Keloids and Hypertrophic Scars

Keloids and hypertrophic scars - UpToDate 1/31/18, 9(22 PM
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Keloids and hypertrophic scars
Authors: Beth G Goldstein, MD, Adam O Goldstein, MD, MPH

Section Editors: Robert P Dellavalle, MD, PhD, MSPH, Moise L Levy, MD
Deputy Editor: Rosamaria Corona, MD, DSc
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Dec 2017. | This topic last updated: Nov 02, 2016.
INTRODUCTION — Keloids and hypertrophic scars represent an excessive tissue response to dermal injury characterized by
local fibroblast proliferation and overproduction of collagen [1,2]. Keloids (from a Greek word meaning "crab's claw") are
fibrous growths that extend beyond the original area of injury to involve the adjacent normal skin. Hypertrophic scars may
have a similar clinical appearance, but in contrast with keloids, remain confined within the boundaries of the wound area and
tend to regress spontaneously over time [3].
Keloids and hypertrophic scars may cause functional impairment and cosmetic disfigurement and are often associated with
low self-reported patient quality of life [4].
This topic will review the pathogenesis, diagnosis, and treatment of keloids and hypertrophic scars. The management of
keloid and hypertrophic scars following burn injuries is discussed separately. (See "Hypertrophic scarring and keloids
following burn injuries".)
EPIDEMIOLOGY — The precise incidence and prevalence of keloids and hypertrophic scars are unknown. Keloids have
been reported in 5 to 16 percent of individuals of Hispanic and African ancestry [5]. An annual incidence of 15 per 10,000 has
been reported in Taiwan [6]. Keloids affect men and women equally and are more common in younger individuals. There is a
familial tendency to develop keloids; family studies suggest an autosomal dominant inheritance with incomplete penetrance
[7].
PATHOGENESIS — The pathogenesis of hypertrophic scars and keloids is incompletely understood. It involves alterations in
the sequential process of wound healing and may be influenced by multiple local and genetic factors [8-10]. In normal wound
healing there is an initial marked local inflammatory reaction, followed by the formation of new blood vessels, activation of
keratinocytes and fibroblasts at the edge of the wound, and synthesis of extracellular matrix components [11]. After the
reepithelialization is completed, the dermal granulation tissue is remodeled into a scar and the replacement tissue adapts to
biomechanical requirements. (See "Basic principles of wound healing".)
Fibroblast proliferation — Fibroblast proliferation and collagen synthesis are greatly increased in hypertrophic scars and
keloids [12-14]. Overexpression of growth factors, such as transforming growth factor-beta (TGF-beta), vascular endothelial
growth factor (VEGF), and connective tissue growth factor (CTGF) appear to play a role in the formation of these lesions [15-
17].
TGF-beta is a regulator of fibroblast proliferation and collagen synthesis and promotes the differentiation of fibroblasts into
myofibroblasts. Myofibroblasts are characterized by contractile actin filaments and a high production of collagen and have a
central role in the contraction and remodeling of the granulation tissue [18]. In normal wound healing, TGF-beta activity
diminishes upon the completion of wound repair, but in keloids TGF-beta is overproduced and poorly regulated [8,19].
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Other factors that may be involved in the pathogenesis of keloids and hypertrophic scars include a decreased production of
molecules that promote matrix breakdown, such as matrix metalloproteinases; increased numbers of platelet-derived growth
factor (PDGF) receptors on fibroblasts; over-activation of signals for insulin-like growth factor-I; decreased fibroblast apoptosis
rate; and increased expression of thymic stromal lymphopoietin and fibrocyte activation via stromal cell-derived factor-1 [20-
22].
Genetics — Keloids occur more frequently in certain ethnic populations; people of African and Asian descent are most
susceptible to the development of keloids [23]. This observation and reports of familial cases suggest a genetic contribution to
keloid development [7,24-26]. Studies of familial keloids have reported varied modes of inheritance; one study of 14 families
suggested an autosomal dominant mode of inheritance with incomplete penetrance and variable expression [24,27].
