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X
- •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

30
Angiogram
Frontal view MRI
S. Akita et al.
e
Fig. 4.3 (continued)
Lateral view

4 Imaging, Vascular Assessment: Extension inDepth andVascular Anomalies
f
31
Fig. 4.3 (continued)

32
S. Akita et al.
References
1. Enjolras O, Mulliken JB.Vascular tumors and vascular malformations. Adv Dermatol. 1997;13:375–423.
2. Wassef M, Enjolrad O.Supercial vascular malformations: classication and histopathology. Ann Pathol.
1999;19:253–64.
3. Chamlin SL, Haggstrom AN, Drolet BA, Baselga E,
Frieden IJ, Garzon MC, Horii KA, Lucky AW, Metry
DW, Newell B, Nopper AJ, Mancini AL. Multicenter
prospective study of ulcerated hemangiomas. J Pediatr.
2007;151:684–9.
4. Maguiness SM, Hoffman WY, McCalmont TH,
Frieden IJ. Early white discoloration of infantile
hemangioma: a sign of impending ulceration. Arch
Dermatol. 2010;146:1235–9.
5. Paltiel HJ, Burrows PE, Kozakewich HP, Zurakowski
D, Mulliken JB.Soft tissue vascular anomalies: utility of US for diagnosis. Radiology. 2000;214:747–54.
6. Kohout MP, Hansen M, Pribaz JJ, Mulliken
JB. Arteriovenous malformations of the head and
neck: natural history and management. Plast Reconstr
Surg. 1998;102:643–54.
7. Akita S, Houbara S, Hirano A.Management of vascular malformations. Plast Reconstr Surg Glob
Open. 2014;2(3):e128. https://doi.org/10.1097/
GOX.0000000000000079. eCollection 2014 Mar.
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Imaging ofHypodermal Fat
Necrosis
XimenaWortsman
5
5.1 Introduction
Fat necrosis is a benign nonsuppurative inammatory entity of the adipose tissue that results
from the aseptic saponication of lipids by
enzymes. The reported causes include trauma,
radiotherapy, anticoagulation, inammatory diseases, surgery, percutaneous interventions, and
perinatal asphyxia, hypoxemia, or hypothermia
[1]. Imaging has been growingly used for studying fat necrosis due to the often variable history
and clinical ndings that can simulate other conditions, which include the differential diagnosis
of palpable lumps and bumps when this entity
affects the hypodermis. Additionally, patients
may not spontaneously refer to an inciting event
such as trauma. Reports on imaging of fat necrosis started with the usage of X-rays, such as
mammography, and have expanded to other
imaging modalities such as ultrasound, magnetic
resonance imaging (MRI), and most recently
positron emission tomography-computed tomography (PET-CT). Besides the support to the clinical diagnosis, the usage of these imaging
techniques may provide an anatomic perspective
for evaluating the extent and characteristics of the
X. Wortsman (*)
Institute for Diagnostic Imaging and Research of the
Skin and Soft Tissues, Department of Dermatology,
Faculty of Medicine, Universidad de Chile,
Santiago, Chile
structural changes in the tissues, as well as a support for assessing the differential diagnosis.
The aim of this chapter is to focus on the
imaging characteristics of hypodermal fat necrosis with different imaging modalities and discuss
some general principles, indications, advantages,
and disadvantages for each method.
5.2 Imaging Methods
5.2.1 X-Ray Mammography
X-rays are the most simple and accessible form
of imaging study and involve the usage of lowdose radiation for diagnostic purposes. Usually,
this modality is not intended for particular study
of fat necrosis; however, there are radiological
signs suggestive of this condition that are frequently and incidentally found in the hypodermis, commonly during mammography
screenings. The most frequent mammographic
characteristic of fat necrosis is the presence of
round- or oval-shaped hypodense structures, frequently showing a hyperdense calcied rim, also
called “eggshell”- or “rim-like”-type calcication that corresponds to calcied lipid cysts
(Fig.5.1). This sign is almost pathognomonic of
fat necrosis; therefore, the patients presenting
this feature may not need additional imaging
studies and should continue with the recommended screening program according to their age
and history. Less frequent forms of presentation
© The Author(s) 2024
L. Téot et al. (eds.), Skin Necrosis, https://doi.org/10.1007/978-3-031-60954-1_5
33

