Transcript Document

‫بسم هللا الرحمن الرحیم‬
‫‪Laser for vascular lesion‬‬
‫دکتر رسول توکلی کیا‬
‫مرکز تحقیقات پوست و سالک‬
Vascular birthmarks
• Vascular birthmarks, or congenital vascular
anomalies, are common lesions that may present
in a variety of fashions.
• There has traditionally been a significant amount
of confusion regarding the nomenclature of
these lesions, and the term ‘hemangioma’ has
been widely used in the medical literature in
reference to a variety of different vascular
anomalies.
classification system for birthmarks
• According to this classification system
vascular birthmarks are divided into
• Tumors
• malformations.
Vascular tumors
• Vascular tumors are neoplasms of the
vasculature. This category includes
• hemangioma of infancy (the most common
vascular tumor),
• kaposiform hemangioendothelioma,
• tufted angioma,
• pyogenic granuloma.
Vascular malformations
• Vascular malformations represent anomalous
blood vessels without any endothelial
proliferation or cellular turnover. In distinction
to infantile hemangioma, these lesions tend to
be present immediately at birth and persist for
a lifetime.
Vascular malformations
• Vascular malformations are further classified
according to their predominant components,
• capillary malformation (port-wine stain,
salmon patch)
• venous malformation
• lymphatic malformation
• arteriovenous malformation.
Infantile hemangioma
• Infantile hemangioma (hemangioma of
infancy) is the most common benign soft
tissue tumor of childhood.
• It occurs in 1–2%of newborns, and at 1 year of
age, 10–12% infants of white skin have one.
• Female infants are three times more likely to
have hemangiomas than male infants, and the
incidence is increased in premature neonates.
Infantile hemangioma
• These lesions vary considerably in their appearance and
significance, relating to their size, depth, location, growth
pattern, and stage of evolution.
• Older descriptive terms for infantile hemangiomas include
strawberry, cavernous, and capillary.
• These terms are no longer useful and should not be used
• Although infantile hemangiomas may occur on any part of
the body, they most commonly involve the head and neck
regions.
• Facial hemangiomas have been noted to have a nonrandom distribution, with the majority of lesions occurring
on the central face at sites of development fusion.
Infantile hemangioma
• Hemangiomas may occur as superficial, deep,
or mixed lesions. Superficial hemangiomas,
when well formed, present as bright red to
scarlet, dome-shaped to plaque-like to
lobulated papules, plaques, and nodules
• They may partially blanch with pressure and
are rubbery or non-compressible
Infantile hemangioma
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Deep hemangiomas usually present as
subcutaneous, partially compressible nodules
and tumors, often with an overlying blue hue,
prominent venous network, or telangiectasias
• These lesions may be warm to palpation.
• Combined hemangiomas have both a superficial
component and a deep component,n and occur
in up to 25–30% of patients.
• They present with both the superficial, bright red
component and a deeper, blue nodularn
component
Infantile hemangioma
• The natural history of infantile hemangiomas is
characteristic. It is notable for a period of growth (the
proliferative phase), a period of stability (the plateau
phase), and a period of spontaneous regression (the
involutional phase).
• The majority of infantile hemangiomas first become
evident at 2–3 weeks of life, with potential continued
growth until around 9–12 months of age.
• The majorty of growth, however, occurs during the first
5 months of age, and in those that continue to grow
beyond this age, the growth rate is markedly slower.
Infantile hemangioma
• Occasional lesions have a proliferative phase that lasts
for >1 year, sometimes as long as 18–24 months.
• Deep hemangiomas tend to exhibit both a delayed
onset of growth, as well as a sustained, longer growth
phase.
• The onset of the involutional phase, which is difficult to
predict in any given patient, is marked by a color
change from bright red to dull red, purple, or marked
by a color change from bright red to dull red, purple, or
gray (for superficial lesions)
Infantile hemangioma
• It is estimated that completed involution of
infantile hemangiomas occurs at a rate of 10%
per year, such that 30% have involuted by 3 years
of age; 50% by 5 years of age; 70% by 7 years of
age, and >90% by 9–10 years of age.
• However, it should be remembered that
involution does not necessarily imply totally
normal skin.
• These possibilities must be explained thoroughly
to the parents of patients with infantile
hemangioma.
Infantile hemangioma
• Treatment decisions regarding an infantile hemangioma
must incorporate many factors.
