Wound healing and dressing

Wound healing and dressing in
dermatology

08/08/2020
-Made by: Dr. Jaspreet Kaur

Content
-Dressings

Ideal dressing

Wound bed preparation

Conventional dressing

Modern dressing

General measures while applying dressings

Choice of dressing

Complications of wound dressing

Advanced wound therapy
-Wound healing

Regeneration and repair

Factors a
ff
ecting wound healing

Cellular and molecular aspect

Components involved in healing

Intention of healing

Impaired healing

Chronic wound

- Regeneration:

During embryogenesis injured foetal skin can heel completely without
fi
brosis

- Repair:

In children and adults wound healing response characteristically leads to
fi
brosis I.e. scar
formation and there may be failure of regeneration of lost adnexal components.

- Normal ageing skin has increased levels of proteases snd elastase with decreased level of
proteolytic inhibitors > proteolytic digestion of dermis > quality of wound healing increase
with reduced scarring.
Regeneration vs Repair

- Wound Depth And Its Effects On Wound Healing:
- Erosion:

Defect a
ff
ects only the epidermis or its portion and heals with regeneration of entire
epidermis

- Ulcer:

Wound extends into the dermis and healing is a reparative process associated with scar
formation. Depending on depth can be of two types:

PARTIAL THICKNESS WOUND FULL THICKNESS WOUND

Epidermis and portion of dermis are missing Epidermis and entire dermis are missing

Ulcer extends into the mid dermis Ulcer extends into the subcutaneous fat

Adnexal structures remain intact Adnexal structures are lost

Preserved adnexal structure serve as source Loss of source of keratinocytes for
of epithelial cells to repopulate the epidermis reepithelialization

Epithelia from wound edge migrate Epithelia from wound edge only is present
for coverage for coverage

Minimal contracture after healing Contractures are characteristically present

-During contraction wound area decreases via centripetal movement of preexisting tissue, not the
formation of new tissue. Contraction occurs in a predictable direction in relation to skin tension lines.

- Time interval until complete re-epithelialization depends upon several factors:

Wound depth:

Wound diameter:

Anatomic infection or foreign body

Vascular supply

Geometric shape of wound

Age and health of patient

Nutritional status

Psychological stress delays wound healing

Medications

Hormones

- There sequential phases of wound healing are:

Coagulative phase

In
fl
ammatory phase

Proliferative phase

Remodelling or maturation phase
Cellular and molecular aspect of skin repair:

The different phases of wound healing
Phases of healing Main cell types involved
Coagulation
phase
Platelets
Platelets
Macrophages
Neutrophils
Macrophages
Fibroblasts
Epithelial cells
Endothelial cells
Fibroblasts
Myofibroblasts
Injury Hours Days Weeks
Inflammatory
phase
Migratory/proliferative
phase
Remodeling
phase

The phases of wound healing and key cells and events involved
Time Phases Main cell types Specific events
Coagulation
Platelets
Fibrin plug formation,
release of growth factors,
cytokines, hypoxia
Days
Weeks
to
months
Platelet aggregation and release of
fibrinogen fragments and other
pro-inflammatory mediators
Selectins slow down blood cells + binding
to integrins diapedesis
Cross-talk between MMPs, integrins,
cells, cytokines cell migration,
ECM production
Phenotypic switch to
myofibroblasts from
fibroblasts
Cell recruitment and
chemotaxis, wound
debridement
Epidermal resurfacing,
fibroplasia, angiogenesis,
ECM deposition, contraction
Scar formation and revision,
ECM degredation, further
contraction and tensile strength
Neutrophils
Monocytes
Macrophages
Keratinocytes
Fibroblasts
Endothelial cells
Myofibroblasts
Inflammatory
Migratory/proliferative
Remodeling
Hemidesomosome break-down
keritinocyte migration
Hours

- Coagulative phase:

- Tissue injury

- Leakage of blood constituents into the wound

- Activation of clotting cascade

- Clotted blood is abundant in platelets

Matrix for cell Rich source of

-Adhesion -Growth factor

-Migration -Pro in
fl
ammatory cytokines

- Mediate recruitment of in
fl
ammatory cells and
fi
broblasts into the wound site
Brief overview of phases of wound h heal healing

Brief overview of phases of wound healing
-Early in
fl
ammatory changes:

-Local activation of innate immune function and chemoattraction

-Early in
fl
ux of PMNL followed by invasion of monocytes

-These monocytes di
ff
erentiate into tissue macrophages

-Role of in
fl
ammatory in
fi
ltrates:

Combat invading microbes

Release cytokines and growth factors which play a critical role in initiation of
proliferative phase of skin repair esp. IL-1, IL-6, VEGF, TNF, TGF-beta

- Proliferative phase:

- Granulation tissue covers and
fi
lls the wound area.

- It consists of invading macrophages,
fi
broblast, endothelial cells(act as vessels precursors)

- Provisional extracellular wound matrix facilitates cell adhesion, migration and proliferation

- Component of provisional extracellular matrix are:

Fibrin

Fibronectin

Vitronectin

Collagen type III

Tenasin


- Re-epithelialization:

- At the wound edge epidermal-mesenchymal interaction

- stimulates keratinocyte proliferation and migration

- re-epthelialization of wound surge

- Upon completion of re-epithelialization cell proliferation and neovascularization ceases
and scar tissue forms and wound enters remodelling or maturation phase.

- Maturation and remodelling phase:

- This phase lasts for several months and is characterised by:

Balance between the synthesis of new components of the scar matrix and their degradation
by proteases

Regression of vascular structures

Transformation of
fi
broblast into myo
fi
broblast

Substitution of provisional extracellular matrix with permanent collagenous matrix

Final resolution of in
fl
ammatory response

- Cellular component

- Chemical mediators

- Growth factors and their receptors

- Extracellular matrix

- Integrins

- Proteases
Various components involved in wound healing:

Components involved in wound healing

Cellular component:
- Keratinocytes

- Endothelial cells

- Leukocytes

PMNL

Blood monocytes

Tissue macrophages

T-cell

Mast cells

- Platelets

- Fibroblast

- Stem cells

- Injury > Keratinocytes at wound edge activated within hours due to alteration in their calcium ion :
magnesium ion ratio

- Activated keratinocytes undergo marked phenotypic and functional alteration to initiate their migration:

Flattening and elongation of keratinocyte

Formation of lamelipodia (aid in cell movement)

Detachment of hemidesmosomes

Migrating keratinocytes express:

MMP: Degrades basement membrane and interstitial collagen

Urokinase type plasminogen activator: enhances keratinocyte migration via inducing hypoxia

Keratinocytes:
Components involved in wound healing : Cellular component

- Replacement of keratinocyte collagen binding receptor with new integrins (alphaV-beta5)
which allows the keratinocytes to adhere to newly formed provisional matrix (
fi
brin,
fi
bronectin, vitronectin). This change is induced by TGF-beta 1.

- Keratinocytes do not express
fi
brin speci
fi
c integrin (alphaV-beta6) and hence instead go
invading the
fi
brin clot the migratory cells dissect the
fi
brin clot from the wound bed.

-
Components involved in wound healing : Cellular component- Keratinocytes

- Markers of activated keratinocytes in wound healing are Keratin6 and 16 (K6 & K16)

- Important GFs include:

Keratinocyte GF/ FGF-7 :

Hepatocyte GF

Epidermal GF

TGF-alpha:induces hsp 90 alpha which promotes epidermal and dermal cell migration

TGF-beta
Components involved in wound healing : Cellular component- Keratinocytes

Mechanisms involved in matrix degradation during keratinocyte migration.

- Precursor for new blood vessels during neoangiogenesis.

- Activated and proliferating endothelial cells express alphaV-beta3 integrin

- Neoangiogenesis within the wound is of two types:

Angiogenesis Vasculogenesis

Sprouting of capillaries from Mobilisation of bone marrow derived

existing blood vessels endothelial progenitor cell

Endothelial cells:

- Innate immunity induces angiogenesis at wound site

- Important angiogenic mediators include:

VEGF-A

IL-6

IL-8

TNF

- ECM degradation during angiogenesis occurs vis MMP, cysteine proteases and serine proteases.
Components involved in wound healing : Cellular component-Endothelial cell

Clinical appearance of a highly
vascularised wound bed
Immunohistochemical
staining demonstrating
endothelial invasion (CD31+
[green]) into a
fi
brin matrix
(red); white arrowheads
indicate sprouting capillaries.
Capillary sprouts invade the
fi
brin/
fi
bronectin-rich provisional wound matrix
and within a few days they organise into a
microvascular network throughout the
granulation tissue.

