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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5191_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Contents
- •2.1 Introduction
- •2.2 Dry Necrosis
- •3.2 Pathophysiology
- •3.3 Clinical Manifestations
- •2.3 Wet Necrosis
- •2.4 Debridement
- •2.4.2 Dissecting Haematomas
- •2.6 Conclusion
- •References
- •3.1 Introduction
- •References
- •4.1 Introduction
- •4.2.1 Conventional X-Rays
- •4.2.2 Duplex Ultrasonography
- •4.2.3 Computed Tomography (CT)
- •4.2.4 Magnetic Resonance Imaging (MRI)
- •4.2.5 Vascular Imaging
- •4.3 Treatment
- •4.3.1 AVM
- •References
- •5.1 Introduction
- •5.2 Imaging Methods
- •5.2.1 X-Ray Mammography
- •5.2.2 Ultrasound
- •5.2.3 Magnetic Resonance Imaging
- •5.3 Conclusion
- •References
- •6.1 Introduction
- •6.10 Revascularization Procedure
- •6.12 Nonoperative Treatment
- •6.13 Conclusion
- •References
- •7.1 Introduction
- •7.2 Metabolic Origin
- •7.3 Pathophysiology
- •7.4 Clinical Diagnosis
- •7.5 Vascular Explorations
- •7.6 Treatment
- •7.7 Conclusion
- •References
- •Reference
- •9.1 Introduction
- •9.4 Conclusion
- •References
- •10.4.1 Primary Necrosis
- •10.4.2 Secondary Necrosis
- •10.4.3 Tertiary Necrosis
- •References
- •11: Electrical Burns
- •11.1 Introduction
- •11.2 Tissue Injury
- •11.2.2 Muscle Injury
- •11.2.3 Myocardial Damage
- •11.2.4 Buccal Mucosa Damage
- •11.2.5 Nerve Damage
- •11.2.6 Deep Damage (Except Viscera)
- •11.2.7 Other Damages
- •11.3 Medical Management
- •11.3.1 Monitoring
- •11.4 Surgical Management
- •11.4.1 First Surgery
- •11.4.2 Second Look
- •11.5 Global Management
- •11.6 Prevention
- •11.7 Conclusion
- •References
- •12: Gunshot Wounds
- •12.1 Introduction
- •12.2 Etiopathogeny
- •12.3 Clinical Detailing
- •12.3.1.1 Cavity
- •12.3.1.2 Abrasion Ring (Marginal Abrasion, Contusion Ring)
- •12.3.1.4 Secondary Shock Wave
- •12.3.1.5 Skin Burn
- •12.3.1.6 Bullet Wipe
- •12.3.1.7 Smudging
- •12.3.1.8 Tattooing
- •12.3.1.9 Retained Foreign Materials
- •12.4.1 Save Life
- •12.5.1 Initial Dressing
- •12.5.2 Wound Surgery
- •12.6 Conclusion
- •References
- •13: Frostbite
- •13.1 Aetiology
- •13.3 Pathology
- •13.3.3 Long-Term Sequelae
- •13.4.1 History
- •13.4.2 Examination
- •13.5 Acute Frostbite Management
- •13.5.3 Pharmacological Support During Rewarming
- •13.6 Post-thaw Frostbite Care
- •14.3 Radiation Ulcers
- •14.4.1 Debridement
- •14.4.2.1 Surgical Treatment
- •14.4.2.2 Stem Cell Therapy
- •14.5 Case Reports
- •14.5.1 Case 1
- •14.5.2 Case 2
- •14.5.3 Case 3
- •14.5.4 Case 4
- •14.6 Conclusion
- •References
- •13.6.2 Physiotherapy Protocols
- •13.6.3 Surgery
- •13.7 Summary Points
- •References
- •14.1 Introduction
- •14.2 Ionizing Radiation
- •15.1 Introduction
- •15.2 Gastroschisis
- •15.3 Dissecting Hematoma
- •15.5 Diabetic Foot Abscesses
