REFERAT

MAY 2017

HEMANGIOMA

Presented By :
Sekar Indah Setyarini

(2015-84-44)

Consulent:

dr. Novriyani Masuku, Sp.KK,

DIBAWAKAN DALAM RANGKA TUGAS KEPANITERAAN KLINIK

PADA BAGIAN LABORATURIUM KULIT KELAMIN
FAKULTAS KEDOKTERAN
UNIVERSITAS PATTIMURA
2017
INTRODUCTION
Vascular anomalies are common
birthmarks. l Their classification has often
been problematic, with contradictory and
confusing descriptive nomenclature. A
classification system first proposed by
Mulliken and Glowacki.
HEMANGIOMA

vascular
Superficial
proliferations
hemangiomas have a
that rapidly enlarge Rarely, they may be
bright red, nodular
Hemangiomas are during the first year associated with
surface and deeper
benign of life and slowly systemic
lesions
spontaneously malformations
may be bluepurple
involute by age 5 to
in color.
10 years.
Synonyms
Infantile hemangioma

Hemangioma of infancy

strawberry nevus

Angioma cavernosum

capillary hemangioma
PREVALENCE
Age 10% to 12% have onset 1 years. Rarely present at
birth.
Gender F M, 2-3:1
Prevalence Seen more in premature infants (30 weeks
gestational age or birthweight 1500 g), infants of
mothers status postchorionic villus sampling, infants
of older mothers, and infants of multiple gestation.
Race More common in Caucasians.
Incidence Most common tumor of infancy.Seen in
2.6% of all newborns.
 10
12% in
1.4% in white
black

0.8 %
in asian

Epidemiology in USA
Etiology
Abnormally increased vascular proliferation. Reports
of familial cases

GLUT-1 (Glucose Transport-1)

has been identified as an immunohistochemical
marker expressed in IH,
Pathogenesis
blood vessels. Extensive study is underway to understand the
signaling mechanisms that cause this benign tumor to grow,
plateau, and then spontaneously involute. Several proposed
mechanisms for hemangioma formation include the
following:

1. A mutation in endothelial cells,

2. A mutation in other cells influencing endothelial
proliferation,
3. Placental origin of proliferative cells, and/or
4. Dysregulation of immature endothelial progenitor cells.
It seems that a combination of these mechanisms,
multiple genes, and local effects all influence the
development, growth, and involution of hemangiomas
2 phase of hemangioma:

Proliferation Involunting
phase phase
Clasification
Hemangioma Clasification
Tipe 1 Neonatal straining

Tipe 2 Intradermal capillary hemangioma

A. Salmon patch
A. Port wine stain
A. Spider angiomas
Tipe 3 Juvenile hemangiomas

A. Strawberry mark
A. Strawberry capillary hemangioma
A. Capillary cavernous hemangioma
Tipe 4 Arteriovenous fistulae

A. Arterial hemangiomas
A. Hemangiomas giantism
Tipe 5 Cirsoid angiomas (racemose aneurysm)
Clasification
Based on its histological appearance:
Capillary Hemangioma
Capillary Hemangioma on child(nevus vasculosus, strawberry nevus)
Granuloma piogenik
Cherry-spot (ruby-spot), angioma senilis

CavernousHemangioma
Cavernous Hemangioma
Hemangioma keratotik
Hemartoma vaskular

Telangiektasis:
Nevus flameus
Angiokeratoma
Spider angioma
Clinical Manifestation

Gambar 1. Infantile Hemangioma (Strawberry hemangioma)

Gambar 2. Granuloma Pyogenik (gambaran nodul vasksular)
Gambar 3. Angiokeratoma, soliter.
Gambar 4. Segmental infantile hemangioma
Diagnose
Skin Findings:

Type Nodule, plaque, may ulcerated.

Color Superficial: pink, red; Deep: bluepurple. Involuting:
white/gray.
Frequency 50% to 60% superficial, 25% to 35% combined, 15%
deep.
Size Average 2 to 5 cm but can grow up to 20 cm in size.
Pattern Focal or segmental.
Palpation Superficial lesions are soft/compressible; deeper
lesions are more firm.
Sites of Predilection Face, trunk, legs, oral, and genital mucous
membranes.
Diagnose

USG MRI

CT scan Foto polos

Biopsi kulit Immunohistochemistry

Differential Diagnose
Another malformasi kapiler,infantile myofibromatosis,
atau pyogenic granuloma.

Deep lession fibrosarkoma, rhabdomiosarkoma,

neuroblastoma, dermatofibrosarkoma protuberans,
nasalglioma, lipoblastoma, venous, limphatik, and
artery venous malformation.
Theraphy
Medikamentosa
Non medikamentosa
Complication
Bleeding the most
Ulcerasi
Ulcus
Secondary Infection
Trombositopenia Rare
Eye sight disorder
Prognosis
The prognosis of most IH is excellent, with spontaneous
involution and little to no sequelae, but a significant
minority can result in permanent disfigurement or
medical sequelae.

Certain characteristics are associated with an increased

risk of complications and need for treatment
THANK YOU