Wound Care and
Hyperbaric Medicine
Miguel G. Madariaga, MD
What is the skin good for?
The epidermis
The epidermis is the tough,
leathery outer surface of the
skin
It has five layers of cells and
appendages
It helps us by:
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Providing a barrier
Regulating fluids
Providing light touch sensation
Controlling temperature
Excretes toxins
Produces vitamin D
Cosmetic apperance
The dermis
It is a 2-4 mm thick layer
below the epidermis
It helps us by:
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Supporting and nourishing the
epidermis
Housing skin appendages
(nails, hair, glands)
Fighting against infection
Controlling temperature
Providing sensation
What is a wound?
How does a wound heal?
What is a chronic wound?
Chronic wounds: the burden of
disease
Chronic wounds represent a silent epidemic (6.5
million in the US)
The amount of money spent on wound care, the
loss of productivity for afflicted individuals and
the families and their diminished quality of life
come at great cost to our society
It is claimed that an excess of US$25 billion is
spent annually on treatment of chronic wounds
Sen, Wound Repair Regen, 2009
Causes of chronic wounds
Diabetes
Arterial insufficiency
Venous disease
Pressure
Radiation
Others
Diabetic ulcers
Diabetes is the sixth leading cause of death in
the United States
7% of the American population have diabetes
and several millions (6) are undiagnosed
Over 85% of all diabetic related lower extremity
amputations are preceded by an ulceration
Risk factors for diabetic ulcers include:
neuropathy, deformity/limited joint mobility,
vascular disease and pivotal trauma
Why do diabetic ulcers occur?
Neuropathy
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Motor: weakness, muscle atrophy (deformity)
Sensory: diminished sensation, pain
Autonomic: dry, fissured skin
Vascular disease
Complications of diabetic ulcers
Venous ulcers
These are the most common cause of ulcers
1-2% of the population has venous insufficiency
14% of people with venous insufficiency develop
ulcers
Women are three times more likely than men to
have venous ulcers
The risk of ulceration is 7.5 times greater in
people older than 65
Why do venous ulcers occur?
Venous ulcers: characteristics
Pressure ulcers
Pressure ulcers are localized areas of dead tissue that
develop when soft tissues is compressed between a firm
surface and a bony prominence
The overall prevalence among hospitalized patients is
15%
Patients at risk: hospitalized patients, individuals in long
term care and patients with spinal cord injury
Pressure ulcer complications may be life-threatening
The cost of caring for each ulcer can be up to 70,000 per
ulcer
Pressure ulcer stages
What is done at the Wound
Center?
Adequate perfusion
Presence of nonviable tissue
Signs of infection or inflammation
Presence of edema
Conduciveness of wound healing environment
Optimization of tissue growth
Appropriateness of pressure offloading
Controllability of pain
Optimization of host factors
Confirm adequate perfusion
Eliminate non-viable tissue
Different types of debridement
Control infection/inflammation
A word about MRSA
Resolve edema
Optimize wound bed
Enhance tissue growth
Graft
Enhance tissue growth: hyperbaric
oxygen
Provide appropriate offloading
Control pain
Optimize host factors
Diabetes mellitus
Renal dysfunction
Ischemic heart disease\Smoking
COPD
Malnutrition
Mobility impairment
Addiction
What to expect when going to the
wound care clinic?
A long initial visit with many questions
A physical exam
Most likely sharp debridement of the ulcer
Initial tests including blood tests and
maybe an ultrasound
Dressing recommendations
Follow up on a weekly basis
Reevaluation of plan at specific time points
Hyperbaric Medicine
What is hyperbaric oxygen
therapy?
…the use of 100% oxygen
breathed at increased
atmospheric pressure
It requires that…
The patient be enclosed in a
pressure vessel
Subjected to an atmospheric
pressure at least 1.5 x sea
level or ambient pressure
And be breathing 100%
oxygen
The “bends”
HBO: Boyle’s law
HBO and carbon monoxide
poisoning
HBO mechanism of action in
wound care
A randomized clinical trial
Faglia, Diabetes Care, 1996
Faglia’s clinical trial
70 DFU patients consecutively admitted
2 subjects withdrew, 35 received HBO, 33 received conventional
care
All patients received initial radical debridement
Standardized wound care protocol for all patients
Infections were treated based on culture results
Optimized metabolic control for all patients
All patients with ABI <.9 or TcPO2 <50mmHg received arteriography
If possible, intervention by angioplasty or bypass graft
HBO treatment protocol was 2.5 ATA 90 minutes initially then 2.4
ATA following
Major amputation decision carried out be consultant surgeon
unaware of HBO status
Faglia, Diabetes Care, 1996
Faglia’s trial results
HBO group: 3/35 (8.6%) had major amputation (2 BKA, 1
AKA)
Conventional group: 11/33 (33%) had major amputation
(7 BKA, 4 AKA)
TcPO2 on dorsum of the foot significantly increased in
HBO treated subjects compared to conventional group
Negative prognostic determinants were poor cruclation
and advanced Wagner grade
Faglia, Diabetes Care, 1996
FDA approved usage of HBO based on UHMS
Report, 2008
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Decompression illness, gas embolism
Carbon monoxide, cyanide poisoning
Blood loss anemia
Clostridial myonecrosis
Other necrotizing soft tissue infections
Refractory osteomyelitis
Prep and preservation of compromised skin
grafts and flaps
Crush injury, compartment syndrome
Other acute traumatic ischemias
Central retinal artery and vein occlusion
Other wounds with demonstrated periwound
hypoxia
Acute thermal burns
Osteoradionecrosis
Soft tissue radionecrosis
Bubble compression,
toxin displacement,
temporary Increase in
oxygen deliver
Enhanced host immune
response, resolution of
infection
Reversal of hypoxia, wound
regeneration effects, tissue