Multiple genes are likely to be involved in the development of keloids, and attempts to definitively identify the genes involved
have been unsuccessful [27]. A genome-wide association study identified four susceptibility loci on chromosomes 1q41,
3q22.3-23, and 15q21.3 in a Japanese population [28]. However, no genes in these regions were definitively linked to keloid
formation.
In contrast with keloids, there is no evidence of a genetic predisposition to develop hypertrophic scars.
PATHOLOGY — Both hypertrophic scars and keloids exhibit excess collagen formation with varying numbers of fibroblasts
and myofibroblasts. In hypertrophic scars, the collagen fibers are arranged in a wavy pattern predominantly oriented parallel
to the epithelial surface. There are also nodular structures containing myofibroblasts and vertically aligned vessels. In
contrast, keloids show characteristic hypocellular zones of fibrous tissue containing thickened, glassy, eosinophilic collagen
bundles (picture 1) [29].
CLINICAL FEATURES — The clinical features and classification of keloids and hypertrophic scars are summarized in the
table (table 1). Hypertrophic scars usually form at sites of surgical wounds, lacerations, burns, or inflammatory or infectious
skin conditions (eg, acne, folliculitis, chicken pox, and vaccinations). They are raised, may be erythematous, and typically do
not exceed the margins of the original wound (picture 2). Hypertrophic scars usually show a rapid growth phase of up to six
months, followed by possible regression over the following 12 to 18 months.
Keloids present as raised dermal lesions that extend beyond the boundaries of the original wound and invade the surrounding
healthy skin (picture 3A). They may arise at sites of minor injuries to the skin, such as earlobe piercings, or may develop in
the absence of an obvious inciting stimulus.
Keloids occur predominantly on the upper chest, shoulders, upper back (picture 3A-B), and head and neck (picture 4C),
especially on the ear (picture 4A-B). Keloids may develop as early as one month after trauma or inflammation, but some may
occur up to one year after the inciting event [5]. In contrast with hypertrophic scars, keloids do not regress spontaneously but
enlarge progressively over time [3].
Pain and pruritus are frequently associated symptoms. Full-thickness burn injuries impair or destroy hair follicles, sweat
glands, sebaceous glands, capillaries, and nerve endings, leading to loss of temperature regulation, dry skin, and neuropathic
pain. These scars may also cause functional impairment from contracture or mechanical irritation.
GENETIC SYNDROMES ASSOCIATED WITH KELOID FORMATION — The formation of keloids can be a clinical clue to
rare inherited syndromes such as Rubinstein-Taybi syndrome and Goeminne syndrome. Rubinstein-Taybi syndrome (MIM
#180849) is a multiple congenital anomalies syndrome, characterized by broad thumbs and big toes, characteristic facies, and
variable growth and intellectual retardation [30]. Individuals with Rubinstein-Taybi syndrome have an increased risk of
malignancies and an increased tendency to develop keloids spontaneously or after minor trauma. Keloids are usually multiple
and mainly located on the chest and shoulders [30]. (See "Microdeletion syndromes (chromosomes 12 to 22)".)
Goeminne syndrome (MIM #314300) is a rare X-linked multiple malformation syndrome characterized by torticollis, multiple
spontaneous keloids, unilateral cryptorchidism, and renal dysplasia [31].
DIAGNOSIS — The diagnosis of keloids and hypertrophic scars is usually clinical, based upon history, scar shape and size,
and growth pattern (table 1). If the diagnosis is uncertain, a skin biopsy for histopathologic examination should be performed
to exclude potentially serious conditions that mimic keloids or hypertrophic scars. (See 'Differential diagnosis' below.)
DIFFERENTIAL DIAGNOSIS — Several benign and malignant conditions may mimic keloids and hypertrophic scars,
including [32]:
● Nodular scleroderma – Nodular scleroderma, also called keloidal scleroderma or keloidal morphea, is a rare form of
scleroderma characterized by multiple firm, nontender nodules or plaques with a predilection for the superior portions of
the thorax (picture 5) [33].
● Dermatofibrosarcoma protuberans – Dermatofibrosarcoma protuberans is a rare, locally aggressive, cutaneous soft

