Modern Concepts of Treating Scars

**55**

**Chapter 5**

*Rei Ogawa*

**Abstract**

**1. Introduction**

Keloids and Hypertrophic Scars

Can Now Be Treated Completely

Surgery, Followed by Radiation

and Corticosteroid Tape/Plaster

by Multimodal Therapy, Including

Keloids and hypertrophic scars are fibroproliferative disorders of the skin. Research over the last decade has markedly improved our understanding of the pathogenesis of these scars, in particular, the fact that both disorders are caused by prolonged inflammation that prevents the orderly healing of injured or irritated skin. This protracted inflammatory response is due to genetic, systemic, and local risk factors. Genetic factors include single nucleotide polymorphisms, while systemic factors include hypertension, pregnancy-related and other hormones, and aberrant cytokine levels. An important local factor is the mechanical force (tension) on the scar. These observations have greatly aided the development of therapies for these once-intractable scars. As a result, these scars are now regarded as being completely treatable. At present, we believe that the following combination of three therapies most reliably achieves a complete cure: surgery followed by radiation and the prolonged daily use of corticosteroid tape/plaster.

**Keywords:** keloid, hypertrophic scar, scar, scar contracture, fibroproliferative

While keloids and hypertrophic scars have some tumor-like properties, they are actually inflammatory conditions that drive the excessive proliferation of dermal fibroblasts and the aberrant accumulation of dermal matrix [1]. These fibroproliferative disorders of the skin are caused by abnormal healing of injured or irritated skin. Common causes of injury and irritation are trauma, burn, surgery, vaccination, skin piercing, acne, and herpes zoster. The risk of developing keloids and hypertrophic scars is particularly high if the wound is deep enough to damage the reticular layer of the dermis and if various genetic, systemic, and/or local risk factors that prolong the inflammatory stage of wound healing are present. The protracted inflammation accelerates angiogenesis and induces the excessive accumulation of collagen. As a result, red and elevated scars that have an unappealing appearance arise. These scars also associate with intermittent pain, persistent itching, and a sensation of contraction. Moreover, if the wounds are located on

disorder, fibrosis, surgery, radiotherapy, corticosteroid, tape, plaster

#### **Chapter 5**

Keloids and Hypertrophic Scars Can Now Be Treated Completely by Multimodal Therapy, Including Surgery, Followed by Radiation and Corticosteroid Tape/Plaster

*Rei Ogawa*

### **Abstract**

Keloids and hypertrophic scars are fibroproliferative disorders of the skin. Research over the last decade has markedly improved our understanding of the pathogenesis of these scars, in particular, the fact that both disorders are caused by prolonged inflammation that prevents the orderly healing of injured or irritated skin. This protracted inflammatory response is due to genetic, systemic, and local risk factors. Genetic factors include single nucleotide polymorphisms, while systemic factors include hypertension, pregnancy-related and other hormones, and aberrant cytokine levels. An important local factor is the mechanical force (tension) on the scar. These observations have greatly aided the development of therapies for these once-intractable scars. As a result, these scars are now regarded as being completely treatable. At present, we believe that the following combination of three therapies most reliably achieves a complete cure: surgery followed by radiation and the prolonged daily use of corticosteroid tape/plaster.

**Keywords:** keloid, hypertrophic scar, scar, scar contracture, fibroproliferative disorder, fibrosis, surgery, radiotherapy, corticosteroid, tape, plaster

### **1. Introduction**

While keloids and hypertrophic scars have some tumor-like properties, they are actually inflammatory conditions that drive the excessive proliferation of dermal fibroblasts and the aberrant accumulation of dermal matrix [1]. These fibroproliferative disorders of the skin are caused by abnormal healing of injured or irritated skin. Common causes of injury and irritation are trauma, burn, surgery, vaccination, skin piercing, acne, and herpes zoster. The risk of developing keloids and hypertrophic scars is particularly high if the wound is deep enough to damage the reticular layer of the dermis and if various genetic, systemic, and/or local risk factors that prolong the inflammatory stage of wound healing are present. The protracted inflammation accelerates angiogenesis and induces the excessive accumulation of collagen. As a result, red and elevated scars that have an unappealing appearance arise. These scars also associate with intermittent pain, persistent itching, and a sensation of contraction. Moreover, if the wounds are located on

the joints or mobile regions, including the neck, the resulting scars can develop into scar contractures. Thus, the primary end-points of treatments for keloids and hypertrophic scars should be functional improvement and relief from pain and itch. Another important goal is the esthetic improvement.

#### **2. Causes of keloids and hypertrophic scars**

A number of genetic, systemic, and local factors that influence the characteristics and quantity of keloids and hypertrophic scars have been identified [2]. The genetic causes of pathological scar development include single nucleotide polymorphisms [3, 4]. Moreover, our study showed that one of these polymorphisms associates significantly with clinically severe keloids [4]. It has been suggested that keloids are more influenced by genetic background than hypertrophic scars. This notion remains to be tested. To test it, it will be necessary to have a critical biomarker that reliably distinguishes keloids from hypertrophic scars. One possibility is keloidal collagen: it seems that this histological feature is only present in lesions that bear other classical hallmarks of keloids, including growth over the edges of the original wound. However, identification of other, nonpathology, biomarkers would be highly useful for addressing questions about the differences between keloids and hypertrophic scars in terms of their etiology, growth characteristics, and treatment responses.

In terms of systemic factors, adolescence and pregnancy appear to associate with a higher risk of developing pathological scars [5, 6]. Our recent study also showed that hypertension associates with the development of severe keloids [7, 8]. I believe that while these factors are not primary causes of keloid and hypertrophic scars, they do worsen the inflammation in the scar tissue, thereby accelerating and increasing angiogenesis and matrix production.

Of the many factors that contribute to pathological scar development is local mechanical forces, I believe that they play a particularly important role [9–11]. Keloids commonly adopt distinct site-specific shapes, namely, the typical butterfly, crab's claw, and dumbbell shapes on the shoulder, anterior chest, and upper arm, respectively. These shapes reflect the region-specific distribution of skin tension that then tugs repetitively or constantly on the wounds/scars. Moreover, keloids are rare on the upper eyelid. This reflects the fact that eyelid skin is always relaxed regardless of whether the eyes are open or closed. An exception may be earlobe keloids: the contribution of mechanical factors to the development of these keloids may be minor. Instead, the most likely local cause of these keloids is the repeated attaching and detaching of the piercing, which repeatedly injures the skin and heightens the risk of infection. Both the skin tension and repeated injury/infection trigger inflammation and the downstream fibroproliferative events. In summary, while skin tension itself may not be a primary cause of keloids and hypertrophic scars, it is likely to be an important local risk factor that worsens and prolongs the inflammation that drives the formation and/or progression of these fibroproliferative scars.

#### **3. Standard treatment of keloids and hypertrophic scars**

These findings have markedly improved our understanding of the pathogenesis of keloids and hypertrophic scars, which in turn has promoted the development of highly effective treatments for these once-intractable scars. At present, I believe that the most reliable approach is a combination of three therapies, namely, surgery, followed by radiation, and prolonged daily use of steroid tape/plaster. The addition

**57**

protocol.

**3.1 Surgery**

regional/local flap transfer.

**3.2 Radiation**

*Keloids and Hypertrophic Scars Can Now Be Treated Completely by Multimodal Therapy…*

of radiation and steroid tape/plaster to surgery reflects the point made above, namely, that keloids and hypertrophic scars are inflammatory disorders, and not tumors. Consequently, anti-inflammatory treatments are most effective for these lesions. Indeed, as will be described below, steroid tapes/plasters/injections on their own work well to reduce the volume of accumulated collagen in keloids and hypertrophic scars, thereby causing their mass to shrink. However, steroid treatments take a long time to achieve mass reduction. Consequently, with large lesions, they are best performed after surgery that rapidly removes the lesion mass. Radiation on its own also has mass-reducing effects because it appears to suppress angiogenesis, and therefore dampens the influx of inflammatory cells and factors into the scar. These anti-inflammatory properties of steroid and radiation mean that their application after mass-reducing surgery (which by itself provokes inflammatory responses) will prevent the recurrence of excised keloids and hypertrophic scars. Below, we will describe each of the three modalities separately. Thereafter, we will describe the three modalities when used in our combination therapeutic

Since surgical treatment itself induces inflammation, surgery alone associates with high rates of keloid and hypertrophic scar recurrence. Worse, the recurrent scars are often much bigger than the original lesions. Thus, unless the scar is a minor hypertrophic scar, the decision to surgically remove a pathological scar should be made very carefully and postoperative radiation therapy should always be performed. However, if keloids and hypertrophic scars have infected areas, such as inclusion cysts, these should be removed surgically. Another key indication for surgery is keloids and hypertrophic scars that result in scar contracture of the joints or mobile areas such as the neck. In this case, the contractures should be released by a combination of subcutaneous/fascial tensile reduction sutures, z-plasties, and

The main objective of surgery for keloids and hypertrophic scars is not only mass reduction, but it is also to reduce the mechanical tension on the scar or the wound that is left after surgical removal of the scar. This is due to the important role of mechanical tension in the development and progression of keloids and hypertrophic scars. This is reflected by the fact that the most effective surgical method for releasing scar contractures is to use a regional or local flap, especially skin-pedicled local flaps: these flaps are particularly useful because they expand naturally after surgery and are therefore not prone to postsurgical contractures [12]. In contrast, skin grafts do not expand, which means that skin grafting tends to generate secondary contractures that result in circular pathological scars around the grafted skin.

Interestingly, keloids respond very well to primary radiation therapy (i.e., radiation monotherapy). This reflects the fact that radiotherapy has a strong anti-inflammatory effect. Primary radiation therapy is suitable for older patients or patients with severe (huge) keloids (**Figure 1**). Since the total radiation dose in these cases is relatively high (e.g., 5 Gy administered once a week for 5 weeks by superficial brachytherapy), it is necessary to apply the radiation carefully to prevent secondary radiation carcinogenesis. However, the risks of primary radiation therapy should be weighed against its tremendous benefits; in particular, the fact that it immediately alleviates the subjective symptoms of keloids such as pain and itching. Moreover, over the following year, it

causes the color and thickness of the scars to progressively normalize.

*DOI: http://dx.doi.org/10.5772/intechopen.84178*

*Keloids and Hypertrophic Scars Can Now Be Treated Completely by Multimodal Therapy… DOI: http://dx.doi.org/10.5772/intechopen.84178*

of radiation and steroid tape/plaster to surgery reflects the point made above, namely, that keloids and hypertrophic scars are inflammatory disorders, and not tumors. Consequently, anti-inflammatory treatments are most effective for these lesions. Indeed, as will be described below, steroid tapes/plasters/injections on their own work well to reduce the volume of accumulated collagen in keloids and hypertrophic scars, thereby causing their mass to shrink. However, steroid treatments take a long time to achieve mass reduction. Consequently, with large lesions, they are best performed after surgery that rapidly removes the lesion mass. Radiation on its own also has mass-reducing effects because it appears to suppress angiogenesis, and therefore dampens the influx of inflammatory cells and factors into the scar. These anti-inflammatory properties of steroid and radiation mean that their application after mass-reducing surgery (which by itself provokes inflammatory responses) will prevent the recurrence of excised keloids and hypertrophic scars.

Below, we will describe each of the three modalities separately. Thereafter, we will describe the three modalities when used in our combination therapeutic protocol.

#### **3.1 Surgery**

*Scars*

responses.

the joints or mobile regions, including the neck, the resulting scars can develop into scar contractures. Thus, the primary end-points of treatments for keloids and hypertrophic scars should be functional improvement and relief from pain and itch.

