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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3722_Библиотеки_им_академика_М_И_Перельмана
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2 Seeing aPatient withaWound
infectious disease referral and surgical
debridement should be considered. Depending
on the wound care specialist’s discretion, patients
may be started on an empiric antibiotic or wait
for a microbiologic diagnosis. A swab culture
allows the physician to identify the underlying
cause of the chronic wound [10].
Site of Cultures: Should be the area of infection in the wound base that may be discolored or
hypertrophic with drainage. Wounds should rst
be washed with sterile water so that the wound
swabs are not taken from heavily contaminated
areas that may give false culture results. Once
resulted, culture-directed antibiotic therapy can
be started or adjusted [10].
13
Fig. 2.9 Chronic wound with bone and joint exposed is
highly suspicious for chronic osteomyelitis
2.7 When Should IBiopsy?
HannahK.Park
Bone biopsy is necessary if there is suspicion of
bone infection. This can be done with:
1. Ronguer
2. Jamshidi needle
3. Trephine
4. Craig needle
When assessing wound infection, wound
biopsy was not shown to assess wound infection
differently from wound cultures taken with a
wound swab. Assessments did not signicantly
differ when specic microorganisms were
cultured nor for different wound types. It is recommended to perform a wound swab initially as
there is less burden on the patient of enlarging the
wound or creating pain/fear compared to a wound
biopsy.
However, if the chronic wound is not healing
with standard methods, and there are clinical
signs of possible skin malignancy, wound biopsy
should be performed. Clinical signs to look out
for are abnormal wound borders, bleeding, abnormal discoloration (black or blue), changing shape
and size, and various levels of thickness (Fig.2.9).
1. Excisional biopsy
2. Incisional biopsy
3. Punch biopsy
2.8 How Do IBiopsy aWound?
NicholasAlianello
Most lower extremity wounds can be classied
by etiology, the majority being in patients with
diabetes in conjunction with peripheral neuropathy, ischemia, and sometimes both. A foot and
ankle deformity and/or area of increased pressure
lends itself to wound formation in the abovementioned patient.
When to biopsy a wound?
1. When a wound presents in atypical anatomical site (e.g., Dorsum of the foot).
2. Etiology and appearance of wound are atypical and do not fall into normal classication.
3. When a wound fails to improve despite strict
adherence to standard wound healing
principles.
How to biopsy the wound:
Cleanse wounds with sterile saline.
Anesthetize the wound with local anesthesia if
needed. Remove full-thickness sample of tissue
from center of lesion/ulcer. It is okay to take samples from multiple areas of the wound if the
14
N. Alianello et al.
lesion is big enough. Use a camera and picture to
document the wound appearance and location of
biopsy to assist pathology in diagnosis.
Incision biopsy: Use a 15-blade and take a
full-thickness section of the ulceration. Send the
sample in formalin to pathology.
Punch biopsy: Type of incisional biopsy by
use of cylindrical blade. Creates full-thickness
sample. Comes in multiple sizes – 4 mm and
6 mm are most commonly used for lower
extremity wounds. This is also sent in formalin to
pathology.
2.9 When Should INot Debride?
NicholasAlianello
1. In ischemic wounds with dry/stable eschars
(Fig.2.10) prior to vascular intervention.
(a) Debridement will only lead to worsening
tissue death and likely expose bone.
(b) Always await vascular intervention to
ensure level of debridement and tissue
removal will be adequate to heal.
2. All pressure ulcers with dry stable eschars.
Even when these ulcers have adequate perfusion you should avoid removing the dry stable
eschar. Removing the dry eschar will likely
expose bone as these pressure injuries occur
at boney prominences of the extremity.
(a) One should focus on enzymatic debride-
ment and avoid sharp debridement until
the periphery of the eschar begins to lift
from the wound base and becomes mobile.
When the eschar breaks down or is loose,
then it is adequate to debride (Figs.2.11,
2.12, 2.13, and 2.14).
Fig. 2.10 Dry eschar of second and fth toe
Fig. 2.11 Dry eschar along the heel. DO NOT debride
lesion. Begin Enzymatic debridement with collagenase
application to wound base daily
Fig. 2.12 Heel eschar after collagenase application.