- •References
- •16.1 Introduction
- •16.3 Tele-Assistance
- •16.4 Technology
- •16.6 Conclusion
- •References
- •18.1 Introduction
- •18.2 Clinical Presentation
- •18.3 The Therapeutic Decision
- •18.3.1 Evolution
- •18.3.3 Surgical Intervention
- •18.3.4 Follow-Up
- •18.4 Conclusion
- •Bibliography
- •19.1 Introduction
- •19.2 Medications
- •19.2.1 Hydroxyurea
- •19.2.2 Anagrelide
- •19.2.3 Coumarins
- •19.2.4 Heparin
- •19.2.5 Methotrexate
- •19.2.7 Hydralazine
- •19.2.8 Amezinium Methylsulfate
- •19.2.9 Diltiazem
- •19.2.10 Propylthiouracil
- •19.2.11 Nicorandil
- •19.2.12 Levamisole
- •19.2.13 Pentazocine
- •19.2.14 Tyrosine Kinase Inhibitors
- •19.3 Therapy
- •19.4 Conclusion
- •References
- •20: Toxic Syndromes
- •20.1.2 Skin Manifestation
- •20.1.2.1 Streptococcal Toxic Shock Syndrome
- •20.1.2.2 Skin Manifestation
- •20.2 Pathophysiology
- •20.3 Treatment
- •20.3.1 Antibiotic Therapy
- •20.3.2 Intravenous Immune Globulin
- •20.3.3 Surgical Therapy
- •References
- •21.1 Introduction
- •21.3 Dry Bite
- •21.4 First Aid
- •21.5 Antivenom Treatment
- •21.7 Surgical Treatment
- •21.9 Case Reports
- •21.9.1 Case 1
- •21.9.2 Case 2
- •21.9.3 Case 3
- •21.10 Conclusion
- •References
- •22.1.2 Habitat
- •22.1.3 Venomous Apparatus
- •22.2.1 General Ideas
- •22.2.2 Circumstances
- •22.2.3 Wound Location
- •22.2.4 Clinical Evidence
- •22.2.5 Diagnosis
- •22.2.7 Medical Complications
- •22.2.8 Treatment
- •22.2.9 Other Used Treatments
- •22.4 Clinical Cases
- •22.4.1 Case 1
- •22.4.2 Case 2
- •22.4.3 Case 3
- •References
- •23.1 Introduction
- •23.2 Case Examination
- •23.4 Conclusion
- •References
- •25.1 Introduction
- •25.2.1 Vasculitis
- •25.2.2 Neutrophilic Dermatoses
- •25.2.3 Venous Stasis
- •25.2.4 Arterial Disease
- •25.2.5 Corticosteroid Therapy
- •25.3.1 Systemic Lupus Erythematosus (SLE)
- •25.3.2 Systemic Sclerosis
- •25.3.3 Dermatomyositis
- •25.3.4 Sjögren’s Syndrome
- •25.3.5 Scleroderma
- •25.3.6 Behcet’s Syndrome
- •25.4.1 Systemic Approach
- •25.4.2 Topical Wound Treatment
- •25.4.3 Occlusive Dressings
- •References
- •26: Giant Cell Arteritis
- •26.1 Introduction/Physiopathology
- •26.2 Diagnosis
- •26.2.1 Medical Context
- •26.2.2 Semiology
- •26.2.4 Routine Evaluation
- •26.3 Treatment
- •26.4 Tocilizumab
- •26.5 Methotrexate
- •References
- •27: Hidradenitis Suppurativa
- •27.1 Introduction
- •27.2 Diagnosis
- •27.3 Pathophysiology
- •27.4 Treatment
- •27.5 Adjuvant Therapy
- •27.6 Conclusion
- •References
- •28: Martorell Hypertensive Ischemic Ulcer
- •28.1 Epidemiology
- •28.2 Etiopathogenesis
- •28.3 Clinical Diagnosis
- •28.4 Histopathology
- •28.6 Evolution
- •28.8 Other Treatments
- •28.9 Conclusion
- •References
- •29: Vasculitis
- •29.2 Pitfalls
- •29.4 Clinical Manifestations
- •References
- •30: Necrobiosis Lipoidica