- PMNL:

- Within hours of injury PMNs transmigrate across the endothelial cell wall of capillaries

- The activation of transmigrated neutrophils produces and release:

IL-8 (proin
fl
ammatory)

TNF (proin
fl
ammatory)

GRO alpha (used by neutrophils to amplify their own recruitment)

MCP-1

- Recruited neutrophils control infections and help in debridement of devitalised tissue by
releasing:

ROS

Cationic peptides

Eicosanoids

Proteases like elastase, cathepsin G, proteinase 3, Urokinase type PA
Leucocytes:

- Blood monocytes and macrophages:

- Major source of chemotactic factors for monocyte:

Platelets trapped in
fi
brin clot

Hyper proliferative keratinocyte at wound edge

Fibroblast

Leukocytes

Macrophages

- Major chemotactic factors:

Various growth factors

Proin
fl
ammatory cytokines

Chemokines:

MIP-1 alpha

MCP-1

RANTES

Fractalkine
Components involved in wound healing : Cellular component-Leukocytes

- Macrophages:

- Macrophages at wound site regulate:

Angiogenesis

Recruitment and activation of immune cells

Synthesis of ECM molecules

Phagocytosis

This regulation is mediated by various growth factors produced by macrophage:

TGF-beta

TNF

PDGF

bFGF

VEGF

Types of macrophages

M1 or Classically activated M2 or Alternatively activated

-Present in early wound changes. Present in late wound changes.

-Proin
fl
ammatory activity. Anti-in
fl
ammatory activity

-Promotes Type 1 immune response Resolves in
fl
ammation and promotes
repair

-Mediatedby: Mediatedby:

IFN-gamma IL-4

TLRmediatedtriggers IL-13

- T-Cells:

- Most frequent leukocyte subset in the human skin wound during the phase of tissue remodelling
(maturation).

- CD4+ Tells can di
ff
erentiate into di
ff
erent subsets thereby in
fl
uencing the wound microenvironment by
secreting distinct cytokine pro
fi
le which in
fl
uence macrophage function and angiogenesis.

- Th 1 cells secrete INF-gamma

- Th 2 cells secrete IL-4, IL-13

- Mast cells:

- Source of prostaglandins, biogenic amine, pro and anti-in
fl
ammatory cytokines which in
fl
uence
in
fl
ammation, tissue modulation and vascular modelling.

- After injury
fi
broblast next to the site of injury become activated, di
ff
erentiate into myo
fi
broblast and
reconstitute new extra cellular matrix

- Conversion to myo
fi
broblast is mediated by:

TGF beta 1

ECM proteins

Mechanical tension

- Following closure of wound healing myo
fi
broblast undergo:

Apoptosis

Reverse di
ff
erentiation into
fi
broblast
Fibroblast:

- Principal stem cells capable of participating in epithelialisation after cutaneous injury are
present at:

Interfollicular epidermis

Within the bulge area at attachment site of arrector pili muscle

Above bulge (isthmus)

- Keratinocytes which can be activated for regeneration are:

Interfollicular epidermal stem cells

Transient amplifying cells

Easy di
ff
erentiated cells
Stem cells:

GROWTH FACTORS INVOLVED IN WOUND HEALING
Growth factor Abbreviation Source Functions
Platelet-derived growth factor PDGF Platelets, keratinocytes, fibroblasts, endothelial
cells, perivascular cells
Fibroblast proliferation, chemotaxis & collagen
metabolism; angiogenesis
Transforming growth factor-β TGF-β Platelets, keratinocytes, fibroblasts, endothelial
cells, macrophages
Fibroblast proliferation, chemotaxis & collagen
metabolism; angiogenesis; immunomodulation
Transforming growth factor-α TGF-α Platelets, keratinocytes Keratinocyte proliferation & migration
Epidermal growth factor EGF Platelets Keratinocyte proliferation & migration
Interleukins IL-1, IL-10 Leukocytes, keratinocytes Fibroblast proliferation; proinflammatory (IL-1);
anti-inflammatory (IL-10)
Tumor necrosis factor TNF Leukocytes, keratinocytes Promotes inflammation
Connective tissue growth factor CTGF Fibroblasts, endothelial cells Fibroblast proliferation, chemotaxis & collagen
metabolism
Fibroblast growth factor FGF Keratinocytes, macrophages Fibroblast & epithelial cell proliferation; matrix
deposition, wound contraction; angiogenesis
Keratinocyte growth factor KGF Fibroblasts Keratinocyte proliferation
Insulin-like growth factor 1 IGF-1 Fibroblasts Keratinocyte proliferation & differentiation
Hepatocyte growth factor HGF Fibroblasts, macrophages Keratinocyte proliferation
Vascular endothelial growth
factor
VEGF Platelets, keratinocytes, macrophages,
neutrophils
Angiogenesis; vascular permeability; macrophage
chemotaxis

- Component of ECM varies continuously as
the healing process evolves.

- In
fl
ammatory phase:

- Initial wound matrix consists of :

Blood vessels

Fibrin

Fibronectin

- This matrix provides a substrate for the
migration and in-growth of various cells
types like macrophages,
fi
broblast
Extracellular matrix:
Component involved in wound healing
- Proliferative phase:

- Granulation tissue formed which acts as
provisional matrix and consists of:

Vitronectin

Tenasin

Glycosaminoglycans

Proteoglycan

Type III. And VI collagen

Thrombospendin 1,2

- Maturation phase:

- Type I collagen increases in amount
resulting in increased wound tensile
strength.

- Transmembrane cell surface receptors.

- Heterodimer consisting of alpha and beta subunits.

- Recognise and bind ECM proteins.
Component involved in wound healing
- Proteases:
- Enzyme that cleave peptide bonds at speci
fi
c site along polypeptides

- Most crucial proteases for skin repair are:

Serine protease

Metalloproteinases

- Involved in:

Matrix degradation

Growth factor activation

Antimicrobial activity

- Integrins:

-Intentions of Healing
-Primary Intention healing:

-Wound closure by approximating the wound edges using side-to-side closure/
fl
aps/grafts

-Secondary intention healing:

When an acute wound is allowed to heal on its own.

Fully re-epithelialised wound
six weeks following surgery.
Three weeks following
surgery. Abundance of pink–
red granulation tissue.
Surgical wound immediately
following Mohs micrographic
surgery; a semi-occlusive
dressing will be applied.

-Tertiary intention healing:

Wounds that are closed with the goal of primary intention healing, but dehiscence occurs and
wound is allowed to heal with secondary intention.

Dehiscence of a surgical excision
that was closed primarily.
Same wound 1 month later, following
second intention healing.

- Post surgical defects that are clean and
free of debris

- Aseptically placed suture

Provide hemostasis

Decrease possibility of wound infections

Improve ultimate cosmetic result

- Sutures removal is followed by the use of
external splinting tape or tension relieving
dressings which supports the tissue

- Enables favourable collagen remodelling

- Limit scar formation and hypertrophy.
First intention healing Second intention healing
- Defects following cutaneous surgical
techniques like:

Tangential biopsy

Cryosurgery

Lazer surgery

Excision and curettage

- Moisture at the wound bed is the key to
optimal spontaneous secondary intention
healing.

- Semiocclusive dressings with topical
application of ointment directly on the wound
is the treatment of choice in these wounds.

- Factors in
fl
uencing wound repair:

- Systemic:

- Most common

Venous insu
ffi
ciency

Advanced age

Atherosclerosis

Diabetes Mellitus associated
microangiopathy

- Less common:

Vasculitis

Hyper coagulability

Malnutrition

Concomitant treatment with drugs
likehydroxyurea,immunosuppressants.
Impaired wound healing:
- Local factors:

Inadequate blood supply

Necrotic tissue

Increased proteolytic activity

Mechanical irritation

Pressure

Bacterial components

Local toxin

Growth factor de
fi
ciencies

- May be a result of impaired process of:

In
fl
ammation

Angiogenesis

Re-epethelialization

Wound remodelling

- Biology of chronic wounds:

Decreased proliferation of
fi
broblast,
endothelial cells, keratinocytes

Fibrin accumulation forms complex that
bind/inactivates other molecules like
growth factors.