34
Fig. 5.1 Fat necrosis on mammography (lateral view)
shows a “rim-like” or “eggshell” type of calcication
(arrow) within the fatty tissue of the breast
of fat necrosis on mammography include focal
asymmetries that may imply parenchymal edema.
However, microcalcications or spiculated dense
masses can also be detected, with the latter being
related to a major presence of brosis or scarring
[2, 3]. Since these occasionally seen mammographic signs may mimic a breast malignancy,
more imaging studies are usually needed in these
particular cases.
5.2.2 Ultrasound
Also called sonography, this widely available
imaging method is based on the properties of
sound waves and has been increasingly used for
studying fat necrosis in soft tissues due to the
high-denition images of the supercial layers
provided by the current machines. Besides its
non-radiating nature and proved safety characteristics, there are several advantages of ultrasound
such as its real-time, 2D, and 3D multiaxial and
dynamic performance as well as its reasonable
balance between resolution and penetration that
allow us to obtain a wide range of anatomical
X. Wortsman
information that can reach from the skin layers to
the bony margin. Also, ultrasound can show the
vascularity of the tissues through its color or
power Doppler capabilities, which include the
detection of the type of vessel (arterial or venous)
and the velocity of blood ow (cm/s) [4, 5]. This
may avoid the adverse reactions due to the use of
contrast media that have been widely reported
with other imaging modalities such as CT or
MRI. The current limitations of ultrasound are
lesions that measure <0.1mm, with only epidermal location, and the detection of pigments such
as melanin [6]. These last two limitations are not
relevant for the study of fat necrosis. In fact, the
hypodermis seems to be a perfect target for ultrasound use, due to its anatomically supercial
location in soft tissue that makes it easily accessible with most of the linear probes that work
with frequencies ≥7.5MHz. Nevertheless, probes
working with higher frequencies (≥12MHz) are
most commonly recommended for studying the
hypodermis due to their higher denition at this
tissue depth. On ultrasound, the most common
sign of fat necrosis is the presence of well-dened
round or oval-shaped anechoic pseudocystic
structures, frequently with posterior acoustic
enhancement, and sometimes surrounded by a
hyperechoic calcied rim. These pseudocystic
structures correspond to the oily cysts produced
by the liquefaction of the fatty tissue. Internal
echoes and a uid–uid level may sometimes be
recognized in these pseudocysts, usually in cases
with a history of trauma where the serohematic
material combines with the liqueed material of
the fatty lobules. Also, increased echogenicity of
the hypodermis and isoechoic pseudonodules,
surrounded by an anechoic or hypoechoic halo,
may be detected. These latter ultrasound features
indicate the degree of hypodermal inammation.
Less frequent sonographic signs are anechoic
masses with a posterior acoustic shadowing artifact due to gross calcication and well- or illdened hypoechoic solid pseudo-masses due to
prominent brosis and scarring. All these characteristics may appear as single or combined features in the affected region (Figs.5.2 and 5.3).
Hypo- or hypervascularity in the hypodermis
may be detected according to the level of

5 Imaging ofHypodermal Fat Necrosis
Fig. 5.2 Fat necrosis on
ultrasound (gray scale,
transverse views)
demonstrates the wide
range of appearance of
this condition. Symbols:
* pseudocyst; o
pseudonodule; x brosis;
arrow calcication; 1
and 2 uid–uid level.
Abbreviations: d dermis;
h hypodermis
35

36
Fig. 5.3 Fat necrosis on 3D ultrasound (gray scale, 5–8-s
reconstruction, transverse views) shows variable forms of
presentation. Symbols: * pseudocyst; o hyperechogenicity
(top) and pseudonodule (middle and bottom locations);
arrows pointing out the lesional sites. Abbreviations: d
dermis; h hypodermis
inammation present in the tissue, with hypervascularity being the most commonly found in
inamed stages [1, 3, 7]. In cases presenting subcutaneous fat necrosis of the newborn, ultrasound
X. Wortsman
has been reported to successfully support the
diagnosis [8–10]. Thus, the main indications for
ultrasound in fat necrosis are to support the early
diagnosis and rule out solid tumors that may be
hard to differentiate on a clinical basis only.
5.2.3 Magnetic Resonance Imaging
This is an imaging method based on the response
of the body’s hydrogen ions in a magnetic eld.
This technique has been widely used in the study
of soft tissues, mainly in the musculoskeletal
eld, due to its high-denition anatomical
images. The main disadvantages of this method
are its high cost and the potential adverse reactions to gadolinium, the usual contrast medium
used in these examinations. Additionally, MRI
has limited ability to show small calcications, a
common nding in fat necrosis which may be
seen in this imaging technique as areas of signal
void or may simply go undetected. On MRI, a
wide spectrum of ndings have been reported in
fat necrosis, and some of the ndings may even
mimic a malignant tumor such as a breast cancer.
The most typical nding on MRI is a round or
oval nodule or mass with hypointense
T1-weighted signal on fat-saturated images that
correspond to a lipid pseudocyst. Also, fat necrosis can show as well- or ill-dened isointense or
hypointense areas or pseudonodules on
T1-weighted images probably due to its inammatory and hemorrhagic characteristics. In case
with strong brosis, architectural distortion, with
or without spiculated margins, and variable
degrees of intensity (low, intermediate, or high
signal) on T1-weighted images are reported. Fat
suppression sequences may help to differentiate
fat necrosis from malignant tumors. On
T2-weighted sequences, isointense, hypointense,
and hyperintense appearances have been
described. Pseudonodular, globular, and laminated appearances have been additionally
reported (Fig. 5.4). After the injection of gadolinium contrast medium, fat necrosis can show
variable appearances that can range from no
enhancement to irregular or peripheral enhancement and from thin to thick rims of enhancement

