Wound Management

Wound Types

 Traumatic Non-Traumatic
Pressure
Sores
Surgical
Skin Disorder
Diabetic
wounds
Infection
Malignant
Vascular lesion
Burns
 Wound Definition
Wound is defined as disruption
of
anatomic or functional
continuity of
living tissues
&
is the product of integrated
response
 Wound Definition

A wound is a physical trauma where the skin is

torn, cut or punctured.

a wound is considered as minor when it is:

superficial;
away from natural orifices;
there is only a minor bleeding;
it was not caused by a tool or an
animal.

Any other wound should be considered as severe.

 Wound Development:
Physiology of capillary
Flow
A. Forces moving the fluid outward from capillary
bed-
*Mean Functional Capillary Pressure =17.0mm of
Hg.
*Negative Interstitial Pressure =7.0mm of
Hg. =28.5mm of
Hg.
*Interstitial fluid colloid osmotic Pressure
B.=4.5mm of Hg the Fluid Inward from capillary
Forces Moving
bed-
* Plasma colloid osmotic Pressure =
28.5mm of Hg.
= 0.5mm of Hg.
e above factors are responsible
Net Outward Pressure=for
A-Bflow of fluid in the capillar
 Wound Development
 By the process of diffusion nutrients
and oxygen are delivered to the
tissues from the capillaries; during
which small amount of fluid enters in
to the surrounding interstitial
spaces. This is done by net outward
pressure of 0.5mm of Hg.
 Wound Development
 Subsequently, lymphatic system
returns this fluid back in to the
venous system.
 Venous system is easily impeded by
external pressure due to small
differential pressure, which depends
upon near total relief of pressure at
frequent intervals to avert anoxia.
 Pressure sore
Development
 When pressure over a given part of
the body exceeds the capillary
pressure at venous end, the blood
flow to the tissue stops; the tissue
becomes anoxic due to lack of
oxygen supply; and if anoxia
persists, necrosis sets-in.
 The whole process takes 1-6hrs
based on combination of factors.
 Pressure sore
Development
 Erythema BlistersBlister Rupture

Necrosis

Eschar
Formation
 Pressure sore
Development
Mechanism of Formation
 Pressure
 Friction by rubbing against bed sheet,
cast, brace, etc., or
 Prolonged exposure to cold.
 Any area of tissue that lies just over a
bone is more likely to develop a
decubitus ulcer.
 These areas include the spine, coccyx or
tailbone, hips, heels, and elbows.
 Pressure sore
Development
Person's body weight presses on the
bone, the bone presses on the tissue
and skin that cover it, and the tissue
is trapped between the bone structure
and bed or wheelchair surface.

The tissue begins to decay due to lack

of blood circulation & formation of
decubitus ulcer sets in.
 Stages of Wounds

Wounds are categorized according to severity

by the use of stages.

The staging system applies to burn wounds,

Decubitus ulcers and several other types of
wounds.
 Stage I

This stage is characterized by

• Skin is unbroken and wound is
superficial
• Would be a light sunburn or a first
degree burn as well as a beginning
Decubitus ulcer
• Burn heals spontaneously or the
Decubitus ulcer quickly fades when
pressure is relieved on the area.
 Key factors to consider in
Stage I wound
o Cause of wound and methods to alleviate
pressure on wound area to prevent it from
worsening.

o Improve nutritional status of individual to

prevent wound worsening.

o Note: The presence of Stage I wound is an

indication or early warning of a problem and
a signal to take preventive action.
 Stage-1: Treatment
• Alleviating pressure and avoiding more
exposure to the cause of the injury by
covering, protecting, and cushioning the
area.

• An increase in vitamin C, proteins, and

fluids is recommended. Increased nutrition
is part of prevention.
 Stage II

This stage is characterized by

• a blister either broken or unbroken.
• partial layer of the skin is now
injured.
• Involvement is no longer superficial.
 Stage II: Treatment
o Goal of care is to cover, protect, and clean the
area.

o Coverings designed to insulate and absorb as

well as protect are used. Additional padding and
protective substances used to decrease the
pressure on the area

o Skin lotions or emollients used to hydrate

surrounding tissues

oClose attention to prevention, protection,

nutrition, and hydration is important
 Stage III
 Wound extends through all of the layers of the
skin.

 Primary site for a serious infection to occur.

The goals and treatments of alleviating pressure

and covering and protecting the wound still apply
as well as an increased emphasis on nutrition and
hydration.