Excess proteases—MMP 1,8,9
Chronic wounds:
Increased levels of:

- gamma and beta chain of
fi
brinogen

- Vitronectin

- Fibronectin

- Lumina

- Alpha 2 HS glycoprotein

- Olfactomedin-4— found exclusively
in non healing wound

Keratinocytes migration failure across
wound bed despite hyper plastic
epithelium

Microbial colonisation of wound

- Infection-related

Bacterial

- Erysipelas bullosa, Necrotizing
fasciitis

Sexually transmitted anogenital
ulceration

- Syphilis

- Granuloma inguinale

- Lymphogranuloma venereum

- Chancroid

Atypical mycobacterial

-Leprosy

-Buruli ulcer

-tuberculosis

Differential diagnosis of chronic wounds
Viral:

- Herpes simplex

- Varicella zoster

- Cytomegalovirus

Fungal:

- Bullous tinea pedis,

- Chromoblastomycosis,

- Sporotrichosis,

- Histoplasmosis,

- Bastomycosis

Protozoan:

-Leishmaniasis,

-Amoebiasis

- Medication-induced

Hydroxyurea

Methotrexate

Chemotherapeutics Immunosuppressives

Bacillus Calmette-Guerin vaccination

- Malignancy-related

Internal malignancy metastasis

Cutaneous malignancy

- Medical conditions

Diabetes mellitus

Neuropathic condition

Hypertension (Martorell ulcer)

Blood disorders

Polycythemia vera

Sickle cell anemia

Thrombocytopenia

- Autoimmune conditions

Scleroderma

Rheumatoid arthritis

Cutaneous lupus erythematosus

- Nutrition

- Pressure

- Primary skin conditions

Sarcoidosis

Pyoderma gangrenosum

Panniculitis

Bullous diseases

SJS and TEN

-Substance abuse related

Skin-popping

Vasoconstrictive cocaine

Bacterial embolism

-Vascular

Venous leg ulcers

Chronic venous insu
ffi
ciency

Congenital valvular insu
ffi
ciency

Trauma-related valvular insu
ffi
ciency

Thrombus-related valvular
insu
ffi
ciency

Arterial leg ulcers
- Atherosclerosis-related

- Embolism-related

Thromboangiitis obliterans

Vasculitis

Small-vessel vasculitis:

- Vasculopathy

Hypercoagulopathic disorders

DIC

Cholesterol emboli

Warfarin-induced necrosis (and heparin necrosis)

-Trauma

-Factitial

- Most common types of lower extremity ulcer are:

Venous leg ulcer (70%-80%)

Arterial ulcer (25%)

Diabetic foot ulcer (5%)
Leg Ulcers

Ulcer type Location Clinical appearance Associated symptoms
Venous
leg ulcer
Gaiter region of the lower
leg (midcalf to 1 in inferior
to the malleolus)
Single or multiple lesions; irregularly
shaped and shallow; commonly
with granulation and fibrinous
tissue and rarely with necrotic
tissue; lower extremity edema;
venous eczema, hemosiderin
deposition, or lipodermatosclerosis;
inverted champagne bottle
appearance of the lower leg
Pain may or may not be present;
aching in the legs after long
periods of standing; leg
heaviness and swelling
Arterial ulcer Distal extremities and sites
of trauma, such as bony
prominences
Sharply demarcated borders; dry,
necrotic wound bed; sparse
granulation tissue; signs of arterial
insufficiency, such as cool extremities
and poor peripheral pulses, hair loss,
atrophic skin, and delayed capillary
refill time
Ulcer pain, often severe;
claudication (leg pain with
exercise or at rest); pain that
worsens with leg elevation and
improves with dependency
Diabetic
foot ulcer
Plantar surfaces and sites
of repetitive trauma and
increased pressure
Often with punched out borders; may
be associated with callus, foot
deformity, or limited joint mobility;
pink, warm, dry skin; signs of fissuring
and skin breakdown
Distal anesthesia or paraesthesia
consistent with diabetic
neuropathy; claudication

Venous ulcer
Arterial ulcer
Diabetic foot ulcer

- Localised areas of tissue necrosis that result from unrelieved pressure, leading to localised
tissue injury

- Risk factors:

Decreased level of consciousness

Malnutrition

Impaired mobility

Fecal incontinence
Pressure wounds
Fig4. Thedistributionofcommonpressureulcers.(ReproducedwithpermissionfromPhillips
TJ. Ulcers. Dermatology, vol 2. Philadelphia: Elsevier; 2008: p 1611.)
Table V. Pressure ulcer classification55
Stage I Nonblanchable erythema
Stage II Partial-thickness, shallow open ulcer with red pink wound bed without slough; may present as a blister
Stage III Full-thickness skin loss. Subcutaneous fat may be visible, but bone, tendon or muscle are not exposed;
slough may be present but does not obscure depth of tissue loss; may include undermining and tunneling
Stage IV Full-thickness tissue loss with exposed bone tendon or muscle; slough or eschar may be present; often
includes undermining and tunneling
Severity grading of pressure ulcers

- Small-vessel vasculitis:

Leukocytoclastic vasculitis

Microscopic polyangiitis

Ganulomatosis with polyangiitis

ChurgeStrauss

Henoch Schonlein purpura

Cryoagglutination

Bechet’s disease

- Small-vessel vasculitis may be associated with super
fi
cial ulceration.

- Medium-sized vessel:

Polyarteritis nodosa

- Medium-vessel disease presents more commonly with nodules favoring the lower extremities,
livedo reticularis, and deep ulcers and poor prognosis.

Vasculitis

- Primary coagulopathy:

- Factor V Leiden de
fi
ciency (most
common)

- Protein C and S de
fi
ciency

- Antithrombin III de
fi
ciency

- Elevated factor VIII, IX, or X

- Dys
fi
brinogenemia

- Plasminogen de
fi
ciency
Vasculopathy
- Secondary Coagulopathy:

- Hospitalisation

- Trauma

- Surgery

- Immobilization

- Obesity

- Malignancy

- Smoking

- Pregnancy

- Medication

- Antiphospholipid antibody syndrome
- Coagulopathies can cause ulcers because of poor tissue perfusion.

- Common causes:

- Various primary skin conditions can result in unhealing chronic wounds:

Ulcerative pyoderma gangrenosum

Necrobiosis lipoidica

Sarcoidosis

Panniculitis (including erythema induratum)

Bullous diseases (bullous pemphigoid, pemphigus, bullous lichen planus, porphyria cutanea tarda)

Stevense Johnson syndrome and toxic epidermal necrolysis
Dermatoses as wounds:

- Pyoderma gangrenosum:

- Rare, ulcerating, neutrophilic dermatosis.

- Usually located on lower extremities, though they may be peristomal.

- Lesions begin as tender nodules, plaques or pustules that become painful ulcers with
undermined, violaceous borders and friable wound beds

- Ulcers are typically multiple, demonstrate pathergy (induction after trauma)

- An ideal dressing should:

- Soak up excess exudate from the wound surface

- Maintain a moist wound–dressing interface

- Not contain organisms or
fi
bres that may contaminate the wound

- Be impermeable to bacteria and provide sterile wound environment

- Cause minimal injury to healing tissue when removed

- Barely need changing

- Comfortable and conformal

- Cost e
ff
ective

- Long shelf life

- Non toxic and non sensitising

- Provided thermal insulation

- Allows gaseous exchange
The ideal dressing

- Majority of wound heal in a timely manner but a proportion of non healing wound need
wound bed preparation which consists of:

- Tissue debridement and wound cleaning

- Infection/ in
fl
ammation

- Moisture imbalance

- Epithelial edge assessment
Wound bed preparation:

- Removal of necrotic, contaminated or foreign material from a wound or area adjacent to the wound.

- 5 types of debridement techniques:

1. Surgical

2. Mechanical

3. Enzymatic

4. Biological

5. Autolytic

- 1. Surgical debridement:

Fastest and most direct method of wound debridement.

- 2. Mechanical debridement:

Done by using dry to wet dressing in wounds with signi
fi
cant necrotic tissue.

Does not distinguish between viable and non viable tissue
Tissue debridement:

3. Enzymatic debridement:

Topical application of an enzymatic agent can be used to supplement autolytic debridement

Only enzymatic agent approved for this purpose by FDA is Collagenase (SantylR).
The Unna boot is a type of compression bandage which has been used for many years in the treatment of stasis ulcers.
It was originally a cotton bandage impregnated with zinc oxide, gelatin and glycerin paste.
Figs. 4.5A and B. Enzymatic debridement using Papain, collagenase dressings. The
photograph is before and after 10 days of papain dressing.
Applied in a semirigid state, Unna boot confers the dual advantage of compression along with the moisture retentive
properties of an occlusive dressing. It should be applied by qualified medical personnel and changed at least weekly.
Nowadays, flexible compression bandages are more preferred (when compared to the rigid nature of Unna's boot).
They come in different varieties—elastic/inelastic, single/multilayered, long- or short-stretch compression, etc. The
major concern is in identifying how much tension is needed while prescribing elastic compression bandages.7
Enzymatic debridement using Papain, collagenase dressings. The photograph is before
and after 10 days of papain dressing.
Dressings in Dermatosurgery
The Unna boot is a type of compression bandage which has been used for many years in the treatment of stasis ulcers.
It was originally a cotton bandage impregnated with zinc oxide, gelatin and glycerin paste.
Figs. 4.5A and B. Enzymatic debridement using Papain, collagenase dressings. The
photograph is before and after 10 days of papain dressing.
Applied in a semirigid state, Unna boot confers the dual advantage of compression along with the moisture retentive
properties of an occlusive dressing. It should be applied by qualified medical personnel and changed at least weekly.
Nowadays, flexible compression bandages are more preferred (when compared to the rigid nature of Unna's boot).
They come in different varieties—elastic/inelastic, single/multilayered, long- or short-stretch compression, etc. The
major concern is in identifying how much tension is needed while prescribing elastic compression bandages.7
The authors have used papain dressings and amniotic membrane dressings to good effect in leg ulcers (Figs. 4.5 and

- 4. Biological debridement:

Most commonly use species is green bottle
fl
y (Lucilia sericata) used in chronic wounds.