tissue sarcoma [34]. It presents as an asymptomatic indurated plaque or nodule that slowly enlarges over months to
years (picture 6). Histology shows monomorphic spindle cells arranged in long fascicles parallel to the epidermis and
infiltrating thick collagen bundles. In the nodular stage, the tumor cells show a characteristic storiform or mat-like
arrangement. (See "Dermatofibrosarcoma protuberans: Epidemiology, pathogenesis, clinical presentation, diagnosis, and
staging".)
● Giant cell fibroblastoma – Giant cell fibroblastoma is an uncommon, locally aggressive, subcutaneous low-grade
sarcoma usually occurring in childhood [35]. It is considered a juvenile form of dermatofibrosarcoma protuberans.
Histologically, it is composed of infiltrating sheets of spindle-shaped fibroblasts and multinucleated cells with
hyperchromatic nuclei.
● Lobomycosis – Lobomycosis is a chronic fungal infection of the skin and subcutaneous tissue occurring in tropical areas
of Latin America. It presents as slow-growing, keloid-like papules, nodules, or plaques in a localized area on exposed
skin (picture 7). A skin biopsy can confirm the diagnosis. (See "Lobomycosis".)
MANAGEMENT — Keloids and hypertrophic scars are conditions that may require treatment if symptomatic. Pain, pruritus,
hyperhidrosis, functional impairment, and cosmetic disfigurement are examples of comorbidities. Although multiple medical
and surgical therapies have been used for the treatment of keloids and hypertrophic scars, none of these treatments has been
adequately evaluated in high-quality studies and there is no universally accepted treatment approach. (See 'Treatment
options' below.)
Patient evaluation and counseling — The evaluation of the patient with a symptomatic scar involves a detailed scar history,
family history of keloids, and scar assessment. The scar location, size, contour, color, pliability, and presence of subjective
symptoms such as pain and itching should be recorded. Baseline photographs may be useful for comparison after treatment
completion.
The Vancouver Scar Scale (VSS) is an objective method for the assessment of scars frequently used in clinical studies [36].
VSS is based upon scar vascularity, pigmentation, pliability, and height. However, this scale does not take into account the
patient's perception about the scar and subjective symptoms such as pruritus and pain.
The clinician should discuss with the patient his/her needs, concerns, and expectations. Patients with keloids should be
informed that there is a high recurrence risk associated with all treatment options and that repeated treatments or multiple
treatment combinations may be necessary to achieve satisfactory results.
Goals of therapy — The goals of therapy should be set with the individual patient, based upon the patient's complaints and
desire for treatment [4]. They may include one or more of the following:
● Relief of symptoms (eg, pain, pruritus)
● Reduction of the scar volume
● Functional improvement
● Cosmetic improvement
As an example, for conservative treatments (eg, intralesional corticosteroids, compression, silicone sheeting), volume
reduction by 30 to 50 percent, symptom reduction by >50 percent, and sufficient satisfaction of the patient may be acceptable
goals after three to six treatments or after three to six months [4].
Treatment options
Intralesional corticosteroids — Intralesional triamcinolone acetonide at a concentration of 10 to 40 mg/mL is the most