• These include the size and location of the lesion or lesions ,
the age of the patient and growth phase of the
hemangioma, associated findings, and the perceived
potential for psychosocial distress both for parents and for
the patient later in life.
• The major goals of management should be to prevent or
reverse life-or function-threatening complications; prevent
disfigurement; minimize psychosocial stress; avoid overly
aggressive procedures; and adequately prevent or treat
ulceration in order to minimize infection, pain, and scarring.
Infantile hemangioma
Infantile hemangioma
Infantile hemangioma
Infantile hemangioma
Infantile hemangioma
Infantile hemangioma
Infantile hemangioma
Infantile hemangioma
Infantile hemangioma
Infantile hemangioma
Infantile hemangioma
• Corticosteroids are the traditional mainstay of
therapy for hemangiomas requiring treatment.
• They are most often used in the oral form,
although both intralesional and topical
preparations may be useful.
• Intralesional corticosteroids are useful for
localized lesions.
• Several injections may be necessary, and
periocular lesions shouldbe treated only by a
physician experienced in their administration,
Infantile hemangioma
• Topical corticosteroid therapy with clobetasol
propionate (a potent, class 1 topical steroid)
may be useful for localized hemangiomas.
• In the authors’ experience,this therapy is
most useful for macular or very thin plaque
heman-giomas in the early proliferative stage
• This medication should beused cautiously with
attention to the risks of atrophy, ocular toxicity, and adrenal suppression.
Infantile hemangioma
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Oral corticosteroids are the traditional ‘gold standard’ for complicated infantile hemangioma treatment, although their mechanism of action is poorly understood.
They are most useful duringt he proliferative phase, and are
generally administered in dosages ranging from 2 to 4 mg/kg per
day of prednisolone or prednisone.
This therapy is usually continued for several months, with gradual
tapering as tolerated.
If corticosteroids are tapered too quickly, rebound growth and
adrenal suppression may occur.
The goals of decreased hemangioma growth or partial shrinkage
must be balanced by the risks of long-term therapy.
Common side-effects include irritability,weight gain, hypertension,
and gastrointestinal upset.
Infantile hemangioma
• An evolving therapy for infantile hemangioma is
propranolol.
• The mechanism of action of propranolol in this setting
is unclear.
• It is most often started at around 0.5 mg/kg per day,
with the dose gradually titrated up to 2 mg/kg per day,
divided into two to three doses daily.
• Potential side-effects include hypotension,bradycardia,
bronchospasm, hypoglycemia and hypothermia, and
this agent should be administered under close
supervision with attention to these possible toxicities.
Infantile hemangioma
Infantile hemangioma
Infantile hemangioma
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Pulsed-dye laser (PDL) therapy may be useful in the treatment of
ulcerated hemangiomas.
This laser emits a wavelength of light specific for oxyhemoglobin,
thus imparting specificity for vascular structures (’selective
photothermolysis’). Since the light penetrates only 1 mm of depth
in the skin, this modality is generally not helpful for non-ulcerated,
elevated, or nodular lesions.
With ulcerated lesions, though, it is useful in accentuating
reepithelialization and decreasing pain.
The choice of PDL therapy must be individualized to the patient,
and occasional patients may show noresponse or even worsening
with this modality.
PDL therapy may also be useful for residual surface vascularity
following hemangioma involution.
Glomus tumor
Glomus tumor
Vascular malformations
• The salmon patch (nevus simplex) is the most
common vascular esion of infancy.
• It occurs in 30–40% of all newborns and
appearsas a flat, dull pink, macular lesion on the
posterior neck and scalp, glabella , forehead,
upper eyelids, and occasionally the nose or
nasolabial regions
• No treatment is necessary, since 95% of facial
salmon patches fade within the first 1–2 years of
life.
salmon patch (nevus simplex)
Nevus flammeus, or port-wine stain
(PWS),
• Nevus flammeus, or port-wine stain (PWS), is a congenital capillary
malformation that may occur as an isolated lesion or in association with a
variety of syndromes.
• These lesions present as macular (non-palpable) stains with a pink to dark
red color.
• Although an early PWS may be indistinguishable from an infantile
hemangioma, these lesions are usually distinguished by their congenital
presence and their static nature, without the rapid proliferation and
thickening that characterizes hemangiomas during the first months of life.
