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E. Cammarata et al.
40.5.2 Pressure Ulcers
Pressure ulcers (PU) are localized lesions that
generally occur as a result of unrelieved and prolonged pressure over bony prominences causing
damage to the skin and/or the underlying tissues.
They usually occur in patients who have
reduced mobility and spend the majority of their
time lying in a bed or in a wheelchair without
shifting their bodyweight. This means that all
patients who are critically unwell in the hospital
setting are potentially at risk [25, 26].
PU is more common in case of coexisting
additional risk factors (e.g., paralysis, peripheral
vascular disease, decreased sensation, poor nutritional status, cognitive impairment, and frailty)
[25–27]. If a patient is conned to bed, the most
frequent areas are the sacrum, the coccyx, the trochanteric region, and the calcaneus, whereas, if a
patient has prolonged periods of sitting in a chair,
the coccyx and the elbows are the areas at higher
risk [28].
Pressure ulcers can present as open ulcers or
can arise on the surface of intact skin, showing
the “tip of the iceberg” effect, where the skin surface is relatively spared compared to the underlying tissue. This is because necrosis often starts at
the site of the highest pressure, which is at the
bone/muscle interface. Accordingly, a pressure
ulcer may be much more severe than rst thought
because the damage to the deeper tissues is not
reected at the surface [29] (Fig.40.3).
Fig. 40.3 Ischiatic ulcer in 60-year-old paraplegic patient
PU are classied into four stages based on
their thickness [30]. National Pressure Ulcer
Advisory Panel’s staging system is provided in
Table40.2.
40.5.2.1 Operative Management
Negative pressure wound therapy (NPWT) is not
routinely used but can be a useful option for
ulcers with high levels of exudate requiring multiple dressing changes a day and for stage 3 or 4
ulcers. NPWT can help optimize the wound bed
for surgical closure or stimulate healing while
waiting for reconstructive surgery.
Ulcerectomy, debridement, and eventual bone
resection are indicated to remove brous scars
and potentially infected tissue, with the aim of
preventing relapses.
Table 40.2 National Pressure Ulcer Advisory Panel’s
updated pressure ulcer staging system
Stages Clinical appearance
Stage 1:
nonblanchable
erythema
Stage 2:
partial
thickness skin
loss
Stage 3: full
thickness skin
loss
Stage 4: full
thickness
tissue loss
Unstageable:
depth
unknown
Skin is intact with non-blanchable
redness localized to an area usually
over bony prominence. The area may
be painful, rm, soft, warmer, or
cooler than adjacent tissue.
Partial thickness loss of dermis
presenting as a shallow ulcer with a
pink wound bed.
Ulcer in which subcutaneous fat may
be visible with or without slough.
However, bone, tendon, or muscle are
not visible.
Ulcer in which muscle, tendon, or
bone is exposed. Ulcer often includes
undermining or tunneling; hence, it is
at risk of causing osteomyelitis.
Ulcer in which base is covered by
slough or necrotic tissue; therefore,
true depth cannot be determined and
therefore classied.
Deep tissue injury presents with a
purple or maroon localized area of
discolored skin or blood blister as a
result of damage to underlying soft
tissue. In darker skin types, it may be
difcult to detect whether nonblanching skin erythema is present,
such as in stage 1 ulcers or a deep
tissue injury, so high suspicion of risk
is required.
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Intraoperative bone specimens should be
obtained for microbiological culture when osteomyelitis is suspected. The removal of bony prominences is recommended to help relieve pressure
points. Care must be taken, however, not to
remove bone in excess, because this may expose
critical deep structures or produce new unnatural
weight-bearing skin surfaces [31, 32].
Although there are no recommendations
regarding a specic type of surgery for this type
of ulcer, reconstruction should provide functional
weight-bearing coverage. Generally, skin grafts
are not indicated because they do not typically
provide enough strength or bulk to cover the
wound.