Medical care is necessary to promote healing and

to treat and prevent infection.
 Stage IV
 Wound extends through the skin and involves
underlying muscle, tendons and bone.

 Diameter of the wound is not as important as

the depth.

 Very serious and can produce life threatening

infection, if not aggressively treated.

 All of the goals of protecting, cleaning and

alleviation of pressure on the area still apply.
Nutrition and hydration is now critical.
Without adequate nutrition, this wound will not
 Stage IV: Treatment
 Needs medical care by professional skilled in
wound care.

 Surgical removal of the necrotic or decayed

tissue is often used on wounds of larger diameter.

 A skilled wound care physician, physical

therapist or nurse can sometimes successfully
treat a smaller diameter wound without the
necessity of surgery.

Surgery is the usual course of treatment.

 Stage V
 Wound is extremely deep, having gone through
the muscle layers and now involves underlying
organs and bone.

 It is difficult to heal.

 Surgical removal of the necrotic or decayed

tissue is the usual treatment.

 Amputation may be necessary is some situations.

 Note

It is possible for a wound to "go

from a stage I wound to a stage
III or IV" without the intermittent
stage[s] being observed.
 Minor wound
First aid
1. Protection: remove the cause of wound so
nobody else gets hurt, or at least to lead
the casualty away and mark out the
dangerous area;
2. Avoid further soiling: the bystander
washes his hands, and makes the
casualty wash his hands;
3. Avoid infection: the wound must be
washed with water and soap or
deinfected with an antiseptic (only one
product should be used, as an antiseptic
 Minor wound
First aid
1. Prevention: Ask whether casualty was
vaccinated against tetanus (the last injection
must be less than ten years old); if not, the
casualty should be vaccinated;
2. Give following advice: "if tomorrow or in the
following days the wound becomes red or hurts,
it is a sign of infection; go to clinician";
3. If there is a risk of dirt (e.g. playing child or
work in contact of any liquid or dusty product),
the wound must be covered with a sticking
plaster, otherwise it can be let in the air.
 Major wound
First aid
1. Avoid an aggravation of the wound and call for
help
2. Remove the cause of wound so nobody else gets
hurt, or lead the casualty away and mark out the
dangerous area; when the casualty cannot walk,
he should not be moved unless the danger is
deadly and real;
3. Avoid aggravation: the casualty is let in the
position he feels comfortable;when there is an
important bleeding, control it (press on the
wound when possible);
4. See general state of the casualty (alertness,
breath) and the wound itself;
 Factors Accelerating Wound
Development
 Anemic status: Compromises oxygen supply
 Malnutrition, fat loss, Vascular insufficiency,
Fecal or urinary Incontinence: causes local skin
irritation and maceration
 Elderly bed ridden patient: due to paucity of
movements and impaired sensation have poor
wound healing capacity
 Shearing forces due to sliding: causes injury to
skin.
 Poor arterial circulation
 Muscular atrophy
 Wound classification
Wagner System
 Grade 0 - intact skin, healed ulcers, bony
deformity
 Grade 1 - superficial ulcer no
subcutaneous involvement 
 Grade 2 - through subcutaneous to bone,
tendon. Ligament, capsule may be
exposed
 Grade 3 - Osteitis, abscess, osteomyelitis
 Grade 4 - gangrene digit
 Grade 5 - gangrene foot
Gangrene Toe
 Wound:
Shea’s Classification
 Grade:1
Irregular ill-defined area of soft
tissue and induration
associated with heat and
erythema overlying a bony
prominence
Reversible lesion
 Wound:
Shea’s Classification
 Grade:2
 Continued intense local pressure

intensifies acute inflammatory response

causing fibroblastic response in all
layers. Shallow full thickness skin
ulceration involving dermis and
subcutaneous fat with distinct edges of
wound margins.
 Early fibrosis and pigmentation changes

causing indistinct area of heat, erythema

and induration.
 Wound:
Shea’s Classification
 Grade:3
 Irregular full thickness skin defect

extending in to subcutaneous fat exposing

a draining, foul smelling, infected necrotic
base and undermining the skin for a
variable distance
 Skin edge is rolled with an altered dark

and light pigmentation that sharply

outlines the ulcer.
 Fever dehydration, anemia and

leukocytosis are compounded by profound

loss of fluid and protein from the opening
 Wound:
Shea’s Classification
 Grade:4
 Resembles clinically like

grade:3 except that bones can

be identified at wound base
with profuse drainage and
necrosis
 Pressure Ulcer
Staging/Grading
 Pressure Ulcer
Staging/Grading
 Wound Healing:3
Phases
 Wound healing process is a complex
series of events that begins at the
moment of injury and can continue for
months to years.
 Phase I: Inflammatory Phase

