show stages in
and swelling process, into the hydrocolloid portions of the the course of wound healing of
a stage II decubitus with vesicu-
dressing, rapid and good wound cleansing takes place. lation on the left heel. Wound
General investigations have shown that the microcircula- treatment was carried out with
tion in the wound area is also improved with enhanced Hydrocoll and was free from com-
cleansing. Particularly in chronic wound conditions with plications. Due to its high absorp-
tion capacity, Hydrocoll could be
a stagnating cleansing phase, the body‘s own cleansing left on the wound for several days,
mechanisms are reactivated. During the granulation phase, 5 6 making treatment simple and, due
the moist environment under Hydrocoll stimulates and to the reduced dressing change
promotes the formation of granulation tissue. This means frequency, more economical
(documentation Gabi Michl,
that with Hydrocoll, a balanced moist wound environment Kötzting).
may be maintained without difficulty and without the dan-
ger of exudate accumulation, even over long treatment pe-
riods, and drying out of the granulation tissue is reliably

7 8

The wound dressing [160.161]

 prevented. In the epithelisation phase, the cell-friendly Treatment of a split-skin graft
moist environment promotes mitosis and migration of the donor site (1) and the recipient
site – an accident injury on the
epithelial cells. In addition, unwanted eschar formation, right knee (2) - with the hydro-
which would impede healing, is prevented. The imperme- active ointment dressing Hydrotul
able to bacteria and liquid top layer acts as a reliable (Case report F. Lang, Leonberg,
barrier against germs and protects the wound against dirt Germany). Complication-free
healing process with cosmetically
and moisture. Mobile patients are able to shower with the very acceptable healing results
dressing in place. 1 2 (3/4). The new epithelium is fine
and uniform and forms conspi-
Hydrocoll is available in different shapes, e.g. as “concave” cuously rapidly from the margin of
the wound.
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 specifically suited
to wounds that are already epithelising.

Hydrotul – hydroactive ointment dressing 3 4

The development of the hydroactive ointment dressing
Hydrotul combines the benefits of conventional ointment
dressing with modern hydrocolloid technology. This opens Treatment of an acute wound
up wide areas of application for the hydroactive ointment (Burst blister as a result of hyper-
keratosis) with Hydrotul (Docu-
dressing. Hydrotul is suitable for the treatment of acute as
mentation from an observational
well as chronic superficial wounds in the granulation and/or study). The condition of the wound
epithelisation phase. before the start of treatment on
30/05 (5) and treatment of the
wound with Hydrotul (6). The
3) The honeycomb like structure of
secondary dressing for absorbing
the carrier material prevents 5 6 wound exudate consisted of gauze
accumulation of exudate.
swabs. First dressing change on
02/06 (7), second change on
06/06 (8), the wound was com-
pletely epithelised.
2) The Hydrotul ointment keeps
the wound margins soft and

1) Hydrocolloid particles keep the

wound moist.

7 8

The wound dressing [162.163]


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).
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 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 difficulties. It can be readily cut to size
using sterile scissors to fit the wound size and shape and
won’t stick to examination gloves.
In observational studies it could also be confirmed 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
1
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
2
of hydrophilic and thus absorbent polymers with a high
water content of 60 %. In spite of this high water content, The mode of action of Hydrosorb.
Hydrosorb can additionally bind large quantities of fluids
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 specific benefit 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 wound dressing [164.165]
Superficial 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
Hydrosorb
2) Good wound cleansing results
after only one week
3) Further treatment with Hydro-
sorb
4) Healing result after one month
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
finally 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.
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
A B C odour molecules.
1 2
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
3 4 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-
5 6 rials or calcium alginates. Hydrogels cannot spontaneously
absorb fluids; their fluid 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- The transparency of Hydrosorb
ods on the wound without the risk of wound irritation. is one important factor for the
economical use. The wound can
Hydrosorb can be removed in its entirety as the gel struc-
be inspected any time through the
ture does not break down because of the absorbed wound
dressing so that Hydrosorb can
7 8 exudate. No residues remain in the wound and the con- stay on the wound for days and
dition of the wound can be assessed safely without prior dressing changes are unnecessary.
rinsing.
The wound dressing [166.167]
 Hydrosorb is available in two versions as Hydrosorb and
Hydrosorb comfort. Hydrosorb does not have a self-adhe-
sive fixing edge and is secured with a conforming bandage,
adhesive tapes or with a compression bandage. Hydrosorb
comfort is fitted with a hypoallergenic adhesive film for a
reliable and impermeable to germs fixation.
Hydrosorb Gel – for rehydration of dry wounds
Hydrosorb 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 fissured 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 benefits: 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.
by the consistency of the gel. The gel is firm 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.