A number of genetic, systemic, and local factors that influence the characteristics and quantity of keloids and hypertrophic scars have been identified [2]. The genetic causes of pathological scar development include single nucleotide polymorphisms [3, 4]. Moreover, our study showed that one of these polymorphisms associates significantly with clinically severe keloids [4]. It has been suggested that keloids are more influenced by genetic background than hypertrophic scars. This notion remains to be tested. To test it, it will be necessary to have a critical biomarker that reliably distinguishes keloids from hypertrophic scars. One possibility is keloidal collagen: it seems that this histological feature is only present in lesions that bear other classical hallmarks of keloids, including growth over the edges of the original wound. However, identification of other, nonpathology, biomarkers would be highly useful for addressing questions about the differences between keloids and hypertrophic scars in terms of their etiology, growth characteristics, and treatment

In terms of systemic factors, adolescence and pregnancy appear to associate with a higher risk of developing pathological scars [5, 6]. Our recent study also showed that hypertension associates with the development of severe keloids [7, 8]. I believe that while these factors are not primary causes of keloid and hypertrophic scars, they do worsen the inflammation in the scar tissue, thereby accelerating and

Of the many factors that contribute to pathological scar development is local mechanical forces, I believe that they play a particularly important role [9–11]. Keloids commonly adopt distinct site-specific shapes, namely, the typical butterfly, crab's claw, and dumbbell shapes on the shoulder, anterior chest, and upper arm, respectively. These shapes reflect the region-specific distribution of skin tension that then tugs repetitively or constantly on the wounds/scars. Moreover, keloids are rare on the upper eyelid. This reflects the fact that eyelid skin is always relaxed regardless of whether the eyes are open or closed. An exception may be earlobe keloids: the contribution of mechanical factors to the development of these keloids may be minor. Instead, the most likely local cause of these keloids is the repeated attaching and detaching of the piercing, which repeatedly injures the skin and heightens the risk of infection. Both the skin tension and repeated injury/infection trigger inflammation and the downstream fibroproliferative events. In summary, while skin tension itself may not be a primary cause of keloids and hypertrophic scars, it is likely to be an important local risk factor that worsens and prolongs the inflammation that drives

the formation and/or progression of these fibroproliferative scars.

**3. Standard treatment of keloids and hypertrophic scars**

These findings have markedly improved our understanding of the pathogenesis of keloids and hypertrophic scars, which in turn has promoted the development of highly effective treatments for these once-intractable scars. At present, I believe that the most reliable approach is a combination of three therapies, namely, surgery, followed by radiation, and prolonged daily use of steroid tape/plaster. The addition

Another important goal is the esthetic improvement.

**2. Causes of keloids and hypertrophic scars**

increasing angiogenesis and matrix production.

**56**

Since surgical treatment itself induces inflammation, surgery alone associates with high rates of keloid and hypertrophic scar recurrence. Worse, the recurrent scars are often much bigger than the original lesions. Thus, unless the scar is a minor hypertrophic scar, the decision to surgically remove a pathological scar should be made very carefully and postoperative radiation therapy should always be performed. However, if keloids and hypertrophic scars have infected areas, such as inclusion cysts, these should be removed surgically. Another key indication for surgery is keloids and hypertrophic scars that result in scar contracture of the joints or mobile areas such as the neck. In this case, the contractures should be released by a combination of subcutaneous/fascial tensile reduction sutures, z-plasties, and regional/local flap transfer.

The main objective of surgery for keloids and hypertrophic scars is not only mass reduction, but it is also to reduce the mechanical tension on the scar or the wound that is left after surgical removal of the scar. This is due to the important role of mechanical tension in the development and progression of keloids and hypertrophic scars. This is reflected by the fact that the most effective surgical method for releasing scar contractures is to use a regional or local flap, especially skin-pedicled local flaps: these flaps are particularly useful because they expand naturally after surgery and are therefore not prone to postsurgical contractures [12]. In contrast, skin grafts do not expand, which means that skin grafting tends to generate secondary contractures that result in circular pathological scars around the grafted skin.

#### **3.2 Radiation**

Interestingly, keloids respond very well to primary radiation therapy (i.e., radiation monotherapy). This reflects the fact that radiotherapy has a strong anti-inflammatory effect. Primary radiation therapy is suitable for older patients or patients with severe (huge) keloids (**Figure 1**). Since the total radiation dose in these cases is relatively high (e.g., 5 Gy administered once a week for 5 weeks by superficial brachytherapy), it is necessary to apply the radiation carefully to prevent secondary radiation carcinogenesis. However, the risks of primary radiation therapy should be weighed against its tremendous benefits; in particular, the fact that it immediately alleviates the subjective symptoms of keloids such as pain and itching. Moreover, over the following year, it causes the color and thickness of the scars to progressively normalize.

**Figure 1.**

*A patient with severe abdominal keloids was effectively treated by radiation monotherapy. (a) View before treatment. (b) 4 months post-treatment. (c) 9 months post-treatment. (d) 14 months post-treatment. (e) 18 months post-treatment. A 68-year-old female was treated with high-dose-rate superficial brachytherapy. A total of 25 Gy was administered in five fractions over 5 days (i.e., 5 Gy was delivered once a week for 5 weeks). After 4 months of treatment, both the subjective and objective symptoms had improved dramatically. The keloids became mature scars 18 months after the treatment.*

Radiation is also useful in the treatment of keloids and hypertrophic scars as a postsurgical modality [13–21]. As mentioned above, the main problem of surgery for pathological scars is recurrence. However, postsurgical radiation therapy can dramatically reduce these rates of recurrence. Use of the linear-quadratic model to calculate the biologically effective doses (BEDs) for various therapeutic radiation regimens after surgical excision of keloids showed that when the BED exceeds 30 Gy, the recurrence rate is less than 10%. Indeed, our review of the literature showed that to ensure maximum efficacy and safety, postoperative radiation for keloids in adults should involve the application of 10–20 Gy *via* daily fractions of 5 Gy.

Currently, we propose that the maximum dose of postoperative radiation therapy for surgically excised keloids is a BED of 30 Gy. A BED of 30 Gy can be obtained in several ways: a single fraction dose of 13 Gy, two fractions of 8 Gy, three fractions of 6 Gy, or four fractions of 5 Gy. In addition, recommended sitedependent dose protocols for the treatment of keloids are as follows: 18 Gy in three fractions over 3 days for the anterior chest wall, shoulder-scapular region, and suprapubic region; 8 Gy in a fraction over a day for the ear lobe; and 15 Gy in two fractions over 2 days for other sites.

It should be noted that the calculated BED of 30 Gy assumes that the α/β ratio for keloids is 10 (the α/β ratio is a measure of the radiosensitivity of a specific tissue). However, when Flickinger [21] investigated the α/β ratio of keloids, they found that it was as low as 2, which suggests that high doses with limited numbers of fractions is the best strategy to achieve low recurrence rates. At present, there is no widely accepted radiation regimen for keloid treatment. Further research on regimens that effectively prevent recurrence without elevating the risk of secondary carcinogenesis is welcome.

#### **3.3 Corticosteroid tapes/plasters**

Corticosteroid injections rapidly reduce the volume of a scar [22]. However, the downsides of corticosteroid injections include pain (caused by the injection itself) and difficulties associated with contraindications such as pregnancy, glaucoma, or Cushing's disease. This problem can be overcome by using steroid tapes/ plasters. Most pediatric and older patients can be treated by steroid tapes/plaster alone because they have much thinner skin, which means that the steroids are easily absorbed (**Figure 2**). Corticosteroid tape/plasters on their own or in combination

**59**

*Keloids and Hypertrophic Scars Can Now Be Treated Completely by Multimodal Therapy…*

with other therapies such as corticosteroid injection are also suitable for adults with minor keloids. Notably, postoperative application of corticosteroid tape/plasters significantly prevents the development of keloids and hypertrophic scars after surgery. Steroid tape/plasters should be changed every day. Important tips regarding the treatment of keloids and hypertrophic scars with steroid tapes/plasters are as follows. First, the patient should continue to use the tapes/plasters until the elevated mass becomes flat and soft. Second, once the mass has become flat and soft, steroid tape/plaster use should be stopped, even if the scar is still red. This reflects the fact that if the patient continues to use the tape just because the scar is still red, capillarectasia will occur. This is because the steroid treatment thins the supporting

*A child with a mild keloid was effectively treated with steroid tape alone. (a) View before treatment. (b) After 16 months of treatment. (c) After 26 months of treatment. This 9-year-old boy had a mild right scapular keloid and was treated by fludroxycortide tape (Drenison® tape). The tape was placed on the keloid 24 h a day and was changed daily. The inflammation resolved completely. After 26 months of treatment, both the subjective and objective symptoms of the patient had improved dramatically (the case was cited from the article: Ogawa R, Akaishi S, Kuribayashi S, Miyashita T. Keloids and Hypertrophic Scars Can Now Be Cured Completely: Recent Progress in Our Understanding of the Pathogenesis of Keloids and Hypertrophic Scars and the Most* 

Steroid tape is available in the following three countries in slightly different preparations [22]. In the UK, the commercially available formulation comprises a

steroid). In our experience, deprodone propionate tape is the most effective tape for

**4. Combination treatment for severe keloids and hypertrophic scars**

epidermis and papillary layer of the dermis is preserved as a thin flap.

If a patient has severe keloids with infected areas or scar contractures, surgery should be performed (**Figure 3**). If the keloids are too large to be removed in their entirety, the surgeon can resect the region of contracture or infection. The resulting defects can then be covered by a regional/local flap. Surgery should also be performed if the keloid growth causes significant deformity and the keloid does not respond to nonsurgical therapies. An example of severely deforming earlobe keloids is shown in **Figure 4**. Such keloids can be treated by the core excision method, where the fibrous reticular layer of the keloid (i.e., the core of the earlobe keloid) is extirpated and the

flurandrenolide (a medium-strength steroid) is available. In Japan, two

). In the USA, a preparation containing

deprodone propionate tape (higher potency

fludroxycortide tape

*DOI: http://dx.doi.org/10.5772/intechopen.84178*

structure of the blood vessels.

4 μg/cm2

**Figure 2.**

fludroxycortide-impregnated tape (4 μg/cm2

(medium-strength) and a 20 μg/cm2

the treatment and prevention of keloids.

steroid tape formulations are available, namely, a 4 μg/cm<sup>2</sup>

*Promising Current Therapeutic Strategy. J Nippon Med Sch. 2016;83(2):46–53).*

*Keloids and Hypertrophic Scars Can Now Be Treated Completely by Multimodal Therapy… DOI: http://dx.doi.org/10.5772/intechopen.84178*

#### **Figure 2.**

*Scars*

**Figure 1.**

Radiation is also useful in the treatment of keloids and hypertrophic scars as a postsurgical modality [13–21]. As mentioned above, the main problem of surgery for pathological scars is recurrence. However, postsurgical radiation therapy can dramatically reduce these rates of recurrence. Use of the linear-quadratic model to calculate the biologically effective doses (BEDs) for various therapeutic radiation regimens after surgical excision of keloids showed that when the BED exceeds 30 Gy, the recurrence rate is less than 10%. Indeed, our review of the literature showed that to ensure maximum efficacy and safety, postoperative radiation for keloids in adults

*A patient with severe abdominal keloids was effectively treated by radiation monotherapy. (a) View before treatment. (b) 4 months post-treatment. (c) 9 months post-treatment. (d) 14 months post-treatment. (e) 18 months post-treatment. A 68-year-old female was treated with high-dose-rate superficial brachytherapy. A total of 25 Gy was administered in five fractions over 5 days (i.e., 5 Gy was delivered once a week for 5 weeks). After 4 months of treatment, both the subjective and objective symptoms had improved dramatically.* 

should involve the application of 10–20 Gy *via* daily fractions of 5 Gy.

*The keloids became mature scars 18 months after the treatment.*

fractions over 2 days for other sites.

carcinogenesis is welcome.