 A) Immediate to 2-5 days

 B) Hemostasis
 Vasoconstriction
 Platelet aggregation
 Thromboplastin makes clot
 C) Inflammation
 Vasodilation
 Wound Healing:3
Phases
 Phase:II. Proliferative Phase
 A) 2 days to 3 weeks
 B) Granulation

Fibroblasts lay bed of collagen
 Fills defect and produces new

capillaries
 C) Contraction
 Wound edges pull together to reduce

defect
 D) Epithelialization

Crosses moist surface
 Wound Healing:3
Phases
 Phase:III. Remodeling Phase
 A) 3 weeks to 2 years
 B) New collagen forms which
increases tensile strength to wounds
 C) Scar tissue is only 80 percent as
strong as original tissue
Wound Type: Pressure
 Wound Type: Pressure
 Combination of situations and factors.
 At cellular level, ischemia occurs when
high pressure is applied to one area for a
prolonged period of time. Ischemia
produced leads to tissue necrosis. These
pressure comes from bony prominence on
one side and a hard surface on the other
side. The soft tissue between these two
surfaces is subjected to abnormal
pressure. The tissue closest to the bone is
typically the first tissue to undergo
necrosis. Skin discoloration or redness
 Wound Type: Pressure
 It has been demonstrated that the
capillary pressure on the arterial side is
around 30-32 mmhg and around 12 mmhg
on the venous side. Sustained pressures
at values higher than these may result in
circulatory compromise and tissue
necrosis.
 Frictional and shearing forces also play
roles in tissue necrosis.
 General health, skin texture and turgor,
patient's mobility, nutritional status and
body weight (too thin and too heavy) are
Wound Type: Arterial Ulcers
Wound Type: Arterial
Ulcers
 Complete or partial arterial blockage leads to
tissue necrosis and / or ulceration. Signs are:
 Pulselessness of extremity
 Painful ulceration
 Small, punctate ulcers well circumscribed
 Cool or Cold skin
 Delayed capillary return time (briefly push on the
end of the toe and release, normal color should
return to the toe in 3 seconds or less)
 Atrophic skin (shiny, thin, dry)
 Loss of digital and pedal hair
 Can occur anywhere, but frequently seen on
Wound Type: Venous
Ulcers
Wound Type: Venous Ulcers
 Common type of ulcer affecting lower
extremities.
 The normal vein has valves that prevent the
backflow of blood. When these valves become
incompetent, the backflow of venous blood
causes venous congestion.
 Hemaglobin from red blood cells escapes and
leaks into the extravascular space, causing the
brownish discoloration.
 Transcutaneous oxygen pressure of skin
surrounding venous ulcer is decreased,
suggesting that there are forces obstructing the
normal vascularity of the area.
 Lymphatic drainage and flow plays a role in these
ulcers.
 The typical venous ulcer appears near the medial
malleolus, is in combination with an edematous
Wound Type: Diabetic
Ulcers
 Wound Type: Diabetic
Ulcers
 Diabetics are prone to foot ulcerations due to
neurologic and vascular complications.
 Peripheral neuropathy causes altered or
complete loss of sensation in the foot and /or leg.
Similar to the feeling of a "fat lip" after a
dentist's anesthetic injection, the diabetic with
advanced neuropathy looses all sharp-dull
discrimination. Any cuts or trauma to the foot
can go completely unnoticed for days or weeks in
a patient with neuropathy. It's not uncommon to
have a patient with neuropathy tell you that the
ulcer "just appeared" when, in fact, the ulcer has
been present for quite some time.
 There is no known cure for neuropathy, but strict
glucose control has been shown to slow the
Wound Type: Diabetic Ulcers
 Charcot foot deformity occurs due to
decreased sensation. People with
"normal" feeling in their feet
automatically determine when too much
pressure is being placed on an area of the
foot. Once identified, our bodies
instinctively shift position to relieve this
stress.
 A patient with advanced neuropathy
looses this important mechanism. As a
result, tissue ischemia and necrosis may
occur leading to plantar ulcerations.
Microfractures in the bones of the foot go
 Wound Type: Diabetic
Ulcers
 Micro vascular disease is a significant
problem for diabetics and can lead to
ulcerations. It is well known that
diabetes is called a small vessel disease.
Most of the problems caused by
narrowing of the small arteries cannot be
resolved surgically. It is critical that
diabetics maintain close control on their
glucose level, maintain a good body
weight and avoid smoking in an attempt
to reduce the onset of small vessel
Wound Type: Traumatic
Ulcers
Wound Type: Traumatic
Ulcers
 Trauma to the body result in a
 Compromise to the arterial, venous or
lymphatic systems.
 Changes to the bony architecture of the
skeleton.
 Loss of tissue layers - epidermis, dermis,
subcutaneous soft tissue, muscle or
bone.
 Damage to body parts or organs.
 Loss of body parts or organs.
 All of the above situations present
different problems, all of which could
Wound Type: Burns
Ulcers

