Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3648_Библиотеки_им_академика_М_И_Перельмана
.pdf
334
ab
cd
H. B. Pasieka et al.
Fig. 24.7 (a) Bullous pemphigoid on the digits of the
lower extremities. You can see here how fresh bullae
reect light. On palpation these bullae are tense and rm
to palpation. Note the hyperpigmentation of the proximal
nail fold of the second digit, suggestive of a previous bulla
associated with bullous pemphigoid, (b) resolving bullae
are less reective and are not as tense and rm as active
lesions. Note that the circular hyperpigmentation around
that resolve with hypopigmented scarring. These
lesions will rarely present on lower extremities if
the more common facial manifestations are not
the lateral malleolus suggests previously healed bullae in
this area, (c) histopathology of bullous pemphigoid with
subepidermal blister formation (arrow). As the epidermis
loses its connection with the underlying dermis, the epidermis will slough off, resulting in ulceration [5], (d)
appearance of blisters after the blister roof has been
removed by trimming, revealing round, shallow ulcerations to the depth of the dermis beneath
associated with systemic disease. If DLE is suspected, a skin biopsy for H&E and DIF evaluation should be performed.
present.
While discoid lupus erythematosus tends to
be a disease limited to the skin [7], it can on
Opportunistic Infections
occasion be associated with underlying systemic
lupus erythematosus, a well-known multisystem
disease. Delphi criteria for the disease as determined by the American College of Rheumatology
in 2019 include arthralgias, fever, leukopenia,
thrombocytopenia, psychosis, and proteinuria
[8]. As is the case with other autoimmune disorders, a thorough history will guide diagnosis
toward or away from DLE, in particular DLE
Opportunistic infection may also be considered
in the evaluation of wounds. Breakdown in the
skin barrier may also yield easier entry to invasive organisms, such as atypical mycobacterial or
fungal species. This section will review common
microorganisms and associated opportunistic
infections along with associated patient history,
risk factors, and presentation.
ab
24 Limb Wounds ofDermatologic Disease: Dermatopathology, Biopsy, andMedical Management
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
335
Fig. 24.8 (a) This gure demonstrates the effect of over-
the-counter Domeboro compresses and 40% urea from
initial presentation, in which the provider desired to disin-
If an infectious etiology is suspected, a tissue
culture specimen should be obtained and cultured
for aerobic and anerobic bacteria, atypical mycobacteria, and fungi. Deep tissue cultures, such as
those obtained via punch or excisional biopsy
technique, are typically sent to the pathology lab
in a sterile cup. They can be placed on a saline
dampened sponge or directly into the sterile cup
with a splash of normal saline to prevent the tissue from desiccation. Tissue for culture should
not encounter formalin. Tissue cultures need to
be sent to the lab as soon as possible for processing, ideally within an hour or two of procurement. Unlike tissue placed in formalin, tissue
cultures cannot be placed on a shelf and await
transport the following day.
In terms of management, debridement and/or
antimicrobials tailored to culture data are eminent treatment options.
Clinical pearl: The sequential application of
Burow’s solution, an antiseptic/astringent compresses, followed by 40% urea cream qHS can be
very benecial in swollen, inamed, or thickened
fect the limb before attempting wound closure, (b) after 2
days of twice daily application of urea and compresses
skin (see Fig.24.8a, b). Burow’s solution can be
obtained over-the-counter or can be purchased as
a convenient powdered formulation in packets to
be mixed with water. The astringent property
decreases swelling and weeping. Additionally,
aluminum acetate is active against S. aureus and
P. aeruginosa, decreasing bacterial colonization
and decreasing inammation at the site. Urea is a
potent keratolytic with humectant properties,
effective at gently lifting and removing retained
hyperkeratosis while hydrating the skin. This
combination can be used to promote de-novo
healing, or prior to planned grafting or amputation to promote a healthy closure. The urea
should be discontinued once the skin is resolved
of hyperkeratosis and smooth.