Maggots digest necrotic tissue via collagenase and trypsin like enzymes.

These also exhibit antimicrobial e
ff
ect.

- 5. Autolytic debridement:

Occlusive dressing provides a moist wound environment which promotes the lytic activity of
enzymes present in the accumulated wound
fl
uid.

- It is a part of local wound care and involves removal of loose debris from the wound surface.

- An optimal wound cleanser has:

Low cytotoxicity

water/isotonic normal saline(0.9%NaCl)

Dilute acetic acid

- 3 methods of wound cleansing:

1. Compresses:

Gauzes soaked and squeezed so that no excess
fl
uid is present are used to clean wound
surface

2. Soaking:

Saturated gauze is used.

3. Irrigation:

Can cause trauma to wound bed and hence not recommended for deep wound as
fl
uid can
get retained within a pocket in wound.
Wound cleansing:

- Bacteria delays wound healing by forming
a bio
fi
lm.

- Prevention:

Topical antibiotics/Systemic antibiotics

Debridement

Antimicrobial dressings
Infection and inflammation:
Bio
fi
lm formation. Colonies of microorganisms with
a surrounding glycocalyx. SEM, scanning electron
micrograph

- This includes assessment and management of wound exudates.

- Acute wound
fl
uid: Chronic wound
fl
uid:

Rich in cytokines and growth factors. Rich in proteases and proin
fl
ammatory cytokines
Promotes cell growth Inhibits cell growth.

Bene
fi
ts from contact with wound
fl
uid Does not bene
fi
t from contact with wound
fl
uid

-
Moisture imbalance:

- Moist wound environment assists reparative process via suppression of tissue desiccation and crust
formation.

- Extra moisture at wound site can hinder healing and can damage peri-wound skin.

- Lack of moisture impairs keratinocyte migration required for re-epithelialization.

A scab is allows the surface to dry out, thus forcing the epidermis to grow under the dry
wound surface. Keratinocytes secrete a proteolytic enzyme which dissolves the base of the
scab; migration ceases when cell–cell contact occurs.

Thicker the scab formed deeper the migration is.
Wound bed preparation:Moisture imbalance:

- Assessment of the non advancing edge and proper use of therapies to advance wound edge.

- Considered that the wound and its epithelial edge can tolerate the trauma that comes with
removal of adhesive dressing.

- Keratinocytes from edge of chronic wound often abnormally express c-myc and treatments such
as debridement which reverse or remove this biomarker can promote keratinocyte migration
Epithelial edge assessment:

-Made of materials like cotton, silk, linen, cellulose, etc
.

-Materials like white petrolatum, antibacterial agents like povidone-iodine, chlorhexidine or balsam of
Peru may be impregnated in the conventional dressings, depending on the indication
.

-Usually a ‘layered’ or composite dressing which is either a ‘pressure’ or ‘non-pressure’ dressing
.

-The 3 layers commonly seen are:

1. A contact interface laye
r

2. The absorbent laye
r

3. The outer ‘wrap’
.

Traditional or conventional wound dressings:

-The middle layer:

Absorb the exudate
s

Mould to the shape of the
wound.

- Composed of materials
like cotton pads or gauze
.

-The contact layer
:

Direct contact with the wound
.

Permeable to
fl
uids

Non adherent.

E.g.
:

- layer of antibiotic ointment,

- contact layer of nonadhesive
material, such as paraf
fi
n gauze
or antibiotic impregnated tulle
.

-The outer layer
:

Secure the dressing in place.

Each layer should be in close
contact with the adjacent layer
with no gaps or air pockets
.

- Like a tape or a roller bandag
e

- In pressure dressings:

- More bulk is added to the absorbent layer with the aim of creating hemostasis.

- Used on scalp and digits.

- Applied immediately after a surgical procedure and changed in 24 hours.

- Can result in schema and necrosis if extensive pressure is applied.

- Antimicrobial dressings

- Occlusive dressing

- Absorbant dressing

- Moist dressing

- Surgical dressing
Modern Dressings:

- Antiseptic impregnated dressings:

Broad spectrum non speci
fi
c

Less associated with resistance

e.g: Silver
Antimicrobial dressing:
- Antibiotic impregnated dressings:

These are anti bacterial agents

Associated with:

- Bacterial resistance

- Risk of allergic contact dermatitis

e.g.: Mupirocin, Retapamulin, Fusidic acid
- These dressings reduce the need for frequent topical application and dressing change.

DRESSINGS THAT CONTAIN ANTISEPTICS
Antimicrobial agent Examples of dressings Coverage spectrum Advantages
Silver Acticoat® Flex 7 Silver,
Actisorb® Silver 220,
Algicell® Ag (alginate),
Aquacel® Ag, Contreet®
Biatain Ag Foam, ColActive®
Plus Ag, Mepilex® Ag,
PolyMem® Silver, SilvaSorb®
(hydrogel), Silvercel®
(alginate), Silverlon®,
UrgoTul® Ag/Silver,
UrgoTul® SSD
Broad-spectrum
antibacterial, including
MRSA and VRE
Release antiba
silver for 3–7
Appear to dec
matrix metal
are upregula
chronic wou
Microbial resis
Variety of prod
different wou
Infrequent app
Chlorhexidine or
polyhexamethylene
biguanide (PHMB), a
chlorhexidine derivative
Bactigras™ (chlorhexidine),
Kendall™ AMD foam (PHMB),
Kerlix™ AMD gauze (PHMB)
Broad-spectrum Low tissue tox
Different forms
foam, ribbon
Comforting so
painful woun
Povidone-iodine*
Cadexomer-iodine
polymer*
Inadine®, Betadine® cream
applied to gauze, Iodoflex™,
Iodosorb®
Broad-spectrum
antimicrobial – bacteria,
fungi, viruses
Less irritating
alone
Cadexomer-io
not inhibit w
Honey Activon Tulle, Medihoney®
Calcium (alginate, hydrogel)
Broad-spectrum
fungi, viruses
Low tissue tox
Autolytic debri
Methylene blue and
gentian violet
Hydrofera Blue® Broad-spectrum
MRSA and VRE, and
anti-candidal
Less irritating
Good absorpti
cavity woun
Hypertonic saline Mesalt® Broad-spectrum Less irritating
DRESSINGS THAT CONTAIN ANTISEPTICS
al agent Examples of dressings Coverage spectrum Advantages Disadvantages
Acticoat® Flex 7 Silver,
Actisorb® Silver 220,
Algicell® Ag (alginate),
Aquacel® Ag, Contreet®
Biatain Ag Foam, ColActive®
Plus Ag, Mepilex® Ag,
PolyMem® Silver, SilvaSorb®
(hydrogel), Silvercel®
(alginate), Silverlon®,
UrgoTul® Ag/Silver,
UrgoTul® SSD
Broad-spectrum
MRSA and VRE
Release antibacterial levels of
silver for 3–7 days
Appear to decrease the levels of
matrix metalloproteinases that
are upregulated in nonhealing,
chronic wounds
Microbial resistance is rare
Variety of products available for
different wound situations
Infrequent application required
Silver may stain tissu
(localized argyria)
Relatively expensive
Slows acute wound
e or
thylene
HMB), a
e derivative
Bactigras™ (chlorhexidine),
Kendall™ AMD foam (PHMB),
Kerlix™ AMD gauze (PHMB)
Broad-spectrum Low tissue toxicity
Different forms available, including
foam, ribbons and gauze
Comforting so recommended for
painful wounds
May cause stinging a
ICD
Cytotoxicity – cornea
ear (in the setting
tympanic membran
rupture), and cartil
Systemic and local
hypersensitivity rea
dine*
iodine
Inadine®, Betadine® cream
applied to gauze, Iodoflex™,
Iodosorb®
Broad-spectrum
fungi, viruses
Less irritating to skin than iodine
alone
Cadexomer-iodine polymer does
not inhibit wound healing
May cause stinging
ICD, ACD
Povidone-iodine can
wound healing