The primary closure of relatively small stage 2
or 3 ulcers may be attempted when immediate
closure is desired. While this relatively simple
procedure can be performed, wound dehiscence
is a common complication [33].
For more extensive stage 3 or 4 pressure
ulcers, surgical management with a regional or
free ap is mandatory in order to ll dead space.
Cutaneous and fasciocutaneous aps are generally preferred over muscle aps, which are generally preserved for recurrent cases or in case of
reconstructive failure as a lifeboat option [34, 35]
(Fig.40.4).
40.5.3 Arterial Ulcers
Arterial ulcers (AU) usually develop from an
imbalance in arterial blood ow: a reduced/inadequate perfusion of the skin and soft tissues leads
to/causes ischemia and subsequent necrosis,
nally resulting in ulceration. The main cause is
represented by peripheral vascular disease/
chronic obstructive disease due to atherosclerosis, diabetic macro- and micro-angiopathy, vasculitis, and microthrombi [36].
If compared to venous ulcers, AU are preferentially located more distally, typically on the
foot (toes, metatarsals, and calcaneus) or, less
frequently, in the anterolateral region of the leg
distal third [37]. AU has a characteristic
“punched-out” appearance, well-demarcated
edges, and a pale bottom. They can present with
an eschar on their surface and deeper structures,
such as fascia, tendons, and muscles may be
involved too.
The surrounding skin appears pale, atrophic,
and hypothermic with altered skin adnexa
(decreased number of hair). The striking clinical
clue is jolting, burning pain, and functional impotence, increased in the supine position.
The most important diagnostic tool in the
evaluation of the arterial nature of an ulcer is rep-
Fig. 40.4 Operative photographs showing the patient in a
prone position with an ischiatic ulcer. (a) Pre-operative
drawing. (b) Advancement of the V–Y ap. (c) Complete
dissection of the perforator ap. (d) Clinical picture 10
weeks after surgery, showing complete healing of the ap
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E. Cammarata et al.
resented by the ankle-brachial pressure index
(APBI): an ABPI <0.6 is strongly suggestive of
arterial insufciency. Other instrumental tests
such as color Doppler ultrasonography, angiography, CT angiography (CTA), or magnetic resonance angiography (MRA) could be useful in
case of doubts regarding the etiology or to preoperatively determine obstruction vessel localization when invasive or surgical intervention is
planned [38].
40.5.3.1 Operative Management
In case of critical vascular impairment, revascularization of the affected arterial segment is
performed rst and is mandatory in order to
repristinate proper blood ow. When necessary,
WPB through surgical debridement, NPWT, and
topical antiseptic treatment is considered prior to
reconstruction. This is possible only after a successful revascularization and is subsequently
achieved through the use of dermal substitutes or
skin grafts (Fig. 40.5). Occasionally, owthrough/bypass aps can be used too, with the
aim to provide soft-tissue coverage, simultaneously preserving the blood ow to distal tissues
[35, 39].
40.5.4 Diabetic Foot Ulcers
Diabetic foot ulcers (DFU) are caused by the
combination of both arterial and nerve damage:
Fig. 40.5 Post-traumatic leg ulcer in a 77-year-old
patient with popliteal artery stenosis. (a) Exposure of the
tibialis anterior muscle. (b) Reconstruction with a split-
thickness skin graft after BWP with NPWT. (c) Final
result 6 months after surgery
40 Surgical Indications inAll Diagnostic andCare Pathways (DTCP) Settings
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461
in fact, the main causes are noted to be peripheral
neuropathy and peripheral vascular disease.
Ulcers and gangrene can be considered one of the
worst complications of diabetes and are the most
common cause of non-traumatic lower limb
amputations in developing countries [40].
Although many classications are currently
available for DFU, Wagner’s classication is one
of the most widespread and can be considered a
useful guide for effective stage-related treatment
[41] (Table40.3).