Another useful tool to prevent colonization
and infection is the use of gentian violet. Gentian
violet has recently gained popularity as a topical
antiseptic due to its effectiveness, low cost, and
availability as an FDA-approved over-the-counter medication. Well known for its antimicrobial
properties, gentian violet has been used to treat
336
H. B. Pasieka et al.
oral candidiasis and in coating urinary catheters
to reduce the risk of urinary tract candidiasis [9,
10]. In terms of antibacterial properties, gentian
violet has been used in the treatment of impetigo
rative/ulcerated/inamed nodules which usually
present at the distal upper extremities and produce
successive proximal lesions along lymphatic
drainage [11, 12] (See Fig.24.9a–c).
as well as demonstrated in randomized controlled
trials to be more effective than iodine in killing
MRSA [9].
Clinical pearl: Gentian violet is also a useful
indicator of patient adherence, as it turns the skin
a characteristic violet after application.
Fungal Infections
The workup of wounds should also include fungal cultures, especially in transplant recipients,
patients with HIV, or other immunocompromised
patients such as patients with uncontrolled diabetes mellitus. See Table24.2 for a relevant sum-
Atypical Mycobacterial Infection
Atypical mycobacterial infections manifest as
single or multiple erythematous lesions. See
Table24.1 for a summary of clinical presentations
and history. In immunocompromised patients,
atypical mycobacterial infections may induce a
distal to proximal “sporotrichoid spread”: suppu-
Table 24.1 Summary of atypical mycobacteria with relevant clinical presentation and history
Mycobacterium Cutaneous presentation History
M. marinum Sporotrichoid spread from point of
inoculation
M. ulcerans Firm, painless, mobile subcutaneous
M. avium complex
(MAC)
M. fortuitum/chelonae
complex
module, may progress to necrosis,
destruction of nervous, musculoskeletal,
vascular tissue
Rare cutaneous involvement, but presents
as necrotic papules with sporotrichoid
spread
Erythematous subcutaneous nodules with
sporotrichoid spread
mary [14].
Clinical pearl: A note on Tinea incognito:
Tinea incognito is a dermatomycosis that can be
exacerbated by the use of systemic or local corticosteroids. Use of these anti-inammatory agents
promotes the proliferation of the dermatophyte
and encourages the Tinea dermatophytes to dive
“Swimming pool granuloma,” cleaning sh
tanks, swimming in freshwater lakes or
unchlorinated swimming pools
Central/West Africa, Japan, SE Asia,
Australia, South America
History of AIDS/immunocompromised
Recent trauma, surgery, injection
abc
Fig. 24.9 (a) A patient with an erythematous right lower
extremity with distinct skip areas and nodularity, inconsistent with venous stasis dermatitis or dermatosclerosis,
(b) skin markings/wrinkles over lesions in the same
patient, inconsistent with lymphedema, (c) deep-seated
indurated nodules with sporotrichoid spread from the
same patient, suggestive of atypical mycobacterial
infection
ab
24 Limb Wounds ofDermatologic Disease: Dermatopathology, Biopsy, andMedical Management
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
337
Table 24.2
Summary of fungal infections in wound care
Fungal organism Cutaneous presentation History
Aspergillus avus/fumigatus Necrotic papules/nodules Immunocompromised, impaired skin
barrier due to wounds, burn, trauma
Mucormycetes spp.
Zygomycetes)
Candida albicans
Tinea pedis Annular supercial erythematous
Tinea incognito
a
(formerly
b
c
Dark eschar at point of inoculation,
commonly in facial/sinus areas
Interdigital superinfection with
satellite lesions
plaques of the feet with scale
Annular erythematous macules/
plaques with hypopigmentation
Immunocompromised, neutropenia,
poorly controlled diabetes
Immunocompromised, high moisture
wound dressing
Male sex, walking barefoot inlocker
rooms, gyms
Misuse of systemic or local
corticosteroids
and diminished/absent scale
a
See Fig.24.10a–d
b
See Fig.24.11
c
See Fig.24.12
c d
Fig. 24.10 (a) Ulcer with dry, necrotic eschar that had
slowly expanded over the course of months in a patient
with poorly controlled diabetes mellitus [13], (b) removal
of the eschar revealed signicant amounts of necrosis
[13], (c) removal of necrotic tissue down to tendon [13],
(d) histology demonstrates broad, non-septate hyphae
consistent with mucormycosis (blue arrow). (d, Courtesy,
Arash Radfar, MD)
338
Fig. 24.11 Erosio interdigitalis blastomycetica due to C.