- •30.1 Introduction
- •30.2 Epidemiology
- •30.5 Treatment
- •References
- •31: Purpura Fulminans
- •31.1 Introduction
- •31.2 Epidemiology
- •31.4 Pathogenesis
- •31.5 Clinical Presentation
- •31.5.1 Workup
- •31.5.2 Management
- •References
- •32.1 Physiopathology
- •32.2 Diagnosis
- •32.3 Treatment
- •33.1 Comorbidity
- •33.2 Exacerbation
- •33.3 Direct Cause
- •33.4 Treatment
- •References
- •34: Calciphylaxis
- •34.1 Introduction
- •34.2 Risk Factors
- •34.3 Clinical Manifestation
- •34.4 Pathophysiology
- •34.5 Diagnosis
- •34.6 Treatment
- •References
- •35: Livedo(id) Vasculitis
- •35.1 Introduction [1]
- •35.2 Histology [1]
- •35.3 Pathogenesis [1, 2]
- •35.4 Clinical Presentation
- •35.4.2 Location
- •35.5 Diagnosis [2, 3]
- •35.6 Treatment [6–11]
- •35.6.1 General Management
- •35.6.2 Therapeutic Modalities
- •35.6.3 Perspectives
- •References
- •36: Pyoderma Gangrenosum
- •36.1 Introduction
- •36.2 Etiopathogenesis
- •36.3 Clinical Detailing
- •36.4 Treatments
- •References
- •37: Cryoglobulinemia
- •37.1 Physiopathology
- •37.2 Diagnosis
- •37.3 Treatment
- •37.3.1 Systemic Treatment
- •37.3.2 Local Treatment
- •References
- •38: Hand Necrosis
- •38.1 Introduction
- •38.2 Vascularization
- •38.3 Mechanisms
- •38.4 Etiologies
- •38.6 Diagnosis
- •38.7 Management
- •References
- •39.1 Introduction
- •39.5 Conclusion
- •References
- •41.1 Introduction
- •41.2 Bacteria
- •41.3 Mycobacteria
- •41.4 Viruses
- •41.6 Yeast
- •41.7 Parasites
- •41.8 Pathological Mechanisms
- •References
- •42: Fusarium solani
- •References
- •43: Fournier Gangrene
- •43.2 Physiopathogenesis
- •43.3 Diagnosis
- •43.4 Treatment
- •43.5 Reconstruction
- •43.6 Conclusion
- •References
- •44: Infection Context: Necrotizing Fasciitis
- •44.1 Introduction
- •44.2 Epidemiology
- •44.3 Symptom
- •44.5.1 Physical Diagnosis
- •44.5.2 Laboratory Tests
- •44.6 Treatment
- •44.6.1 Medical Therapy
- •44.6.2 Surgical Therapy
- •References
- •46: Skin Necrosis Over Osteosynthetic Material
- •46.1 Introduction
- •46.2 Postoperative Skin Necrosis
- •46.2.1 Debridement
- •46.2.2 NPWTi
- •46.2.3 Hardware Removal
- •46.2.4 Soft Tissue Reconstruction
- •46.3 Delayed Skin Necrosis
- •46.4 Conclusion
- •References
- •47: Necrotic Complications After Skin Grafts
- •47.1 Introduction
- •47.2 Graft Survival
- •47.3.1 Recipient Site
- •47.3.3 Graft Shearing
- •47.3.4 Infection
- •47.3.5 Poor Systemic Conditions
- •47.3.6 Technical Errors
- •47.4 Graft Rescue
- •48: Arterial Leg Ulcers
- •48.1 Introduction
- •48.3 Clinical Findings
- •48.4 Diagnosis
- •48.5 Treatment
- •References
- •49.1 Introduction
- •49.1.1 Aesthetic Procedures
- •49.1.2 Filling Products
- •49.1.4.1 Ablative Lasers
- •49.1.4.2 Non-ablative Thermal Lasers
- •49.1.4.3 Vascular Lasers
- •49.1.4.4 Pigment Lasers
- •49.1.4.5 Radiofrequency
- •49.1.5 EBD