Dry wounds or wounds at risk of drying out particularly

Hydrosorb Gel serves for efficient
rehydration of dry wounds and
is available in easy to use dosing
syringes with 15 g and 8 g.
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 fissured wounds. This reliable application is supported
The wound dressing [168.169]

Wound dressings for chronic problematic wounds/wound pattern
Wound cleansing
Necrosis
superficial wounds
 TenderWet 24 active
(if needed in combination
with Atrauman Ag*)
deep or gaping wounds
 TenderWet active cavity
 Hydrosorb Gel
Further products
Cosmopor steril
Granulation Epithelisation
Self-adhesive wound dressing with
Infection Fibrin coating high absorption capacity and good
cushioning effect for postoperative
wound treatment as well as for
sterile treatment of minor injuries.
Hydrofilm plus
Self-adhesive, waterproof, trans-
parent wound dressing with good
absorption and padding effect
Exudate ++ for postoperative care of slightly
 TenderWet 24 active intact wound site intact wound site intact wound site secreting wounds and for protec-
 Sorbalgon  PermaFoam comfort  PermaFoam comfort  Hydrocoll thin tion against secondary infection.
 Atrauman Ag*  PermaFoam sacral  PermaFoam sacral  Hydrosorb comfort Rolta Soft
 PermaFoam  PermaFoam concave  PermaFoam concave  Hydrofilm** Very soft, skin-friendly synthetic
(in infected wounds only  TenderWet 24 active previously damaged  Hydrotul* padding bandage, which is
under medical supervision) previously damaged wound site previously damaged particularly suitable as padding
wound site  PermaFoam wound site material under support bandages
 PermaFoam  Hydrotul*  Hydrosorb and compression dressings.
Exudate +  Hydrotul* Cosmopor I.V:
Medicomp Drain
 TenderWet 24 active  TenderWet 24 active intact wound site
Peha-Slit dressing
 Atrauman Ag*  Hydrocoll
PermaFoam tracheostomy
 Hydrocoll sacral
For the use with drainages and
 Hydrocoll concave
extensions
previously damaged
wound site Fixation
 Hydrosorb normal skin:
 Hydrotul* Omnifix elastic, Omniplast,
Omnisilk, Peha-haft, Stülpa-fix
sensitive skin:
Pehalast, Omnipor, Peha-crepp,
Extremities:
Peha-haft, Pehalast, Stülpa-fix
Joints:
Lastodur straff, Stülpa-fix,
Omnifix elastic
Exudate ++
Fingers and toes:
 TenderWet active cavity  TenderWet active cavity  PermaFoam cavity Stülpa Fertigverband, Peha-haft
 Sorbalgon/Sorbalgon T  PermaFoam cavity  Sorbalgon/Sorbalgon T Sacral region:
 Atrauman Ag*  Sorbalgon/Sorbalgon T Omnifix elastic, Stülpa-
 PermaFoam cavity fix,Molipants (inco-system),
Exudate +
* As primary wound dressing in
 TenderWet active cavity  TenderWet active cavity  Hydrosorb Gel combination with absorbent wound
dressings
 Atrauman Ag*  Hydrosorb Gel ** For wounds with almost no exudate
The wound dressing [170.171]
 Zetuvit
Products for
dry wound
treatment
Product characteristic Wound compatible absorbent
dressing with non-adherent non-
woven cover and absorbent core
of cellulose fluffs.
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.
Presentations Zetuvit, sterile and non-sterile,
10x10, 10x20, 13.5x25, 20x20
and 20x40 cm
Zetuvit Plus
Combined absorbent dressing
pad consisting of four layers of
different materials: Absorbent
core consisting of cellulose fluffs,
blended with super absorber,
non-woven covering of the
absorbent core, water-repellent