ab
5 Imaging ofHypodermal Fat Necrosis
37
Fig. 5.4 (a, b) Fat necrosis on MRI (axial views). (a)
T1-weighted sequence shows isointense pseudonodule
with a hypointense rim located in the hypodermis of the
right side of the lower back (arrow, fat necrosis area). In
the vicinity, a hypointense oval-shaped hypodermal structure is detected that corresponds to a hematoma (hm). (b)
[1–3, 7, 11, 12]. The most frequent indications
for MRI regarding fat necrosis are to complete
the imaging study in cases with mammographic
abnormalities, especially the ones where a malignancy must be ruled out, and to assess the differential diagnosis in cases presenting palpable
large lumps or extensive trauma.
T2-weighted image of the same case shows a change in
the intensity of the hematoma (hm) with a uid–uid level
(hyperintense/hypointense) and no change in the intensity
of the pseudonodule (arrow, fat necrosis site) in comparison with the T1-weighted sequence. (Courtesy of Drs.
Raul Valenzuela and Herly Pulgar)
the need for intravenous contrast media. On CT,
fat necrosis has been reported as a well-dened
hypodense mass with rim enhancement or a globular mass with central fat density [11].
Positron emission tomography (PET) is a
nuclear imaging modality that registers the
gamma rays emitted by a positron-emitting radionuclide, also called tracer. The most commonly
used tracer is uorodeoxyglucose (FDG), an ana-
5.2.4 Computed Tomography
andPositron Emission
Tomography
log of glucose. However, this is a radiating
modality that also requires injection of an agent.
In recent years, the combination of these two
modalities (PET-CT) has gained adepts due to the
Computed tomography (CT) implies the crosssectional usage of X-rays and has a broad range
of applications, mainly in the neurological, cardiac, and abdominal elds. Thus, CT has been
extensively used for staging malignant conditions. However, there are few reports in literature
on the usage of CT for studying hypodermal fat
necrosis, mostly showing isolated case reports.
Advantages of CT are its wide availability and
relatively short time of examination due to the
new multi-slice machines that can acquire and
process the images very rapidly. Disadvantages
of CT are its high cost, its radiating nature, and
mix of the anatomical and biological images that
have been widely used in the staging of cancer-
ous lesions [13]. However, PET-CT has certain
notable shortcomings, including the inability to
perform simultaneous data acquisition and the
signicant radiation dose to the patient [14].
PET-CT is now used in the staging of melanoma,
showing high sensitivity especially in advanced
stages [15, 16]. Nevertheless, there are several
reports of false positives of PET-CT due to the
glycolytic activity present in inammation that
can easily mimic a malignancy in this modality
[17–19]. These inammatory features are