albicans infection
H. B. Pasieka et al.
into adnexal structures such as hair follicles [9]
causing a fungal folliculitis. See Fig.24.12.
When situated in the dermis, Tinea may be
more difcult to detect as the characteristic erythema and round morphology may be obscured.
Additionally, tinea treated with steroids is usually
lacking the characteristic scale on the surface of
the skin. Fungal folliculitis usually requires systemic antifungal medications for several weeks to
cure, as antifungal medications applied topically
do not reach the depth of the infection. Therefore,
dermatologists generally discourage the use of
combination or concomitant use of anti-inammatory/antifungal creams.
Ecthyma Gangrenosum
Ecthyma gangrenosum is a cutaneous manifestation of septic Pseudomonas aeruginosa angioinvasion. Lesions may initially develop on the
extremities as hemorrhagic vesicles/bullae that
progress into a central black eschar surrounded
by tender and erythematous tissue [15].
Fig. 24.12 Conuent faint erythematous patch without
scale overlying the lateral left lower extremity from a
patient with Tinea incognito
Allergic Contact Dermatitis
Allergic contact dermatitis is another useful consideration in the management of atypical wounds.
In contrast to pyoderma gangrenosum and DLE,
allergic contact dermatitis is a sterile reaction to a
foreign but innocuous antigen. The type IV
delayed hypersensitivity reaction associated with
allergic contact dermatitis can hinder wound
healing. Furthermore, the impaired protective
skin barrier in the setting of wound care may further facilitate sensitization to allergens.
Several components of routine wound care are
potential causes of allergic contact dermatitis: topical antibiotics such as neomycin and bacitracin,
ointments containing balsam of Peru, hydrogels
containing propylene glycol, and hydrocolloids
containing colophonium. Moisturizing substances
such as lanolin or wood alcohols can cause periwound maceration [16].
According to North American Contact
Dermatitis Group (NACDG) patch testing data
from 2017 to 2018, balsam of Peru and topical
antibiotics are the most common causes of allergic
contact dermatitis. Balsam of Peru is of particular
concern to the wound care provider because it may
24 Limb Wounds ofDermatologic Disease: Dermatopathology, Biopsy, andMedical Management
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
339
be found in combination ointments [16], whether
applied in clinic or at home. Per NACDG patch
testing data from 2017 to 2018, 7.1% of allergic
contact dermatitis patients experienced reactions
to balsam of Peru [16]. Colophonium/resin may be
found in some hydrocolloid dressings and may
cross react with balsam of Peru [16].
Antibiotics constitute a key component of
wound care, although common topical antibiotics
such as neomycin and bacitracin may induce
allergic contact dermatitis and impede normal
wound healing (see Fig.24.13). Of the two, neomycin is especially of note as it is the most used
topical antibiotic. NACDG patch testing results
up to 2018 have demonstrated that 5.4% to 13%
of patch-tested patients exhibit a contact dermatitis reaction to this aminoglycoside and that it
consistently appears within the top 15 most common causes of contact dermatitis [17–19]. The
associated contact dermatitis reaction can mani-
fest with extensive inammation and skin breakdown, but neomycin reaction may not necessarily
be the rst thought that comes to mind.
In addition to neomycin and bacitracin, other
antibiotics that may cause contact dermatitis
include polymyxin B and gentamicin, a known
cross-reactant with neomycin.