• PWS may darken progressively over many years, and occasional lesions
develop secondary proliferative(pyogenic granuloma-like) vascular blebs
on their surface .
• They may also become somewhat thickened and raised later in life.
• Port-wine stains are often, but not always, unilateral and the most
common site of involvement is the face, although they may occur on any
cutaneous surface.
Nevus flammeus, or port-wine stain
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PWS lesions show little tendency toward spontaneous improvement or
involution,
Laser therapy has revolutionized the treatment of these lesions, and the
flashlamp-pumped tunable pulsed-dye laser (PDL) is the most accepted
laser for PWS treatment.
PDL allows the targeting of short bursts of energy at intravascular
hemoglobin (because of the specific wavelength of the emitted
light)within the lesional vessels, while sparing other tissue components
and thus allowing for precise therapy.
Treatment of PWS with PDL is usually performed in conjunction with local
or general anestheia, depending on the size and location of the lesion and
the age of the patient.
Some smaller lesions can be treated without the need for anesthesia.
PDL therapy is usually performed over several sessions, separated in time
by 6–8 weeks, and can be quite effective in lightening these lesions,
thereby minimizing their cosmetic and psychosocial significance109
Nevus flammeus, or port-wine stain
Nevus flammeus, or port-wine stain
• Some authors have reported optimal treatment response in
patients<1 year of age, whereas others have found no
evidence that treat-ment during early childhood is more
effective than treatment at alater age.
• In general, lesions over bony areas of the face (i.e.,the
forehead), lateral cheeks, chest and proximal arms seem to
respond best to PDL therapy, while those over the mid-face
and distal extremities respond less.
• PWS of the central face may not respond as well, given the
deeper vessels which may escape the effect of the PDL.
Sturge–Weber syndrome
• Sturge–Weber syndrome (SWS, encephalofacial
or encephalotrigeminal angiomatosis) is a
neuroectodermal syndrome characterzed by a
PWS in the distribution of the first (ophthalmic)
branch of the trigeminal nerve (V1) in association
with leptomeningeal angiomatosis (presenting
usually with seizures) and glaucoma.
• There are rare reports of patients with classic
brain and ophthalmic findings of SWS in the
absence of facial PWS.
Port wine stain on face before treatment. (b) Portwine stain on
face after pulsed dye laser treatment
Nevus flammeus, or port-wine stain
• The potassium titanyl phosphate (KTP) laser emits greenlight at 532
nm.
• High fluences are available with this laser and the pulse durations
may be more appropriatefor some PWSs.
• The KTP laser has been shown to produce further lightening in PDLresistant lesions .
• In this study, 30 patients with PWS that had failed to lighten after
at least five treatments with the PDL at 0.5-ms pulse widths were
treated with the KTP laser. Fluences rangedfrom 18 to 24 J cm−2
with pulse widths of 9–14 ms.
• Five patients (17%) showed more than 50% response.
• In general, patients preferred the KTP laser because there was less
discomfort and purpura.
• However, two patients (7%)developed scarring.
Nevus flammeus, or port-wine stain
• A study comparing the PDL with a frequency-dou-bled
Nd:YAG laser showed similar response rates among43
patients; however, a substantially higher scarring ratewith
the 532-nm Nd:YAG laser was noted [13].
• Longer-wavelength lasers such as the alexandrite(755 nm)
and Nd:YAG (1,064 nm) may have a role in PWS treatment.
In the milli second modes these lasers have been widely
used for hair removal and leg vein telangiectasia.
• These lasers may be particularly useful in the treatment of
bulky malformations and mature PWSs, lesions that are
typically more resistant to PDL because of the
predominance of larger and deeper vessels and higher
content of deoxygenated hemoglobin.
Nevus flammeus, or port-wine stain
• Yang et al. [22] treated 18 patients with
PWSs,comparing a 595-nm PDL to a longpulsed Nd:YAGlaser with contact cooling.
• Similar clearance rates were achieved.
• Patients preferred the Nd:YAG laser because
of the shorter recovery period between
treatments.
Nevus flammeus, or port-wine stain
• Intense pulsed light (IPL) has also been used
to treatPWSs. Unlike laser systems, these flash
lamps producenoncoherent broadband light
with wavelengths in therange of 515–1,200
nm and permit various pulsewidths.
• Filters are used to remove unwanted wavelengths.