Is there any treatment for post operative keloid?

there is a keloid in chest caused by the open heart surgery. any plastic surgery or injection is there for curing.

Is there any treatment for post operative keloid?
Hey Bey the guy had asked for a treatment n not for a keloid journal from you.





I'll tell u a simple and effective treatment....inject steroid topically into the keloid, it will regress in sometime.
Reply:No treatment of keloids has been shown to be uniformly effective. Surgery is unfortunately associated with a high risk of recurrence. It may be of use in keloids that occur as a result of post-operative wound infection or from poorly placed incisions. If further surgery is contemplated post-operative pressure from elastic compression garments may help to prevent recurrence. Physiotherapy may be a useful adjunct as also may be topical silicone gel sheets. These have been shown to be particularly useful in post-burn hypertrophic scars. Cryotherapy, laser and both external beam and intra-lesional radiotherapy have been used. The use radiotherapy is controversial as it does induce regression of keloid scars but concerns exist that it may induce skin tumours.





The most extensively used drug treatment is topical or intra-lesional injection of the long-acting steroid, triamcinolone. Steroids reduce collagen synthesis by decreasing mRNA production and shifting collagen metabolism in favour of lysis. Whilst reducing the extent of keloid scarring complications including skin atrophy, hypopigmentation and telangiectasia are not uncommon. Interferon-gamma has recently been used with encouraging results.


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No single therapeutic modality is best for all keloids. The location, size, and depth of the lesion; the age of the patient; and the past response to treatment determine the type of therapy used. Prevention is key, but therapeutic treatment of hypertrophic scars and keloids includes occlusive dressings, compression therapy, intralesional corticosteroid injections, cryosurgery, excision, radiation therapy, laser therapy, interferon therapy, imiquimod 5% cream, and other promising but lesser-known therapies directed at collagen synthesis.





Prevention: This is the first rule in keloid therapy.





Avoid performing nonessential cosmetic surgery in patients known to form keloids; however, do not consider patients who have only earlobe lesions to be among those who form keloids.





Close all surgical wounds with minimal tension.





Incisions should not cross joint spaces.





Avoid making midchest incisions, and ensure that incisions follow skin creases whenever possible.


Standard treatments: These include occlusive dressings, compression therapy, and intralesional corticosteroid injections.





Occlusive dressings include silicone gel sheets and dressings, nonsilicone occlusive sheets, Cordran tape, and Scarguard. These measures have been used with varied success. Antikeloidal effects appear to result from a combination of occlusion and hydration, rather than from an effect of the silicone.





Previous studies have shown that in patients treated with silicone occlusive sheeting with pressure worn 24 h/d for up to 12 months, 34% showed excellent improvement, 37.5% showed moderate improvement, and 28% demonstrated no or slight improvement.





Of patients treated with semipermeable, semiocclusive, nonsilicone-based dressings for 8 weeks, 60% experienced flattening of keloids, 71% had reduced pain, 78% had reduced tenderness, 80% had reduced pruritus, 87.5% had reduced erythema, and 90% were satisfied with the treatment.





Cordran tape is a clear surgical tape that contains flurandrenolide, a steroid that is uniformly distributed on each square centimeter of the tape, and it has been shown to soften and flatten keloids over time.





Scarguard is a topical medication containing silicone, hydrocortisone, and vitamin E. In an in vitro study, Scarguard stimulated the release of inactive collagenase precursors that may inhibit new scars from forming and may reduce existing scars. In a pilot study of 12 patients, Scarguard was applied twice daily after the removal of a mole and nothing was applied after the removal of a second mole. After 2 months, 9 of 12 patients reported that the treated scar was less red and less noticeable compared with the untreated scar.


Compression therapy involves pressure, which has long been known to have thinning effects on skin. Reduction in the cohesiveness of collagen fibers in pressure-treated hypertrophic scars has been demonstrated by electron microscopy.





Compression treatments include button compression, pressure earrings, ACE bandages, elastic adhesive bandages, compression wraps, Lycra bandages, and support bandages. In one study, button compression (2 buttons sandwiching the earlobe applied after keloid excision) prevented recurrence during 8 months to 4 years of follow-up observation.





Other pressure devices include pressure earrings and pressure-gradient garments made of lightweight porous Dacron, spandex (also known as elastane), or bobbinet fabric (usually worn 12-24 h/d) and zinc oxide adhesive plaster. Overall, 60% of patients treated with these devices showed 75-100% improvement.





Corticosteroids, specifically intralesional corticosteroid injections, have been the mainstay of treatment. Corticosteroids reduce excessive scarring by reducing collagen synthesis, altering glucosaminoglycan synthesis, and reducing production of inflammatory mediators and fibroblast proliferation during wound healing. The most commonly used corticosteroid is triamcinolone acetonide (TAC) in concentrations of 10-40 mg/mL administered intralesionally with a 25- to 27-gauge needle at 4- to 6-week intervals.





Intralesional steroid therapy as a single modality and as an adjunct to excision has been shown to be efficacious in various studies. Response rates varied from 50-100%, with recurrence rates of 9-50% in completely resolved scars.