Eschar begins to loosen from peripheral of wound base
and becomes mobile
2 Seeing aPatient withaWound
15
Fig. 2.13 Heel eschar is now mobile enough to remove
without exposing bone. Continue collagenase application
to assist in brotic tissue removal
Fig. 2.14 Heel eschar with wound base now granular
with no exposed bone. It is now ok to return to sharp
debridement
3. Pyoderma gangrenosum wounds: Wound
management should focus on pathergy avoidance. NO debridement, dressing management,
and overall disease management with systemic medications are mainstay treatment.
2.10 Identifying andManaging
Calciphylaxis
NicholasAlianello
Identication: Start off as small plaques/eschar
that worsen and form larger lesions. They form a
lacy appearance and are acutely painful
(Fig. 2.15). Eventually, the plaques form deep,
Fig. 2.15 Calciphylaxis of lower extremity
ischemic ulcers. Normally found on areas of
body with high amounts of adipose tissue (trunk
and thighs).
Wound Management: Due to intense pain
associated with wounds, sharp debridement is
difcult. Enzymatic debridement of brous tissue and eschar is best performed with “collagenase” applied during daily dressing changes.
Proper wound dressings are paramount to control
moisture balance. Hyperbaric oxygen therapy
should be used when wound healing stalls.
The complexity of the diagnosis calls for a
total team approach to treat underlying systemic
disease.
2.11 When Do IWound Vac?
NicholasAlianello
A wound vac should be used in wounds with
depth that need assistance in increasing
granulation tissue within the wound base.
In most cases, the wound vac is used as
adjunctive therapy after aggressive surgical
debridement that leaves a wound with a deep
decit (Figs.2.16 and 2.17).
To allow for epidermal growth, a wound base
must be granular and must be at the level of the
skin. A wound vac uses negative pressure therapy
to promote granulation through capillary budding
at the wound site. The goal is to increase granulation tissue to eliminate wound depth.
16
Fig. 2.16 Deep wound after fourth digit amputation
N. Alianello et al.
Standard treatment protocol calls for pressure
to be set at 125mmHg with oscillation between
continuous and intermittent suction.
2.12 Ooading
NicholasAlianello
When to ofoad: When wounds occur on the
plantar surface of the foot, there is a need to eliminate the vertical plantar peak pressure associated
with walking (diabetic neuropathic foot ulcers).
2.12.1 Options forOoading
1. Total Non-weight Bearing: Crutches,
Wheelchair, Knee Scooter.
2. Total Contact Cast: Gold standard for ofoad-
ing DFUs.
3. Wedge Shoes (Half shoes).
4. Removable Cam Walker with ofoading
pad.
5. Felt/foam pads and donut pads were applied
to surgical shoe.
6. Extra-depth shoe with custom cut-out tri-
laminate insert.
Fig. 2.17 Wound vac placement along wound base of
fourth digit amputation
2.12.2 When toMake aChange?
The issue with aggressive ofoading is the
impractical nature of requesting a patient to
remain off the foot for the lifetime of the wound.
Non-compliance is high. The recommendation is
that you aggressively ofoad immediately when
a wound forms. Recommend strict non-weight
bearing (NWB) or Total Contact Cast during the
initial treatment plan. As the wound heals and
becomes smaller, you can transition to the wedge
shoe or ofoading pads (Figs. 2.18, 2.19, 2.20,
and 2.21).
Large deep wounds: Strict NWB, Total
Contact Cast, Wedge Shoes.
Small, shallow wounds: Felt/Foam Pads,
Removable Cam walker, Extra-depth shoe.
