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Malnutrition
Symptoms: limb swelling, extremity heaviness, skin
tightness, skin infections
Examination
Nonpitting edema that usually affects hands/feet.
Usually not painful.
Minimal pigment change or ulceration.
Often unilateral (can measure limb circumference to
document progression of disease).
Fluid protein content is 1-5 g/dL.
*Positive Stemmer sign: inability to grasp the skin
of the second toe or finger due to thickening of the
subcutaneous tissues.
Limb circumference/volume changes: measure at standardized
intervals between limbs, and a difference of 2 cm in
circumference or volume difference of 200 mL is significant.
Prone to discrepency due to user variation in
measurements
Bioimpedance spectroscopy: noninvasive method used to
measure fluid content of a limb by measuring electrical current
transmission through tissues.
Lymphoscintigraphy (gold standard): injection of radiolabeled
colloid into distal effected limb to evaluate uptake at draining
lymph node.
Sensitivity: 96%; specificity: 100%
MR lymphangiography: uses gadolinium-based contrast agents
injected into web spaces to help specifically visualize lymphatic
vessels.
CT/US: used to evaluate thickness of skin/subcutaneous tissues
and appearance of fluid stasis and rule out other causes for limb
asymmetry (eg, deep venous thrombosis, venous stasis).
Indocyanine Green (ICG) Lymphography: ICG is injected into
the interdigital webspaces and a near-infrared camera is used to
visual lymphatic vessels.
DIFFERENTIAL DIAGNOSIS
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Venous insufficiency.
Lipedema: excessive deposition of adipose tissue typically in the
extremities sparing the hands and feet; affects females > males;
can have a normal BMI.
Obesity-induced lymphedema: bilateral lower extremity typically
in patients with BMI > 40; mainstay treatment is weight loss.
Myxedema: swelling of skin and soft tissue secondary to
deposition of mucopolysaccharides in severe hypothyroidism.
STAGING
Multiple classification schemes have been described:
International Society of Lymphology, Koshima, MD
Anderson, Cheng Classification System (Table 8-1)
Table 8-1 Lymphedema Staging Classifications
COMPLICATIONS
Cellulitis
Can be severe so prompt antibiotic therapy is key
Patients with more than three episodes of cellulitis, consider
prophylactic antibiotics
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Hyperkeratosis
Lymphangiosarcoma: <1% incidence but biopsy any suspicious
lesions in the setting of lymphedema
Decreased patient quality of life
TREATMENT
Non-surgical Management
Elevation of the extremity and proper skin hygiene to
decrease risk of infection
Use low pH solutions and water-based products to
keep skin clean and daily moisturizers.
Avoid skin damage.
Treat any dermatologic conditions as they arise.
Complete decongestive therapy: key component of
lymphedema management
Multimodality approach overseen by certified
lymphedema therapist
Involves education, skin care, manual lymphatic
drainage, multilayered short stretch bandages,
specialized exercises
Divided into two phases
Phase I: decongestion—employing the above
components to achieve maximal volume
reduction usually with daily therapy
Phase II: maintenance—continued manual
lymphatic drainage, exercises, skin care, and
compression to maintain improvement
Can result in reduction of extremity volume by
25%-60%
Need compression >20 mm Hg
Intermittent pneumatic compression: inflatable device in
which the extremity is placed in and is filled with air to
compress the extremity
Exercise: important component to increase muscle
strength, increase lymph movement, and increase joint
mobility
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Surgical Management: Physiologic vs Excisional
Indications: loss of function, frequent infections, failure of
conservative/nonsurgical management, significant
psychological burden
Physiologic
Lymphovenous bypass (LVB)/lymphovenous
anastomosis (LVA)
Employs principle that lymphatics drain
interstitial fluid back to the venous system via
the thoracic duct
Utilizes supermicrosurgery to anastomose
functioning lymphatic vessels to adjacent
venules
Vascularized lymph node transfer
Vascularized free tissue transfer of donor
lymph nodes to lymphedematous extremity.