**3.3 Corticosteroid tapes/plasters**

Currently, we propose that the maximum dose of postoperative radiation therapy for surgically excised keloids is a BED of 30 Gy. A BED of 30 Gy can be obtained in several ways: a single fraction dose of 13 Gy, two fractions of 8 Gy, three fractions of 6 Gy, or four fractions of 5 Gy. In addition, recommended sitedependent dose protocols for the treatment of keloids are as follows: 18 Gy in three fractions over 3 days for the anterior chest wall, shoulder-scapular region, and suprapubic region; 8 Gy in a fraction over a day for the ear lobe; and 15 Gy in two

It should be noted that the calculated BED of 30 Gy assumes that the α/β ratio for keloids is 10 (the α/β ratio is a measure of the radiosensitivity of a specific tissue). However, when Flickinger [21] investigated the α/β ratio of keloids, they found that it was as low as 2, which suggests that high doses with limited numbers of fractions is the best strategy to achieve low recurrence rates. At present, there is no widely accepted radiation regimen for keloid treatment. Further research on regimens that effectively prevent recurrence without elevating the risk of secondary

Corticosteroid injections rapidly reduce the volume of a scar [22]. However, the downsides of corticosteroid injections include pain (caused by the injection itself) and difficulties associated with contraindications such as pregnancy, glaucoma, or Cushing's disease. This problem can be overcome by using steroid tapes/ plasters. Most pediatric and older patients can be treated by steroid tapes/plaster alone because they have much thinner skin, which means that the steroids are easily absorbed (**Figure 2**). Corticosteroid tape/plasters on their own or in combination

**58**

*A child with a mild keloid was effectively treated with steroid tape alone. (a) View before treatment. (b) After 16 months of treatment. (c) After 26 months of treatment. This 9-year-old boy had a mild right scapular keloid and was treated by fludroxycortide tape (Drenison® tape). The tape was placed on the keloid 24 h a day and was changed daily. The inflammation resolved completely. After 26 months of treatment, both the subjective and objective symptoms of the patient had improved dramatically (the case was cited from the article: Ogawa R, Akaishi S, Kuribayashi S, Miyashita T. Keloids and Hypertrophic Scars Can Now Be Cured Completely: Recent Progress in Our Understanding of the Pathogenesis of Keloids and Hypertrophic Scars and the Most Promising Current Therapeutic Strategy. J Nippon Med Sch. 2016;83(2):46–53).*

with other therapies such as corticosteroid injection are also suitable for adults with minor keloids. Notably, postoperative application of corticosteroid tape/plasters significantly prevents the development of keloids and hypertrophic scars after surgery.

Steroid tape/plasters should be changed every day. Important tips regarding the treatment of keloids and hypertrophic scars with steroid tapes/plasters are as follows. First, the patient should continue to use the tapes/plasters until the elevated mass becomes flat and soft. Second, once the mass has become flat and soft, steroid tape/plaster use should be stopped, even if the scar is still red. This reflects the fact that if the patient continues to use the tape just because the scar is still red, capillarectasia will occur. This is because the steroid treatment thins the supporting structure of the blood vessels.

Steroid tape is available in the following three countries in slightly different preparations [22]. In the UK, the commercially available formulation comprises a fludroxycortide-impregnated tape (4 μg/cm2 ). In the USA, a preparation containing 4 μg/cm2 flurandrenolide (a medium-strength steroid) is available. In Japan, two steroid tape formulations are available, namely, a 4 μg/cm<sup>2</sup> fludroxycortide tape (medium-strength) and a 20 μg/cm2 deprodone propionate tape (higher potency steroid). In our experience, deprodone propionate tape is the most effective tape for the treatment and prevention of keloids.

#### **4. Combination treatment for severe keloids and hypertrophic scars**

If a patient has severe keloids with infected areas or scar contractures, surgery should be performed (**Figure 3**). If the keloids are too large to be removed in their entirety, the surgeon can resect the region of contracture or infection. The resulting defects can then be covered by a regional/local flap. Surgery should also be performed if the keloid growth causes significant deformity and the keloid does not respond to nonsurgical therapies. An example of severely deforming earlobe keloids is shown in **Figure 4**. Such keloids can be treated by the core excision method, where the fibrous reticular layer of the keloid (i.e., the core of the earlobe keloid) is extirpated and the epidermis and papillary layer of the dermis is preserved as a thin flap.

#### **Figure 3.**

*A patient with an upper limb keloid was effectively treated by surgery and postoperative radiotherapy. (a) Preoperative view. (b) Removal of the hand and wrist keloids and harvest of the flap. (c) Flap rotation. (d) The recipient site immediately after surgery. (e–i) 5 years after the operation. This 63-year-old female had hypertension together with severe keloids of an unknown origin (folliculitis was suspected) that covered her right elbow, wrist joint, and thumb and made it difficult for her to use her right hand. The contractures were released by surgery with a distally based radial forearm flap followed by adjuvant 4-MeV electron beam irradiation therapy (15 Gy/three fractions for 3 days) (the case was cited from the article: Ogawa R, Arima J, Ono S, Hyakusoku H. CASE REPORT Total Management of a Severe Case of Systemic Keloids Associated With High Blood Pressure (Hypertension): Clinical Symptoms of Keloids May Be Aggravated by Hypertension. Eplasty. 2013 Jun 3;13:e25).*

While these surgical approaches on their own associate with a relatively high risk of recurrence, this risk can be significantly reduced by combining surgery with postoperative radiotherapy and prolonged corticosteroid tape/plaster application. Thus, after the operation, both the donor and recipient sites of the flap should be irradiated to prevent the new formation of keloids. Notably, when partial resection or core extirpation is followed by postoperative radiotherapy, any remaining keloids around the flap (which do not undergo radiotherapy) also improve (**Figure 3**). This

**61**

**Figure 4.**

*Keloids and Hypertrophic Scars Can Now Be Treated Completely by Multimodal Therapy…*

reflects the fact that the flap releases tension, which in turn decreases the inflammation in the remnant keloids. The high risk of recurrence in these severe cases can be further reduced by the routine application of corticosteroid tape/plasters on the operated area that are changed daily. In general, we recommend patients to use tape/plasters for at least 6 months after the surgery and radiotherapy, or until the scar becomes soft. Long-term follow-up is necessary because if the scars start to stiffen again, corticosteroid tape/plasters should be re-applied. In general, it will

*Keloid Risk Factor. Plast Reconstr Surg Glob Open. 2017 May 16;5(5):e1336).*

*A patient with bilateral ear keloids was effectively treated by surgery and postoperative radiotherapy.* 

*(a, b) Preoperative view of the left ear. (c) Design of the incision on the left ear. (d) Intraoperative view of the left ear. (e, f) The left ear immediately after surgery. (g) Preoperative view of the right ear. (h) Design of the incision on the right ear. (i) Intraoperative view (the right ear). (j, k) The right ear immediately after surgery. (l, m) The right ear 14 months after surgery. (n, o) The left ear 14 months after surgery. A 37-year-old Japanese woman with multiple keloids was diagnosed with multicentric type Castleman's disease. She was treated with systemic administration of steroid for Castleman's disease but the treatment did not improve her keloids. We removed both auricular keloids by using the core excision method. On postoperative days 1, 2, and 3, the patient received a total radiation dose of 15 Gy in three fractions over 3 days. The radiation was delivered by a 4 MeV electron beam. Histopathological examination of the resected tissues showed the absence of abnormal lymphocytes or plasma cell infiltration. Consequently, the auricular lesions were diagnosed definitively as keloids (the case was cited from the article: Quong WL, Kozai Y, Ogawa R. A Case of Keloids Complicated by Castleman's Disease: Interleukin-6 as a* 

*DOI: http://dx.doi.org/10.5772/intechopen.84178*

*Keloids and Hypertrophic Scars Can Now Be Treated Completely by Multimodal Therapy… DOI: http://dx.doi.org/10.5772/intechopen.84178*

#### **Figure 4.**

*Scars*

**60**

**Figure 3.**

*Eplasty. 2013 Jun 3;13:e25).*

While these surgical approaches on their own associate with a relatively high risk of recurrence, this risk can be significantly reduced by combining surgery with postoperative radiotherapy and prolonged corticosteroid tape/plaster application. Thus, after the operation, both the donor and recipient sites of the flap should be irradiated to prevent the new formation of keloids. Notably, when partial resection or core extirpation is followed by postoperative radiotherapy, any remaining keloids around the flap (which do not undergo radiotherapy) also improve (**Figure 3**). This

*A patient with an upper limb keloid was effectively treated by surgery and postoperative radiotherapy. (a) Preoperative view. (b) Removal of the hand and wrist keloids and harvest of the flap. (c) Flap rotation. (d) The recipient site immediately after surgery. (e–i) 5 years after the operation. This 63-year-old female had hypertension together with severe keloids of an unknown origin (folliculitis was suspected) that covered her right elbow, wrist joint, and thumb and made it difficult for her to use her right hand. The contractures were released by surgery with a distally based radial forearm flap followed by adjuvant 4-MeV electron beam irradiation therapy (15 Gy/three fractions for 3 days) (the case was cited from the article: Ogawa R, Arima J, Ono S, Hyakusoku H. CASE REPORT Total Management of a Severe Case of Systemic Keloids Associated With High Blood Pressure (Hypertension): Clinical Symptoms of Keloids May Be Aggravated by Hypertension.*  *A patient with bilateral ear keloids was effectively treated by surgery and postoperative radiotherapy. (a, b) Preoperative view of the left ear. (c) Design of the incision on the left ear. (d) Intraoperative view of the left ear. (e, f) The left ear immediately after surgery. (g) Preoperative view of the right ear. (h) Design of the incision on the right ear. (i) Intraoperative view (the right ear). (j, k) The right ear immediately after surgery. (l, m) The right ear 14 months after surgery. (n, o) The left ear 14 months after surgery. A 37-year-old Japanese woman with multiple keloids was diagnosed with multicentric type Castleman's disease. She was treated with systemic administration of steroid for Castleman's disease but the treatment did not improve her keloids. We removed both auricular keloids by using the core excision method. On postoperative days 1, 2, and 3, the patient received a total radiation dose of 15 Gy in three fractions over 3 days. The radiation was delivered by a 4 MeV electron beam. Histopathological examination of the resected tissues showed the absence of abnormal lymphocytes or plasma cell infiltration. Consequently, the auricular lesions were diagnosed definitively as keloids (the case was cited from the article: Quong WL, Kozai Y, Ogawa R. A Case of Keloids Complicated by Castleman's Disease: Interleukin-6 as a Keloid Risk Factor. Plast Reconstr Surg Glob Open. 2017 May 16;5(5):e1336).*

reflects the fact that the flap releases tension, which in turn decreases the inflammation in the remnant keloids. The high risk of recurrence in these severe cases can be further reduced by the routine application of corticosteroid tape/plasters on the operated area that are changed daily. In general, we recommend patients to use tape/plasters for at least 6 months after the surgery and radiotherapy, or until the scar becomes soft. Long-term follow-up is necessary because if the scars start to stiffen again, corticosteroid tape/plasters should be re-applied. In general, it will



#### **Figure 5.**

*Algorithm for selecting keloid and hypertrophic scar treatment modalities. Particular care should be taken when selecting the treatment for growing children and pregnant women with keloids and hypertrophic scars. In our facility, pediatric patients (<20 years of age) and pregnant women are not treated with radiation. Invasive surgery in pregnant women is also avoided. In these cases, the primary treatment choice should be steroid tape/ plaster together with stabilization/compression therapy that reduces the tension on the scar.*

**63**

**Author details**

School Hospital, Tokyo, Japan

Rei Ogawa

provided the original work is properly cited.

\*Address all correspondence to: r.ogawa@nms.ac.jp

© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

Department of Plastic, Reconstructive and Aesthetic Surgery, Nippon Medical

*Keloids and Hypertrophic Scars Can Now Be Treated Completely by Multimodal Therapy…*

take at least 2 years before combination therapy-treated keloids and hypertrophic scars mature. It is important to make clear to the patient before this therapy starts that the protocol has a long duration. Nevertheless, close monitoring and assiduous re-application of steroid tape/plasters have an excellent chance of converting

It should be noted that our combination therapy is not suitable for growing children and pregnant women. In our facility, we do not treat pediatric patients (<20 years of age) or pregnant women with radiation. Moreover, invasive treatments such as surgery are not performed during pregnancy. The primary choice of treatment for children and pregnant women with keloids and hypertrophic scars

*DOI: http://dx.doi.org/10.5772/intechopen.84178*

postoperative keloid sites into mature scars.

should be steroid tape/plaster on its own (**Figure 5**).

*Keloids and Hypertrophic Scars Can Now Be Treated Completely by Multimodal Therapy… DOI: http://dx.doi.org/10.5772/intechopen.84178*

take at least 2 years before combination therapy-treated keloids and hypertrophic scars mature. It is important to make clear to the patient before this therapy starts that the protocol has a long duration. Nevertheless, close monitoring and assiduous re-application of steroid tape/plasters have an excellent chance of converting postoperative keloid sites into mature scars.