Removing the offending allergen and continued
avoidance will alleviate allergic contact dermatitis.
Use of topical steroid ointment such as clobetasol or
triamcinolone twice daily can speed the resolution
of the eruption and provide relief of pruritus. Be
sure to avoid placing steroid ointment directly on
surgical incisions in the immediate post-operative
period; we recommend sparing the area 1cm around
the incision. Discontinue steroids as soon as the
rash is no longer pruritic to avoid side effects from
topical steroids. If these allergens constituted a
component of previous wound care, the wound care
provider may need to consider non-allergy-provoking substitutes. Patch testing is a further step that
can establish a patient’s allergy proles and personalize wound treatment regimens going forward.
Clinical pearl: It is important to distinguish
irritant contact dermatitis from allergic contact
dermatitis. Irritant contact dermatitis is caused by
direct tissue damage following exposure to a
known irritant—for this reason irritant contact
dermatitis tends to be localized. Because allergic
contact dermatitis is mediated through immunologic mechanisms, allergic contact dermatitis
tends to involve skin beyond the area of application. Allergic contact dermatitis also tends to be
intensely pruritic.
Cutaneous Malignancy
The wound care provider should also consider
that skin malignancies may be another source of
wounds. The protective skin barrier that is caught
in the vicious cycle of barrier disruption and
chronic inammation may continue to deterio-
Fig. 24.13 Contact dermatitis on the abdomen of a
patient who had laparoscopic surgery. He was applying
Neosporin™ to his surgical sites. You can see the intense
inammation at the site of his surgical wounds and also an
“id reaction,” also known as an “autoeczematous
response,” manifesting as innumerable small papules, in
the surrounding skin. The treatment for both conditions is
withdrawal of the offending topical allergen
rate, or it may exit the cycle via malignant transformation. Lesions in these cases tend to present
as fungating wounds.
Squamous Cell Carcinoma
Areas which have undergone radiation or thermal
treatment are at heightened risk for squamous
340
ab
H. B. Pasieka et al.
Fig. 24.14 (a) Multinodal cutaneous squamous cell car-
cinoma in a patient with a history of pyoderma gangrenosum, with a fungating central lesion suggestive of
Fig. 24.15 Depicted is an example of squamous cell carcinoma on histopathology which shows a markedly atypical with a lack of maturation, large keratinocytic islands
and squamous eddies as well as thick overlying crust [20]
cell carcinoma due to increased keratinocyte
activity. Persistent ulceration or inammation in
the context of hidradenitis suppurativa, especially
in the inguinal folds, may be another driver of
keratinocyte activity and risk for squamous cell
carcinoma. See Figs.24.14a, b and 24.15.
Marjolin’s Ulcer
Marjolin’s ulcer describes a delayed malignant
transformation associated with scarred tissue.
Most Marjolin’s ulcers are squamous cell carci-
squamous cell carcinoma, deemed unresectable, (b) Posttreatment appearance after administration of systemic
immunotherapy
Fig. 24.16 Here on the left buttock of a young man is a
large, crateriform non-healing wound at the center of surrounding sinus tracts. Biopsy revealed that this was a
Marjolin’s ulcer. This poorly differentiated squamous cell
carcinoma developed after several years of uncontrolled
hidradenitis suppurativa. Further workup revealed metastatic disease
nomas and occur over lower extremity scars.
While Marjolin’s ulcer is primarily associated
with old burn trauma and secondarily with osteomyelitis, they may also arise from venous stasis
ulcers, pressure ulcers, hidradenitis suppurativa
(see Fig.24.16), or trauma.
Malignant transformation takes on average
30–35years to manifest, but acute variations of
24 Limb Wounds ofDermatologic Disease: Dermatopathology, Biopsy, andMedical Management
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
341
Marjolin’s ulcer exist with some reports of disease following 6months after injury [15]. Given
this variable range, a patient who presents with
more than 3months of a triad including nodularity, induration, and ulceration over an area of
scarring should warrant consideration of
Marjolin’s ulcer.