Possible mechanism of actions: transplanted
lymph nodes act as sump pump collecting
lymph and directing into the venous system or
they may result in lymphangiogenesis and
reestablishing new functional lymphatic
vessels.
Lymph node donor sites: groin, thoracic,
submental, supraclavicular, and omental.
Complications: donor site lymphedema.
Excisional
Charles procedure: removes entire skin and soft
tissue with skin grafting to cover underlying muscle
Rarely used due to morbidity of procedure
Wedge resection
Staged subcutaneous excision ± skin grafting
First line for penile/scrotal lymphedema
Liposuction: useful for later stages of lymphedema
where main component is adipose deposition
VASCULAR ANOMALIES
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Classification: Mulliken and Glowacki described a histology-based
classification system in 1982, which was most recently updated by
the International Society for the Study of Vascular Anomalies
(ISSVA) in 2014 classifying vascular anomalies as vascular tumors
and vascular malformations (Fig. 8-1).
Figure 8-1 Flowchart of vascular
anomalies.
VASCULAR TUMORS
Infantile hemangioma (IH): benign proliferation of endothelial
cells, which is present after birth
Most common tumor of infancy
Incidence: 1:10 infants
10% of White infants
2% of Black infants
3:1 female to male ratio
Most commonly found in the head and neck
Phases of growth: typically present within the first week of
life followed by rapid postnatal growth switching to slow
involution
Proliferative phase (0-12 months)
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Rapid expansion of endothelial cells and pericytes
(mostly during 6-8 months of age).
Vascular endothelial growth factor (VEGF) drives
proliferation.
80% of growth completed by 3 months.
Involuting phase (12 months to 10 years)
Progressive shrinking of lesion volume with
deposition of fibrous tissue and degeneration of
endothelial cells (continues to 5-10 years of age).
Mast cells downregulate endothelial cell turnover.
Involuted phase (>10 years)
Loose fibroadipose tissue replaces previous
parenchymal tissue.
Dogma suggests 50% involution by age 5, 70% by age
7, and >90% by age 9; little data to support this, and
likely involution starts earlier around 8-9 months with
completion in most individuals by 3-5 years.
Diagnosis
*Primarily based on history and physical
examination → lesions that are present after birth
and enlarge during infancy.
Additional testing is not necessarily required, but MRI
with contrast (gold standard) for evaluation especially if
visceral hemangioma are suspected.
Ultrasound can be used to show shunting pattern of
flow but can be difficult to distinguish hemangioma
from arteriovenous malformation (AVM) due to both
being high-flow lesions.
Congenital hemangioma
Rapidly involuting (RICH)—similar histological
appearance to IH except GLUT-1 negative; will typically
involute by 1 year of age.
Noninvoluting (NICH)—similar histological appearance to
IH except GLUT-1 negative; lesions grow in proportion to
the child.
Partially involuting (PICH)—as the name suggests, these
lesions begin as RICH but do not completely involute and
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become more like NICH.
Other associated conditions with hemangiomas
Spina bifida occulta—associated with lumbar
hemangioma.
PHACES—posterior fossa anomalies, hemangiomas,
cardiac anomalies, eye abnormalities, sternal cleft.
Kasabach-Merritt syndrome: hemangioma +
thrombocytopenia.
Platelet count <10 000, normal PT/PTT.
Diagnosis can be confirmed with MRI.
von Hippel-Lindau disease: retinal hemangiomas,
hemangioblastomas of the cerebellum, visceral cysts,
mental retardation.
Cutaneous visceral hemangiomas: Multiple
hemangiomas (>5) should elicit concern for visceral
hemangiomas.
Associated with: congestive heart failure,
hepatomegaly (intrahepatic hemangiomas), anemia
Treatment
Observation is appropriate in most cases.
Reassurance to parents is important.
Serial photographs to monitor progress.
Minor ulceration/bleeding can be treated with topical
antibiotics ± hydrocolloid dressing to improve healing.
Indications for treatment
Bleeding/ulceration (5% cases): mostly seen in
hemangiomas in the lip or anogenital areas.