It should be noted that our combination therapy is not suitable for growing children and pregnant women. In our facility, we do not treat pediatric patients (<20 years of age) or pregnant women with radiation. Moreover, invasive treatments such as surgery are not performed during pregnancy. The primary choice of treatment for children and pregnant women with keloids and hypertrophic scars should be steroid tape/plaster on its own (**Figure 5**).

#### **Author details**

#### Rei Ogawa

*Scars*

**62**

**Figure 5.**

*Algorithm for selecting keloid and hypertrophic scar treatment modalities. Particular care should be taken when selecting the treatment for growing children and pregnant women with keloids and hypertrophic scars. In our facility, pediatric patients (<20 years of age) and pregnant women are not treated with radiation. Invasive surgery in pregnant women is also avoided. In these cases, the primary treatment choice should be steroid tape/*

*plaster together with stabilization/compression therapy that reduces the tension on the scar.*

Department of Plastic, Reconstructive and Aesthetic Surgery, Nippon Medical School Hospital, Tokyo, Japan

\*Address all correspondence to: r.ogawa@nms.ac.jp

© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

### **References**

[1] Ogawa R. Keloid and hypertrophic scars are the result of chronic inflammation in the reticular dermis. International Journal of Molecular Sciences. 2017;**18**(3):E606

[2] Huang C, Murphy GF, Akaishi S, Ogawa R. Keloids and hypertrophic scars: Update and future directions. Plastic and Reconstructive Surgery. Global Open. 2013;**1**(4):e25

[3] Nakashima M, Chung S, Takahashi A, Kamatani N, Kawaguchi T, Tsunoda T, et al. A genome-wide association study identifies four susceptibility loci for keloid in the Japanese population. Nature Genetics. 2010;**42**(9):768-771

[4] Ogawa R, Watanabe A, Than Naing B, Sasaki M, Fujita A, Akaishi S, et al. Associations between keloid severity and single-nucleotide polymorphisms: Importance of rs8032158 as a biomarker of keloid severity. The Journal of Investigative Dermatology. 2014;**134**(7):2041-2043

[5] Moustafa MF, Abdel-Fattah MA, Abdel-Fattah DC. Presumptive evidence of the effect of pregnancy estrogens on keloid growth. Case report. Plastic and Reconstructive Surgery. 1975;**56**(4):450-453

[6] Mendelsohn ME, Karas RH. Estrogen and the blood vessel wall. Current Opinion in Cardiology. 1994;**9**(5):619-626

[7] Arima J, Huang C, Rosner B, Akaishi S, Ogawa R. Hypertension: A systemic key to understanding local keloid severity. Wound Repair and Regeneration. 2015;**23**(2):213-221

[8] Huang C, Ogawa R. The link between hypertension and pathological scarring: Does hypertension cause or promote keloid and hypertrophic scar pathogenesis? Wound Repair and Regeneration. 2014;**22**(4):462-466

[9] Ogawa R, Okai K, Tokumura F, Mori K, Ohmori Y, Huang C, et al. The relationship between skin stretching/ contraction and pathologic scarring: The important role of mechanical forces in keloid generation. Wound Repair and Regeneration. 2012;**20**(2):149-157

[10] Ogawa R, Akaishi S, Huang C, Dohi T, Aoki M, Omori Y, et al. Clinical applications of basic research that shows reducing skin tension could prevent and treat abnormal scarring: The importance of fascial/subcutaneous tensile reduction sutures and flap surgery for keloid and hypertrophic scar reconstruction. Journal of Nippon Medical School. 2011;**78**(2):68-76

[11] Akaishi S, Akimoto M, Ogawa R, Hyakusoku H. The relationship between keloid growth pattern and stretching tension: Visual analysis using the finite element method. Annals of Plastic Surgery. 2008;**60**(4):445-451

[12] Yoshino Y, Kubomura K, Ueda H, Tsuge T, Ogawa R. Extension of flaps associated with burn scar reconstruction: A key difference between island and skin-pedicled flaps. Burns. 2018;**44**(3):683-691

[13] Ogawa R. The most current algorithms for the treatment and prevention of hypertrophic scars and keloids. Plastic and Reconstructive Surgery. 2010;**125**(2):557-568

[14] Norris JE. Superficial x-ray therapy in keloid management: A retrospective study of 24 cases and literature review. Plastic and Reconstructive Surgery. 1995;**95**(6):1051-1055

[15] Enhamre A, Hammar H. Treatment of keloids with excision and postoperative X-ray irradiation. Dermatologica. 1983;**167**(2):90-93

**65**

*Keloids and Hypertrophic Scars Can Now Be Treated Completely by Multimodal Therapy…*

*DOI: http://dx.doi.org/10.5772/intechopen.84178*

Treatment of keloids by high-dose-rate brachytherapy: A seven-year study. International Journal of Radiation Oncology, Biology, Physics. 2001;**50**(1, 1):

[17] Kuribayashi S, Miyashita T, Ozawa Y, Iwano M, Ogawa R, Akaishi S, et al. Post-keloidectomy irradiation using high-dose-rate superficial brachytherapy. Journal of Radiation Research. 2011;**52**(3):365-368

[18] Ogawa R, Miyashita T, Hyakusoku H, Akaishi S, Kuribayashi S, Tateno A. Postoperative radiation protocol for keloids and hypertrophic scars: Statistical analysis of 370 sites followed for over 18 months. Annals of Plastic

[19] Ogawa R, Mitsuhashi K, Hyakusoku H, Miyashita T. Postoperative electronbeam irradiation therapy for keloids and hypertrophic scars: Retrospective study of 147 cases followed for more than 18 months. Plastic and Reconstructive Surgery. 2003;**111**(2):547-553

[20] Lo TC, Seckel BR, Salzman FA, Wright KA. Single-dose electron beam irradiation in treatment and prevention of keloids and hypertrophic scars. Radiotherapy and Oncology.

[21] Flickinger JC. A radiobiological analysis of multicenter data for postoperative keloid radiotherapy. International Journal of Radiation Oncology, Biology, Physics. 2011;**79**(4):1164-1170

[22] Goutos I, Ogawa R. Steroid tape: A promising adjunct to scar management. Scars, Burns & Healing.

2017;**3**:2059513117690937

1990;**19**(3):267-272

Surgery. 2007;**59**(6):688-691

167-172

[16] Guix B, Henríquez I, Andrés A, Finestres F, Tello JI, Martínez A. *Keloids and Hypertrophic Scars Can Now Be Treated Completely by Multimodal Therapy… DOI: http://dx.doi.org/10.5772/intechopen.84178*

Treatment of keloids by high-dose-rate brachytherapy: A seven-year study. International Journal of Radiation Oncology, Biology, Physics. 2001;**50**(1, 1): 167-172

[17] Kuribayashi S, Miyashita T, Ozawa Y, Iwano M, Ogawa R, Akaishi S, et al. Post-keloidectomy irradiation using high-dose-rate superficial brachytherapy. Journal of Radiation Research. 2011;**52**(3):365-368

[18] Ogawa R, Miyashita T, Hyakusoku H, Akaishi S, Kuribayashi S, Tateno A. Postoperative radiation protocol for keloids and hypertrophic scars: Statistical analysis of 370 sites followed for over 18 months. Annals of Plastic Surgery. 2007;**59**(6):688-691

[19] Ogawa R, Mitsuhashi K, Hyakusoku H, Miyashita T. Postoperative electronbeam irradiation therapy for keloids and hypertrophic scars: Retrospective study of 147 cases followed for more than 18 months. Plastic and Reconstructive Surgery. 2003;**111**(2):547-553

[20] Lo TC, Seckel BR, Salzman FA, Wright KA. Single-dose electron beam irradiation in treatment and prevention of keloids and hypertrophic scars. Radiotherapy and Oncology. 1990;**19**(3):267-272

[21] Flickinger JC. A radiobiological analysis of multicenter data for postoperative keloid radiotherapy. International Journal of Radiation Oncology, Biology, Physics. 2011;**79**(4):1164-1170

[22] Goutos I, Ogawa R. Steroid tape: A promising adjunct to scar management. Scars, Burns & Healing. 2017;**3**:2059513117690937

**64**

*Scars*

**References**

[1] Ogawa R. Keloid and hypertrophic

[9] Ogawa R, Okai K, Tokumura F, Mori K, Ohmori Y, Huang C, et al. The relationship between skin stretching/ contraction and pathologic scarring: The important role of mechanical forces in keloid generation. Wound Repair and Regeneration. 2012;**20**(2):149-157

[10] Ogawa R, Akaishi S, Huang C, Dohi T, Aoki M, Omori Y, et al. Clinical applications of basic research that shows reducing skin tension could prevent and treat abnormal scarring: The importance of fascial/subcutaneous tensile reduction sutures and flap surgery for keloid and hypertrophic scar reconstruction. Journal of Nippon Medical School. 2011;**78**(2):68-76

[11] Akaishi S, Akimoto M, Ogawa R, Hyakusoku H. The relationship between keloid growth pattern and stretching tension: Visual analysis using the finite element method. Annals of Plastic Surgery. 2008;**60**(4):445-451

[12] Yoshino Y, Kubomura K, Ueda H, Tsuge T, Ogawa R. Extension of flaps associated with burn scar reconstruction: A key difference between island and skin-pedicled flaps.

Burns. 2018;**44**(3):683-691

1995;**95**(6):1051-1055

of keloids with excision and postoperative X-ray irradiation. Dermatologica. 1983;**167**(2):90-93

[16] Guix B, Henríquez I, Andrés A, Finestres F, Tello JI, Martínez A.

[13] Ogawa R. The most current algorithms for the treatment and prevention of hypertrophic scars and keloids. Plastic and Reconstructive Surgery. 2010;**125**(2):557-568

[14] Norris JE. Superficial x-ray therapy in keloid management: A retrospective study of 24 cases and literature review. Plastic and Reconstructive Surgery.

[15] Enhamre A, Hammar H. Treatment

inflammation in the reticular dermis. International Journal of Molecular

[2] Huang C, Murphy GF, Akaishi S, Ogawa R. Keloids and hypertrophic scars: Update and future directions. Plastic and Reconstructive Surgery.

[3] Nakashima M, Chung S, Takahashi A, Kamatani N, Kawaguchi T, Tsunoda T, et al. A genome-wide association study identifies four susceptibility loci for keloid in the Japanese population. Nature Genetics. 2010;**42**(9):768-771

[4] Ogawa R, Watanabe A, Than Naing B, Sasaki M, Fujita A, Akaishi S, et al. Associations between keloid severity and single-nucleotide polymorphisms:

Importance of rs8032158 as a biomarker of keloid severity. The Journal of Investigative Dermatology.

[5] Moustafa MF, Abdel-Fattah MA, Abdel-Fattah DC. Presumptive evidence of the effect of pregnancy estrogens on keloid growth. Case report. Plastic and Reconstructive Surgery.

[6] Mendelsohn ME, Karas RH. Estrogen and the blood vessel wall. Current Opinion in Cardiology.

[7] Arima J, Huang C, Rosner B, Akaishi S, Ogawa R. Hypertension: A systemic key to understanding local keloid severity. Wound Repair and Regeneration. 2015;**23**(2):213-221

[8] Huang C, Ogawa R. The link

between hypertension and pathological scarring: Does hypertension cause or promote keloid and hypertrophic scar pathogenesis? Wound Repair and Regeneration. 2014;**22**(4):462-466

2014;**134**(7):2041-2043

1975;**56**(4):450-453

1994;**9**(5):619-626

scars are the result of chronic

Sciences. 2017;**18**(3):E606

Global Open. 2013;**1**(4):e25

**67**

**Chapter 6**

**Abstract**

esthetic surgery

**1. Introduction**

Plastic Surgery

*Gustavo E. Prezzavento*

Scars: A New Point of View in

The issue of achieving esthetically pleasing surgical scars has gained prominence

in recent years, with the emergence of the concept of the "imperceptible scar," which is expected by patients of not only cosmetic but also reconstructive surgery. Current research in reconstructive surgery focuses on obtaining high-quality results in the minimum number of steps, with a view to "doing it right the first time." However, there is no uniform approach to scar treatment, which is partly due to a lack of consensus regarding the most effective healing methods. This chapter aims at shedding new light to discussion by putting forward two different procedures that enhance scar results in cosmetic and reconstructive surgeries by applying a topical treatment with active ingredients and by combining cadaver and artificial skin as dermal substitutes, respectively. The effectiveness of these treatments is shown by means of objective, quantifiable data collected as a result of studies and

postoperative follow-ups carried out at Hospital Alemán in Buenos Aires.