38
X. Wortsman
a
b
Fig. 5.5 (a, b) Fat necrosis on 3D ultrasound and
PET-CT. Patient with a history of removed in situ mela-
noma in the left leg. (a) 3D ultrasound (gray scale, 5–8-s
reconstruction, longitudinal view) shows two anechoic
pseudocysts (*) surrounded by a hyperechoic pseudonodular structure (o) consistent with fat necrosis. (b) PET-CT
(coronal view) demonstrates a false-positive uptake of
FDG in the hypodermis of the left thigh with two hypermetabolic pseudonodules (arrows). Abbreviations: d dermis; h hypodermis. (PET-CT image courtesy of Dr. Vicky
Roizen)
common in fat necrosis; therefore, this condition
seems to be one of the most common pitfalls for
PET-CT. These reports mention pseudonodular
solid images with hypermetabolic activity and
increased uptake of FDG (Fig. 5.5). Besides fat
necrosis, other causes of false positives of
PET-CT have been reported. Among them are
acute and chronic inammation or infection,
physiologic lactation, and benign breast masses,
including silicone granuloma, broadenoma, and
postsurgical or radiotherapy changes. Therefore,
the usage of PET-CT is not recommended as a
rst imaging modality in fat necrosis. Moreover,
the usage of this imaging modality may cause
diagnostic dilemmas in oncologic imaging [20].
5.3 Conclusion
There are several imaging methods that can
reveal the anatomical characteristics of hypoder-
mal fat necrosis. The usage of imaging in this
condition is intended for the assessment of the
differential diagnosis of lumps and bumps in the
soft tissues and also to try to rule out malignant
tumors. The advantages and disadvantages of
each technique as well as the availability of these
modalities in the medical institutions should be
considered, when selecting the appropriate imag-
ing modality for each case.
References
1. Atasoy MM, Oren NC, Ilica AT, Güvenç I, Günal A,
Mossa-Basha M. Sonography of fat necrosis of the
breast: correlation with mammography and MR imaging. J Clin Ultrasound. 2013;41(7):415–23. https://
doi.org/10.1002/jcu.22061.
2. Taboada JL, Stephens TW, Krishnamurthy S, Brandt
KR, Whitman GJ.The many faces of fat necrosis in
the breast. AJR Am J Roentgenol. 2009;192:815–25.
3. Tan PH, Lai LM, Carrington EV, etal. Fat necrosis of
the breast—a review. Breast. 2006;15:313–8.
4. Wortsman X.Common applications of dermatologic
sonography. J Ultrasound Med. 2012;31:97–111.
5. Wortsman X. Ultrasound in dermatology: why,
how, and when? Semin Ultrasound CT MR.
2013;34:177–95.
6. Wortsman X, Wortsman J. Clinical usefulness of
variable- frequency ultrasound in localized lesions of
the skin. J Am Acad Dermatol. 2010;62:247–56.
7. Walsh M, Jacobson JA, Kim SM, Lucas DR, Morag Y,
Fessell DP.Sonography of fat necrosis involving the
extremity and torso with magnetic resonance imaging and histologic correlation. J Ultrasound Med.
2008;27:1751–7.
8. Marszałek A, Maciejewska J, Bowszyc-Dmochowska
M, Prokurat A. Subcutaneous fat necrosis of the
newborn—a case report and review of literature. Pol J
Pathol. 2010;61:240–4.
9. Vasireddy S, Long SD, Sacheti B, Mayforth RD.MRI
and US ndings of subcutaneous fat necrosis of the
newborn. Pediatr Radiol. 2009;39:73–6.

5 Imaging ofHypodermal Fat Necrosis
39
10. Avayú E, Rodríguez C, Wortsman X, et al.
Newborn fat necrosis: case-report. Rev Chil Pediatr.
2009;80:60–4.
11. Chan LP, Gee R, Keogh C, Munk PL. Imaging
features of fat necrosis. AJR Am J Roentgenol.
2003;181:955–9.
12. Daly CP, Jaeger B, Sill DS.Variable appearances of
fat necrosis on breast MRI. AJR Am J Roentgenol.
2008;191:1374–80.
13. Bockisch A, Beyer T, Antoch G, etal. Positron emission tomography/computed tomography—imaging
protocols, artifacts, and pitfalls. Mol Imaging Biol.
2004;6:188–99.
14. Pichler BJ, Wehrl HF, Kolb A, Judenhofer
MS. Positron emission tomography/magnetic resonance imaging: the next generation of multimodality
imaging? Semin Nucl Med. 2008;38:199–208.
15. Schröer-Günther MA, Wolff RF, Westwood ME,
et al. F-18-uoro-2-deoxyglucose positron emission
tomography (PET) and PET/computed tomography
imaging in primary staging of patients with malignant
melanoma: a systematic review. Syst Rev. 2012;1:62.
https://doi.org/10.1186/2046- 4053- 1- 62.
16. Hinz T, Voth H, Ahmadzadehfar H, et al. Role of
high-resolution ultrasound and PET/CT imaging
for preoperative characterization of sentinel lymph
nodes in cutaneous melanoma. Ultrasound Med Biol.
2013;39:30–6.
17. Kashyap R, Lau E, George A, et al. High FDG
activity in focal fat necrosis: a pitfall in interpretation of posttreatment PET/CT in patients with nonHodgkin lymphoma. Eur J Nucl Med Mol Imaging.
2013;40(9):1330–6.
18. Akkas BE, Ucmak Vural G.Fat necrosis may mimic
local recurrence of breast cancer in FDG PET/
CT.Rev Esp Med Nucl Imagen Mol. 2013;32:105–6.
19. Lee SA, Chung HW, Cho KJ, et al. Encapsulated
fat necrosis mimicking subcutaneous liposarcoma:
radiologic ndings on MR, PET-CT, and US imaging.
Skeletal Radiol. 2013;42(10):1465–70.
20. Adejolu M, Huo L, Rohren E, Santiago L, Yang
WT.False-positive lesions mimicking breast cancer
on FDG PET and PET/CT.AJR Am J Roentgenol.
2012;198:W304–14.
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