commonly used treatment for hypertrophic scars and keloids [37]. (See "Intralesional injection", section on 'Injection
techniques'.)
Corticosteroids soften and flatten the scar by diminishing collagen and glycosaminoglycan synthesis and by inhibiting
fibroblast proliferation. Due to their antiinflammatory and vasoconstrictive properties, intralesional corticosteroids are effective
in reducing pain and pruritus. Treatment is usually repeated several times at four to six-week intervals, but the optimal
concentration and number of treatments has not been determined.
Data from observational studies indicate response rates to intralesional corticosteroids of 50 to 100 percent, with a recurrence
rate of up to 50 percent at five years [38,39]. In a series of 94 patients with 109 keloids treated with intralesional triamcinolone
acetonide 1 to 10 mg/mL every four weeks, 83 percent of patients receiving more than 10 injections reported reduction of
itching and pain [40]. Excellent or good improvement of prominence and redness was observed in 39 percent of patients who
received 20 to 30 injections over three to five years.
Intralesional corticosteroid injections are painful. Other adverse effects include dermal atrophy, skin ulceration, hypo- or
hyperpigmentation, and development of telangiectasias.
Intralesional 5-fluorouracil — Intralesional 5-fluorouracil (5-FU) has been used for scars that do not respond to
intralesional corticosteroids [41,42]. Intralesional 5-FU appears to induce fibroblast apoptosis without necrosis and inhibit
transforming growth factor (TGF)-beta signaling in the production of collagen type I [41].
In one randomized study, 40 patients were treated with intralesional triamcinolone acetonide 40 mg/mL or 5-FU 50 mg/mL
tattooing every four weeks for a total of three treatments [43]. After 44 weeks, both groups showed a reduction in height,
surface area, erythema, and induration of lesions, with good to excellent response reported in 95 percent of patients in the 5-
FU group versus 50 percent in the triamcinolone group. Patient satisfaction with treatment was greater in the 5-FU group than
in the triamcinolone group, with 85 and 40 percent of patients rating the response to treatment as good or excellent,
respectively.
A 2015 systematic review of 18 small randomized trials and case series (482 patients) found that a good or excellent outcome
was achieved by 45 to 78 percent of patients treated with intralesional 5-FU alone and 50 to 96 percent of those treated with
intralesional 5-FU and triamcinolone acetonide (0.9 mL of 5-FU 50 mg/mL with 0.1 mL triamcinolone 40 mg/mL) [44]. All
studies were of poor quality and seven did not report recurrence rates. Recurrence rates of 25 to 47 percent were found in
studies with a follow-up of one year or longer.
Adverse effects of intralesional 5-FU include pain and hyperpigmentation. Intralesional 5-FU can be used in combination with
intralesional corticosteroids [45,46].
Silicone gel sheets — Silicone gel sheeting is frequently used for the treatment and prevention of hypertrophic scars and
keloids [47-50]. The mechanism by which silicone gel sheeting might exert an anti-scarring effect is unknown, but may be
related to occlusion and hydration of the stratum corneum, generation of static electricity, or reduction of mast cells
[47,48,51,52].
Fluid silicone gel formulations have been developed as an alternative to silicone sheets for use on exposed or large areas.
The silicone gel is applied to the scar area in a thin layer that dries forming a transparent, flexible, gas permeable but water
impermeable silicone sheet.
Silicone gel sheeting and silicone gel are available by prescription and over-the-counter. The sheeting is clear and sticky and
should be cut to fit the size of the keloid and fixed with tape.
A 2013 Cochrane systematic review of 20 controlled trials including 873 patients found some evidence that silicone gel
sheeting may reduce the thickness and improve the appearance of hypertrophic scars and keloids, but concluded that any
estimate of effect was uncertain because the underlying trials were of poor quality and highly susceptible to bias [53].
Pressure therapy — Pressure therapy is usually performed with pressure garments, bandages, or special devices for
certain locations such as the ear. A type of pressure earrings for earlobe keloids called Zimmer splints can be molded to the
appropriate size and cosmetically altered to appear as earrings [54]. Other devices using magnets with or without silicone
sheeting have also been used as post-surgery adjuvant therapy for ear keloids [55-57]. Several types of pressure earrings are
commercially available (eg, Delasco acrylic pressure earrings).
The mechanism of action of pressure may involve the reduction of oxygen tension in the wound through the occlusion of small
blood vessels, resulting in a decreased fibroblast proliferation and collagen synthesis. However, the optimal amount of
pressure is difficult to determine. It should exceed the inherent capillary pressure without diminishing the peripheral blood
circulation (20 to 30 mmHg). In one study, the applied pressure was 35 mmHg, which was estimated using a digital
manometer [56].
The evidence to support the use of pressure therapy is limited. A 2009 meta-analysis of six high quality randomized trials
including 316 burn patients did not demonstrate a difference in the global scar assessment between patients treated with
pressure garments and untreated patients [58]. Observational studies of patients with ear keloids have shown that custom-
made pressure devices may be beneficial to reduce the risk of recurrence after surgical excision [54-56,59].
Cryotherapy — Cryotherapy is most useful in combination with other treatments for keloids [60,61], although up to 50
percent of patients may respond to cryotherapy alone [38,62,63]. A 10- to 30-second freeze-thaw cycle is used and can be
repeated up to three times per treatment session. Treatment is repeated at intervals of four to six weeks until response
occurs. The major side effects are pain and permanent hypopigmentation, the latter of which limits its use in patients with
darker skin.
Intralesional cryotherapy is a newer technique that allows the focused destruction of keloid scar tissue with minimal surface