**Keywords:** scars, surgical wound, wound healing, reconstructive surgery,

functional limitations, which patients often perceive as a problem.

Thus, when the scar has unfavorable characteristics, scar revision is often indicated. Furthermore, as poor-quality healing of an incision can constitute a disabling pathology [3], scar treatment should not be considered as a trivial part of the intervention. On the contrary, wound treatment and care after surgery of any kind, including esthetic or reconstructive interventions, should be initiated early.

Scars are a natural part of dermal healing following lacerations, incisions, or tissue loss. Wound healing, which is a natural process of tissue repair, consists of three phases: inflammation, fibroplasia, and maturation. The healing tissue generates changes in the cutaneous architecture, which renders the skin surrounding the scar different from the rest of the skin in terms of color, thickness, elasticity, texture, and degree of contraction [1]. In surgical procedures, scars, which are the only visible sequela of the intervention, result from the reparation process undergone by the skin to heal the wounds caused by surgery or trauma. Because of its impact in scarring, considerable importance is placed on the closure of a surgical incision, which is the final phase of the intervention [2]. The ideal scar is narrow, flat, level with surrounding tissue, and difficult for the untrained eye to see due to color match and placement parallel to relaxed skin tension lines. In contrast, hypertrophic, keloidal, dyspigmented, widened, contracted, or atrophic scars can be unsightly and/or cause

#### **Chapter 6**

## Scars: A New Point of View in Plastic Surgery

*Gustavo E. Prezzavento*

#### **Abstract**

The issue of achieving esthetically pleasing surgical scars has gained prominence in recent years, with the emergence of the concept of the "imperceptible scar," which is expected by patients of not only cosmetic but also reconstructive surgery. Current research in reconstructive surgery focuses on obtaining high-quality results in the minimum number of steps, with a view to "doing it right the first time." However, there is no uniform approach to scar treatment, which is partly due to a lack of consensus regarding the most effective healing methods. This chapter aims at shedding new light to discussion by putting forward two different procedures that enhance scar results in cosmetic and reconstructive surgeries by applying a topical treatment with active ingredients and by combining cadaver and artificial skin as dermal substitutes, respectively. The effectiveness of these treatments is shown by means of objective, quantifiable data collected as a result of studies and postoperative follow-ups carried out at Hospital Alemán in Buenos Aires.

**Keywords:** scars, surgical wound, wound healing, reconstructive surgery, esthetic surgery

#### **1. Introduction**

Scars are a natural part of dermal healing following lacerations, incisions, or tissue loss. Wound healing, which is a natural process of tissue repair, consists of three phases: inflammation, fibroplasia, and maturation. The healing tissue generates changes in the cutaneous architecture, which renders the skin surrounding the scar different from the rest of the skin in terms of color, thickness, elasticity, texture, and degree of contraction [1]. In surgical procedures, scars, which are the only visible sequela of the intervention, result from the reparation process undergone by the skin to heal the wounds caused by surgery or trauma. Because of its impact in scarring, considerable importance is placed on the closure of a surgical incision, which is the final phase of the intervention [2]. The ideal scar is narrow, flat, level with surrounding tissue, and difficult for the untrained eye to see due to color match and placement parallel to relaxed skin tension lines. In contrast, hypertrophic, keloidal, dyspigmented, widened, contracted, or atrophic scars can be unsightly and/or cause functional limitations, which patients often perceive as a problem.

Thus, when the scar has unfavorable characteristics, scar revision is often indicated. Furthermore, as poor-quality healing of an incision can constitute a disabling pathology [3], scar treatment should not be considered as a trivial part of the intervention. On the contrary, wound treatment and care after surgery of any kind, including esthetic or reconstructive interventions, should be initiated early.

In order to arrive at an effective esthetic and functional outcome, surgeons must be familiar with the different scar treatments available, and they must also know how to prevent scars and how to reduce them after surgery. In this sense, it should be borne in mind that, while there exist multiple treatment modalities, none of them guarantees a 100% success rate. Current guidelines suggest a multimodal approach to treating scars but there is no gold standard for their treatment. In this chapter, we will present two new ways to treat scars following plastic surgery. As explained in the following sections, these techniques were successfully implemented in a number of cases, and their comparative advantages regarding other methods were also evaluated. We hope that our contribution will help point in the direction toward an effective, uniform standard.

The first part of our research deals with cosmetic surgery scars, which generally receive different topical treatments that help maintain the moisture and the plasticity of the wound. Besides, these treatments prevent wound contamination or infection, which would delay healing. We have analyzed and compared the results of two of these treatment options and found that the best functional and esthetic results are obtained when using a cream with active ingredients. The second part of our research revolves around the combined use of two skin substitutes, cadaver skin and artificial skin, so as to obtain improved results in reconstructive surgery after trauma injuries with abnormal wound healing in response to skin trauma or inflammation. Employing dermal substitutes result in a better regeneration of the dermis and in dermal fibroblast optimization. In the next sections, we will present a detailed account of the two studies we have carried out, which will allow us to further discuss the aforementioned techniques to optimize surgical scars.

#### **2. Topical treatment of cosmetic surgery scars**

As we have already mentioned, the first study involved the comparison and evaluation of two topical treatments applied to scars resulting from cosmetic surgery. One was a cream containing 1 g of silver sulfadiazine, 248,000 IU of vitamin A and 0.666 g of lidocaine in each 100 g of product (Platsul-A®, Soubeiran Chobet Laboratory, Autonomous City of Buenos Aires, Argentina) (cream A), and the other was a moisturizing cream based on petrolatum, keto-stearyl alcohol, glycerin, and water without any active ingredient (cream B). About 32 patients participated in the study; 24 with bilateral breast implants and 8 with face and neck lifts, hence totaling 64 scars. The study included patients of both sexes: 31 women and 1 man, with ages ranging from 22 to 64 years (mean of 41 years). All patients received both topical treatments under study, each of their postsurgical scars (right and left) being applied one of the creams at random. We monitored patients for 1 month after the beginning of treatment, meeting them at an initial appointment and at subsequent appointments after 3, 6, 9, 16, 23, and 30 days from the intervention. Each patient's progress was checked by the same medical examiner.

In these appointments, we measured the length and width of the scars to determine their total surface and assessed them in accordance with the Vancouver scar scale (VSS) and the patient and observer objective assessment scale (POSAS). We evaluated (1) the surface area of each scar by multiplying its length by its width, as measured with a ruler with graduation, (2) the quality of each scar as assessed by the VSS, [4] taking into account the parameters of pigmentation, vascularity, and thickness, and (3) the patient's perception of each scar as appraised by the POSAS, [5] by having them rank a series of symptomatic and esthetic parameters. The results are reported as follows, discriminated on the basis of the type of surgery performed.

**69**

**Table 1.**

*Scars: A New Point of View in Plastic Surgery DOI: http://dx.doi.org/10.5772/intechopen.84127*

In the group of patients with breast implants, the percentage of change did not differ significantly between the two treatments studied in the appointments of days 3, 6, 9, 16, and 23. On day 30, however, we detected a statistically significant difference (P = 0.017). The percentage of decrease was significantly higher in the scars treated with the cream with silver sulfadiazine, vitamin A, and lidocaine (cream A) than in those treated with the cream without active ingredients (cream B) (18.6 and 9.5%, respectively) (**Table 1**). In the group of patients with face and neck lift, there was no significant difference between the percentage of change achieved due to the two treatments on days 3, 6, 9, and 16. Nevertheless, on days 23 and 30, we encountered a statistically significant difference (P = 0.026 and P = 0.007, respectively). The percentage of decrease was significantly higher in the scars treated with cream A than in those that had been treated with cream B. On day 23, the surface area of the scars treated with cream A had decreased, on average, by 14.8%, while that of the scars treated with cream B had increased, on average, by 24.9%. On day 30, the surface area of the scars treated with cream A had decreased, on average, by 19.1%, whereas that of the scars treated with cream B had increased, on average, by 22.2% (**Table 2**). **Figure 1** shows the changes in the surface area of each patient's scars on days 23 and 30 with respect to the initial appointment and classifies the results according to the type of surgery undergone and the treatment received. As we can see, more favorable results were obtained with cream A than with cream B, except in the case of two patients with breast

The VSS assigns values to the scar pigmentation, vascularity, and thickness, which are then added to obtain a total. Although the score may vary between 0 and 10, the average of the initial scores in our study was 2.7 and the maximum value observed throughout the study was 5. We conducted the analysis taking into account the absolute change in the VSS score with respect to the initiation of treatment (day 0). Results are expressed in absolute values. The analysis is carried out separately for each group of patients, depending on the type of surgery, on days 3,

In the breast implant patient group, the VSS score change did not differ significantly between treatments on days 3, 6, 9, and 16. On days 23 and 30, nonetheless,

**P**

**(breast implant)**

**Cream A (%) Cream B (%)** 4.2 0.0 0.97 (NS) 2.6 3.7 0.37 (NS) −1.8 −6.0 0.40 (NS) −12.8 −7.2 0.089 (NS) −18.6 −9.5 0.017\*

*Average percentage of change of the surface area of the scars treated with silver sulfadiazine, vitamin A, and lidocaine (cream A) and with a cream without active ingredients (cream B) in patients with breast implants* 

**Days Average percentage of change of the surface area as from treatment onset** 

**2.1 Surface area of each scar**

implants (patients No. 7 and 12).

**2.2 Vancouver scar scale**

6, 9, 16, 23, and 30.

*NS: not significant.\**

*Significant: at 5%.*

*after 3, 6, 9, 16, 23, and 30 days from the onset of the topical treatment.*

#### **2.1 Surface area of each scar**

*Scars*

effective, uniform standard.

**2. Topical treatment of cosmetic surgery scars**

In order to arrive at an effective esthetic and functional outcome, surgeons must be familiar with the different scar treatments available, and they must also know how to prevent scars and how to reduce them after surgery. In this sense, it should be borne in mind that, while there exist multiple treatment modalities, none of them guarantees a 100% success rate. Current guidelines suggest a multimodal approach to treating scars but there is no gold standard for their treatment. In this chapter, we will present two new ways to treat scars following plastic surgery. As explained in the following sections, these techniques were successfully implemented in a number of cases, and their comparative advantages regarding other methods were also evaluated. We hope that our contribution will help point in the direction toward an

The first part of our research deals with cosmetic surgery scars, which generally receive different topical treatments that help maintain the moisture and the plasticity of the wound. Besides, these treatments prevent wound contamination or infection, which would delay healing. We have analyzed and compared the results of two of these treatment options and found that the best functional and esthetic results are obtained when using a cream with active ingredients. The second part of our research revolves around the combined use of two skin substitutes, cadaver skin and artificial skin, so as to obtain improved results in reconstructive surgery after trauma injuries with abnormal wound healing in response to skin trauma or inflammation. Employing dermal substitutes result in a better regeneration of the dermis and in dermal fibroblast optimization. In the next sections, we will present a detailed account of the two studies we have carried out, which will allow us to further discuss the aforementioned techniques to optimize surgical scars.

As we have already mentioned, the first study involved the comparison and evaluation of two topical treatments applied to scars resulting from cosmetic surgery. One was a cream containing 1 g of silver sulfadiazine, 248,000 IU of vitamin A and 0.666 g of lidocaine in each 100 g of product (Platsul-A®, Soubeiran Chobet Laboratory, Autonomous City of Buenos Aires, Argentina) (cream A), and the other was a moisturizing cream based on petrolatum, keto-stearyl alcohol, glycerin, and water without any active ingredient (cream B). About 32 patients participated in the study; 24 with bilateral breast implants and 8 with face and neck lifts, hence totaling 64 scars. The study included patients of both sexes: 31 women and 1 man, with ages ranging from 22 to 64 years (mean of 41 years). All patients received both topical treatments under study, each of their postsurgical scars (right and left) being applied one of the creams at random. We monitored patients for 1 month after the beginning of treatment, meeting them at an initial appointment and at subsequent appointments after 3, 6, 9, 16, 23, and 30 days from the intervention.