growth
Wound regeneration effects,
tissue growth, reversal of
fibrosis
HBO technique
Single occupancy chambers are most appropriate for the
treatment of chronic medical conditions in stable patients
Acute therapy may require only one or two treatments,
while chronic medical conditions may warrant up to 30 or
more sessions
Treatment is given 3-5 times a week, usually once a day
for stable patients
Chamber pressure is usually maintained between 2.0
and 2.5 ATM, with treatment lasting 90 to 120 minutes
depending upon the indication
Air breaks are given every 30 mins to prevent
complications
Most common complication:
barotrauma
Observe TM
movement during
valsalva
If unable to
demonstrate auto
inflation refer to ENT
for myringotomy
Other complications of HBO
Reversible myopia due to direct toxicity to the
lens; recovers in weeks to months
Pulmonary barotrauma is unusual
Pulmonary oxygen toxicity (chest tightness,
cough, reversible decline of pulmonary function),
occurs in patients receiving multiple treatments
or previously exposed to high oxygen levels
Seizures are a rare but dramatic consequence
of HBO treatment; estimates of incidence range
from 1 in 11,000 to 2.4 per 100,000 treatments
Decompression sickness may occur in patients
breathing compressed air that contains nitrogen
Scleroderma
Scleroderma comprises a heterogeneous group of conditions linked by the
presence of thickened, sclerotic skin lesions
Classification:
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Localized scleroderma
Linear scleroderma
Localized and generalized morphea
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Systemic sclerosis
Limited cutaneous SSc — skin sclerosis restricted to hands (and face and neck). They
may suffer from the CREST syndrome (Calcinosis cutis, Raynaud phenomenon,
Esophageal dysmotility, Sclerodactyly, and Telangiectasia)
Diffuse cutaneous SSc — extensive skin sclerosis and greater risk for the development
of significant renal, lung, and cardiac disease
Others including overlap syndromes
The classification of SSc may ultimately be based upon genetic and
immunologic markers associated with an increased risk of specific
complication
Scleroderma pictures
Linear
scleroderma
Morphea
Skin involvement in Scleroderma
Skin involvement is a nearly universal feature of SSc. It
is characterized by variable extent and severity of skin
thickening and hardening. The fingers, hands, and face
are generally the earliest areas of the body involved.
Edematous swelling and erythema may precede skin
induration.
Other prominent skin manifestations include:
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Itching in the early stages
Edema in the early stages
Sclerodactyly
Digital ulcers
Pitting at the fingertips
Telangiectasia
Calcinosis cutis
Scleroderma skin involvement
Ulcers
Telangiectasias
Sclerodactily
Calcinosis
Treatment of sclerotic skin
Localized disease:
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The lesions of localized scleroderma,
including morphea, appear to soften with
ultraviolet-A (UVA) light therapy
Other options include highly potent topical
glucocorticoids, calcipotriol (a vitamin D
analog), and methotrexate.
Widespread disease: Immunomodulatory
and antifibrotic approaches have yet to be
shown to be more beneficial than harmful
Treatment of other symptoms
Pruritus:
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Antihistamines may help, but can cause drowsiness
Maintaining adequate lubrication of the skin is essential
Low-dose oral glucocorticoids are sometimes effective, topical steroids are rarely
helpful
Telangiectasia:
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Green foundation make-up
Laser or other light therapy may be useful for large lesions
Calcinosis:
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Medications are unhelpful
Suitably located lesions can be removed surgically, sometimes by using a dental
drill; this technique causes less tissue damage than conventional methods
Raynaud phenomenon:
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Avoidance of cold, stress, nicotine, caffeine, and decongestants
Medications help for symptomatic relief: diltiazem, ACE inhibitors, ketanserin,
fluoxetine
Different forms of sympathectomy (surgery) have been tried in an attempt to treat
severe Raynaud phenomenon.
Adequate perfusion:
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Ultrasound and referral to vascular surgery if larger vessels are
affected
Presence of nonviable tissue:
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Debridement is important, but it may be contraindicated if there
is vascular disease
Signs of infection or inflammation
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A biopsy needs to be considered to rule out vasculitis
Presence of edema
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Venous insufficiency is a common but unrelated problem
Compression therapy is indicated
Conduciveness of wound healing environment
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Dressings depending on the wound environment
Optimization of tissue growth
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Hyperbaric oxygen therapy is not indicated for
scleroderma, but it may be considered if there is a
coexistent disease or evidence of poor oxygenation in
the wound
Byosinthetic substitutes may be of use
Appropriateness of pressure offloading
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Usually not an issue
Controllability of pain
Optimization of host factors
The most important message:
prevention
Wash skin daily using warm water and a mild
soap
Use a moisturizer daily (lactic acid, urea,
dimethicone). Avoid perfumed moisturizers
Wear wide comfortable shoes
Prevent triggering Raynaud’s syndrome
Consult a podiatrist for nail care and callus
removal
Do not attempt to remove calcinosis by yourself.
Consider wearing orthotics
Seek prompt attention for skin openings