damage to the epidermis [64,65]. Delivery of liquid nitrogen to the scar tissue is performed under local anesthesia using a
special cryosurgery needle probe consisting of a long, uninsulated, double-lumen cryo-needle equipped with a sharp distal tip,
cryogen vent, and adaptor to a cryogen source. The freezing time may vary, depending on the keloid size, but is typically
longer than external cryotherapy.
Following a single intralesional cryotherapy session, mean scar volume reductions ranging from 50 to over 60 percent and
improvement of pain and itching have been reported [66-68]. Treatments can be repeated at two- to three-week intervals. In
contrast with conventional cryotherapy, postinflammatory hypopigmentation is infrequent after intralesional cryotherapy and
occurs most frequently in patients with darker skin types [68,69]. The reported recurrence rates after intralesional cryotherapy
range from 0 to 24 percent [68].
Excision — Surgical excision of hypertrophic scars and keloids may be indicated if conservative therapies alone are
unsuccessful or unlikely to result in significant improvement. Surgical excision of keloids is associated with recurrence rates of
up to 100 percent [60]. The combination of surgery with adjunctive perioperative therapies can significantly lower the risk of
recurrence:
● Intralesional corticosteroids – Surgical excision combined with preoperative, intraoperative, and postoperative
intralesional injection triamcinolone acetonide has been reported in several small, uncontrolled studies using various
dosages, schedules, and concentrations of the drug [70-75]. In all reports, the perioperative intralesional injection
resulted in a markedly reduced recurrence rate.
● Intralesional 5-fluorouracil (5-FU) – In one study, 80 patients with keloids of one- to four-year duration underwent
surgical excision followed by a single injection of 5-FU and botulinum toxin eight days postsurgery [76]. Recurrence
occurred in three (4 percent) patients after a follow-up time of 17 to 24 months.
● Cryotherapy – Surgical excision followed by immediate freezing of the open wound was performed in one study of 66
patients with 97 large ear keloids [77]. After a median follow-up time of 12 months, 36 percent of lesions recurred and
required further treatment.
● Imiquimod – A few small observational studies have reported that postoperative use of imiquimod with daily or alternate
day applications may reduce the rate of recurrence of keloids [78,79]. However, other studies have provided conflicting
results [80,81].
● Radiation therapy – Brachytherapy (ie, the treatment with radioactive implants in the tissue) or external beam
radiotherapy administered after surgical excision appear to be highly effective in reducing keloid recurrence, as
discussed below.
Postoperative radiation therapy — Several studies have found radiation therapy to be highly effective in reducing keloid
recurrence when administered immediately after surgical excision [82-86]. A variety of techniques, doses, and schedules of
radiation have been used in the treatment of keloids [83,87]. These include megavoltage external beam radiation therapy,
lower energy external radiation sources (radiographs, Co-60), electron beam, and various brachytherapy techniques. Reviews
of the literature have found that the effectiveness in preventing recurrence is related to the biologically effective dose (BED)
and is influenced by the site of the keloid. As an example, one report found that recurrence of keloids in the earlobe could be
prevented in 90 percent of cases with a dose of approximately 16 Gy, given in three fractions using electron beam techniques
[83]. A second review reached a similar conclusion, with a BED of about 30 Gy reducing the recurrence rate to <10 percent
[87].
The control of keloids using postoperative radiation is illustrated by several studies:
● In a study of 80 patients with earlobe keloids treated with a single-fraction 10 Gy dose within 24 hours of the surgical
excision, the recurrence rate was 9 percent at one year and 16 percent at five years [88]. In another study, 174 earlobe
keloids were treated with a total dose of 15 Gy delivered in three fractions or 10 Gy in two fractions [89]. At 18 months,
the recurrence rate was four percent.
● In a study of 45 patients with chest keloids, radiation therapy consisting of 6-MV electron-beam irradiation, 0.5 cm outside
the incision border at a source-to-skin distance of 10 cm, was given in fractions of 5 Gy once daily for three to four
consecutive days to a total dose of 15 to 20 Gy [90]. One case of relapse was observed during a follow-up period of two
years.
● In a study of 612 patients with 892 keloids, patients were treated with Sr-90 brachytherapy after surgical excision [91].
After a median follow-up time of 61 months, the overall recurrence rate was 12 percent. Factors associated with a less
favorable response were the scar location (thorax), size (large), and etiology (result of a burn injury).
● In a study of 43 patients with 67 keloids, high-dose brachytherapy (12 Gy) was administered in two fractions of 6 Gy
given within 4 and 24 hours after surgery [92]. The recurrence rate was 3.1 percent after a mean follow-up of 34 months.
● In another study using iridium-192 high-dose-rate brachytherapy, 28 patients with 32 keloids, 15 of which on the ear,
received a total dose of 12 Gy in two fractions starting immediately after surgery. The overall recurrence rate after a
mean follow-up time of 34 months was 3 percent.
Concerns regarding the potential long-term risks associated with the use of radiation therapy limit its utilization for these
lesions [93]. Several cases of malignancy that may have been associated with radiation therapy for keloids have been
reported [94]. Although causation cannot be confirmed in these cases, caution should still be used when prescribing adjuvant
radiation therapy for keloids, particularly when treating younger patients [88].
Radiation therapy may occasionally be indicated for lesions that are not amenable to resection [95].
Laser therapy — Pulsed dye laser (PDL) and neodymium-yttrium-aluminum-garnet (Nd:YAG) laser treatment has been
reported to be beneficial for hypertrophic scars and keloids [96-98]. The underlying mechanism of laser therapy involves the