special non-woven and two-layer
outer non-woven.
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.
Zetuvit Plus, sterile, 10x10,
10x20, 20x25 und 20x40 cm
Cosmopor steril
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.
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 first aid.
Cosmopor steril, 7.2x5, 10x6,
15x6, 10x8, 15x8, 20x8, 20x10,
25x10 and 35x10 cm
Atrauman
Wound compatible ointment
dressing made of hydrophobic
polyester tulle, impregnated with
an ointment mass that is free
from active agents.
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.
Atrauman, sterile,
5x5 and 7.5x10 cm
Atrauman Ag
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.
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.
Atrauman Ag, sterile, 5x5,
10x10 and 10x20 cm
The wound dressing [172.173]
 TenderWet
Products for
hydroactive wound
treatment
Product characteristic Wound dressing pad with
absorbing 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.
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.
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
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 swelling process, germs
are also securely enclosed within
the gel structure.
High absorption capacity with ef-
ficient 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.
Sorbalgon, sterile, 5x5, 10x10
and 10x20 cm; Sorbalgon T
ribbons, sterile, 1 g/30 cm and
2 g/30 cm
PermaFoam
Hydroactive foam dressing made
from foam materials of differing
structure, with high vertical
capillary effect and retention for
reliable fluid binding, top layer
impermeable to germs.
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 difficult to treat,
the respective specific sizes.
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; PermaFoam
concave, sterile, 16.5x18 cm;
PermaFoam cavity, sterile,
10x10 cm; PermaFoam trache-
ostomy, sterile, 8x8 cm
Hydrocoll
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.
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.
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
Hydroactive ointment dressing
with integrated hydrocolloid
particles in the wide-meshed
polyamide carrier tissue and non-
medicated ointment impregna-
tion based on triglyceride.
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 superficial, acute and chronic
wounds in the granulation and
epithelisation phase.
Hydrotul, sterile, 5 x 5 cm,
10 x 12 cm und 15 x 20 cm
The wound dressing [174.175]
 Hydrosorb
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.
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 efficiency because of
longer dressing change intervals),
ideal for keeping granulation and
epithelium moist after therapy
with TenderWet, Sorbalgon or
PermaFoam.
Presentations Hydrosorb, sterile, 5x7.5, 10x10
and 20x20 cm; Hydrosorb
comfort, sterile, 4.5x6.5, 7.5x10,
12.5x12.5 and 21.5x24 cm
Hydrosorb Gel
Clear, viscous and sterile
hydrogel based on carboxymethyl
cellulose, Ringer’s solution and
glycerine.
Rehydrates wounds at risk of
drying out and dry deep and
fissured wounds; fibrinous 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.
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 difficulties.
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 influence 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 wound dressing [176.177]