2 Seeing aPatient withaWound
17
Fig. 2.20 Ofoading pads
Fig. 2.18 Total contact cast
Fig. 2.19 Wedge shoe
Fig. 2.21 Accommodative padding
18
N. Alianello et al.
2.13 Oxygen Therapy
intheTreatment ofChronic
Wounds
J.KarimEad and DavidG.Armstrong
Wound healing represents a comprehensive series
of well-orchestrated physiological reactions that
create an orderly healing cascade [11]. This process theoretically includes four key overlapping
phases: hemostasis, inammation, proliferation,
and remodeling. It progresses along a continuum
that should result in the restoration of anatomical
and functional integrity [12]. Acute wounds in a
relatively healthy host will continue through the
wound healing cascade quickly due to the robust
utilization of intrinsic growth factors, cytokines,
and matrix proteins that keep the wound on a
well-regulated trajectory [11].
In contrast, chronic wounds manifest when
the normal healing cascade is interrupted at one
or more points during the phases of wound healing (often stagnating in the inammatory or proliferative phases [13]. Various theories have
been proposed to explain why some wounds
become chronic and non-healing. Despite the
etiological differences in chronic wounds, they
often share common pathogenic features.
Common causes for chronic inammation
include various inammatory-based comorbidities, infection, an externally induced pressure
injury, devitalized tissue that has been incom-
pletely debrided, mechanical insults from
retained foreign body, and hypoxia secondary to
ischemia [14]. Initial efforts should focus on
correcting or ruling out these causes of wound
chronicity. Normal tissue repair is a dynamic
process that balances decient and excessive
healing (Fig.2.22).
2.13.1 The Simple SALSA Wound
Treatment Guideline: Vertical
andHorizontal Approach
• If a wound does not reduce in size by 40% or
more after 4 weeks of standard-of-care
treatment, consider the utilization of alternative advanced therapies [15, 16].
– The “Vertical” approach is to ll/provide
coverage for vital structures using negative
pressure wound therapy (NPWT).
NPWT promotes localized perfusion,
increased granulation tissue formation,
and facilitates wound closure.
– The “Horizontal” component is achieved
via skin grafting (bioengineered or autologous split-thickness skin grafts).
Ofoading is a vital component of
wound healing that should be integrated
in any treatment algorithm.
• If the wound is older than 3–4months or not
responsive after 4weeks of therapy; consider
biopsy to rule out malignancy).
Fig. 2.22 Wound
healing is a balance
2 Seeing aPatient withaWound
19
*SALSA=The Southwestern Academic Limb
Salvage Alliance (SALSA).
Chronic wounds are comprised of proinammatory cytokines and proteases that disrupt
extracellular matrix communication with other
cells in the wound [16]. During these inammatory
states, there is increased oxygen consumption
and vascular dysfunction within the wound
environment causing hypoxic tissue formation
[17]. Oxygen is recognizably essential for life
itself, and it is no less essential for wound healing
and tissue repair. It is a necessary co-factor for
several oxygen-dependent biochemical processes
that are vital in the wound healing cascade. The
two main oxygen-based therapies include
hyperbaric oxygen and topically based oxygen
therapies.
2.13.2 Hyperbaric Oxygen Therapy
Hyperbaric oxygen therapy (HBOT) might be
considered in situations of chronic wounds that
have not responded to the standard of care. Today
there are several approved applications and
indications/contraindications for HBOT [18].
HBOT mechanism of action on chronic wounds
includes localized vascular modulation,
angiogenesis, leukocyte oxidative killing, growth
factor proliferation, and immune cell revitalization
(Fig.2.23) [19]. Treatment protocols for HBOT
vary depending on the suspected pathophysiology.
Simply put, HBOT is utilized to help restore
abnormal tissue oxygen tension by applying
basic physical gas laws. In certain circumstances,
hyperbaric oxygen therapy represents the primary
treatment modality, while in others it is an adjunct
to surgical or pharmacologic interventions.
Treatment is typically performed in either a
mono- or a multi-place chamber. In a monoplace
chamber, a single patient occupies an entire
chamber and is pressurized with 100% oxygen.
The patient breathes the ambient chamber oxygen directly. Whereas a multi-place chamber
holds two or more people and is pressurized with
compressed air while patients breathe 100%
oxygen (with masks, head hoods, or endotracheal
tubes) [20]. It should be noted that HBOT studies
have been ridiculed for signicant bias and large
numbers of dropouts or adverse events. There
will likely be a decline in the use of HBOT
therapy without robust evidence regarding
optimal therapy for specic wounds.