Each patient's progress was checked by the same medical examiner.

In these appointments, we measured the length and width of the scars to determine their total surface and assessed them in accordance with the Vancouver scar scale (VSS) and the patient and observer objective assessment scale (POSAS). We evaluated (1) the surface area of each scar by multiplying its length by its width, as measured with a ruler with graduation, (2) the quality of each scar as assessed by the VSS, [4] taking into account the parameters of pigmentation, vascularity, and thickness, and (3) the patient's perception of each scar as appraised by the POSAS, [5] by having them rank a series of symptomatic and esthetic parameters. The results are reported as follows, discriminated on the basis of the type of surgery

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performed.

In the group of patients with breast implants, the percentage of change did not differ significantly between the two treatments studied in the appointments of days 3, 6, 9, 16, and 23. On day 30, however, we detected a statistically significant difference (P = 0.017). The percentage of decrease was significantly higher in the scars treated with the cream with silver sulfadiazine, vitamin A, and lidocaine (cream A) than in those treated with the cream without active ingredients (cream B) (18.6 and 9.5%, respectively) (**Table 1**). In the group of patients with face and neck lift, there was no significant difference between the percentage of change achieved due to the two treatments on days 3, 6, 9, and 16. Nevertheless, on days 23 and 30, we encountered a statistically significant difference (P = 0.026 and P = 0.007, respectively). The percentage of decrease was significantly higher in the scars treated with cream A than in those that had been treated with cream B. On day 23, the surface area of the scars treated with cream A had decreased, on average, by 14.8%, while that of the scars treated with cream B had increased, on average, by 24.9%. On day 30, the surface area of the scars treated with cream A had decreased, on average, by 19.1%, whereas that of the scars treated with cream B had increased, on average, by 22.2% (**Table 2**). **Figure 1** shows the changes in the surface area of each patient's scars on days 23 and 30 with respect to the initial appointment and classifies the results according to the type of surgery undergone and the treatment received. As we can see, more favorable results were obtained with cream A than with cream B, except in the case of two patients with breast implants (patients No. 7 and 12).

#### **2.2 Vancouver scar scale**

The VSS assigns values to the scar pigmentation, vascularity, and thickness, which are then added to obtain a total. Although the score may vary between 0 and 10, the average of the initial scores in our study was 2.7 and the maximum value observed throughout the study was 5. We conducted the analysis taking into account the absolute change in the VSS score with respect to the initiation of treatment (day 0). Results are expressed in absolute values. The analysis is carried out separately for each group of patients, depending on the type of surgery, on days 3, 6, 9, 16, 23, and 30.


In the breast implant patient group, the VSS score change did not differ significantly between treatments on days 3, 6, 9, and 16. On days 23 and 30, nonetheless,

#### **Table 1.**

*Average percentage of change of the surface area of the scars treated with silver sulfadiazine, vitamin A, and lidocaine (cream A) and with a cream without active ingredients (cream B) in patients with breast implants after 3, 6, 9, 16, 23, and 30 days from the onset of the topical treatment.*


*NS: not significant. \**

*Significant at 5%. \*\*Significant at 1%.*

*+ No surface area changes were perceived in any patient in either of the treatments.*

#### **Table 2.**

*Average percentage of change of the surface area of the scars treated with silver sulfadiazine, vitamin A, and lidocaine (cream A) and with a cream without active ingredients (cream B) in patients with face lift after 3, 6, 9, 16, 23, and 30 days from the onset of the topical treatment.*

#### **Figure 1.**

*Percentage changes of the scar surface area, per patient after 23 and 30 days from treatment onset.*

we noticed a statistically significant difference (P = 0.02 and P = 0.006, respectively). The decrease was significantly higher in the scars treated with cream A in comparison with those treated with cream B. On day 23, the score of the scars treated with cream A decreased by 1.13 points average, while that of the scars treated with cream B increased by 0.04 points average. On day 30, the average score decrease was of 1.88 points in those treated with cream A and of 0.42 points in those treated with cream B (**Table 3**).

In the group of patients with face and neck lift, the change in the VSS score did not differ significantly between treatments after 3 days. Yet, in all of the following appointments, a statistically significant difference (P ˂ 0.05) was observed. The reduction of the score was significantly higher in scars treated with cream A than in

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results obtained when applying each cream.

*Scars: A New Point of View in Plastic Surgery DOI: http://dx.doi.org/10.5772/intechopen.84127*

*and 30 days from the onset of the topical treatment.*

*VSS: Vancouver scar scale. NS: not significant.*

*VSS: Vancouver scar scale. NS: not significant.*

*30 days from the onset of the topical treatment.*

*Significant at 5%. \*\*Significant at 1%.*

*\**

**Table 4.**

*Significant at 5%. \*\*Significant at 1%.*

*\**

**Table 3.**

those treated with cream B. On day 23, scars treated with cream A had decreased by 0.86 points average, while those treated with cream B had increased by 1.75 points average. On day 30, the average score decrease of scars treated with cream A was 1.88 points, while the score of scars treated with cream B increased by 1.88 average points (**Table 4**). **Figure 2** displays the changes in the VSS scores for each patient with breast implants on 23 and 30 days, compared to the initial control. In a majority of patients, we see a favorable effect with the cream A treatment compared to cream B, except for three cases (patients No. 16, 28, and 30). **Figure 3** illustrates the changes in the VSS scores for each patient with face and neck lifts on days 6, 9, 16, 23, and 30 with respect to the initial appointment. In most cases, cream A shows a more favorable effect in comparison with cream B. Regardless of whether cream A or B had been used, in general, the changes observed in the VSS, either increase or decrease, were homogeneous in the three variables that make up this scale: pigmentation, vascularity, and thickness of the scar. **Figures 4–6** illustrate the different

*Average change in the VSS score of scars treated with silver sulfadiazine, vitamin A, and lidocaine (cream A) and with a cream without active ingredients (cream B) in patients with face lift after 3, 6, 9, 16, 23, and* 

**Days Average change in the VSS score as from treatment onset (breast implant) P Cream A Cream B** 0.33 0.21 0.80 (NS) 0.13 0.29 0.30 (NS) −0.21 0.46 0.10 (NS) −0.42 0.29 0.09 (NS) −1.13 0.04 0.02\* −1.88 −0.42 0.006\*\*

*Average change in the VSS score of scars treated with silver sulfadiazine, vitamin A, and lidocaine (cream A) and with a cream without active ingredients (cream B) in patients with breast implants after 3, 6, 9, 16, 23,* 

**Days Average change in the VSS score as from treatment onset (face and neck lift) P**

 0.50 1.50 0.17 (NS) 0.13 1.50 0. 048\* −0.13 2.00 0.029\* −0.50 1.88 0.029\* −0.86 1.75 0.020\* −1.88 1.88 0.007\*\*

**Cream A Cream B**


*\* Significant at 5%.*

*\*\*Significant at 1%.*

#### **Table 3.**

*Scars*

*NS: not significant.*

*Significant at 5%. \*\*Significant at 1%.*

*\**

*+*

**Table 2.**

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**Figure 1.**

those treated with cream B (**Table 3**).

we noticed a statistically significant difference (P = 0.02 and P = 0.006, respectively). The decrease was significantly higher in the scars treated with cream A in comparison with those treated with cream B. On day 23, the score of the scars treated with cream A decreased by 1.13 points average, while that of the scars treated with cream B increased by 0.04 points average. On day 30, the average score decrease was of 1.88 points in those treated with cream A and of 0.42 points in

*Percentage changes of the scar surface area, per patient after 23 and 30 days from treatment onset.*

**Days Average percentage of change of the surface area as from treatment onset** 

*No surface area changes were perceived in any patient in either of the treatments.*

*9, 16, 23, and 30 days from the onset of the topical treatment.*

**(face and neck lift)**

**Cream A (%) Cream B (%)** 12.5 12.5 + 12.5 12.5 + 12.3 12.4 0.60 (NS) 2.1 24.9 0.07 (NS) −14.8 24.9 0.026\* −19.1 22.2 0.007\*\*

*Average percentage of change of the surface area of the scars treated with silver sulfadiazine, vitamin A, and lidocaine (cream A) and with a cream without active ingredients (cream B) in patients with face lift after 3, 6,* 

**P**

In the group of patients with face and neck lift, the change in the VSS score did not differ significantly between treatments after 3 days. Yet, in all of the following appointments, a statistically significant difference (P ˂ 0.05) was observed. The reduction of the score was significantly higher in scars treated with cream A than in *Average change in the VSS score of scars treated with silver sulfadiazine, vitamin A, and lidocaine (cream A) and with a cream without active ingredients (cream B) in patients with breast implants after 3, 6, 9, 16, 23, and 30 days from the onset of the topical treatment.*


*Significant at 5%.*

*\*\*Significant at 1%.*

#### **Table 4.**

*Average change in the VSS score of scars treated with silver sulfadiazine, vitamin A, and lidocaine (cream A) and with a cream without active ingredients (cream B) in patients with face lift after 3, 6, 9, 16, 23, and 30 days from the onset of the topical treatment.*

those treated with cream B. On day 23, scars treated with cream A had decreased by 0.86 points average, while those treated with cream B had increased by 1.75 points average. On day 30, the average score decrease of scars treated with cream A was 1.88 points, while the score of scars treated with cream B increased by 1.88 average points (**Table 4**). **Figure 2** displays the changes in the VSS scores for each patient with breast implants on 23 and 30 days, compared to the initial control. In a majority of patients, we see a favorable effect with the cream A treatment compared to cream B, except for three cases (patients No. 16, 28, and 30). **Figure 3** illustrates the changes in the VSS scores for each patient with face and neck lifts on days 6, 9, 16, 23, and 30 with respect to the initial appointment. In most cases, cream A shows a more favorable effect in comparison with cream B. Regardless of whether cream A or B had been used, in general, the changes observed in the VSS, either increase or decrease, were homogeneous in the three variables that make up this scale: pigmentation, vascularity, and thickness of the scar. **Figures 4–6** illustrate the different results obtained when applying each cream.

#### **Figure 2.**

*Changes in VSS scores for each patient with breast implants after 23 and 30 days from treatment onset of treatment. VSS: Vancouver scar scale.*

#### **Figure 3.**

*Changes in VSS scores for each patient with cervical-facial stretch and after 6, 9, 16, 23, and 30 days from treatment onset. VSS: Vancouver scar scale.*

#### **2.3 Patient and observer objective assessment scale**

This scale allowed us to evaluate numerically, based on the patient's own answers, scar characteristics related to pain, itching, color, stiffness, and thickness. The treating physician recorded the data reported for each variable and for each scar during the corresponding appointments. Although the score may vary between 0 and 60, the average of the initial scores was 16 and the maximum value observed throughout the study was 25. We carried out the analysis taking into account the

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percentage change in the score of the scale with respect to that of the beginning of the treatment (day 0). We evaluated the results separately for each group of patients, depending on the type of surgery performed, and we considered the results obtained on days 3, 6, 9, 16, 23, and 30 of the postoperative period.