Other forms of skin cancer that could present
as a non-healing wound include basal cell carcinoma and rarer malignancies such as epithelioid
angiosarcoma. Nonmalignant causes of fungating wounds include pseudoepitheliomatous
hyperplasia, a close, but benign mimic of squamous cell carcinoma. For this reason, we prefer
that such biopsies be sent to an experienced
dermatopathologist.
Vascular Diseases
Venous and arterial ulcers are commonly seen
and therefore will not be discussed here. This
section will focus on less common dermatologic
entities caused by vascular diseases such as calciphylaxis, vasculopathy, and vasculitis.
A common and nonspecic manifestation of
vascular disease in the setting of atypical wounds
is retiform purpura, a net-like lesion with nonblanching and visible hemorrhage into the skin
and mucous membranes. The non-blanching purpuric characteristic of retiform purpura differentiates it from livedo reticularis, another net-like
lesion.
Retiform purpura occurs from thrombus formation in small cutaneous vessels and carries
with it a broad differential ranging from vasculitis to vessel occlusion. When the wound care provider suspects a vascular etiology with retiform
purpura, a sample for direct immunouorescence
should be obtained and sent in Michel’s/Zeus
transport media in addition to a sample for hematoxylin and eosin staining.
Calciphylaxis
Calciphylaxis typically presents as extremely
painful, edematous, retiform, non-blanching purpura, plaques, or livedo reticularis. Of note, retiform purpura is not a specic nding of
calciphylaxis and heads a broad differential,
which will be covered further in this chapter.
In later stages of calciphylaxis, the wound
may form a central, leathery, bound down eschar
with a surrounding dusky, reticular plaque (see
Fig.24.17a–c). Traditional locations of calciphylaxis have a predilection for areas with high
amounts of adipose tissue, such as the thigh, buttocks, trunk, and upper extremities, but may
involve atypical locations like the penis, digits,
and lower extremities.
Calciphylaxis can be further characterized
into uremic and nonuremic disease. Risk factors
for uremic disease revolve around hypercalcemic
conditions such as end-stage renal disease and
secondary hyperparathyroidism to calcium and/
or vitamin D supplementation (see Fig.24.18a).
Nonuremic etiologies can arise due to liver dis-
abc
Fig. 24.17 (a–c) Retiform, “star-like” eschar as seen in calciphylaxis
342
a b
H. B. Pasieka et al.
Fig. 24.18 (a) Faint dusky retiform plaques with overly-
ing dried serosanguineous crust on leg of a patient with
renal failure, early calciphylaxis lesion, (b) this photomi-
ease, warfarin, or malignancy. Elevated alkaline
phosphatase and low serum albumin have also
been identied as risk factors for calciphylaxis.
Patients undergoing hemodialysis or the use of
calcium-based phosphate binders such as calcium carbonate will place patients at a higher risk
of vascular calcium deposition and calciphylaxis
(see Fig.24.18b). Additional risk factors identied include female gender, hyperphosphatemia,
obesity, and diabetes mellitus [22].
Management of calciphylaxis focuses on
removing the underlying source of hypercalcemia and preventing secondary infection of
wounds. Whether to debride the wounds is
debated, as in some cases this causes pathergy.
Partnership with dermatology is recommended.
Vasculitis
Small to medium vessel vasculitis describe endothelial inammation in postcapillary vasculature
that can cause retiform purpura [23].
IgA vasculitis/Henoch-Schönlein purpura is
thought to induce retiform purpura through IgA
immune complex deposition.
ANCA vasculitis such as microscopic polyangiitis, granulomatosis with polyangiitis/
Wegener’s granulomatosis, and eosinophilic
granulomatosis with polyangiitis/Churg-Strauss
crograph shows calciphylaxis with calcium deposits in the
vessel in the deep dermis (see arrow) which have resulted
in overlying dermal and epidermal necrosis [21]
Fig. 24.19 This gure shows a massively inamed
medium caliber artery in the subcuticular tissues characteristic of vasculitis/polyarteritis nodosa. Inammation of
vessels can lead to vessel destruction which eventually
can result in ulceration of the skin [25]
syndrome may also present with retiform purpura
[24]. Both microscopic polyangiitis and granulomatosis with polyangiitis may present with
glomerulonephritis.