Sun Burn

Boiling water burn

 Wound Type: Burns
Ulcers
 1st degree burn......is a superficial,
reddened area of skin like a
sunburn.
 2nd degree burn.....is a blistered
injury site which may heal
spontaneously after the blister fluid
has bee removed.
 3rd degree burn......is a burn
through the entire skin and will
 Wound Type: Burns
Ulcers
 Scald..occur from scalding hot water,
grease or radiator fluid.
 Thermal..occur from flames, usually deep
burns.
 Chemical..from acid and alkali, usually
deep burns.
 Electrical..Either low voltage around a
house or high voltage at work
 Explosion Flash.. superficial injuries.
 Contact Burns..Usually deep and occur
from muffler tail pipes, hot irons and
 Wound Management: Wound Debridement

 Autolytic Debridement:
 Autolysis uses the body's own enzymes and
moisture to re-hydrate, soften and finally liquefy
hard eschar and slough.
 Autolytic debridement is selective; only necrotic
tissue is liquefied.
 It is virtually painless for the patient.
 Autolytic debridement can be achieved with the
use of occlusive or semi-occlusive dressings
which maintain wound fluid in contact with the
necrotic tissue.
 Autolytic debridement can be achieved with
hydrocolloids, hydrogels and transparent films.

Wound Management: Wound Debridement

 Autolytic Debridement:
 Advantages:

 Very selective, with no damage to surrounding

skin.
 Process is safe, using the body's own defense
mechanisms to clean the wound of necrotic
debris.
 Effective, versatile and easy to perform
 Little to no pain for the patient
 Disadvantages:

 Not as rapid as surgical debridement

 Wound must be monitored closely for signs of
infection
Wound Management: Wound Debridement

 Enzymatic Debridement:
 Chemical enzymes are fast acting
products that produce slough of necrotic
tissue. Some enzymatic debriders are
selective, while some are not.
 Best Uses:

 On any wound with a large amount of

necrotic debris & Eschar formation
Wound Management: Wound Debridement

 Enzymatic Debridement:
 Advantages:
 Fast acting
 Minimal or no damage to healthy tissue with
proper application.
 Disadvantages:

 Expensive
 Requires a prescription
 Application must be performed carefully only to
the necrotic tissue.
 May require a specific secondary dressing
 Inflammation or discomfort may occur
Wound Management: Wound Debridement

 Mechanical Debridement:
 Used for decades in wound care. Allowing
a dressing to proceed from moist to wet,
then manually removing the dressing
causes a form of non-selective
debridement.
 Hydrotherapy is also a type of mechanical
debridement.
 Best Uses:

 Wounds with moderate amounts of

necrotic debris
Wound Management: Wound Debridement

 Mechanical Debridement:
 Advantages:

 Cost of the actual material (ie. gauze) is low

 Disadvantages:

 Non-selective and may traumatize healthy or

healing tissue
 Time consuming
 Can be painful to patient
 Hydrotherapy can cause tissue maceration.
Also, waterborne pathogens may cause
contamination or infection. Disinfecting
Wound Management: Wound Debridement

 Surgical Debridement:
 Sharp surgical debridement and laser
debridement under anesthesia are the fastest
methods of debridement.
 Are very selective, meaning that the person
performing the debridement has complete
control over which tissue is removed and which
is left behind
 Surgical debridement can be performed in the
operating room or at bedside, depending on the
extent of the necrotic material.
 Best Uses:

 Wounds with a large amount of necrotic tissue.