Antimicrobial Dressings:
SLIVER DRESSINGS
Silvercel®
PolyMem®
MAX® Silver
Acticoat® Flex 7 Silver,
ColActive® Plus Ag
Restore® Silver.
CHLORHEXIDINE DRESSING

- These are also known as moisture retentive dressings or passive dressings

- These are of 6 categories:

Alginates

Hydrogels

Hydrocolloids

Films

Foams

Hydro
fi
bers

Occlusive dressings:

Consist of a hydrophilic
foam with a hydrophobic
backing, which can
prevent leakage, provide
a barrier against bacterial
penetration, and provide
the moist environment.
Ideally, once a foam
dressing has absorbed
some amount of exudate,
it should be able to retain
that
fl
uid, even if exposed
to pressure. Change in 1-3 days
96% of its content
is water
Provides poor bacterial
barrier

Composites
The designs of occlusive dressings are constantly changing with the
goal of improved and simplified care for a greater range of wounds.
Several new types of composite dressings, which combine two or more
types of semi-occlusive dressings into one product, are commercially
available. They have three components: (1) a semi- or non-adherent
layer that contacts the wound (like a hydrogel, hydrocolloid, foam or
alginate; Fig. 145.10); (2) an absorptive layer; and (3) an outer layer
(like a film with an adhesive border). This maximizes the efficiency and
comfort of the dressing by expanding absorbency as well as lessening
the chance of maceration50
. Other features include the lack of need for
secondary retention dressings and better waterproof coverings, which
enable the patient to shower or bathe.
Dressings That Reduce Wound Protease Levels
Matrix metalloproteinases (MMPs) are a family of proteolytic enzymes
that play a role in cellular migration during the inflammatory phase of
healing and whose levels are elevated in non-healing chronic wounds
(see Ch. 141). Dressings composed of a mixture of extracellular matrix
proteins, bovine collagen, and oxidized regenerated cellulose have been
designed which act as a substrate (sink) for MMPs51
. In addition, the
enzymatic activity of MMPs is reduced via ion exchange.
ADVANCED WOUND THERAPIES
particles to the continuous medium and to the proportion of water
within that medium. This property accounts for the absorptive and
expansive capacity of colloid gels, which function as a semipermeable
membrane. Gel swelling occurs because the particle concentration of
the gel is usually higher than that of the surrounding medium, thereby
drawing water from the surroundings into the gel.
Hydrocolloid dressings were first employed as ostomy products and
are now available in multiple forms. The most commonly used hydro-
colloid dressings (e.g. DuoDERM®) are available as sheets with an inner
adhesive layer consisting of a hydrophilic colloid base that is a mixture
of pectin, karaya, guar or carboxymethyl cellulose plus an adhesive con-
taining polyisobutylene, styrene isoprene, or ethylene vinyl acetate (Fig.
145.9). The outer layer is composed of a thin semipermeable material
such as polyurethane. A gel is formed in the presence of wound exudate,
and as a unit, the dressing is semipermeable to water vapor and gases45
.
Another type of hydrocolloid dressing is a synthetic, non-adherent,
high-density plastic woven polymer (e.g. N-Terface®). Fluid is able to
flow through this matrix to be absorbed by an overlying dressing
without adherence to the new epithelial surface.
Advantages/disadvantages
When in sheet form, these dressings can be cut and conformed to the
shape of the wound. They are waterproof and adhere directly; as a
result, they do not require a secondary dressing. In addition, these
dressings have a cushioning or pressure-relieving effect (especially at
bony sites), which increases as the dressing absorbs exudate. The result-
ing colloidal gel that forms prevents the dressing from adhering to the
wound base. Accumulation of the exudate itself in a moist, semiperme-
able environment becomes a source of phagocytic cells and endogenous
enzymes. This feature, along with the gel, results in autolytic debride-
ment that can be washed away with saline irrigation of the wound
Fig. 145.9 Hydrocolloid dressing placed over a healing wound on the ankle.
This example is DuoDERM®.
Fig. 145.10 Choice of dressing based on wound depth and exudate. Courtesy,
Gregg M Menaker, MD.
CHOICE OF DRESSING BASED ON WOUND DEPTH AND EXUDATE
Wound
depth
Wound drainage
Foam
Hydrocolloid
Alginate
Film
Gel
Thin Thick
Fig. 145.7 Hyd
A Hydrogel she
B Premixed am
hydrogel.
A
CHAPTER
145
Dressings
Fig. 145.7 Hydrogels.
A Hydrogel sheet.
B Premixed amorphous
hydrogel.
A
B
Fig. 145.8 Collagen–alginate complex dressing. Alginate dressings have
hemostatic effects and can be used post
N
1
Fig. 145.5 A transparent film dressing is used to occlude a dry wound. This
example is Tegaderm™.
Fig. 145.6 Polymer foam dressing. It consists of hydrophilic foam with a
hydrophobic backing (pink).
dressing; permeability to water vapor; and tendency to reduce postop- Ideally, once a foam dressing has absorbed some amount of exudate, it
SEC TION
21
SURGERY
Fig. 145.5 A transparent film dressing is used to occlude a dry wound. This
example is Tegaderm™.
Fig. 145.6 Polymer foam dressing. It consists of hydrophilic foam with a
hydrophobic backing (pink).
dressing; permeability to water vapor; and tendency to reduce postop-
erative pain. It is also thought to enhance re-epithelialization of graft
donor sites, with a reported increase in healing rates of 25–45%36
. One
disadvantage of film dressings is that they are difficult to place properly,
requiring uniform tension on the film to prevent wrinkling and its
adherence to itself (similar to what is experienced with Saran™ Plastic
Wrap). As the film usually only adheres to intact skin, a 1–2 cm appli-
cation margin is recommended. In addition, due to shearing forces, it
is best to avoid using films on thin or fragile skin.
Films may adhere to the wound as drying progresses, thereby risking
disruption or stripping of the newly formed epithelium that is not yet
tightly bound to the underlying dermal layer. It is also possible to trau-
matize newly grafted skin tissue during dressing changes. For these
reasons, it is advisable to allow the film dressing to remain in place
until it spontaneously falls off, which occurs after 1–2 weeks37
. Any
wrinkling of the film during placement can create a conduit for bacterial
penetration and leakage of wound exudate. It is therefore recommended
that for exudative wounds the film have a complete 2–3 cm adhesion
margin to prevent this leakage.
Another disadvantage of film dressings is that they are non-absorbent;
therefore, wound fluid can accumulate under the dressing layer, espe-
cially with highly exudative wounds. This is often the case during the
first 7–10 days after the creation of a wound, with the adherent proper-
ties of film dressings making frequent changing undesirable.
Foams
Polymer foams are semi-occlusive, bilaminate, and polyurethane- or
silicone-based dressings. They consist of a hydrophilic foam with a
hydrophobic backing, which can prevent leakage, provide a barrier
against bacterial penetration, and provide the moist environment
afforded by films, but with the addition of some absorbency (Fig. 145.6).
The inner layer is composed of an absorbent, gas-permeable polyure-
thane foam mesh, which lies adjacent to the wound. The outer layer
is a semipermeable, non-absorbent membrane composed of polyure-
thane, polyester, silicone or Gore-Tex®, surrounded by a polyoxyethyl-
Ideally, once a foam dressing has absorbed some amount of exudate, it
should be able to retain that fluid, even if exposed to pressure. Some
brands are described as having such a quality.
Although very absorbent, there is a limit to the amount of wound
exudate this type of dressing can absorb. Therefore, it should be changed
every 1–3 days. The permeability of foams to both gas and water vapor
makes them suitable for mild to moderately exudative wounds, although
there are brands designed for heavily exudative wounds.
Silicone-based rubber foams, known as silastic foams, are composed
of a silicone mixture to which a stannous octoate catalyst has been
added. This type molds and contours to the shape of the wound and
therefore can be used for packing cavities or deep ulcers such as piloni-
dal sinuses. The additional advantages are absorbency, non-adherence,
increased comfort for the patient, a tendency to be less expensive,
and dressing changes that do not generally require skilled nursing
care38
.
The disadvantages of foam dressings are the inability to use them
with dry wounds, their opacity, which prevents visual monitoring of
the wound, and the need for frequent changing, perhaps as often as
every day. Infrequent changing could risk incorporation of the dressing
material into the wound itself. There is also the possibility of an unde-
sirable drying effect of the wound if drainage is insufficient to maintain
a moist environment.
Hydrogels
As their name implies, hydrogels are composed primarily of water – up
to 96% of the content. This dressing type consists of a cross-linked
hydrophilic polymer network composed of polyvinyl alcohol, polyacryl-
amide, polyethylene oxide or polyvinyl pyrrolidone; it is produced as
sheets, amorphous gels (pre-mixed or dry), or as impregnated dressings
(Fig. 145.7). Hydrogels are semitransparent (allowing visual inspection
of the wound), have a high absorptive capacity (between 100% and
Transparent
fi
lm
Hydro collide dressing
Polymer foam dressing
Hydrogel sheet
Collagen alginate complex dressing
In general, the sheet form of a hydrogel dressing is constru
sandwiching the hydrophilic polymer between two removab
sheets of polyethylene film, with some types containing a su
inner gel mesh. For application to the wound, the film on the
side is removed, leaving the outer film in place. With this m
application, the dressing is semipermeable to gases (including
and water vapor. If the outer film is also removed, then the
becomes permeable to fluid as well; as a result, exudate can p
secondary gauze dressing. The polymer sheets can be remove
without trauma to the wound bed.
The amorphous type of hydrogel is composed of a cornstarch-
polymerized compound that forms a gel upon hydration at the
its use. It is available commercially in a powdered or pre-mixe
is applied wet to the wound defect, requires a secondary outer d
and requires water application to the surface for removal.
One significant advantage of hydrogel dressings is a reduction
operative pain and inflammation. Another is that hydrogels ha
shown to accelerate the rate of wound healing when compared
A
B
Permitted amorphous hydrogel