- •49.1.5.1 LEDs
- •49.1.5.2 High-Intensity Focused Ultrasound (HIFU)
- •49.1.5.3 Cryolipolysis
- •49.1.6 Peelings
- •49.1.6.1 Epidermal Peel
- •49.2 Complications
- •49.2.2 Scars
- •49.2.3 Infectious
- •49.3 Conclusion
- •References
- •50.1 Introduction
- •50.4 Clinical Indications
- •50.5 Conclusion
- •References
- •References
- •52: Skin Reconstruction Using Dermal Substitutes After Skin Necrosis
- •52.1 Introduction
- •References
- •53.1 Introduction
- •References
- •54.1 Introduction
- •54.3 Clinical Presentation
- •54.3.1 Detecting Early Change
- •54.3.2 Wet Necrosis
- •54.3.3 Dry Necrosis
- •54.4.1 Debridement
- •54.4.2 Vascular Intervention
- •54.4.3 Reconstruction Using Free Flaps
- •References
- •55: Exposed Necrotic Tendons
- •55.1 Introduction
- •55.3.1 Immobilization
- •55.3.2 Negative Pressure Wound Therapy
- •55.3.4 Flaps
- •55.4.1 Burns
- •55.4.2 Trauma
- •55.4.3 Miscellaneous
- •References
- •56.1 Introduction
- •56.2 Clinical Signs
- •56.4 Complementary Exams
- •56.5 Surgical Management
- •References
- •57.1 Introduction
- •57.3.1.2 Postoperative Management
- •57.3.1.3 Patient-Inherent Irreversible Causes
- •57.3.1.4 Vascular Disease
- •57.3.1.5 Systemic Disease
- •57.4.1 Repeat Free Flap Procedure
- •57.4.2 Non-microsurgical Therapy
- •References
- •59.1 Introduction
- •59.2.1 Hydrating Dressings
- •59.2.1.1 Hydrogels
- •59.2.1.2 Hydrogel-Like Devices
- •59.2.2.1 Irrigo-Absorbents
- •59.2.2.2 Hydrocolloids
- •59.2.3 Absorbent Dressings
- •59.2.3.1 Alginates
- •59.2.3.2 Fiber Dressings
- •Dressings Containing Salts
- •Medical Honey Dressings
- •References
- •60: Surgical Debridement
- •60.1 Introduction
- •60.2.1 Burns
- •60.2.2 High-Energy Trauma Wound
- •60.2.3 Pressure Injury
- •60.2.4 Diabetic Foot Ulcer
- •60.2.5 Leg Ulcer
- •References
- •61.1 Introduction
- •61.4 Clinical Indications Outside Burns
- •61.4.1 Arterial Leg Ulcer
- •61.4.3 Diabetic Foot Ulcer
- •61.5.1 Malignant Wound
- •61.5.2 Radionecrosis
- •61.8 Conclusion
- •References
- •62: Honey Debridement
- •62.1 Introduction
- •62.2 Antibacterial Properties
- •62.3 Debridement
- •62.4 Tissue Growth
- •62.5 Deodorizing
- •62.7 Contraindications
- •62.8 Conclusion
- •References
- •63.1 Introduction
- •63.3 Clinical Indications
- •References
- •References
- •65.1 Introduction
- •65.2.1 General Aspects
- •65.2.2 Predisposing Factors
- •65.2.3 Laboratory Examinations
- •65.2.4 Diagnosis
- •65.3.3 Epidemiology
- •65.3.5 Care
- •65.3.6 Physiology of Extravasation
- •65.3.9 Dangerous Substances
- •65.3.10 Treatments
- •65.4.1 Introduction
- •65.4.2 Care
- •References
- •66: Neonatal Pressure Ulcer
- •66.1 Introduction
- •66.2 Risk Assessment Scales
- •66.3.1 Topic Treatment
- •66.3.2 Surgical Treatment
- •66.4.1 The Nose
- •66.5 Conclusion
- •References
- •67.1 Introduction