Wound Management: Wound Debridement

 Surgical Debridement:
 Advantages:
 Fast and Selective
 Can be extremely effective
 Disadvantages:

 Painful to patient
 Costly, especially if an operating room is
required
 Requires transport of patient if operating room
is required.
Physical Therapy Modalities in Wound
Care

 Electrical Stimulation
 Ultrasound
 Whirlpool
 Hyperbaric Oxygen
 Laser
 Ultra violet Radiation
Electrical stimulation: Wound Healing
 Electrical stimulation affects the biological
phases of wound healing in the following ways:
 Inflammation phase

 Initiates the wound repair process by its effect

on the current of injury,Increases blood
flow,Promotes phagocytosis,Enhances tissue
oxygenation,Reduces edema from reduced
microvascular leakage,Attracts and stimulates
fibroblasts and epithelial cells, Stimulates DNA
synthesis,Controls infection,Solubilizes blood
products including necrotic tissue
Electrical stimulation: Wound Healing
 Proliferation phase
 Stimulates fibroblasts and epithelial cells
 Stimulates DNA and protein synthesis
 Increases ATP generation
 Improves membrane transport
 Produces better collagen matrix organization,
 Stimulates wound contraction
 Epithelialization phase

 Stimulates epidermal cell reproduction and

migration
 Produces a smoother, thinner scar
 Electrical stimulation: Treatment
Protocol
 Inflammation phase
 Wound progresses to the

Proliferation phase
 Proliferation phase

 Polarity - negative
 Pulse rate - 100 - 128 pps
 Intensity - 100-150 volts
 Duration - 60 minutes
 Frequency 5-7 x per week, once
 Electrical stimulation: Treatment
Protocol
 Epithelialization phase
 Polarity - alternate every three days
ie 3 days negative followed by 3
days positive
 Pulse rate - 64 PPS
 Intensity - 100-150 volts
 Duration - 60 minutes
 Frequency 5-7 x per week, once
Electrical stimulation: CONTRAINDICATIONS
 Placement of electrodes
 tangential to the heart
 Along regions of the phrenic nerve
 over the carotid sinus
 over the laryngeal musculature
 over topical substances containing metal
ions
 over osteomyelitis
 Presence of a cardiac pacemaker or
malignancy
 Ultra Sound: Wound Healing
 Inflammatory Phase
 causes a degranulation of mast cells resulting in the
release of histamine. Histamine and other chemical
mediators released from the mast cell are felt to play a
role in attracting neutrophils and monocytes to the injured
site. These events accelerate acute inflammatory phase
and promote healing.
 Proliferative Phase

 accelerates fibroblasts and stimulate them to secrete

collagen. It leads to wound contraction and increase tensile
strength of the healing tissue. Connective tissue will
elongate better if both heat and stretch are combined.
 Continuous ultrasound at higher therapeutic intensities
provides and effective means of heating deeper tissue
prior to stretch.
 Ultra Sound: Wound Healing
 Frequency
 As the frequency of ultrasound is
increased, the penetration of the
signal decreases.
 For most dermal wounds, it is
preferable therefore, to utilize a
frequency of 3 MHz.
 1 MHz wound be more effective on
deeper structures or peri-wound
 Whirlpool: Wound Healing
 Objectives of whirlpool treatment:
 vasodilitation
 increased blood flow
 softening and loosening of necrotic
tissue
 mechanical debridement
 wound cleansing: debris and topical
agents
 exudate removal --- > reduced infection

 Whirlpool: Wound Healing
 Theory behind whirlpool's effectiveness:
 effects the Inflammation Phase of healing
 Warm water increases vasodilitation of the superficial
vessels; Increased blood flow brings oxygen and nutrients
to the tissues and removes metabolites
 Increased blood flow brings antibodies, leukocytes and
systemic antibiotics
 Fluid shifts into the interstitial spaces leading to edema
 Softening and loosening of necrotic tissue aides
phagocytosis
 Cleansing and removal of wound exudate controls infection
 Mechanical effects of whirlpool stimulate granulation
tissue formation
 Sedation and analgesia are induced by the warm water
 Hyperbaric oxygen therapy:Wound
Healing
 In an hypoxic environment, wound healing is
halted by decreased fibroblast proliferation
collagen production, and capillary angiogenesis.
 Hypoxia also allows growth of anaerobic
organisms, further complicating wound healing.
 Hyperbaric oxygen therapy provides a
significant increase in tissue oxygenation in the
hypoperfused, infected wound. It influences the
rate of collagen deposition, angiogenesis, and
bacterial clearance in wounds. The greatest
benefits are achieved in tissues with
compromised blood flow and oxygen supply.