When combined with excision, postoperative intralesional TAC injections yielded a recurrence rate of 0-100%, with most studies citing a rate of less than 50%.





Complications of repeated corticosteroid injections include atrophy, telangiectasia formation, and pigmentary alteration.


Recent innovations: New treatments for keloids and hypertrophic scars include intralesional interferon, verapamil, bleomycin, 5-fluorouracil (5-FU), retinoic acid, imiquimod, tacrolimus, and botulinum toxin.





Interferon therapy, including interferon alfa, interferon beta, and interferon gamma, has been demonstrated in in vitro studies to reduce keloidal fibroblast production of collagen I, III, and VI mRNA.





Interferon alfa and interferon beta also reduce fibroblast production of glycosaminoglycans (GAGs), which form the scaffolding for deposition of dermal collagen. Interferon gamma enhances GAG production.





Interferon alfa, interferon beta, and interferon gamma have been shown to increase collagenase activity. Studies have shown that interferon gamma modulates a p53 apoptotic pathway by inducing apoptosis-related genes. p53 is a protein synthesized following DNA damage. Once damage is repaired, p53 is degraded. Mutations of this protein are believed to predispose cells to hyperproliferation, possibly resulting in keloid formation. In addition, p53 is a potent suppressor of interleukin (IL)–6, a cytokine implicated in hyperproliferative and fibrotic conditions.





Interferon injected into the suture line of keloid excision sites may be prophylactic for reducing recurrences. Berman and Flores reported statistically significant fewer keloid recurrences in a study of 124 keloid lesions after postoperative interferon alfa-2b injection treatment (5 million U, 1 million U injected per cm of scar) into keloid excision sites (18%) versus excision alone (51.1%) and TAC treatment (58.4%).





Verapamil is a calcium channel blocker that blocks the synthesis/secretion of extracellular matrix molecules (eg, collagen, GAGs, fibronectin) and increases fibrinase. In a study of 22 patients with keloids, patients were treated with surgical excision and 5 treatments of verapamil at 2.5 mg/mL (doses varied from 0.5-5 mL, depending on the size of the keloid) over a 2-month period and were evaluated at 2-year follow-up. Two patients had keloids that decreased in size from the original lesion, 2 patients had hypertrophic scars, 4 patients had pruritus, and 1 patient had a keloid on the donor site.





Bleomycin injections cause necrosis of keratinocytes with a mixed inflammatory infiltrate. In 2 studies, bleomycin was used to treat keloids and hypertrophic scars. In one study, bleomycin was given at a concentration of 1.5 IU/mL to 13 patients using the multiple-puncture method. Bleomycin was dripped onto the lesion, and then multiple punctures were made on the lesions by means of a syringe. Seven patients had complete flattening, 5 patients had highly significant flattening, and 1 patient had significant flattening. In another study of 31 keloids, patients were treated with 3-5 infiltrates of bleomycin within a 1-month period. Total regression occurred in 84% of the keloids, and both keloid volume and functional impairment were reduced.





5-FU, a pyrimidine analog, inhibits fibroblastic proliferation in tissue culture and is believed to reduce postoperative scarring by decreasing fibroblast proliferation. 5-FU has also been shown to be safe and effective in the treatment and prevention of hypertrophic scars and to be somewhat responsive in small keloids. Two studies have shown the effectiveness of 5-FU.





In one prospective, randomized, uncontrolled trial, 28 patients were treated with weekly injections of 0.5-2 mL at a 50-mg/mL concentration of 5-FU for 12 weeks. At the 24-week follow-up, 70% of the patients had more than 50% improvement in keloid size.





In the other retrospective study of 1000 patients with hypertrophic scars and keloids over a 9-year period, the most effective regimen was found to be 0.1 mL of TAC (10 mg/mL) and 0.9 mL of 5-FU (50 mg/mL) up to 3 times a week.





Retinoic acid decreases normal tonofilament and keratohyalin synthesis, increases production of mucoid substances and epidermal cell growth rate, and inhibits DNA synthesis in vitro. In a clinical trial involving 21 patients with 28 keloids and hypertrophic scars, topical retinoic acid was applied for at least 3 months twice daily and showed favorable results in 77-79% of the lesions. This includes a decrease in the size and symptoms of the scar.





Imiquimod induces tumor necrosis factor-alpha (TNF-alpha), interferon-alpha and interferon-gamma, IL-1, IL-6, IL-8, and IL-12 and alters the expression of markers for apoptosis. In one study, 13 keloids were treated with excision in combination with nightly applications of imiquimod for 8 weeks. Ten patients with 11 keloids completed the 6-month study, and no keloids recurred after 6 months. Mild irritation was experienced with the application of imiquimod, and some patients needed a vacation period from the medication. Hyperpigmentation was experienced by more than half of the patients in the study.





Tacrolimus is an immunomodulator that inhibits TNF-alpha. gli-1, an oncogene, has been found to be overexpressed in fibroblasts of keloids. Rapamycin, a close analogue of tacrolimus, was used in an in vitro study and was found to inhibit the gli-1 oncogene, thus giving a rationale to initiate clinical trials of topical tacrolimus and rapamycin. In an open-label pilot study, 11 patients used tacrolimus 0.1% ointment twice daily for 12 weeks on their keloids. Although the results were not statistically significant, the study showed a decrease in induration, tenderness, erythema, and pruritus for most patients.