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, 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 first.
The practical performance of dressing change

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 fluids (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
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
fingers 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.

The wound dressing [178.179]

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 flowers 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 filled 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, firm)
▪ extent of epithelial formation
▪ degree of bleeding tendency
▪ painfulness of the wound
▪ signs of infection (swelling, erythema, yellowish or
greenish sloughy deposits, odour)
The wound dressing [180.181]

Removal of necrotic tissue and
slough is best done with a scalpel
in order to avoid tissue crushing
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 sufficient for prima-
rily healing aseptic wounds. Disinfection of the wound
surroundings 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.
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.
Irrigation with Ringer‘s solution contributes to efficient
wound cleansing. The irrigation fluid 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 fluid 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 sufficiently large to adhere to non-greasy skin.
The wound dressing [182.183]

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
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 influences 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 find 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.
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.
Reverdin‘s method for wound clo-
sure: Epidermal flaps are obtained
If there is no spontaneous epithelialisation or the process
with a scalpel and transplanted
is stagnating, which is frequently the case with chronic onto the well-conditioned wound.
wounds, plastic surgical measures (e.g. skin grafting) Further epithelisation is able to
should be considered to achieve wound closure. spread out from these islands of
epithelium
The wound dressing [184.185]

The wound dressing must provide
optimum fit 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.
Application of the new dressing Possible dressing fixations: Even
The new dressing is chosen which has a mode of action dressing with the adhesive tape
Omniplast which ensures secure
meeting specific wound requirements (see overview wound fixation because of its adhesive
dressing p. 170 – 176). It should be ensured that the strength (left). The hypoallergenic
selected dressing fits the wound surface well, for wound adhesive tape Omnipor made of
secretion can only be absorbed when there is good contact highly air and water vapour permea-
ble non-woven support is well-suited
between the dressing and the wound. Deep and gaping for patients with hypersensitive skin
wounds should be packed carefully with suitable dressings (right).
such as Sorbalgon to ensure absorption of infected secre-
tions even deep within the wound. The non-woven for dressing reten-
tion Omnifix elastic is easy to use.
It fits securely and without creases
In the case of deep, gaping wounds, particular care should even to joints and conical parts of
be taken that they are not too firmly packed. The pressure the body by means of the transver-
of excessive packing impairs the microcirculation of the sely elastic support of non-woven
wound surface and particularly of the granulation tissue. fabric.
White sloughy deposits and necrosis appear as a result
of the compression. If the firm packing continues, sepsis
may occur. Moreover, it should be possible to remove the
packing without cell stripping and increased pain, which is The cohesive elastic conforming
ensured with Sorbalgon. bandage Peha-haft* holds securely
without end-fixation and is par-
ticularly economical to use (left).
Securing the dressing Simple securing with elastic
Securing the dressing using adhesive tapes is usually bandages over joints, in this case
sufficient in the case of primarily or small secondarily with Pehalast (right).
healing wounds.
In the case of larger injuries, adhesion over the entire area
with adhesive dressing retention sheets or conforming The highly elastic net tubular
bandages is indicated. Dressings which are not secured bandage Stülpa-fix only needs to
be lifted to change the wound
firmly can cause irritation of the wound leading to disturb- dressing (left). The tubular band-
ances and delays in wound healing. age Stülpa is indispensable espe-
cially for special fixations, e.g. as
a finger bandage (right).
* 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.
The wound dressing [186.187]
In some wounds, it is necessary to prevent the occurrence
of oedema at the wound edges by slight flat 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 final 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 difficult 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- The formation of a blister in the
sorb also allows problem-free observation of the wound hydrocolloid dressing Hydrocoll
indicates that the dressing needs
because of its transparency. It gives the doctor and nursing to be changed
staff the security of knowing that any complications can be
recognised immediately.
The wound dressing [188.189]
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 simplifies
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 findings 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,
stagnation or set-backs in the treatment to be assessed reli-
ably, so that treatment measures may possibly be amended
accordingly.
The documentation also, above all, ensures an information
flow 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 significance. However, this frequently
presents difficulties in practice and the statements are
The wound dressing [190.191]
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.
1 2 3

Additional photographic documentation is also particularly

well suited to recording the condition as well as the healing ▪ With regard to the settings used it must be ensured that
process of the wound clearly and precisely. Misinterpreta- not only the central wound area is sharply defined but
tions that can arise in purely written wound descriptions also the near and further way areas of the body.
are avoided. Certain legal aspects need to be paid regard ▪ If there is not sufficient daylight available, a flash can
to in the context of photographic documentation, mainly be used for illumination if necessary, whereby it must be
relating to the consent of the patient. ensured that no reflections occur. The use of special
colour cards is also useful which in the case of differing
Here are a few tips for carrying out the documentation: light conditions allow the images to be corrected to
▪ Basically it has to take care that photographs which “standard conditions” and can thereby be compared.
record the progress of a wound are always taken under ▪ The selected background should be as “quiet” as possible
the same conditions in order that, even if the dates of – i.e. without any structure (2).
the photography are different, useful comparisons can be ▪ The camera should be held with its exposure plane as far
made. as possible parallel to the subject. If the exposure plane
▪ Digital photography has been become the standard and the subject are not parallel, the image will be dis-
means of imaging, allowing photographs to be produced torted and will not show the exact size relationships (3).
and filed 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 sufficient.
▪ Perhaps, all pictures have to retain their evidential value
even years later. Therefore it is important that the files are
carefully administered. This includes meaningful naming
of the files (e.g. “Surname_Forename_Date.jpg” instead
of “DSC35469.jpg”), regularly backing up all files (e.g. on
CD-ROM or DVD) and if necessary keeping print-outs pro-
duced with suitable photo printers in the patient files (1).

The wound dressing [192.193]