eFig.145.2Apolymer
filmisusedtooccludea
woundthathasbeen
coveredbycotton
gauze.Courtesy,GreggM
Menaker,MD.
eFig.145.3Afoamdressing.
eFig
film
wou
cove
gau
Mena
eFig.
145.4
Example
of
a
collagen–alginate
complex
dre
can
be
used
to
pack
deep
wounds.
Courtesy,
Gregg
M
Menaker,
M
eFig.145.4 Exampleofacollagen–alginatecomplexdressing.The rope form
can be used to pack deep wounds. Courtesy,GreggMMenaker,MD.
A polymer
fi
lm is used to
occlude a wound that has
been covered by cotton
gauze
Collagen-alginate complex
dressing
Foam dressing

Online only content
A B C
Antibiotic ointment
applied over sutures
help tp prevent infection
and prevents contact
slyer from adhering
directly to the wound
Three layer of paper tape
comprise the contact layer
-Rolled gauze or cotton
dental roll can be used to:

Provide hemostasis

Aid conforming the
dressing to the wound

Absorbe excess exudate

-The entire dressing is
secured with additional
layers of tape
Online
only
content
B
infection
and
prevents
the
contact
layer
from
adhering
directly
to
the
dental
roll
can
be
used
to:
(i)
provide
pressure
for
hemostasis;
(ii)
aid
in
is
secured
with
additional
layers
of
tape.
Courtesy,
Gregg
M
Menaker,
MD.
C
45.3
A
foam
dressing.

- Combine two or more types of semiocclusive dressings.

- Expand absorbency and lessens maceration.

- No need for secondary retention dressings

- Better waterproof covering-enables the patient to
shower or bathe.

- They have three components:

Semi/non-adherent layer- contacts the wound. e.g.
hydrogel, hydrocolloid, foam, alginate

Absorptive layer

Outer layer:
fi
lm with adhesive border

e.g. Leukomed Tplus
Composite occlusive dressing:
Composite dressing with a pad and
a
fi
lm.

- Hand hygiene must be practised before and after the dressing change.

- The tape or adhesive portion of the previous dressing, is removed by pulling it parallel to the skin
surface and in the direction of hair growth.

- Alcohol wipes or nonirritating solvents help in removing the adhesive quickly and painlessly.

- The old dressing is removed and placed in the appropriate biomedical waste disposal bin. A
dressing should never be handled by an ungloved hand.

General Measures while Applying/Changing
Dressings:

- Clean the wound area with saline or antimicrobial solution; look for any signs of infection.

- In modern dressings, the sticky side of the dressing which adheres to the paper should sticks to
the wound.

- Tape used to secure the dressing, is placed at the center of the dressing and pressed down on
both sides, applying tension evenly away from midline.

General Measures while Applying/Changing Dressings

- An elastic adhesive bandage may be used to hold the dressings in place on mobile areas, or where
pressure is required.

-To avoid the formation of bubbles/air pockets while applying dressings use the proximal end of the
thumb forceps and move it from one side to the other end of the dressing (like applying butter with
a knife).

-The skin surrounding a highly exuding wound may be further protected through the use of
emollients (such as 50:50 mix of white soft para
ffi
n and liquid para
ffi
n) or the application of barrier
fi
lms.

-Hydrogel dressings have two removable thin sheets of polyethylene
fi
lm, For application to the
wound, the
fi
lm on the contact side is removed, leaving the outer
fi
lm in place. With this mode of
application, the dressing is semipermeable to gases and water vapour.

- If the outer
fi
lm is also removed, then the dressing becomes permeable to
fl
uid too.


-
CHOICE OF DRESSING BASED ON WOUND DEPTH AND EXUDATE
Wound
depth
Wound drainage
Foam
Hydrocolloid
Alginate
Film
Gel
Thin Thick

Leg Ulcers:

- Moisture retention can be best achieved by occlusive dressings preferably simple non-adherent
dressings.

- Provide strongest compression that maintains patient concordance. An ankle pressure of 30 to 40
mm Hg should be achieved

- Compression can be achieved by layered( single or multi) pressure dressings .

- Graduated compression stockings, can be worn independently

- Combining compression with occlusive dressings augments the healing rates of venous ulcers.
Choosing a suitable dressing:

- The NICE guideline development group recommend a dressing that promotes the optimum
healing environment rather than a speci
fi
c type of dressing

- A dressing that promotes warm, moist, healing environment should be considered for grade 2,
3 and four pressure ulcers.

- Hydrocolloid,
fi
lms and foam dressings prevent pressure ulcer

- Turning and repositioning, skin care, good nutrition and continence management are essential
for pressure ulcer healing.

- Gauze dressings should not be used in pressure ulcers.
Pressure sores:

-Dressings allow proper immobilisation and secure the grafts
and improving cosmetic outcome.

-Cyanoacrylate tissue glue:

Quick and e
ff
ective immobilization of donor grafts

Secures grafts over areas that are di
ffi
cult to treat, like
the genitalia, groin, eyelids, palms, and
fi
ngertips.

In split thickness grafting and suction blister grafting,
octyl cyanoacrylate gel can be used to secure the graft in
position in place of sutures.

-
Vitiligo surgery:
Choosing a suitable dressing: Fig. 4.7. Cyanoacrylate tissue glue.
The tiny droplets of octyl cyanoacrylate are expressed from the needle tip; broken further into even smaller droplets
by taking it on another sterile needle tip, and applied only at four points, at 12, 3, 6 and 9 o'clock positions between the
edges of the donor grafts and the recipient wells. The adhesion between the graft and the recipient wells start within
10 seconds and is complete within 1 minute of application. No dressing or immobilization is required in any patients.
Apart from the adhesive property, octyl cyanoacrylate also exhibits antimicrobial properties against staphylococci,
Pseudomonas, and E. coli.23
Alternatively, paraffin embedded nonadherent sterile gauze (Jelonet®
) can be applied as a primary dressing followed
by surgical pad and elastic adhesive dressings to immobilize the area (Fig. 4.8).
In split thickness grafting and suction blister grafting, octyl cyanoacrylate gel can be used to secure the graft in position
in place of sutures (Figs. 4.9A and B). Adhesive film dressings like Opsite®
can be used as secondary dressings over the
recipient site. Opsite is a transparent, adhesive film. The film is moisture vapor permeable, conformable and extensible
which is widely used to provide a moist wound environment for superficial wounds. Opsite provides moisture vapor
permeability, allowing the excess exudate to evaporate, helping to prevent skin maceration. The grafts can also be
placed in position using sutures or without sutures and further dressed with absorbent pads and hydrofilm dressings.
Lukomed T plus®
is a film dressing with absorbent pad which can be directly applied over a grafted site.
14
- 19-July-2019 10:25:15
Cyanoacrylate tissue glue
Figs. 4.9A and B. Tissue glue for securing grafts in SBEG, ultrathin epidermal grafting—
applied over the periphery of grafts to secure them in place.
Tissue glue for securing ultra thin
epidermal grafting

-Paraf
fi
n embedded non-adherent sterile gauze
(Jelonet®)
:

can be applied as a primary dressing followed by
surgical pad and elastic adhesive dressings to
immobilise the are
a

-Opsite:

It is a transparent, adhesive
fi
lm.

Moisture vapour permeable (prevents skin
maceration), conformable and extensible
.