- •67.2.1 Progeroid Syndromes
- •67.2.2 Vascular Anomalies
- •67.2.3 Metabolic Disorders
- •67.2.5 Harlequin Ichthyosis
- •67.2.6 Olmsted Syndrome
- •67.2.8 Other Genetic Diseases
- •References
- •68.1.1 Physiopathology
- •68.1.2 Clinical Presentation
- •68.1.3 Diagnosis
- •68.1.4 Treatment
- •68.2 Ulcerated Congenital Hemangiomas
- •68.2.1 Physiopathology
- •68.2.2 Clinical Presentation
- •68.2.3 Diagnosis
- •68.2.4 Treatment
- •68.3 Arteriovenous Malformations
- •68.3.1 Physiopathology
- •68.3.2 Clinical Presentation
- •68.3.3 Diagnosis
- •68.3.4 Treatment
- •References
- •70.1 Background
- •70.2 Etiology/Pathophysiology
- •70.3 Presentation
- •70.5 Prevention
- •70.6 Treatment
- •References
- •71.1 Pathophysiology
- •71.2 Epidemiology
- •71.3 Clinical Signs
- •71.5 Complications
- •71.6 Additional Examinations
- •71.7.1 Medical Management
- •71.7.2 Surgical Management
- •71.7.3 Healing
- •71.8 Prevention
- •71.9 Conclusion
- •References
- •72: Introduction
- •References
- •References
- •74.1 Introduction
- •74.3 Conclusion
- •References
- •75.1 Introduction
- •75.2.1 Autolytic Debridement
- •75.2.2 Enzymatic Debridement
- •75.2.3 Mechanical Debridement
- •75.2.4 Biological Debridement
- •References
- •76.1 Introduction
- •76.4 Who Can Debride?
- •76.6 Assess
- •76.7 Pain Relief
- •76.10 Conclusions
- •References
- •77.1 Introduction
- •77.4 Regulations
- •77.5 Conclusion
- •References
- •78: Distance Skin Necrosis Management
- •78.1 Introduction
- •78.2 Who Is Concerned?
- •78.2.1 The Patients
- •78.2.2 Local or First-Line Caregivers
- •78.2.3 The Experts
- •78.4 When? How? ‘OR’ What?
- •78.5 Conclusion
- •References
- •Index

ab
71 Deep Dissecting Haematoma: AFrequent Cause ofNecrosis inElderly Patient
463
DDH [1, 3]. The lack of specicity of these clinical signs and the lack of knowledge about the disease frequently lead to delays in diagnosis and
management.
There are several clinical forms, depending on
the extent, age and whether or not the affected
limb has been operated on [3]:
(a) Early closed form: swelling or tumefaction on
the affected limb with normal skin coloration
(b) Advanced closed form: swelling or pucker-
ing, with changes in skin colour (erythema,
purplish appearance) (Fig.71.2)
(c) Advanced form with necrosis of the haema-
toma roof: appearance of an area of skin
necrosis above the swelling or curvature
(Fig.71.3)
(d) Spontaneous open form or after surgery
(e) Lastly, there are forms of late revelation [17]
Fig. 71.2 Advanced closed form of DDH: tumefaction or
swelling, with change in skin color (erythema, purplish
appearance). Note pen mark to monitor evolution of the
dissection
71.4 Dierential Diagnosis
All the clinical signs and a lack of awareness of
this common condition are the cause of many
misdiagnoses, with a signicant delay in treatment [3, 7].