destruction of small blood vessels by photodermolysis followed by hypoxemia and altered local collagen production, which
leads to improved scar color, height, pliability, and texture [9].
Evidence from high-quality studies to support the use of lasers for the treatment of hypertrophic scars and keloids is limited. A
systematic review of 13 clinical trials examining seven different types of lasers found that treatment with PDL 585 nm and 595
nm induced a low to moderate improvement of pliability, texture, erythema, and symptoms of hypertrophic scars [99]. A
subsequent meta-analysis of 28 studies including 919 patients showed that the 585/595 nm PDL and 532 nm laser reduced
the total Vancouver Scar Scale scores, scar height, and scar erythema of hypertrophic scars [100]. However, because of the
low quality and heterogeneity of the included studies, the efficacy of laser treatment for hypertrophic scars remains uncertain.
Combination treatments — Recalcitrant keloids that do not respond to intralesional corticosteroids alone may be treated
with a combination of intralesional triamcinolone acetonide and 5-FU (0.9 mL of 5-FU 50 mg/mL plus 0.1 mL of triamcinolone
acetonide 40 mg/mL). In a few randomized trials and observational studies, this combination was more effective than
intralesional corticosteroids alone in reducing the keloid size, induration, erythema, and pruritus [46,101-103].
Limited evidence from small retrospective studies supports the use of pulsed dye laser (PDL) or fractional ablative laser
treatment in combination with postoperative intralesional triamcinolone [104,105].
Other — Other therapies that have been used for keloids include intralesional bleomycin [106-108], mitomycin C [109],
and topical imiquimod cream [80,81]. There is insufficient evidence to make definitive recommendations about these therapies
when used alone, although they may provide benefit when used after surgical excision. (See 'Excision' above.)
Two small randomized trials indicated that intralesional verapamil, a calcium channel blocker, may be as effective as
intralesional triamcinolone acetonide with fewer adverse effects [110]. However, a subsequent randomized trial showed a
higher risk of recurrence for intralesional verapamil compared with triamcinolone [111].
A single intralesional injection of a collagenase preparation approved for the treatment of Dupuytren contracture, followed by
compression, has been evaluated in a small study of six patients with earlobe keloids [112]. An average reduction of over 50
percent in keloid volume was observed at 12 months. Although these results appear promising, further and larger studies are
needed to evaluate the efficacy and safety of this treatment.
Approach — The approach to management of the patient with symptomatic scars is based upon the type and size of scar
(table 1), the patient's characteristics, and the patient's desire for treatment [109].
Linear or small hypertrophic scars — Hypertrophic scars without scar contractures may improve somewhat
spontaneously over time. However, the maturation process is slow and may take months to years to complete, if at all. The
goal of treatment is to accelerate the maturation process and improve subjective symptoms.
First-line therapies for linear or small hypertrophic scars resulting from surgery or trauma include silicone gel sheeting and
pressure therapy.
● Silicone gel sheets should be cut to fit the size of the keloid. The sheet is placed on top of the scar, taped into place, and
left on for 12 to 24 hours per day for two to six months. The sheet is washed daily and replaced every 10 to 14 days.
Silicone gel may be used as an alternative to sheets in body areas in which the application of silicone sheets is not
possible.
● Pressure therapy with pressure garments, bandages, or devices for special locations, if feasible and tolerated by the
patient, may be an alternative to silicone sheeting. Pressure between 20 to 30 mmHg should be maintained for 12 to 24
hours per day for 6 to 12 months.
Second-line therapies include intralesional corticosteroids, laser therapy, and surgical excision.
● Intralesional triamcinolone acetonide 10 to 40 mg/mL can be injected using a 27- or 30-gauge needle with the bevel
directed up toward the skin until skin blanching is noted. Injections can be repeated at three- to four-week intervals as
needed.
● Laser therapy with pulsed dye laser (PDL) may be useful to reduce persistent redness. Laser therapy may also improve
the scar pliability and texture [99].
● The surgical correction of hypertrophic scars should be performed at least one year after the development of the scar to
allow time for spontaneous regression [11]. However, early surgical excision and plastic reconstruction may be performed
for hypertrophic scars that cause cosmetic disfigurement or significant functional impairment.
Minor keloids — We suggest intralesional corticosteroid injections as first-line therapy for the treatment of minor keloids
(<0.5 cm) [11,113]. Triamcinolone acetonide 10 to 40 mg/mL can be injected using a 27- or 30-gauge needle with the bevel
directed up toward the skin until skin blanching is noted (usually 0.1 to 0.5 mL) (picture 8). Injections can be repeated at four-
week intervals. Silicone gel sheeting may be used as adjunctive treatment.
Intralesional corticosteroid injections are painful. For local anesthesia, EMLA cream may be applied under occlusion for 1.5
hours before injection. A Luer-Lok (twist on) type of syringe should be used since injections are often made under pressure.
Superficial cryotherapy immediately before the triamcinolone injection may facilitate the injection through the development of
edema. (See "Intralesional injection".)
For small earlobe keloids, compression with custom-made devices is often used as an adjunctive treatment after intralesional
corticosteroids. Compression for at least 20 hours per day may reduce the need for additional corticosteroid injections.
Second-line therapies include intralesional 5-FU in combination with intralesional corticosteroids (0.9 mL of 5-fluorouracil 50
mg/mL plus 0.1 mL of triamcinolone acetonide 40 mg/mL), contact or intralesional cryotherapy, or laser therapy [114]. Small-
based keloids may be treated with surgical excision and postoperative adjuvant therapy with intralesional corticosteroids,