40.5.4.1 Operative Management
As for arterial ulcers, rst-line treatment often
includes a revascularization procedure, the critical reduction of the arterial ow caused by diabetic angiopathy one of the main characteristics
of the disease [42].
Surgical procedures of debridement, bone
resection, WBP, and treatment of any infectious
foci are highly recommended when they are
necessary.
Either direct closure, skin grafts, and local or
free aps are feasible options for reconstruction,
according to Wagner’s grade of severity [41, 43].
However, ap reconstruction is possible only
after revascularization.
In regard to the amount of soft tissue and bone
to be resected or otherwise preserved during
debridement, the patient’s functional needs
should always be considered: in fact, in the case
of walking patients, a functional reconstruction
that allows to bear weight has always to be preferred over a non-functional one, if possible (e.g.,
avoiding tendon resection on the dorsum of the
Table 40.3 Wagner’s classication of diabetic foot
ulcers
Grade Clinical appearance
Grade 0 Skin intact but bony deformities leading
to “foot at risk”
Grade 1 Supercial ulcer
Grade 2 Deeper, full-thickness ulcer
Grade 3 Deep abscess formation of osteomyelitis
Grade 4 Partial gangrene of forefoot
Grade 5 Extensive gangrene
foot in order to allow nger extension; preserving
rst and fth metatarsal heads and choosing not
to perform forefoot or midfoot amputations to
maintain the weight-bearing tripod; preserving
plantar skin or reconstructing it with aps; and
trying not to graft heel ulcers).
Finally, we have to remember that about 80%
of DFUs have a neuropathic origin. Therefore,
further association of nerve decompression procedures at anatomic sites of nerve entrapment
(e.g., tarsal tunnel release), thanks to the improvement in the sensation of the foot, may help to
reduce the risk of recurrence after reconstructive
surgery [44–46].
40.5.5 Neoplastic Ulcers
A neoplastic ulcer is dened as a lesion whose
origin is not caused by circulatory, metabolic, or
traumatic causes, but an expression of the
malignant degeneration of one of the components
of the skin or expression of a tumor process originating elsewhere and reaching the skin metastatically (lymphatic or hematogenous) to the skin.
It is possible to distinguish primitive forms,
which are ulcers that have arisen themselves, and
secondary forms, represented by chronic ulcers,
from which a carcinoma takes its origin.
Among primitive forms, basal cell carcinoma
(BCC), squamous cell carcinoma (SCC), malignant melanoma (MM), T cell and B cell lymphoma, and Kaposi’s sarcoma are the most
frequent types of neoplastic ulcers. Metastatic
ulcers are very rare and, in the majority of cases,
derive from a primitive breast adenocarcinoma
[47].
In the case of secondary forms, neoplastic
degeneration arises on skin damaged by chronic
inammation or scarring, as in the case of radiation dermatitis, burns, venous ulcers, osteomyelitis, and chronic diseases including discoid lupus
and sclero-atrophic lichen. Generally, SCC is a
tumor that originates from chronic wounds, and
in this case, the ulcer is named “Marjolin’s ulcer”
[48] (Fig.40.6).
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Fig. 40.6 Photograph showing a case of Marjolin’s ulcer
in a 72-years-old man
Suggestive characteristics of a neoplastic
ulcer are:
– Atypical localization, often unusual for vascu-
lar ulcer.
– Irregular margins and hemorrhagic borders.
– Abnormal granulation tissue, extending
beyond the margins.
– Presence of vegetative, exophytic, thick
lesion, covering the entire surface of the ulcer.
– Rapid increase of the lesion despite adequate
treatment.
– Presence of purulent fundus and fetid scent.
– Locoregional lymphadenopathy [31].
40.5.5.1 Operative Management
A tissue biopsy followed by histological examination in the suspicion of a neoplastic ulcer is
always mandatory to rule out malignancy. To
obtain greater diagnostic accuracy, multiple
biopsy sampling at several points of the lesion is
recommended [49].