The main differential diagnoses are as
follows:
(a) The diagnosis of erysipelas (bacterial
dermo-hypodermatitis) is often made in
the rst instance, mainly in the lower limb
[1, 3, 10] (Fig. 71.4a). In the series by
Kaya et al., almost half the patients had
been treated for erysipelas before the DDH
was diagnosed. The average delay between
the onset of clinical signs and the diagnosis of cutaneous dissecting haematoma was
2weeks [1]
(b) A simple haematoma appears as a more or
less coloured bulge, without extension or
necrosis. Drawing the outline of the bulge
with a pen on the skin allows you to monitor
its development and determine whether it is
dissecting or not (Fig.71.2)
(c) c] Deep vein thrombosis (DVT) is also
sometimes suspected with a tense, painful
calf and the presence of a Homans’s sign±an
indurated cord. Doppler examination is used
to rule out this diagnosis
(d) More rare, Morel-Lavallée syndrome
occurs following violent trauma with shearing of the skin on the deep planes. It often
occurs in young people practicing a violent
Fig. 71.3 Example of advanced DDH with complete moist necrosis of the skin cover (a) and appearance of the base-
ment after partial mechanical debridement (b)

464
H. Colboc and S. Meaume
a
b
c
Fig. 71.4 Differential diagnosis. (a) Erysipelas in an elderly patient. (b, c) Necrosis and underlying cavity on Morel-
Lavallée in an elderly patient
sport during a slip (motorbike, skiing, etc.).
Diagnosis is usually late, often >1year. Men
are more often affected. They consult their
doctor because of skin puckering and func-
tional or cosmetic discomfort. The surround-
ing skin is rarely necrotic unless it occurs in
an elderly person with atrophic skin
(Fig.71.4b, c).
71.5 Complications
(a) Deglobulation in DDH is a classic compli-
cation. ln the vast majority of cases,
patients receive at least one transfusion of
red blood cells [2]. However, DDH is
rarely the cause of major deglobulation
during active bleeding, with hemorrhagic
shock or hypovolemic shock leading to
death [1, 3, 4]
Fig. 71.5 DDH complicated by infection
(b) Infection, which can progress to severe sep-
sis, is also a possible complication. A cutaneous breach (spontaneous or provoked)
associated with the collection of blood, constitutes a real “culture broth” often at the origin of the infection (Fig.71.5). The infection

71 Deep Dissecting Haematoma: AFrequent Cause ofNecrosis inElderly Patient
465
a
b
c
Fig. 71.6 Complicated DDH with compartment syndrome (a). But unfortunatly aponeurotomy will not (b, c) prevent
amputation
may be acute, with the onset of erysipelas,
manifested by erythema, skin heat, pain,
fever with hyperleukocytosis, and the possi-
ble presence of adenopathy. It can also
develop quietly, leading to endocarditis in
the absence of rapid, appropriate antibiotic
treatment.
(c) Compartment syndrome in the lower limb
occurs when there is a large and often rapid
increase in haematoma in a conned space,
which interrupts the blood supply to the mus-
cles. Clinically, it manifests itself as intense
pain, resistant to morphine, with a persistent
pedal pulse. MRl conrms muscle damage
and treatment consists of emergency aponeu-
rotomy, which does not always prevent
amputation (Fig.71.6a–c)
(d) Delayed healing of the attened haema-
toma, in the case of DDH of the lower
limbs, if associated with arterial disease or
chronic venous insufciency with delayed
healing if the arterial disease (revascularisa-
tion) or venous disease (compression) is not
treated.
71.6 Additional Examinations
They are not systematic, but are selected according to the terrain and the clinic.
1. A blood sample is often taken urgently in the
event of DH in order to carry out a blood
count, blood crase, AB0, and rhesus blood
group to consider a blood transfusion if necessary [3].
2. Emergency imaging is necessary in cases of
large and/or rapidly expanding DDH [3]. This
conrms the diagnosis, claries the lesion status, and should not delay medical and surgical
management.
(a) Ultrasound of the soft tissues allows the
haematoma to be located and the extent of
the haematoma to be determined.
(b) An angio-TDM or angio-MRl angiogram
is used to determine whether or not there
is active bleeding.
(c) An X-ray can be used to check for associ-
ated fractures.

466
H. Colboc and S. Meaume
3. There is no indication for a skin biopsy; the diag-
nosis is made clinically and radiologically [3].
71.7 Medical andSurgical
Management
71.7.1 Medical Management
While some DDH can be managed on an outpatient basis, serious or potentially serious haemorrhage requires hospital treatment.