Glossary & Index
A Betahaemolysis, betahaemolytic
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 inflammation
Antiseptics ➞ 77
Apocrine sweat glands ➞ 20
Arterioles ➞ the smallest arterial
blood vessels, splitting into capilla-
ries (Latin: arteriola = little artery)
Asepsis ➞ 168
B about by enzymes
Basal layer ➞ 10
Basal membrane ➞ 10
➞ 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 or removal of part of a tissue or
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
granulation 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 Embolism ➞ sudden occlusion of
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
Dermatome, mesh dermatome ➞
surgical cutting instrument
for removing skin flaps 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 instrument
Electrocoagulation ➞ (thermo-
coagulation), surgical procedure
for destruction of tissue with a
powerful electric current; heating
of the protein also stops bleeding
an artery by a blocking particle,
e.g. a thrombus
Emphysema ➞ inflation, 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
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
organ with the aid of a sharp
Execution ➞ 169
Exogenous ➞ medical: exerting
an influence 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-
tive 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 classification
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 flow
➞ 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 Leukocytosis ➞ increase in the
Ileus ➞ intestinal obstruction ➞
57, 63
Immune status ➞ 56
Immunosuppressant ➞ medica-
tion for artificial 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
Inflammatory reactions ➞ 38
Inflammatory stage ➞ 36
Influences 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 insufficiency or ischaemia
K return of a disease
Keloids ➞ 64
Krause‘s corpuscles ➞ 19
L (Latin: proliferatus = sprouting,
Langer‘s lines ➞ 14, 63
Leukocytes (white blood
corpuscles) ➞ 24
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 ➞ inflammation of
the lymphatic vessels
Lymphocytes ➞ 24
M 183
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)
Myofibroblasts ➞ 47
N Peritonitis ➞ inflammation of
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 influences ➞ harmful-
ness, disease cause (Latin: noxa =
harm, cause of disease)
Nutrition ➞ 55
O Phases of wound healing ➞ 35
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
inflammation of bone marrow
including the bone tissue and the
periosteum
P Predisposition ➞ proneness/
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
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
Photographic documentation ➞
Physiological ➞ relating to
normal (natural) life processes,
not diseased
Platelets ➞ 22, 26
Pneumonia ➞ lung inflammation
Post(-) ➞ Latin: after Postopera-
tive wound-healing impairments
➞ 61
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
inflammatory processes, e.g. in
the context of wound healing
following the inflammatory stage
overgrown)
Proliferative stage ➞ 42
Provisional wound treatment ➞
82
Putrid infection ➞ 73
Pyogenic infection ➞ 73
Q exudation)
Quantitative classification 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 flaps
obtained with a scalpel (named
after Jacques-Louis Reverdin,
1842 – 1908) ➞ 176
Reversible ➞ able to reverse
(lat. reversibilis = able to reverse)
Recurrent ➞ relapse, medical:
Red blood corpuscles
(erythrocytes) ➞ 23
Ruffini‘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 =
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 flattened,
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
Superficial wounds ➞ 28
Sweat glands ➞ 20
T Wunde, in WundForum 1/1996
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 fibrinogen-free fluid 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 insufficiency/acute renal
failure (Greek: uraemia = urea
poisoning of blood)
V fahrung bei chronischen Wunden,
Vascularisation ➞ 43
Vasculogenesis ➞ 43
Vasoactive ➞ affecting vascular
tone
Vater Pacini corpuscles ➞ 18
Virulence ➞ 69
W thoden, in WundForum 3/1995
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
Bibliography
Blank, I.: Postoperative Wundhei-
lungsstörungen und Komplikati-
onen, in WundForum 4/1997