After diagnosis is conrmed, in well-
differentiated and less aggressive forms, surgical
removal with a wide margin followed by reconstruction is preferred, although cases of relapse
are reported.
More radical treatment is indicated in patients
with poorly differentiated and, therefore, more
aggressive forms. In these cases, major amputation is to be considered, due to the risk of metastasis and death [50].
E. Cammarata et al.
40.5.6 Vasculitic Ulcers
Vasculitis is a rare case of ulceration. Ulcer formation is caused by the injury of cutaneous
microvessels in the context of various systemic
conditions, such as connective tissue diseases
(systemic lupus erythematosus, rheumatoid
arthritis, and Sjögren syndrome), antiphospholipid antibodies syndrome, panarteritis nodosa,
and Wegener’s granulomatosis.
40.5.6.1 Operative Management
Surgical treatment of vasculitic ulcers follows the
general principles applied for venous ulcers and
is based on debridement, NPWT, and grafts.
However, it is recommended to cautiously manage the donor areas, due to the difcult healing of
secondary lesions. Regenerative surgery has a
fundamental role: in selected cases, it is possible
to use cultures of broblasts, platelet-rich plasma
(PRP), and fat grafting (lipolling/ADSCs) to
help skin regeneration [51] (Figs.40.7 and 40.8).
40.5.7 Infected Ulcers
All chronic ulcers contain bacteria but their presence does not necessarily indicate the existence
of infection and does not necessarily entail a
delay in healing [4]. For this reason, one should
distinguish between contamination, colonization,
and infection.
Contamination is dened by the presence of
non-replicative microorganisms, while colonization is dened by the presence of replicative
microorganisms without signs of reaction by the
host. Infection of the ulcer is nally dened by
the presence of replicative microorganisms with
the reaction of the host. It should never be forgotten that the majority of venous ulcers are colonized by bacteria rather than infected [52].
There are many factors that together with the
bacterial load determine the appearance of infection: they include the amount of necrotic tissue
and exudate, the number of microorganisms, the
pathogenicity of the bacteria, and the host organism’s defenses. Host resistance can be conditioned by both local factors (location, size, depth,
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40 Surgical Indications inAll Diagnostic andCare Pathways (DTCP) Settings
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463
Fig. 40.7 Photographs showing a 48-year-old lady
affected by SLE with chronic ulcers on the anterior surface of her legs. (a) Post-debridement ulcer. (b)
ab
Fig. 40.8 Vasculitic ulcer in a female patient. (a)
Preoperative photograph. (b) Intraoperative photograph
showing PRP injection after ulcer debridement. (c)
time of ulcer onset, and vascular situation) and
systemic factors (metabolic disorders, diabetes
mellitus, vascular disease, edema, malnutrition,
smoking, drug use or abuse of alcohol, and
immunosuppressive drugs).
The diagnosis of infection is substantially
clinical, and the signs that identify its presence
are at least two of the following: onset or increase
of pain, increased exudate and edema, appearance of an unpleasant odor, change in color of the
Reconstruction with autologous skin graft. (c) Recurrent
ulcer 3months after surgery
c
Autologous skin graft 1 week after surgery. (d) Final
result 3months after surgery
ulcer base, appearance of a peri-wound erythema,
change in the appearance of the granulation tissue, and observation of a slow healing process or
its sudden stop.
It is, therefore, advisable to take at least one
swab of the wound, enriched with exudate and
with the material obtained from the curettage of
the edges of the ulcer or with the aspiration of
purulent material, after having thoroughly
cleaned the wound with saline solution [53].
d
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E. Cammarata et al.