If the patient is on anticoagulation, its continuation must be assessed on the basis of the benet/risk balance and adapted in the event of
overdose, which must be investigated [2].
A blood transfusion may be necessary if the
patient develops deglobulation [1–3].
There is no place for antibiotics in the treatment of DDH, in the absence of fever or associated erysipelas.
a
71.7.2 Surgical Management
The indication for surgical management depends
on the age and stage of the DH (see above) [1, 3]
may be performed in the patient’s bed or in the
operating room [18].
In the rst case, when the DDH is small and
often old (dry necrosis), the procedure can be
carried out by a nurse or doctor trained in the
procedure.
ln the case of an extensive or complicated
haematoma, it is essential to have a team of
experienced surgeons: orthopaedic surgeon,
vascular surgeon, general surgeon, or plastic
surgeon.
Necrotic tissue must be excised and debridement down to the muscle plane must be performed, often resulting in signicant skin
breakdown. In the presence of an old HD (redcurrant jelly appearance), debridement down to the
healthy layer is carried out (Fig.71.7a–c).
b
c
Fig. 71.7 Old DDH constituted: the necrotic tissue is excised (a) a declotting of the coagulated blood (appearance of
currant jelly) until the healthy plan is carried out (b, c)

71 Deep Dissecting Haematoma: AFrequent Cause ofNecrosis inElderly Patient
467
It should be noted that if DDH is diagnosed
early and treated at an early stage, it will spread
less and surgery will be less disruptive [3].
ln general, the following management can
be proposed, depending on the stage of the
DDH:
• Early or advanced stage, closed, small: no
surgery
a
c
de
• Advanced stage, large, extensive: experienced
surgeon ± vascular surgeon
• Advanced stage with skin necrosis
– Limited old dry necrosis: nurse at the bed-
side (Fig.71.8a–d)
– Extensive necrosis with large haematoma:
experienced surgeon
• Open stage: experienced surgeon, major risk
of infection
b
fgh
Fig. 71.8 Necrotic DDH (a) bedside clean (b, c, d) with NPWT placement (e), granulation tissue (f) then mesh graft
(g) and complete healing (h)

468
ac
H. Colboc and S. Meaume
There are no data in the literature on the benets of limb compression or ice bag placement in
the initial phase of DDH management.
71.7.3 Healing
The method chosen for healing the wound after
attening depends on the extent of the wound and
the type of surgery (dislocating or not).
The use of Negative Pressure Wound Therapy
(NPWT) is very effective in large wounds with
signicant loss of substance (Fig.71.8e, f). After
obtaining granulation tissue (Fig. 71.8g), it can
be followed by a skin graft: often a mesh graft
(Figs. 71.8h and 71.9a) or split skin graft
(Fig.71.9b) performed by a team of plastic surgeons, or else pinch grafts (Fig.71.9c) in case of
smaller wounds.
Wound healing can be obtained using
advanced dressings (alginate, bre dressing) in
case of small wounds [18]. It is usually performed
in geriatric wards to ensure comprehensive care
for patients, who are often elderly and disabled.
However, despite careful management, healing is often slow and may be delayed by malnu-
trition or in patients with associated venous and/
or arterial insufciency. This difculty in healing
has been observed in half of all patients, and is
associated with diabetes, venous insufciency,
and the presence of arterial disease [1–3].
71.8 Prevention
Care also involves prevention, particularly
against minor trauma in people identied as
being at risk of DDH.Education of nursing staff,
protection of the lower limbs, prevention of the
risk of falls by adapting home furnishings and
correcting visual problems. Dosage of anticoagulant treatment must be adjusted in elderly
patients, who are therefore at risk of renal failure
and drug interactions.
Detection and management of dermatoporosis
are also essential. Photoprotection is a key factor
in preventing the worsening of dermatoporosis if
it is applied early enough in life. The use of local
retinoids thickens the epidermis and stimulates
epidermal differentiation. The maximum effect is
obtained after 6 months, but this topical often
causes skin irritation, which limits its use.
b
Fig. 71.9 Different types of grafts used to close DDH-related defects. Mesh graft (a) or split skin graft (b) for large
DDH.Pinch graft (c) for small DDH

71 Deep Dissecting Haematoma: AFrequent Cause ofNecrosis inElderly Patient
469
Conversely, dermocorticoid treatments that
increase skin atrophy should be avoided wherever possible.