Radiation therapy





Using radiotherapy to treat keloids remains controversial. Although many studies have demonstrated efficacy and decreased recurrence rates, the safety of radiotherapy has been questioned.





In one retrospective study of superficial x-ray therapy of 24 excised keloids, the author reported a recurrence rate of 53%. Use of iridium Ir 192 interstitial irradiation after excisional surgery resulted in a 21% recurrence rate after 1 year. Excisional surgery and preoperative hyaluronidase solution (150 U/mL NaCl) followed by external radiation (7.2-10.8 Gy) had a 0% recurrence rate. Adjunctive high dose rate brachytherapy (192Ir) used after excision and closure resulted in a 12% reoccurrence rate after 26 months.





When excisional surgery is followed by postoperative radiation therapy, the total fractionated dose should be a minimum of 12 Gy, according to a comparative study showing a higher recurrence rate for patients treated with total doses less than 12 Gy.


Surgical Care:





Cryotherapy





Cryosurgical media (eg, liquid nitrogen) affects the microvasculature and causes cell damage via intracellular crystals, leading to tissue anoxia.





Generally, 1, 2, or 3 freeze-thaw cycles lasting 10-30 seconds each are used for the desired effect. Treatment may need to be repeated every 20-30 days. Take care to administer liquid nitrogen in short application periods because of the possibility of reversible hypopigmentation. Cryotherapy can cause pain and depigmentation in selected patients.





As a single modality, cryosurgery led to total resolution with no recurrences in 51-74% of patients after 30 months of follow-up observation.


Excision


Apply basic soft tissue handling techniques at primary wound repair sites.





Carefully plan closure with minimal tension, paralleling the relaxed skin tension lines.





Use buried sutures when necessary for layered closure and to reduce tension.





Whenever feasible, apply pressure dressings and garments during the immediate postoperative period to wounds of patients in whom hypertrophic scars and keloid formation occur.





Decreased recurrence rates have been reported with excision in combination with other postoperative modalities, such as radiotherapy, injected interferon, or corticosteroids.





Excisional surgery alone has been shown to yield a 45-100% recurrence rate and should very rarely be used as a solitary modality, although excision in combination adjunct measures can be curative. Most studies in which excisional surgery was combined with injected steroids indicated less than 50% recurrence.


The authors recently reported the effects of topically applied imiquimod 5% cream (Aldara), which induces local production of interferons at the site of application, on the postexcision recurrence rates of 13 keloids excised surgically from 12 patients.





Starting the night of surgery, imiquimod 5% cream was applied for 8 weeks. Patients were examined at weeks 4, 8, 16, and 24 for local erythema, edema, erosions, pigment alteration, and/or recurrence of keloid.





Of the 11 keloids evaluated at 24 weeks, none (0%) recurred. The rate of hyperpigmentation was 63.6%. Two cases of mild irritation and superficial erosion cleared with temporary discontinuation of imiquimod. Both patients completed the 8 weeks of topical therapy and the final 24-week assessment.





At 24 weeks, the recurrence rate of excised keloids treated with postoperative imiquimod 5% cream was lower than recurrence rates previously reported in the literature.


Laser therapy


Ablation of keloids and hypertrophic scars using a carbon dioxide laser (10,600 nm) can cut and cauterize the lesion, creating a dry surgical environment with minimal tissue trauma. When used as a single modality, the carbon dioxide laser was associated with recurrence rates of 39-92%, and when combined with postoperative injected steroids, it was associated with recurrence rates of 25-74%.





The argon laser (488 nm), similar to the carbon dioxide laser, can induce collagen shrinkage via generation of excessive localized heat. The argon laser has demonstrated recurrence rates of 45-93%.





The pulsed dye laser (585 nm) provides photothermolysis, resulting in microvascular thrombosis. Beginning in the 1980s, authors noted that scars became less erythematous, more pliable, and less hypertrophic after treatment with the 585-nm pulsed dye laser. The findings were later confirmed using objective measurements of erythema by reflectance spectrometry readings, scar height, and pliability measurements. The pulsed dye laser remains the laser treatment of choice for hypertrophic scars, because of its efficacy, safety, and relatively low cost.





The Nd:YAG laser (1064 nm) has demonstrated recurrence rates of 53-100%.


Other potential therapies


Additional potential therapeutic options for treating hypertrophic and keloidal scarring that have been shown in vitro to affect collagen synthesis include the use of proline-cis-hydroxyproline and azetidine carboxylic acid, tranilast (antiallergic drug shown to decrease collagen and GAG synthesis), and pentoxifylline (inhibits DNA replication).


In addition, wounds treated with anti–transforming growth factor healed with minimal scar tissue formation and without affecting wound tensile strength. A possible candidate for affecting wounds via the neutralizing effect of transforming growth factor is the proteoglycan termed decorin.