2.13.3 Topical Oxygen Therapy
Over the years, there has been some controversy
as to whether topical oxygen therapy (TOT) can
be utilized as a wound healing agent (Fig.2.24).
TOT has been in clinical use for over 50years
with encouraging pre-clinical and clinical studies
[21]. However, early studies were observational,
including several comparative cohort studies.
Even when conducted prospectively, lack of
randomized (blinded) studies have led many to
suspect its efcacy in the treatment of chronic
wounds [22].
There are three general types of delivery sys-
tems for TOT:
1. Continuous delivery of oxygen (CDO) at negligible pressures.
2. Low constant pressure delivery in a contained
chamber.
3. Higher cyclically pressurized (humidied
delivery in a contained extremity chamber).
As previously mentioned, chronic wounds are
typically hypoxic, in that the partial pressure of
HBOT
Fig. 2.23 Oxygen and its potential effects on wound healing
fibroblast
replaction
collagen angiogensis
immune
cell
modulation
Wound
Healing
20
N. Alianello et al.
O2 Modality
Topical O2 Therapy
HBOT
Fig. 2.24 Head-to-head HBOT vs TOT
Indications Relative Cost Level of evidence
VLU, DFU
(Neuro/Neuro ischemic)
Neuropathic, ischemic
ulcers
oxygen (pO2) at the central aspect of the wound is
often insufcient to support vital biochemical processes required for wound healing and tissue
repair. Providing localized topical oxygen can
potentially raise pO2 levels to better optimize
enzymatic/cellular function. It should be emphasized that on a molecular level, oxygen is the rate
limiting substrate for many vital biochemical reactions in cellular metabolism. Molecular oxygen is,
of course, also necessary for the synthesis of nitric
oxide (NO) that regulates vasodilation [22].
Oxygen-dependent processes, relevant to
wound healing, include the following:
Problems w/
evidence
+++
+++
Several RCTs,
observational, meta-
analysis positive results
Few RCT's showing
efficacy
Numerous devices
difficult to compare
Observer bias, high
drop out rates/ adverse
events
• Vascular endothelial growth factor (VEGF)
levels.
• Angiogenesis.
• Enhance collagen deposition.
Three recent systematic reviews with metaanalyses focused on the clinical effectiveness of
TOT for healing chronic diabetic foot ulcers
(DFUs) [22–24]. All three studies indicated that
TOT (using CDO and cyclically pressurized
devices) can signicantly improve wound healing
among people with chronic DFUs [23, 25].
• Mitochondrial-driven adenosine triphosphate
(ATP).
– Production for chemical/cellular energy.
• Nicotinamide adenine dinucleotide phosphate
(NADPH) oxidase.
– Production of ROS (“respiratory burst”)
involved in signal transduction of growth
factors, cellular recruitment, and bacterial
killing.
In animal models, TOT mechanism of action
has been demonstrated to increase/improve the
following:
• Central wound pO2 from a baseline of
5–7mmHg to levels of >40mmHg 4min into
treatment.
2.14 Skin Substitutes
andMatrixes Demystied
J.KarimEad and DavidG.Armstrong
Advances in cell biology and tissue engineering
have led to an increase in the quantity and quality
of biological wound dressings, also referred to as
biologics, skin substitutes, or matrixes [26]. Skin
substitutes are a diverse group of biologics or
biosynthetic materials that can provide temporary or permanent coverage of open or ulcerated
skin lesions (Fig. 2.25) [27]. These advanced
modalities can be a combination of cellular or
acellular tissue products, both human and animal
derived such as from human placenta, foreskin
allografts, sh scales, and other sources. It is
2 Seeing aPatient withaWound
21
Skin
Substitutes
Tissue
Layer
Epidermal Dermal Epi-Derm
Fig. 2.25 Skin substitutes
essential purpose is to stimulate the host to
regenerate lost tissue and replace the wound with
functional skin.