Brychta, P.: Die Verbrennungs-
wunde – Pathophysiologie und
Therapieprinzipien, in WundForum
3/1995
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-
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
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-
fige Probleme bei der Behandlung
chronischer Wunden, in WundFo-
rum 1/1996
Lang, F., Röthel, H.: Der Ver-
bandwechsel – Anregung für die
Entwicklung von Standards, in
WundForum 3/1996
Mast, B. A., Schultz, G. S.: Inter-
aktionen von Zytokinen, Wachs-
tumsfaktoren und Proteasen in
akuten und chronischen Wunden,
in WundForum 3/1997
Miller, M. and Glover D.: Wound
management theory and practice,
Nursing Times Books 1999
Niedner, R., Vanscheidt, W.: Die
Wundinfektion – folgenschwerste
Komplikation der Wundheilung, in
WundForum 2/1994
Nusser, B.: Die Fixierung von
Wundauflagen – Material und Me-
Rietzsch, H.: Diabetische Fußläsi-
onen – Pathogenese und Therapie,
in WundForum 2/1995
Röthel, H.: Verbandstoffsysteme
für die feuchte Wundbehandlung,
in WundForum 2/1996
Röthel, H., Schenck, K.: Passive
und interaktive Wundauflagen
– Aufbau, Wirkung und Einsatzbe-
reiche, in WundForum 2/1994
Röthel, H., Vanscheidt, W.: Ba-
sisinformationen zum Wundma-
nagement (I): Die Reinigung der
Wunde, in WundForum 1/1997
Röthel, H., Vanscheidt, W.: Basis-
informationen zum Wundmanage-
ment (II): Defektauffüllung und
Reepithelisierung, in WundForum
2/1997
Schenck, K.: Verbandstoffkunde
Teil I: Calciumalginate zur feuch-
ten Wundbehandlung, in WundFo-
rum 4/1994
Schenck, K.: Verbandstoffkunde
Teil II: Hydrogele zur feuchten
Wundbehandlung, in WundForum
1/1995
Schenck, K.: Verbandstoffkunde
Teil III: Hydrokolloide zur feuchten
Wundbehandlung, in WundForum
2/1995
Seiler, W. O.: Chronische Hautul-
cera: Die Feuchttherapie als
wesentliches Element moderner
Ulcusbehandlung, in WundForum
3/1995
Seiler, W. O.: Impaired wound
healing bei Dekubitalulzera, in
WundForum 2/1994
Tautenhahn, J., Bürger, Th., Pi-
atek, S., Lippert, H., Halloul, Z.:
Diagnostik und Therapie des Ulcus
cruris arteriosum, in WundForum
1/1997
White R.: Skin care in wound
management: assessment, preven-
tion and treatment, Wounds-UK
Books 2006
Wilde, J., Wilde jun., J.: Wundhei-
lungstörungen I und II, in Wund-
Forum 1/1995 und 2/1995
Bibliography [198.199]
Pictures sources
Abbey, M. / NAS / Okapia (S. 19)
akg images (S. 65)
Baschong, W. (S. 31)
Bavosi, J. / SPL / Focus (S. 34)
Beddow, T. / SPL / Focus (S. 80)
Bildarchiv Preußischer Kulturbesitz
(S. 137)
Biophoto Ass. / Okapia (S. 12)
Blank, I. (S. 29, 84, 176)
Brain Dr., T. & Parker, D. / SPL
(S. 77)
Brychta, P. (S. 29, 31, 63, 90-93,
151, 177)
Butcher, M. (S. 151)
Camazine, S. / NAS / Okapia
(S. 26)
CNRI / SPL / Focus (S. 18, 44, 68,
79)
Deutschle, G. (S. 45, 59)
Dex, A. / SPL / Focus (S. 105)
Dowsett, A. B. / SPL / Focus (S. 23)
Durham, J. / SPL / Focus (S. 79)
Eward, K. / Okapia (S. 20)
Franke, R. P. (S. 17)
Germann, G. (S. 29, 86, 130, 133)
Gray, D. (S. 31)
Gschmeissner, S. / SPL / Focus
(S. 18)
Kage, M. B. / Okapia (S. 38, 41)
Kaufmann, S. H. E. & Golecki, J. R.
/ SPL / Focus (S. 96)
Lang, F. (S. 29, 31, 59, 63, 73,
74, 75, 82, 86, 98, 100, 102, 142,
153, 156, 173, 175, 177, 180)
Lippert, H. (S. 39, 52, 94, 135)
Looks, A. (S. 97)
LWA-Dann Tardif / Corbis (S. 7)
Mackowski, M. S. (S. 95)
Mähr, R. (S. 33)
Marazzi Dr., P. / SPL / Focus (S. 39)
Mauritius / Phototake (S. 23, 104)
Meckes, O. / EOS / Focus (S. 111)
Michl, G. (S. 159)
Michler, A. u. H.-F. / Okapia (S. 9,
12, 13)
Michler, A. u. H.-F. / SPL / Focus
(S. 18)
Morbach, S. (S. 124)
Motta, P. / Dept. of Anatomy /
University La Sapienza Rome /
SPL / Focus (S. 16)
Murti Dr., G. / SPL / Focus (S. 15)
NIBSC / SPL / Focus (S. 24)
Nishinaga, S. / SPL / Focus (S. 21)
Piatek, S. (S. 62, 103, 108)
Rath, E. (S. 124)
Röhrig, C.-W. / Okapia (S. 110)
Schepler, H. (S. 33, 119)
Seiler, W. O. (S. 52)
Syred, A. / SPL / Focus (S. 12)
Tautenhahn, J. (S. 112, 114, 120)
Terry, S. / SPL / Focus (S. 8)
Teschner, M. (S. 52)
Thinkstock (S. 7)
Vanscheidt, W. (S. 33)
Velzen van, C. J. (S. 183)
VVG / SPL / Focus (S. 11, 19, 20)
Wilde, J. (S. 63, 64)
Winter, H. (S. 75, 135, 153)
Zimmermann; M. (S. 156)
All other illustrations from
the PAUL HARTMANN AG
picture archive.
The wound dressing [200.201]