Kaya etal raised the possibility of using topical treatments comprising intermediate-sized
hyaluronic acid fragments to correct the cutaneous atrophy of dermatoporosis by a CD44dependent mechanism in elderly subjects [7].
The patients who respond best are those aged
between 74 and 86years [19].
A synergistic action has recently been shown
in mice, and also in patients suffering from dermatoporosis, when retinaldehyde and
intermediate- sized hyaluronic acid fragments are
applied [20].
71.9 Conclusion
DDH is a serious and often overlooked complication of anticoagulant therapy. It most often
occurs on the lower limbs of elderly subjects
with skin fragility linked to dermatoporosis. lt
generally follows trauma, but this may be minimal or even absent in the case of spontaneous
haematomas.
ln extreme cases, it can lead to hemorrhagic
shock and extensive skin necrosis around the
haematoma.
Management should be as early as possible
and is mainly surgical, with evacuation of the
haematoma, debridement of necrotic tissue, granulation encouraged by NWPT.
Prevention is based on adjusting the dosage
of anticoagulant treatments, preventing the risk
of elderly people falling and limiting, as far as
possible, the factors that aggravate
dermatoporosis.
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Part X
Education on Debridement

Introduction
SebastianProbst
72
In recent years, a range of wound care courses,
study days, and conferences have been developed in an attempt to update health care professionals about advances in wound management.
One of the knowledge and skills that have to be
acquired are the techniques of the debridement.
Debridement is an important element of the
wound bed preparation paradigm [1] and
describes any method by which devitalized tissues/necrosis are removed [2]. In addition, tissue necrosis in the wound bed serves as an area
ideal for bacterial overgrowth and infection; it
can contribute to protein losses in wound exudate and often delays healing [3]. They also
form a barrier to prevent angiogenesis, the formation of granulation tissue or the extracellular
matrix, as well as the re-epithelialization [4].
Necrotic tissue may inhibit the direct contact of
agents applied in the wound bed and hamper the
clinician from making a proper assessment, for
example, in masking a possible underlying
infection [2]. There is a growing body of evi-
S. Probst (*)
HES-SO University of Applied Sciences and Arts
Western Switzerland, Geneva, Switzerland
University Hospital Geneva, Geneva, Switzerland
University of Geneva, Geneva, Switzerland
University of Galway, Galway, Ireland
Monash University, Melbourne, Australia
e-mail: sebastian.probst@hesge.ch
dence and agreement among wound clinicians
and scientists that debridement represents a necessary process in reducing bacteria, infection,
and a biolm within a wound and promotes a
stimulatory environment for healing [5].
The main methods of debridement are autolytic, chemical/enzymatic, mechanical/sharp/
hydro-surgery, and bio-surgery. In the following,
the different methods are outlined:
– Autolytic debridement is widely used in
clinical practice. Wound dressings such as
hydrogels, alginates, or hydrocolloids support
the maintenance of moisture and provide opti-
mal conditions to activate the wound debride-
ment [6].
– When using a chemical debridement, exog-
enous enzymes such as brinolytic enzymes
or collagenase are applied the wound bed.
Enzymatic debridement is part of the chemi-
cal debridement and is a selective method for
debridement of necrotic tissue [7].
– Mechanical debridement method includes
wet-to-dry dressing, irrigation (high-pressure
irrigation and pulsatile high-pressure lavage),
whirlpool, and wound scrubbing [6]. Sharp
debridement is considered as a surgical
wound debridement. It is the most aggressive
type of debridement [2], but is generally con-
sidered to be the most rapid and effective
method even though there is a risk of injury of
the healthy tissue [7]. Hydro-surgery
© The Author(s) 2024
L. Téot et al. (eds.), Skin Necrosis, https://doi.org/10.1007/978-3-031-60954-1_72
473
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