Polyarteritis nodosa (PAN) is a medium vessel
vasculitis (see Fig.24.19) that may exhibit systemic manifestations with fever, arthralgias,
24 Limb Wounds ofDermatologic Disease: Dermatopathology, Biopsy, andMedical Management
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
343
myalgias, abdominal pain, and renovascular
hypertension or may simply be limited to cutaneous signs like retiform purpura. Cutaneous PAN
tends to be a chronic and benign disease and
recently has been theorized to be an altogether
separate process from systemic PAN [26].
Other vasculitides that can cause retiform purpura include rheumatoid vasculitis or septic
vasculitis.
Vasculopathies
In contrast to vasculitis, vasculopathies describe
an occlusion of the vasculature that can manifest
as retiform purpura. This can arise from angioinvasive organisms or occlusive conditions such as
calciphylaxis or thrombophilia.
Heparin-induced thrombocytopenia (HIT)
may induce platelet activation and subsequent
thrombocytopenia and should be consistent with
the patient’s medication history.
Cryoglobulinemia/cryofibrinogenemia
describes the excessive vascular deposition of
antibodies or brinogen in response to cold
temperature.
Underlying coagulation disorders such as protein C/S deciencies, antiphospholipid syndrome
[27], livedoid vasculopathy, and use of levamisole-adulterated cocaine may also contribute
toward a presentation of livedo reticularis.
Angioinvasive organisms include fungi such
as Aspergillus and Mucor spp. These infections
and their associated cutaneous manifestations are
covered in the “Opportunistic Infections” section
above.
The context of thrombophilia as well as an
accurate patient history is important to the consideration of thrombophilia.
Workup
This section ties together a summary of biopsy
locations and appropriate media to use for dermatopathology evaluation. Once the wound care
provider has considered the possibility of a dermatologic wound before debridement, the next
step is to obtain three specimens for histopathologic analysis (see Table24.3).
It is important to keep each specimen organized in its correct transport media. A common
mistake is to send a sample in an inappropriate
medium, such as a sample intended for DIF or
culture, incorrectly sent in formalin rather than
correctly sent in Michel’s/Zeus transport media
or sterile cup, respectively.
All specimen containers should be labeled
with the patient’s name and the site from which
they were procured. It is also helpful for the clinician to provide an adequate history (i.e. concern
for calciphylaxis) along with the specimen, as
this can focus pathology evaluation.
Obtaining Specimens: Recommended
Sites andTransport Media
For larger wounds, the main specimen should be
obtained via an elliptical wedge incision at the
ulcer edge (see Fig.24.20). This specimen should
be from a wound that is over 72h old and should
be sent in a formalin bottle for H&E analysis.
A tissue culture specimen should be obtained
from a representative site and should be about
4–6 mm in size. This should be submitted in a
sterile urine cup with sterile gauze/saline with
orders for tissue culture for bacteria, fungi, and
Table 24.3 Summary of the three different biopsy specimens, sites, and recommended transport media
Main specimen Tissue culture specimen Peripheral specimen
Purpose Is there pyoderma
gangrenosum, malignancy, or
calciphylaxis?
Specimen
site
Media Formalin Sterile urine cup with sterile
Orders H&E Mycobacterial, fungal, and
Elliptical wedge incision at
ulcer edge, >72h old
Is there an opportunistic
infection?
Representative site,
4–6mm
gauze/saline
bacterial cultures
Is there underlying vasculitis,
vasculopathy, or autoimmune
process?
Representative site,
<24h old
Michel’s/Zeus transport media
DIF
Соседние файлы в папке Библиотека им академика М.И. Перельмана