-Lukomed T plus®
:

Film dressing with absorbent pad which can be
directly applied over a grafted site.
Fig. 4.8. Paraffin embedded nonadherent sterile gauze (Jelonet®
) can be applied as a primary
dressing in miniature punch grafting.
In cellular grafting techniques, primary dressing is done using collagen dressings. After applying the basal layer cell
suspension, collagen sheets are used as primary covers to create a biological environment (Fig. 4.10). Alternatively,
amniotic membrane can also be used (Figs. 4.11A and B). Mepitel dressing is also used in places where collagen sheets
are not available (Figs. 4.12A and B). This is then covered with a sterile pad and finally with Tegaderm (3M) dressing.
Nail Surgeries
In nail surgery, the postoperative dressings must have these properties: nonadherent, absorbent, perfectly fixed and
with adequate pressure to prevent bleeding.
Application of an antiseptic ointment covered with a paraffin embedded nonadherent sterile gauze (Jelonet®
,
Bactigrass®
, Sofratulle®
) as a first layer will protect the wound from drying and will allow easy and painless removal.
Mepitel®
is another nonabsorbent, porous, semitransparent flexible poyamide net, silicon- coated dressing useful as a
primary dressing in nail surgeries and cellular grafting surgeries in vitiligo.
Para
ffi
n embed non adherent sterile
gauze— JelonetR
Choosing a suitable dressing: Vitiligo surgery

Choosing a suitable dressing: Vitiligo surgery
16
- 19-July-2019 10:25:15
Figs. 4.11A and B. Amniotic membrane dressings in vitligo surgery.
Figs. 4.12A and B. Mepitel dressings.
Recently, authors have found a new self-adhesive bandage without any chemical adhesive namely Coban®
to be very
effective in nail surgeries. The advantage being nonallergic and can be easily reapplied if the patient feels the dressing
too tight without disturbing the inner layers of the dressing. It is a stretchable and self-adhesive dressing suitable for
pressure dressings and also provides effective hemostasis (Figs. 4.13A to D).
Figs. 4.11A and B. Amniotic membrane dressings in vitligo surgery.
Figs. 4.12A and B. Mepitel dressings.
Recently, authors have found a new self-adhesive bandage without any chemical adhesive namely Coban®
to be very
effective in nail surgeries. The advantage being nonallergic and can be easily reapplied if the patient feels the dressing
too tight without disturbing the inner layers of the dressing. It is a stretchable and self-adhesive dressing suitable for
pressure dressings and also provides effective hemostasis (Figs. 4.13A to D).
-In cellular grafting techniques
:

Primary dressing is done using collagen dressings after
applying the basal layer suspension

Amniotic membrane can also be used

Mepitel dressing is also used in places where collagen
sheets are not available. This is then covered with a sterile
pad and
fi
nally with Tegaderm (3M) dressing.
Collagen dressing
Amniotic membrane dressing in vitiligo
Mepitel

- The post operative dressings must have these properties:

Non adherent

Absorbent

Perfectly
fi
xed

Adequate pressure to prevent heeling.

- Layers of nail dressing:

- First layer:

Antiseptic ointment covered with para
ffi
n embedded non adherent sterile gauze.

Will protect the wound from drying

Allows easy and painless removal

E.g.: JelonetR, BactigrassR, SofratulleR

-
Nail surgery:

- Second layer:

Made of 3 or 4 layers of absorbent mesh gauze that will absorb exudate and bleed and
provide protection against trauma.

- Third layer:

Made of elastic adherent plate that will keep the surgical area secure and exert su
ffi
cient
pressure so that post -operative bleeding can be prevented.

- Care should be taken to leave the tip of the toes and the
fi
ngers uncovered so as to inspect for
cyanosis if the dressing of too tight

Choosing a suitable dressing: Nail surgery

Figs. 4.14 A to E. Nail dressing to provide protection to the wounds and the toes.
Figs. 4.14 A to E. Nail dressing to provide protection to the wounds and the toes.
• If the dressing is highly absorptive, then more frequent dressing c
and management of the cause of the exudate (such as infection).
l dressing to provide protection to the wounds and the toes.
Nail dressing to provide protection to the wound and toes

- Latest dressings in nail surgeries:

- New self adhesive bandage without any
chemical adhesive namely CobanR to be very
e
ff
ective in nail surgeries.

- Advantages of CobanR:

Nonallergic

Can be easily reapplied if patient feels the
dressing is too tight without disturbing the
inner layers of the dressing.

Stretchable

Suitable for pressure dressing
Figs. 4.13 A to D. Coban®
dressings in nail surgeries.
18
- 19-July-2019 10:25:15
18
- 19-July-2019 10:25:15
18
- 19-July-2019 10:25:15
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- 19-July-2019 10:25:15
CobanR dressing in nail surgeries

- Laser surgery:

- The dressing maybe open or close.

- Open dressing:

Wound is left alone after applying cream and ointment without covering it.

Application is repeated in frequent intervals.

- Closed dressing:

Any of the occlusive dressing, except alginate and hydro
fi
bers ,maybe used

Dressing is placed immediately after procedure and on postoperative day 1 and 2 the wound is
cleansed and the dressing is changed.

This replacement dressing remains in place till day 5, when the dressing is changed to an open
dressing.

- Hair transplant:

- Pressure dressing may be given on the donor site after hair transplant surgery.

- The recipient area is generally left uncovered with the newer techniques but sometimes non
adherent dressing may be given depending on the preference of the surgeon.

- Liposuction:

- Absorbent dressings are generally given on the incision sites to facilitate drainage.

- Patient may also be required to wear compression garments in postoperative period.

-Maceration of the skin surrounding a wound may occur, if a dressing with a low absorptive capacity
is used on a heavily exuding wound.

-If the dressing is highly absorptive, then more frequent dressing changes may be needed, in
addition to investigation and management of the cause of the exudate (such as infection).

-Use of a highly absorptive dressing on a dry wound may lead to disruption of healthy tissue on the
wound surface and cause pain on removing.

-Iodine containing dressings should not be used in young children, pregnant or lactating women, or
patients with known or suspected iodine sensitivity.

-As iodine is absorbed, caution must be taken when using these dressings in large wounds, wound
with cavities, patients with a history of thyroid disease.
Complications of wound dressing:

- PRP

- Topical growth factors

- Tissue-engineered skin equivalent or skin substitutes

Epidermal graft

Dermal replacement

Composite graft

- Negative pressure wound therapy

- Hyperbaric oxygen therapy

- Compression therapy
Advanced wound therapies:

- Platelet-rich plasma (PRP) is plasma which is rich in growth
factors and also referred to as autologous platelet gel
.

- Platelets are natural sources of growth factors (GFs) and play
a fundamental role in
:

hemostasi
s

wound healing/regenerative processes
.

It also contains plasma proteins like
fi
brin,
fi
bronectin and
vitonectin which act as scaffold for connective tissue and
epithelial migratio
n

PRP in wound healing:
• Chronic ulcers of various aetiologies35–41
• Acne scars or traumatic scars and contour defects of fac
• Skin rejuvenation of face.46–53
Statistically significant improvement in management of
the face have been seen. However study conducted by
fractional CO2 laser treatment did not produce statistical
side effects and a longer downtime.47
• Miscellaneous indications
• Striae distensae54–56
• Lichen sclerosus57
(A)Chronic nonhealing traumatic ulcer. (B) Chronic
nonhealing ulcer post three sittings of intralesional
PRP.
Platelet Rich Plasma
Figs. 10.14A and B. (A) Chronic nonhealing traumatic ulcer. (B) Chronic nonhealing ulcer
post three sittings of intralesional PRP.

Topical growth factors:
- Growth factors stimulate
fi
broblasts, promote angiogenesis, and encourage migration of
keratinocytes.

- A topical formulation of recombinant human PDGF, becaplermin (Regranex®) gel, has been shown to
increase the complete closure rate of diabetic foot ulcers by 43%.

- Its current FDA indication is for non-healing diabetic neuropathic foot ulcers.
Advanced wound therapies

-A true skin substitute provides both the physiologic and mechanical functions akin to an
autologous skin graft.

-Advantages:

No painful donor sites

Potential for providing coverage of large areas.

-Edge e
ff
ect: characterised by promotion of epithelialisation from the edge of the ulcer toward its
center, likely due to a release of cytokines in chronic wounds treated with engineered dressings.
Skin substitutes:

-There are currently three types of skin substitutes:

Epidermal grafts

Dermal replacements (acellular or cellular)

Composite grafts (with both an epidermal and dermal component)

-Tissue- engineered dressings can also be classi
fi
ed as :

Autologous

Allogeneic

Xenogeneic
Advanced wound therapies: Skin substitutes

STIMULATION OF TISSUE REGENERATION VIA CELL THERAPY
Chronic ulcer
Cell Culture
• Modification in vitro
• Propagation of cells
Tissue engineering
Combination of cells and/or
growth factors with synthetic
scaffold or biomaterial
Transplantation
of composite
graft
Local application
of isolated
hematopoietic
stem cells
Bone
marrow cells
Cell isolation
Biopsy
Local
application of
differentiated
cells
Keratinocytes
Fibroblasts
Adipose cells
Mesenchymal
stem cells

-Epicel® :

-Epidermal autograft

-Skin biopsy is obtained from the patient.