cryotherapy, or pressure therapy.
Major keloids — For major keloids, intralesional triamcinolone acetonide 40 mg/mL is the first-line therapy to control
pruritus and pain, increase scar pliability, and reduce volume [113]. Injections are repeated at intervals of three to four weeks
for four to six months. Adjunctive treatments include intralesional 5-FU and contact or intralesional cryotherapy.
For large earlobe keloids (picture 4A) that cause considerable cosmetic disfigurement, the initial treatment is often surgical
excision in combination with postoperative intralesional corticosteroids, cryotherapy, compression, or radiation therapy
[56,115].
Widespread burn hypertrophic scars and keloids — The management of extensive hypertrophic burn scars and keloids
is discussed in detail separately. (See "Hypertrophic scarring and keloids following burn injuries".)
PREVENTION — Individuals with a history of hypertrophic or keloid scarring should avoid unnecessary trauma or surgery (eg,
ear piercing, removal of a benign cutaneous lesion for cosmetic reasons). Any skin problems in predisposed individuals (eg,
acne, infections) should be treated as early as possible to minimize areas of inflammation [116].
For at-risk patients undergoing surgery, general preventive measures include:
● Keeping wounds moist – Keeping wounds moist and covered during the early healing phase appears to hasten wound
healing and potentially decreases scar formation [117]. Plain petrolatum is an appropriate lubricant for uninfected
wounds. A nonadherent dressing such as Telfa can be held in place by occlusion with tape, DuoDerm, or silicone gel
pads.
● Avoiding stretching tension on the wound – To limit skin stretching during healing and facilitate appropriate wound
resting, wounds should be covered by protective materials, including tape, bandages, garments, or silicone gel sheets.
Silicone gel sheets can be applied to the wound after completion of reepithelialization and maintained for at least one
month.
● Avoiding sun exposure – Hyperpigmentation after wound healing is common and may be increased by sun exposure.
Sun protection measures include covering the scar with tape or an adhesive dressing or using a broad-spectrum
sunscreen with an SPF of 50 or higher. (See "Selection of sunscreen and sun-protective measures".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the
Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they
answer the four or five key questions a patient might have about a given condition. These articles are best for patients who
want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer,
more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for
patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your
patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the
keyword(s) of interest.)
● Basics topic (see "Patient education: Keloids (The Basics)")
SUMMARY AND RECOMMENDATIONS
● Keloids and hypertrophic scars represent an excessive tissue response to dermal injury characterized by local fibroblast
proliferation and overproduction of collagen. (See 'Introduction' above.)
● Keloids present as raised dermal lesions that extend beyond the boundaries of the original wound and invade the
surrounding healthy skin (picture 3A-B, 4A, 4C). In contrast, hypertrophic scars are usually confined within the margins of
the original wound (table 1). Symptoms include pain, tenderness, and pruritus. (See 'Clinical features' above.)
● The diagnosis of keloids and hypertrophic scars is usually clinical. However, a skin biopsy should be performed if the
diagnosis is uncertain. (See 'Diagnosis' above and 'Differential diagnosis' above.)
● Multiple medical and surgical therapies have been used for the treatment of keloids and hypertrophic scars. However,
data on the efficacy of these treatments are limited and there is no universally accepted treatment approach. (See
'Treatment options' above.)
● For linear or small hypertrophic scars resulting from surgery or trauma, silicone gel sheeting may be used as initial
treatment. Pressure therapy, if feasible and tolerated by the patient, may be an alternative first-line treatment. Second-
line therapies include intralesional corticosteroids, laser therapy, and surgical excision. (See 'Linear or small hypertrophic
scars' above.)
● For minor keloids (<0.5 cm), we suggest intralesional corticosteroids as the first-line therapy (Grade 2C). Triamcinolone
acetonide 10 to 40 mg/mL is injected using a 27- or 30-gauge needle until skin blanching is noted (usually 0.1 to 0.5 mL).
Silicone gel sheeting or pressure therapy may be used as adjunctive therapies. Second-line therapies include
intralesional 5-fluorouracil (5-FU) in combination with intralesional corticosteroids, contact or intralesional cryotherapy, or
laser therapy. (See 'Minor keloids' above.)
● For major keloids (>0.5 cm), intralesional triamcinolone acetonide 40 mg/mL is the first-line therapy to control pruritus
and pain, increase scar pliability, and reduce volume. Adjunctive treatments include intralesional 5-FU and contact or
intralesional cryotherapy. For large earlobe keloids (picture 4A) that cause considerable cosmetic disfigurement, the initial
treatment is often surgical excision in combination with perioperative intralesional corticosteroids, compression, or
radiation therapy. (See 'Major keloids' above.)
● The management of extensive hypertrophic burn scars and keloids is discussed separately. (See "Hypertrophic scarring
and keloids following burn injuries".)
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Topic 5569 Version 19.0
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GRAPHICS
Histopathologic features of keloids
(A) Nodules of spindle cells with abundant collagen are present in the dermis
with prominent hyalinization.
(B) Glassy eosinophilic and hyalinized collagen fibers are interspersed with
swathes of fibroblasts.
Reproduced with permission from: Beer TW, Lam MH, Heenan PJ. Tumors of fibrous
tissue involving the skin. In: Lever's Histopathology of the Skin, 10th ed, Elder DE,
Elenitsas R, Johnson B Jr, et al (Eds), Lippincott Williams & Wilkins, Philadelphia
2009. Copyright © 2009 Lippincott Williams & Wilkins. www.lww.com.
Graphic 97006 Version 3.0
Classification of scars
Characteristics*
Scar type Maturation
Mature Light in color