Major ulceration, destruction, or distortion of
surrounding structures, and/or obstruction of vital
structures (10% cases). Most commonly occurs in the
eyelid, nose, lip, and ear.
Eye/eyelid: Obstruction can cause deprivation
amblyopia in as little as 1 week; hemangiomas can
directly distort the cornea and damage vision.
Airway: Subglottic hemangioma can cause
stridor/obstruction of the airway.
Nonsurgical management
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*β-Blockers—has become the first-line treatment;
effective at reducing bulk during the proliferative
phase
Propranolol—2 mg/kg/d
Topical timolol—0.5% twice a day
Side effects: hypotension, bradycardia,
hypoglycemia
Consider admitting patient for observation.
Systemic corticosteroids—historically used as firstline therapy but has fallen out of favor due to improved
side effect profile of β-blockers
2-3 mg/kg/d for 4-6 weeks.
Initial response visible after 7-10 days.
85% of hemangiomas respond by regression or
stabilization of growth after completion of
corticosteroid therapy.
Side effects: cushingoid facies, myopathy,
cardiomyopathy, premature thelarche, and
hirsutism.
Intralesional steroid injection—alternative option
with less systemic side effects
1-2 mg/kg injected into the hemangioma at low
pressure.
Care should be taken when injecting near the eye
to avoid retinal artery occlusion.
Interferon α-2A—alternative therapy when failed other
options
Effective in Kasabach-Merritt syndrome.
1-3 million units/m2 injected subcutaneously daily.
Response seen over 6-10 months; 80% of patients
demonstrate a response.
Side effects: fever on initiation (pretreat with
acetaminophen), transaminitis, transient
neutropenia, anemia, spastic diplegia (must stop
immediately).
Vincristine—alternative therapy when failed other
options
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>80% response rate
Given through central line
Side effects: peripheral neuropathy, sepsis, hair
loss, central line complications (eg, infections,
placement complications)
Laser therapy—typically pulse dye lasers targeting
oxyhemoglobin (585-595 nm)
Lightens the color of the hemangioma but does not
reduce size or bulk
Only penetrates 0.75-1.2 mm into the dermis
Surgical management
Excision of the hemangioma
Indications
Infancy
Obstruction or deformation of a critical/vital
structure (eg, eye, subglottic airway)
Bleeding/ulceration that is unresponsive to
medical management
Easily excisable area with acceptable scar
Childhood (includes the above plus)
Excision of resultant scar from ulceration or
residual fibroadipose tissue
Staged excision and reconstruction of large
lesions
Locally aggressive or borderline
Kaposiform hemangioepithelioma—result in platelet
consumption; often have a lymphatic component; potential
for malignant transformation
Retiform hemangioepithelioma—slow growing, low-grade
vascular neoplasm that presents as singular nodule or
plaque
Kaposi sarcoma—neoplasm associated with painless,
purple raised, or flat lesions; associated with human
herpesvirus 8
Malignant
Angiosarcoma—typically solitary limb mass, locally
recurrent
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VASCULAR MALFORMATIONS
Common features
*Vascular malformations are always present at birth,
which helps distinguish from hemangiomas (are not
seen at and grow after birth).
Lesions grow proportional to infant, and they do not
involute.
1:1 female:male ratio.
Vessels are inherently abnormal due to aberrant signaling
pathways that determine apoptosis and proliferation
pathways.
Diagnosis
Clinical history and physical examination
Imaging
Doppler ultrasound: can differentiate high-flow vs lowflow lesions
MRI with contrast: gold standard for evaluation of
vascular malformations; allows for differentiation
between different forms of vascular malformations
Arteriography: invasive study; usually performed in
conjunction with embolization
Classification: simple vs combined
Simple
Capillary malformation → low-flow lesion
Appearance: dilated, thin-walled capillaries
localized to the papillary and superficial reticular
dermis.
Must be differentiated from other common macular
stains of the face (eg, nevus flammeus).
The autonomic nervous system influences the
development of this lesion, which is why it is often
localized to distinct nerve distributions (eg, port-
wine stains of the face associated with V1 nerve
distribution).
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