*Same patient's evolution with cream A (left) versus cream B (right) following a breast implant intervention* 

*Same patient's evolution with cream A (left) versus cream B (right) following a breast implant intervention* 

*Same patient's evolution with cream A (left) versus cream B (right) following a face lift intervention.*

In the group of patients with breast implants, the percentage change of the score of the POSAS did not differ significantly between the treatments on days 3 and 6, but in the remaining appointments, we found a statistically significant difference (P < 0.05) in favor of cream A. The percentage decrease in the score was significantly higher in those scars treated with cream A than in those treated with cream B. On day 23, the score of scars treated with cream A decreased by

*Scars: A New Point of View in Plastic Surgery DOI: http://dx.doi.org/10.5772/intechopen.84127*

**Figure 4.**

**Figure 5.**

**Figure 6.**

*(periareolar incision).*

*(submammary incision).*

#### **Figure 4.**

*Scars*

**Figure 2.**

*treatment. VSS: Vancouver scar scale.*

**72**

**Figure 3.**

**2.3 Patient and observer objective assessment scale**

*treatment onset. VSS: Vancouver scar scale.*

This scale allowed us to evaluate numerically, based on the patient's own answers, scar characteristics related to pain, itching, color, stiffness, and thickness. The treating physician recorded the data reported for each variable and for each scar during the corresponding appointments. Although the score may vary between 0 and 60, the average of the initial scores was 16 and the maximum value observed throughout the study was 25. We carried out the analysis taking into account the

*Changes in VSS scores for each patient with cervical-facial stretch and after 6, 9, 16, 23, and 30 days from* 

*Changes in VSS scores for each patient with breast implants after 23 and 30 days from treatment onset of* 

*Same patient's evolution with cream A (left) versus cream B (right) following a breast implant intervention (submammary incision).*

#### **Figure 5.**

*Same patient's evolution with cream A (left) versus cream B (right) following a face lift intervention.*

#### **Figure 6.**

*Same patient's evolution with cream A (left) versus cream B (right) following a breast implant intervention (periareolar incision).*

percentage change in the score of the scale with respect to that of the beginning of the treatment (day 0). We evaluated the results separately for each group of patients, depending on the type of surgery performed, and we considered the results obtained on days 3, 6, 9, 16, 23, and 30 of the postoperative period.

In the group of patients with breast implants, the percentage change of the score of the POSAS did not differ significantly between the treatments on days 3 and 6, but in the remaining appointments, we found a statistically significant difference (P < 0.05) in favor of cream A. The percentage decrease in the score was significantly higher in those scars treated with cream A than in those treated with cream B. On day 23, the score of scars treated with cream A decreased by


*NS: not significant.*

*\* Significant at 5%.*

#### *\*\*Significant at 1%.*

#### **Table 5.**

*Average POSAS score change rate for scars with silver sulfadiazine, vitamin A, and lidocaine (cream A) and with a cream without active ingredients (cream B) in patients with breast implants after 3, 6, 9, 16, 23, and 30 days from the onset of the topical treatment.*


*POSAS: patient and observer scar assessment scale. NS: not significant. \* Significant at 5%.*

#### **Table 6.**

*Average POSAS score change rate for scars with silver sulfadiazine, vitamin A, and lidocaine (cream A) and with a cream without active ingredients (cream B) in patients with face lift after 3, 6, 9, 16, 23, and 30 days from the onset of the topical treatment.*

21.8 points average, while that of the scars treated with cream B did so by 1.3 points average. On day 30, the average score decrease was of 37.7 points in scars treated with cream A while, in those treated with cream B, the decrease was 7.3 points average (**Table 5**).

In the group of patients with face and neck lifts, the percentage change in the POSAS score did not differ significantly between the treatments on days 3, 6, 9, 16, and 23. On day 30, however, we detected a statistically significant difference (P = 0.021) in favor of cream A. The percentage decrease was significantly higher in cases treated with cream A versus those treated with cream B. On day 30, the score of scars treated with cream A decreased, on average, by 14.4%, while that of the scars treated with cream B increased, on average, by 26.6% (**Table 6**). **Figure 7** presents the percentage changes of the POSAS scores for each patient with breast implants on days 9, 16, 23, and 30 with respect to the initial appointment,

**75**

**Figure 8.**

*observer objective evaluation scale.*

**Figure 7.**

differentiated according to the treatment applied. In most patients, we see that the treatment with cream A resulted in a more favorable effect than that obtained with

*POSAS score changes for each patient with face lift after 30 days from treatment onset. POSAS: patient and* 

*Percentage POSAS score changes for each patient with breast implants after 9, 16, 23, and 30 days from the* 

*beginning of treatment. POSAS: patient and observer objective evaluation scale.*

No. 13, day 16). **Figure 8** shows the percentage changes of the POSAS scores for each patient with face and neck lift between the onset of the treatment and day 30 and organizes the results based on the cream employed. In most cases, a better outcome was reached with cream A than with cream B. Irrespective of the cream applied, in general, the changes observed, either increase or decrease, reflected homogeneous

cream B, except for two cases (patient No. 15, days 9 and 16; and patient

changes in the variables that constitute this scale.

*Scars: A New Point of View in Plastic Surgery DOI: http://dx.doi.org/10.5772/intechopen.84127*

#### **Figure 7.**

*Scars*

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average (**Table 5**).

*NS: not significant.*

*Significant at 5%.*

*\**

**Table 6.**

21.8 points average, while that of the scars treated with cream B did so by 1.3 points average. On day 30, the average score decrease was of 37.7 points in scars treated with cream A while, in those treated with cream B, the decrease was 7.3 points

*Average POSAS score change rate for scars with silver sulfadiazine, vitamin A, and lidocaine (cream A) and with a cream without active ingredients (cream B) in patients with face lift after 3, 6, 9, 16, 23, and 30 days* 

**Days Average change in the POSAS score as from treatment onset (face and neck** 

*POSAS: patient and observer scar assessment scale.*

*30 days from the onset of the topical treatment.*

*POSAS: patient and observer scar assessment scale.*

*from the onset of the topical treatment.*

*NS: not significant.*

*Significant at 5%. \*\*Significant at 1%.*

*\**

**Table 5.**

**lift)**

**Cream A Cream B** 2.5 8.5 1.0 (NS) 1.7 7.8 0.129 (NS) −6.2 7.1 0.026\* −9.9 6.6 0.037\* −21.8 −1.3 0.005\*\* −37.7 −7.3 0.0007\*\*

*Average POSAS score change rate for scars with silver sulfadiazine, vitamin A, and lidocaine (cream A) and with a cream without active ingredients (cream B) in patients with breast implants after 3, 6, 9, 16, 23, and* 

**Days Average change in the POSAS score as from treatment onset (breast implant) P Cream A Cream B** 22.1 18.2 0.66 (NS) 18.2 20.2 0.40 (NS) 19.0 26.3 0.26 (NS) 18.0 23.9 0.36 (NS) −1.4 32.7 0.07 (NS) −14.4 26.6 0.021\*

**P**

In the group of patients with face and neck lifts, the percentage change in the POSAS score did not differ significantly between the treatments on days 3, 6, 9, 16, and 23. On day 30, however, we detected a statistically significant difference

(P = 0.021) in favor of cream A. The percentage decrease was significantly higher in cases treated with cream A versus those treated with cream B. On day 30, the score of scars treated with cream A decreased, on average, by 14.4%, while that of the scars treated with cream B increased, on average, by 26.6% (**Table 6**). **Figure 7** presents the percentage changes of the POSAS scores for each patient with breast implants on days 9, 16, 23, and 30 with respect to the initial appointment,

*Percentage POSAS score changes for each patient with breast implants after 9, 16, 23, and 30 days from the beginning of treatment. POSAS: patient and observer objective evaluation scale.*

#### **Figure 8.**

*POSAS score changes for each patient with face lift after 30 days from treatment onset. POSAS: patient and observer objective evaluation scale.*

differentiated according to the treatment applied. In most patients, we see that the treatment with cream A resulted in a more favorable effect than that obtained with cream B, except for two cases (patient No. 15, days 9 and 16; and patient No. 13, day 16). **Figure 8** shows the percentage changes of the POSAS scores for each patient with face and neck lift between the onset of the treatment and day 30 and organizes the results based on the cream employed. In most cases, a better outcome was reached with cream A than with cream B. Irrespective of the cream applied, in general, the changes observed, either increase or decrease, reflected homogeneous changes in the variables that constitute this scale.

The results showed an improvement of all the evaluated variables when we used the cream with silver sulfadiazine, vitamin A, and lidocaine as treatment [6]. In all the scars treated in this way, we observed a greater percentage decrease of the surface area as compared with those treated with the cream without active principles. In addition, the scars treated with silver sulfadiazine, vitamin A, and lidocaine obtained a lower POSAS score, associated with a better scar quality. Such decrease in the POSAS score throughout the treatment is indicative not only of a more positive perception by the patient of the healing process but also of improvement of all the parameters evaluated: pain, itching, color, stiffness, thickness, and irregular scarring [7]. Therefore, our results indicate that performing a topical treatment with a cream containing silver sulfadiazine, vitamin A, and lidocaine from the beginning of treatment decreases wound size faster, improves the quality of the scar and the overall perception of the patients. In other words, such a treatment of postcosmetic surgery scars yields better esthetic and functional outcomes [8].

#### **3. Combining skin substitutes for dermal reconstruction**

The other treatment we are concerned with involves using different dermal substitutes in reconstructive surgery. Soft tissue impairment after an accident requires fast radical treatment and often multiple surgical procedures related to necrotic and poorly perfused tissue. Traditionally, dermal reconstruction meant harvesting grafts and flaps, which left major sequelae in donor sites. However, modern understanding of the composition of the skin has enabled researchers to develop numerous cutaneous substitutes which allow for the reconstruction of the dermis by providing a scaffold that promotes new tissue growth, thus compensating for the functional and physiological impairments caused by damaged tissue. Moreover, they offer the attractive possibility of employing grafts to treat large burns.

Skin substitutes are biomatrices that may be used to replace the damaged epidermis or dermis (or both) partially or totally, transitory or definitively. Although they can be classified in different ways [9], they fall broadly into two groups, either decellularized dermis derived from human or animal sources or artificially constructed scaffolds comprised of highly purified biomaterials or synthetic polymers. Many of these substitutes act by guiding the patient's own cells to form a neodermis, both reducing pain and improving healing by avoiding excessive scarring [10]. They allow practitioners to create a controlled environment appropriate for physiology and cellular function, as well as to identify and properly manipulate the cells so that parenchyma, stroma, and vascular components are generated, and to produce materials malleable by the cells.

One such cutaneous substitute is Integra®, which consists of a matrix of purified collagen from bovine tendon cross-linked with glycosaminoglycan obtained from shark cartilage and a silicone layer that functions as a temporary epidermis. It is a bilayer membrane system, consisting of an inner dermal substitute layer and a temporary outer epidermal substance layer. The inner layer is composed of a threedimensional matrix of cross-linked bovine tendon collagen plus a glycosaminoglycan, and the outer layer is made of silicone. Integra® was introduced by Burke and Yannas in the early 1980s. The aim of their research was to find a substitute for the skin of patients with massive burns [11]. Nowadays, Integra® is a fundamental part of the "reconstructive ladder" and is utilized for treating skin loss resulting from burns, trauma and oncologic and pressure sore surgery [12]. After application of Integra®, the patient's native fibroblasts, macrophages, and lymphocytes infiltrate and new capillary growth occurs into the matrix of the inner layer. The inner layer becomes degraded and an endogenous collagen matrix is deposited by the patient's

**77**

**Figure 9.**

*Full-thickness trauma in lower limbs.*

*Scars: A New Point of View in Plastic Surgery DOI: http://dx.doi.org/10.5772/intechopen.84127*

own fibroblasts, forming a neodermis. Once engraftment is complete, 2–3 weeks after application, the outer silicone layer needs to be removed and an epidermal autograft must be placed over the neodermis. One of the advantages of this process is that successful neodermis formation requires only a thin skin graft which provides epidermal coverage which also prevents infections. Furthermore, as no donor

Another skin substitute is cadaver skin or homograft, which was included in protocols for the first time in the year 1981 in Philadelphia, United States. By virtue of the processing of cadaver skin through a skin bank, a suitable substitute is obtained and distributed to potential receptors [13]. Depending on the way in which they are processed, these "acellular dermal homografts" (as Takami describes them [14]) can be used transiently or permanently. To reduce the probability of graft rejection, cadaveric grafts undergo a cell-removal process and the resulting acellular tissue is irradiated with gamma rays, which destroy the immunogenic potential of the tissue. Employing cadaver skin to treat severe trauma of lower limbs with skin impairment has a number of advantages. To begin with, this treatment produces a biological closure after escharectomy. Furthermore, it helps reduce the loss of fluids, proteins, and electrolytes, as well as the pain experienced by the patient. Apart from this, it prevents the desiccation of the wound bed, since it functions as a biological cover for complex wounds, ultimately improving the preparation of the wound bed before definite reconstruction [15]. Finally, the addition of artificial skin over the vascularized homologous dermis creates a dermal structure of greater thickness and elasticity. Another recent development which is of great importance for reconstructive surgery is vacuum therapy (VAC), which improves wound healing by means of two main mechanisms. In the first place, it acts on the interstitial level eliminating edema, inflammatory mediators, and bacteria. It thus combats the vicious cycle of increased interstitial edema and pressure, cell death, and necrosis which is begotten by the inflammatory response triggered after a lesion. In addition, this treatment promotes mitogenesis and granulation tissue formation [16]. VAC is relevant to our research since, as Morykwas explains, it can be used to help incorporate Integra® and skin grafts as permanent replacements. Using a vacuum system after the escharectomy and the homograft placement and 1 week after positioning the artificial skin and the ultrathin autograft favors the arrest of these two substitutes. Moreover, negative pressure wound therapy can help augment the healing process and prepare the wound for definitive closure. A review published in Cochrane in 2007 [21] reported that, after 6 months of treatment, a 71% success rate had been observed in wounds treated with both artificial skin and negative pressure through

site is created, it eliminates the risk of donor site wound complications.