Flat
Immature Red Many mature in time

Pruritic Become flat
Painful Pigmentation generally similar to surrounding skin
Slightly elevated, indicating remodeling Pigmentation may be paler or darker than skin
Linear, Red Increases in size rapidly for first three to six months
hypertrophic Raised After a static phase, regresses
Example: Pruritic Full maturation in approximately two years
Surgical or Confined to the border of the original scar
traumatic scar Generally matures to an elevated, slightly rope-
like appearance
Mature scar has increased width (variable)
Widespread, Widespread
hypertrophied Red
Example: Burn Raised
Pruritic
Remains within the borders of the burn injury
Minor keloid Focally raised May develop one year after burn
Pruritic Does not regress spontaneously
Extends beyond burn borders Recurrence generally follows surgical excision
May have genetic component for keloid
development
Typical site: Earlobes
Major keloid Large (>0.5 cm) Does not spontaneously regress

Painful Can continue to progress in size over years
Pruritic
Extends beyond burn borders over normal tissue
Can result even from minor trauma
* Characteristics may be variable in symptoms (eg, pruritus, pain) for each patient.
From: Mustoe TA, Cooter RD, Gold MH, et al. International clinical recommendations on scar management. Plast Reconstr Surg 2002;
110:560. Adapted with permission from Lippincott Williams & Wilkins. Copyright © 2002 American Society of Plastic Surgeons, Inc.
Unauthorized reproduction of this material is prohibited.
Hypertrophic scar
Hypertrophic scar at the site of a surgical wound. Multiple telangiectasias are

visible on the scar surface.
Reproduced with permission from: Diepgen TL, Yihune G, et al. Dermatology Online
Atlas. Published online at: www.dermis.net. Copyright © 1996-2015 DermIS. All
rights reserved.
Keloids
Patient with large spontaneous keloids on the upper back.
Reproduced with permission from: www.visualdx.com. Copyright Logical Images, Inc.
Keloids from acne
Reproduced with permission from: Stedman's Medical Dictionary. Copyright © 2008

Lippincott Williams & Wilkins.
Keloid scar
A large keloid is present on the neck of this patient.
Keloid
A large keloid of the ear lobe.
Small keloid on the ear lobe
Lower lobe piercing resulting in a small keloid. Piercing hardware was removed one month after piercing and picture was taken
approximately one year later.
Nodular scleroderma
Hyperpigmented nodules and plaques on the chest of a 51-year-old man with nodular scleroderma.
From: Wriston CC, Rubin AI, Elenitsas R, Crawford GH. Nodular scleroderma: A report of 2 cases. Am J Dermatopathol
2008; 30:385. DOI: 10.1097/DAD.0b013e3181766177. Reproduced with permission from Lippincott Williams & Wilkins.
Copyright © 2008 International Society of Dermatopathology. Unauthorized reproduction of this material is prohibited.
Dermatofibrosarcoma protuberans
Dermatofibrosarcoma protuberans on the trunk presenting as a red-brown plaque with nodules.
Reproduced with permission from: www.visualdx.com. Copyright © 2014 Logical Images, Inc.
Lobomycosis
Keloid-like plaques on the extremity, consistent with lobomycosis.
Courtesy of Fabio Francesconi, MD.
Injection of kenalog in a hypertrophic scar
The appearance of the hypertrophic scar is similar to that of keloids, but does
not extend beyond the margin of the scar. The scar is being injected with
kenalog.
Courtesy of Beth G Goldstein, MD, and Adam O Goldstein, MD.

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Authors: Beth G Goldstein, MD, Adam O Goldstein, MD, MPH

spontaneous keloids, unilateral cryptorchidism, and renal dysplasia [31].

● Dermatofibrosarcoma protuberans – Dermatofibrosarcoma protuberans is a rare, locally aggressive, cutaneous soft

● Relief of symptoms (eg, pain, pruritus)

● Reduction of the scar volume

Intralesional corticosteroids — Intralesional triamcinolone acetonide at a concentration of 10 to 40 mg/mL is the most

The control of keloids using postoperative radiation is illustrated by several studies:

For at-risk patients undergoing surgery, general preventive measures include:

● Basics topic (see "Patient education: Keloids (The Basics)")

SUMMARY AND RECOMMENDATIONS

'Treatment options' above.)

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Topic 5569 Version 19.0

Histopathologic features of keloids

Graphic 97006 Version 3.0

Mature Light in color

Immature Red Many mature in time

Major keloid Large (>0.5 cm) Does not spontaneously regress

Graphic 95115 Version 5.0

Hypertrophic scar at the site of a surgical wound. Multiple telangiectasias are

Graphic 97014 Version 2.0

Patient with large spontaneous keloids on the upper back.

Reproduced with permission from: www.visualdx.com. Copyright Logical Images, Inc.

Graphic 97537 Version 1.0

Keloids from acne

Reproduced with permission from: Stedman's Medical Dictionary. Copyright © 2008

Graphic 61382 Version 4.0

A large keloid is present on the neck of this patient.

Reproduced with permission from: www.visualdx.com. Copyright Logical Images, Inc.

Graphic 97009 Version 2.0

A large keloid of the ear lobe.

Reproduced with permission from: www.visualdx.com. Copyright Logical Images, Inc.

Graphic 54044 Version 3.0

Small keloid on the ear lobe

Graphic 109966 Version 1.0

Graphic 97529 Version 2.0

Dermatofibrosarcoma protuberans on the trunk presenting as a red-brown plaque with nodules.

Graphic 96386 Version 1.0

Keloid-like plaques on the extremity, consistent with lobomycosis.

Courtesy of Fabio Francesconi, MD.

Graphic 96226 Version 2.0

Injection of kenalog in a hypertrophic scar

Courtesy of Beth G Goldstein, MD, and Adam O Goldstein, MD.

Graphic 55411 Version 3.0

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