Fig. 40.9 Infected chronic venous ulcer in a 78-year-old
female suffering from type II diabetes. (a) Chronic ulcer
on the later side of the leg. (b) Post-debridement ulcer. (c)
40.5.7.1 Operative Management
In case of conrmed infection, the initial therapy
of the ulcer, regardless of its type, is based on the
administration of topical and systemic antibiotics
and a good wound bed preparation (WBP),
through the execution of a good debridement
with either sharp technique or high-pressure
water jet dissection, the control of the bacterial
load and the adequate management of the exudate through NPWT, eventually enriched with
antibiotic instillation. Topical silver- and iodinebased agents and advanced dressings containing
slow-release antiseptics can also be useful for the
control of the infection and the reduction of biolms [34, 54–56]. Dermal substitutes can be used
Dermal regeneration template. (d) Clinical picture 1 week
after surgery. (e) Staged autologous skin grafting 1month
after rst surgery. (f) Final result 6 months after surgery
of life. The management of patients with skin
ulcers is complex and often leads to poor outcomes. The implementation of a DTCP in daily
clinical practice allows for the delivery of more
effective care to these patients thanks to the cooperation between the hospitals and the territory
and the constant interaction between different
healthcare professionals. According to the DTCP,
each patient with a complex or complicated ulcer
should be referred in a timely way to a secondlevel center for a multidisciplinary review in
order to receive the most appropriate surgical
treatment, which is always tailored to the patient’s
specic condition and varies between ulcer
subtypes.
as a bridge to the nal reconstruction with autologous skin grafts, which is usually deferred in a
second surgical stage [57–59] (Fig.40.9).
40.6 Conclusion
Skin ulcers are very common in the general population and represent a cause of long-term illness,
functional impairment, and reduction of quality
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Microsurgery inWound Healing
https://t.me/medicina_free
JoonPioHong andAsliDatli
41
Key Points
• Microsurgery is a surgical approach or a
specialty using surgical microscopes to
manipulate small tissues such as vessels
of the ap to reconstruct a defect caused
by various reasons.
• Flap reconstruction for wounds is frequently considered in cases of lacking
healing progress despite good wound
care or complex wounds when timely
coverage will benet the overall healing
process.
• Along with a multidisciplinary approach
and good principle of wound care, the
repair and restoration strategies using
aps and microsurgery have widened
the possibilities for good esthetic and
functional results for complex wounds.
J. P. Hong (*)
Department of Plastic Surgery, Asan Medical Center,
University of Ulsan, Seoul, South Korea
A. Datli
Department of Plastic and Reconstructive Surgery,
Istinye University School of Medicine,
Istanbul, Turkey
41.1 Introduction
Frequently considered chronic wounds for reconstruction are wounds lacking healing progress
despite good wound care. In addition, those needing aps or microsurgical reconstruction are
wounds that are unable to close by skin grafts,
wounds with an exposed vital structure such as
tendon and bones, and wounds that have prolonged infections, such as osteomyelitis and skin
necrosis. These wounds have become a major
challenge to healthcare professionals all over the
world. Reports show that in the United States
alone, these wounds affect an estimated 2.4–4.5
million people [1, 2]. Acute wounds are often
straightforward involving good principles of
wound care: debridement, infection control, adequate vascularity, and wound preparation for
reconstruction followed by the reconstruction
itself [3]. The big challenges involved in wound
healing is often chronic wounds, especially in the
lower extremity [4]. Chronic leg and foot ulcers
occur in many adults with vascular disease or diabetes and are attributed to chronic venous insufciency, arterial disease, prolonged pressure, or
neuropathy [2, 5]. Thus, chronic wounds can be
classied as vascular ulcers (venous and arterial),
diabetic ulcers, and pressure ulcers [6]. These
ulcers last on average 12–13months, recur in up
to 60–70% of patients, can lead to loss of function and decreased quality of life, and are a signicant cause of morbidity [2, 5]. Moreover, care
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M. Maruccia et al. (eds.), Pearls and Pitfalls in Skin Ulcer Management,
https://doi.org/10.1007/978-3-031-45453-0_41
467
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