Cellular-based therapies, also called bioengineered cellular therapies are comprised of skin
cells (broblasts, keratinocytes, or both) that create a new source of growth factors, cytokines,
and enzymes that promote wound healing and
tissue regeneration. For example, one possible
treatment option for non-healing ulcers is the use
of platelet-rich plasma or platelet-rich brin,
which have recently been developed into
multilayered patches comprising autologous
leucocytes, platelets, and brin. These patches
can be made at the bedside without adding any
reagents. This autologous therapy can potentially
aid in the release of several key cytokines and
growth factors involved in tissue repair,
angiogenesis, and inammation [27].
Goals for treating acute and chronic wounds
with skin substitutes are to:
• Provide temporary coverage or permanent
wound closure.
• Reduce healing time.
• Reduce post-operative contracture.
• Improve function.
• To decrease morbidity from more invasive
treatments such as skin grafting.
Chronic non-healing wounds are often secondary to systemic pathological processes, it is critical
that skilled medical personnel encompass a holis-
Origin
Allograft Autograft Xenograft
tic approach in their treatment pathways. In 2019,
Samsell etal. conducted a cost-effectiveness study
on eight skin substitutes, they found that the costs
of a skin substitute itself did not necessarily correlate with its healing efcacy. Snyder etal. conducted a follow-up head-to-head comparative
analysis on ve skin substitutes and found that an
autologous-based graft was more cost-efcient as
an advanced therapy in the treatment of diabetic
foot ulcers when compared to four other advanced
cellular- based tissue products [28].
Armstrong etal. retrospectively analyzed data
from the Medicare Limited Dataset [29]. They
took a close look at patients receiving care for
lower extremity diabetic foot ulcerations treated
with advanced treatment (AT) versus no advanced
treatment (NAT). The advanced treatment
included patients receiving skin substitutes
(cellular and acellular dermal grafts) derived
mostly from human placental membranes and
animal tissue sources [22].
Key variables in the study included major and
minor amputations, emergency department (ED)
visits, and hospital readmissions. It was
discovered that AT for diabetic ulcers resulted in
fewer Major and Minor amputations, ED visits,
and Re-Admissions when compared to NAT.
These ndings emphasize the importance of
choosing the appropriate advanced skin
substitutes that are both effective and cost
efcient when considering a treatment plan for
patients with non-healing lower extremity
wounds.
22
N. Alianello et al.
2.15 This Patient Needs
tobeAdmitted Now
J.KarimEad and DavidG.Armstrong
The incidence of skin and soft tissue infections
(SSTI) in the general population has been
increasing in recent years. Consequently, increasing the number of patients being seen and treated
in the Emergency Department (ED), as well as
admitted to the hospital. It is vital for medical
personnel to utilize evidence-based consensus
guidelines for the management of suspected SSTI
[30]. These conditions are subdivided into specic categories (non-purulent, purulent, ulcerative, and recurrent/refractory SSTI) (Fig.2.26).
Recent data suggests that lower extremity-based
ED visits generate 81.2% hospital admission rate
with an annual bill of at least $1.2 billion in the
United States alone [12].
The likelihood of hospital admission, amputation, and other subsequent adverse outcomes is
associated with three key factors [31]:
The Infectious Diseases Society of America
(IDSA) recommends clinicians to consider the
possibility of infection occurring in any foot/
lower extremity wound (especially in the diabetic
patient) [29]. If an in-ofce patient presents with
signicant tissue loss, a thorough history and
physical exam should be performed. If there are
obvious signs of either infection or ischemia,
hospital admission should be advised (Fig.2.27).
Redness/Pain
Skin Warmth
Swelling/
Purulence
1. Wound severity (degree of tissue loss)
2. Ischemia
3. Foot infection
Non Purulent SSTI:
• cellulitis
• ersipelas
Purulent SSTI:
• Abscesses
• Cellulitis w/ pustules
Ulcerative SSTI
• Chronic ulceration (lower extremity)
Recurrent/Refactory SSTI
• More than 3 occurences per year of either non-purulent or purulent SSTI
Classic Signs of Infection
Fig. 2.27 Evidence of infection includes classic signs of
inammation
Fig. 2.26 SSTI denitions
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