-The autologous keratinocytes are co-cultured with irradiated murine
fi
broblasts

-A 2-8 cells thick sheet of keratinocytes forms.

-This is attached to petrolatum gauze.

-The graft is then sutured in place and the gauze backing is removed at 1 week

-Disadvantages include:

Several-week period required to culture the keratinocytes

Graft fragility

Short shelf life

Cost of processing

-Other e.g.: Laserskin®, CeladermTM:
Epidermal grafts:

Epicel®


-Dermal replacement
:

-Xenogeneic
:

-Composed of porcine or bovine collagen
.

-Advantages:

Effect hemostasis

Provide immediate closure

Cosmetically acceptable scars with second
intention healin
g

Safety from potential human pathogen
transmissio
n

Adequate shelf lif
e

-e.g.: Oasis® Wound Matrix, EZ DermTM,
Biobrane® ,IntegraR
of both Laserskin® and Celaderm™ are limited, improved healing of
diabetic foot ulcers and venous leg ulcers was noted when compared to
saline gauze59
. These epidermal grafts are also used for partial- and
full-thickness burns.
Dermal replacements
There are two types of dermal replacements: xenogeneic and allogeneic
(Table 145.7). Neither of these is permanent: DNA analysis of wounds
after the application of non-autologous skin substitutes shows almost
complete disappearance of the grafted cells after two months60
. The
goal of these dermal grafts is to provide a temporary biologic dressing
in order to stimulate the healing process. They are placed over the
wound, extending slightly onto normal skin, and then bolstered into
place. Secondary dressings must be applied. The major component of
dermal replacements is collagen; other elements of the extracellular
matrix, e.g. glycosaminoglycans, may be included and in the case of
cellular products, fibroblasts.
Xenogeneic
Although other sources are available, xenogeneic grafts are usually
composed of porcine or bovine collagen (see Table 145.7). The advan-
tages of these products are: (1) their ability to effect hemostasis and to
provide immediate closure as well as cosmetically acceptable scars with
second intention healing; (2) safety from potential human pathogen
transmission due to their animal origin; and (3) an adequate shelf life,
facilitating off-the-shelf access.
Fig. 145.11 An acellular xenogeneic dressing. This particular wound matrix is
derived from porcine small intestine submucosa (Oasis®) and serves as a
dermal graft.
Oasis® Wound Matrix, EZ Derm™, and Biobrane® are examples
of acellular matrices derived from porcine collagen (Fig. 145.11).
They have significant elasticity, enabling a full range of motion of the
covered body part, and there is no requirement for dressing changes
once it has adhered to the wound bed. However, Biobrane® may
An acellular xenogeneic dressing. This
particular wound matrix is derived from
porcine small intestine submucosa (Oasis®)
and serves as a dermal graft.


-Allogenic
:

-Composed of cadaveric dermis or neonatal foreskin
fi
broblast
.

-Advantages are similar to xenogeneic graft but there is a risk of graft rejection due to T-cell
recognition of donor T-cell
.

-e.g.: AlloDermR, Graftjacket (both are FDA classi
fi
es banked human tissue for transplant
)

tiveness of HBOT68
. More studies are needed to examine the role of
HBOT in the treatment of chronic wounds and proper indications.
this sponge are human dermal fibroblasts that also produce multiple
matrix proteins and growth factors. As with all of the allogeneic and
Fig. 145.12 Example of an engineered composite (xenogeneic and
allogeneic) graft sutured into place (Apligraf®). Courtesy, Gregg M Menaker, MD.
Fig. 145.13 Negative pressure wound therapy. In negative pressure wound
therapy, a polyurethane (this patient) or polyvinyl alcohol foam is cut and
placed on the wound surface. The foam is then sealed over by a transparent
drape. A vacuum pump, connected via a plastic tube, provides a negative
pressure environment. The sterile polyurethane foam has large pores and
stimulates granulation
Example of an engineered composite
(xenogeneic and allogeneic) graft sutured
into place (Apligraf®)

This composite graft produces its own

matrix proteins and growth factors and, if
wounded, it can repair itself.

-This is a vacuum-assisted closure (VAC) system based on
the delivery of sub-atmospheric pressure to the wound
bed.

-A polyurethane or polyvinyl alcohol foam is cut and
placed on the wound surface.

-The foam is then sealed over by a transparent drape in
order to provide a closed air-tight system.

-A vacuum pump, connected to this space via a plastic
tube, provides a negative pressure environment.

-NPWT removes interstitial
fl
uid, stimulates angiogenesis,
and enhances circulation as well as lymphatic drainage.
Negative pressure wound therapy:
Fig. 145.12 Example of an engineered composite (xenogeneic and
Fig. 145.13 Negative pressure wound therapy. In negative pressure wound
therapy, a polyurethane (this patient) or polyvinyl alcohol foam is cut and
placed on the wound surface.The foam is then sealed over by a transparent
drape. A vacuum pump, connected via a plastic tube, provides a negative
pressure environment.The sterile polyurethane foam has large pores and
NPWT

- Patients are placed in a pressure chamber where they breath oxygen at one atmospheric
pressure.

- Systemic HBOT sessions last 45-120 minutes and are conducted once or twice daily for 20-30
sessions.

- Oxygenation of hypoxic tissue induces vasoconstriction which reduces oedema and congestion.

- At cellular level there is:

Increased
fi
broblast replication,

Collagen synthesis

Neovascularization

Regulation of growth factor.

-Response to HBOT: Transcutaneous oxygen levels measured in the peri-wound region both at
base-line and while breathing 100% oxygen; at least a doubling of the levels is preferred.
Hyperbaric oxygen chamber:

Compression therapy:
Short stretch (inelastic) bandages
:

-Advantages
:

Comfortable so better tolerate
d

Minimal interference with daily activitie
s

-Disadvantages
:

Some (e.g. Viscopaste®) can generate
high working pressur
e

Can lose compression after applicatio
n

Not good for highly exudative wound
s

Viscopaste®/Unna boot needs to be
applied by well-trained staff
Types of compression system:

- Long stretch (elastic) bandages:

- Advantages:

Base of the toes to knee
s

Low working pressur
e

High resting pressur
e

100–200% extensibilit
y

Can be applied as spiral or
fi
gure-of-
eigh
t

Inexpensive; washable and reusable
forms availabl
e

-Disadvantages
:

Tend to unrave
l

Do not provide a sustained
compression

Risk of incorrect applicatio
n

Can lose elasticity with continued us
e

Advanced wound therapies: Compression therapy

fibers. In contrast, inelastic bandages such as
stretch bandage (more commonly used in Euro
that resists lateral expansion of the calf musc
tions. Of note, contractions of the calf muscle
ates a propelling force to promote venous retu
Compression bandages may be composed o
multiple combined components. In a recen
stretch bandages were found to be as efficacio
of venous leg ulcers as more complex mul
systems, in both ambulatory and non-ambul
Cochrane reviews suggest that the evidence su
systems (over single-component systems) and
component (over those with an inelastic band
Compression devices
Intermittent pneumatic compression (IPC) d
pressure to the limb. IPC is a beneficial adjunc
pression in the treatment of venous leg ulc
ambulatory patients80,81
. When the calf muscl
use of a dynamic compression system is more
or abnormal pressure to the limb, compromised circulation, skin
breakdown, additional ulcer formation, or further limb deterioration
Fig. 145.14 Unna boot. Nonelastic compression therapy with a zinc-
impregnated compression wrap.
eFig. 145.3 A foam dressing.
eFig. 145.4 Example of a collagen–alginate complex dressing. The rope form
can be used to pack deep wounds. Courtesy, Gregg M Menaker, MD.
eFig. 145.5 Graduated compression stockings being applied.
Unna boot
Graduated compression dressings
Advanced wound therapies: Compression therapy

- Rook’s Textbook of Dermatology 9th Edition

- Bolognia’s Dermatology 4th Edition

- Fitzpatrick’s Dermatology 9th Edition

- ACS(I) Procedural Dermatosurgery

- Wound healing and treating wounds by Laurel M. Morton, MD, and Tania J. Phillips, MD
Chestnut Hill and Boston, Massachusetts
Reference:

Wound healing and dressing

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