#### *Scars: A New Point of View in Plastic Surgery DOI: http://dx.doi.org/10.5772/intechopen.84127*

*Scars*

The results showed an improvement of all the evaluated variables when we used the cream with silver sulfadiazine, vitamin A, and lidocaine as treatment [6]. In all the scars treated in this way, we observed a greater percentage decrease of the surface area as compared with those treated with the cream without active principles. In addition, the scars treated with silver sulfadiazine, vitamin A, and lidocaine obtained a lower POSAS score, associated with a better scar quality. Such decrease in the POSAS score throughout the treatment is indicative not only of a more positive perception by the patient of the healing process but also of improvement of all the parameters evaluated: pain, itching, color, stiffness, thickness, and irregular scarring [7]. Therefore, our results indicate that performing a topical treatment with a cream containing silver sulfadiazine, vitamin A, and lidocaine from the beginning of treatment decreases wound size faster, improves the quality of the scar and the overall perception of the patients. In other words, such a treatment of postcosmetic surgery scars

yields better esthetic and functional outcomes [8].

**3. Combining skin substitutes for dermal reconstruction**

The other treatment we are concerned with involves using different dermal substitutes in reconstructive surgery. Soft tissue impairment after an accident requires fast radical treatment and often multiple surgical procedures related to necrotic and poorly perfused tissue. Traditionally, dermal reconstruction meant harvesting grafts and flaps, which left major sequelae in donor sites. However, modern understanding of the composition of the skin has enabled researchers to develop numerous cutaneous substitutes which allow for the reconstruction of the dermis by providing a scaffold that promotes new tissue growth, thus compensating for the functional and physiological impairments caused by damaged tissue. Moreover,

Skin substitutes are biomatrices that may be used to replace the damaged epidermis or dermis (or both) partially or totally, transitory or definitively. Although they can be classified in different ways [9], they fall broadly into two groups, either decellularized dermis derived from human or animal sources or artificially constructed scaffolds comprised of highly purified biomaterials or synthetic polymers. Many of these substitutes act by guiding the patient's own cells to form a neodermis, both reducing pain and improving healing by avoiding excessive scarring [10]. They allow practitioners to create a controlled environment appropriate for physiology and cellular function, as well as to identify and properly manipulate the cells so that parenchyma, stroma, and vascular components are generated, and to produce materials malleable by the cells. One such cutaneous substitute is Integra®, which consists of a matrix of purified collagen from bovine tendon cross-linked with glycosaminoglycan obtained from shark cartilage and a silicone layer that functions as a temporary epidermis. It is a bilayer membrane system, consisting of an inner dermal substitute layer and a temporary outer epidermal substance layer. The inner layer is composed of a threedimensional matrix of cross-linked bovine tendon collagen plus a glycosaminoglycan, and the outer layer is made of silicone. Integra® was introduced by Burke and Yannas in the early 1980s. The aim of their research was to find a substitute for the skin of patients with massive burns [11]. Nowadays, Integra® is a fundamental part of the "reconstructive ladder" and is utilized for treating skin loss resulting from burns, trauma and oncologic and pressure sore surgery [12]. After application of Integra®, the patient's native fibroblasts, macrophages, and lymphocytes infiltrate and new capillary growth occurs into the matrix of the inner layer. The inner layer becomes degraded and an endogenous collagen matrix is deposited by the patient's

they offer the attractive possibility of employing grafts to treat large burns.

**76**

own fibroblasts, forming a neodermis. Once engraftment is complete, 2–3 weeks after application, the outer silicone layer needs to be removed and an epidermal autograft must be placed over the neodermis. One of the advantages of this process is that successful neodermis formation requires only a thin skin graft which provides epidermal coverage which also prevents infections. Furthermore, as no donor site is created, it eliminates the risk of donor site wound complications.

Another skin substitute is cadaver skin or homograft, which was included in protocols for the first time in the year 1981 in Philadelphia, United States. By virtue of the processing of cadaver skin through a skin bank, a suitable substitute is obtained and distributed to potential receptors [13]. Depending on the way in which they are processed, these "acellular dermal homografts" (as Takami describes them [14]) can be used transiently or permanently. To reduce the probability of graft rejection, cadaveric grafts undergo a cell-removal process and the resulting acellular tissue is irradiated with gamma rays, which destroy the immunogenic potential of the tissue. Employing cadaver skin to treat severe trauma of lower limbs with skin impairment has a number of advantages. To begin with, this treatment produces a biological closure after escharectomy. Furthermore, it helps reduce the loss of fluids, proteins, and electrolytes, as well as the pain experienced by the patient. Apart from this, it prevents the desiccation of the wound bed, since it functions as a biological cover for complex wounds, ultimately improving the preparation of the wound bed before definite reconstruction [15]. Finally, the addition of artificial skin over the vascularized homologous dermis creates a dermal structure of greater thickness and elasticity.

Another recent development which is of great importance for reconstructive surgery is vacuum therapy (VAC), which improves wound healing by means of two main mechanisms. In the first place, it acts on the interstitial level eliminating edema, inflammatory mediators, and bacteria. It thus combats the vicious cycle of increased interstitial edema and pressure, cell death, and necrosis which is begotten by the inflammatory response triggered after a lesion. In addition, this treatment promotes mitogenesis and granulation tissue formation [16]. VAC is relevant to our research since, as Morykwas explains, it can be used to help incorporate Integra® and skin grafts as permanent replacements. Using a vacuum system after the escharectomy and the homograft placement and 1 week after positioning the artificial skin and the ultrathin autograft favors the arrest of these two substitutes. Moreover, negative pressure wound therapy can help augment the healing process and prepare the wound for definitive closure. A review published in Cochrane in 2007 [21] reported that, after 6 months of treatment, a 71% success rate had been observed in wounds treated with both artificial skin and negative pressure through

**Figure 9.** *Full-thickness trauma in lower limbs.*

**Figure 10.** *Pulaski and Tennison's Rules of Nines.*

#### **Figure 11.**

*(1) Escharectomy, (2) cadaver skin, (3) vacuum system, (4) epidermolysis, (5) neovascularized homodermis, and (6) artificial skin over vascularized homodermis—final result with autograft.*

a vacuum system, whereas the success rate of wounds treated solely with negative pressure had been, at 37%, significantly lower. In terms of wound healing, even better results were obtained when Integra® was used as a dermal substitute [22].

As a consequence of the benefits we have mentioned, dermal substitutes have now been extended to treat other pathologies. Furthermore, the use of cutaneous substitutes added to the vacuum therapy has been incorporated into the "Modified Ladder of Reconstruction" [17]. However, the usefulness of treating large wounds with deep skin impairment with both cadaver skin and artificial skins has not been, to date, exhaustively studied. Therefore, we wish to contribute to this line of research by reporting the successful esthetic and functional results we have obtained when treating extensive skin lesions with both substitutes. Our study involved the follow-up of the wound healing of four patients (N:4) who had suffered high impact trauma in their lower

**79**

*Scars: A New Point of View in Plastic Surgery DOI: http://dx.doi.org/10.5772/intechopen.84127*

bedside

Grade 4b Multiorgan dysfunction Grade 5 Death of a patient

*Dindo classification of surgical complications.*

**Table 7.**

**Grade Definition**

limbs (**Figure 9**) and who were treated at Hospital Alemán in the city of Buenos Aires. All of them were females with ages ranging from 19 to 73 years (median: 32 years). All of their lesions belonged to Group 4 of Benaim's severity classification and ranked as full-thickness burns in Benaim's depth classification [18]. The affected body surface was calculated based on the rule of nines described by Pulaski and Tennison in 1949 [19] (**Figure 10**) with the following results: 8% in the 19-year-old patient, 24% in the

Grade 1 Any deviation from the normal postoperative course without the need for pharmacological treatment or surgical, endoscopic, and radiological interventions

Grade 2 Requiring pharmacological treatment with drugs other than such allowed for grade 1

Grade 3 Requiring surgical, endoscopic, or radiological intervention

a follow-up to fully evaluate the complication

Grade 3a Intervention not under general anesthesia Grade 3b Intervention under general anesthesia

Grade 4a Single organ dysfunction (including dialysis)

complications. Blood transfusions and total parenteral nutrition are also included

Grade 4 Life-threatening complications including brain hemorrhage, ischemic stroke, subarachnoid

attacks) requiring intermediate care or intensive care unit management

Suffix "d" If the patient suffers from a complication at the time of discharge, the suffix "d" (for

bleeding, and central nervous system complications (but excluding transient ischemic

"disability") is added to the respective grade of complication. This label indicates the need for

Allowed therapeutic regiments are: drugs and antiemetics, antipyretics, analgetics, diuretics, electrolytes, and physiotherapy. This grade also includes wound infections opened at the

In all cases, escharectomy was performed on fascia within the first 48 h of the accident. Immediately afterward, the wounds were covered with cadaver skin from the tissue bank. Over the next 5–9 days, epidermolysis was observed (i.e., spontaneous removal of the epidermis), as well as vascularization and arrest of the homologous dermis on the receptor bed. In the second stage, the artificial skin was placed on the built-in vascularized homologous dermis. Once the artificial skin had been placed, we waited for 21 days before removing the silicone layer and completing the third and last surgical stage with the placement of a 1/4-thick autograft, obtained with an electric dermatome, over the heterologous vascularized neodermis. **Figure 11**

We used a grid of manual design to evaluate the arrest of the cadaver and artificial skin (expressed in percentages). The arrest of the cadaver skin was of 95% and the placement of the heterologous matrix with an ultrathin autograft was of 94%. The average hospital time was 46 days. No major complications were present, but only minimal difficulties belonging to grades 3b, 4, and 5 of the Dindo and Clavien table [20] (**Table 7**). After a year of follow-up, we observed that favorable functional results had been obtained in highly complex articular areas such as ankles or knees due to the contribution of homologous and heterologous matrixes that provided adequate scaffolding. With respect to the esthetic results, no depression of the covered surfaces was observed with respect to the adjacent normal dermal tissue. Furthermore, there was no

22-year-old, 28% in the 43-year-old, and 8% in the 73-year-old (**Table 4**).

illustrates the procedure we followed and the results we obtained.

evidence of pathological scarring (such as keloids or hypertrophic scars).


#### **Table 7.**

*Scars*

**Figure 10.**

*Pulaski and Tennison's Rules of Nines.*

**78**

**Figure 11.**

*(1) Escharectomy, (2) cadaver skin, (3) vacuum system, (4) epidermolysis, (5) neovascularized homodermis,* 

a vacuum system, whereas the success rate of wounds treated solely with negative pressure had been, at 37%, significantly lower. In terms of wound healing, even better results were obtained when Integra® was used as a dermal substitute [22]. As a consequence of the benefits we have mentioned, dermal substitutes have now been extended to treat other pathologies. Furthermore, the use of cutaneous substitutes added to the vacuum therapy has been incorporated into the "Modified Ladder of Reconstruction" [17]. However, the usefulness of treating large wounds with deep skin impairment with both cadaver skin and artificial skins has not been, to date, exhaustively studied. Therefore, we wish to contribute to this line of research by reporting the successful esthetic and functional results we have obtained when treating extensive skin lesions with both substitutes. Our study involved the follow-up of the wound healing of four patients (N:4) who had suffered high impact trauma in their lower

*and (6) artificial skin over vascularized homodermis—final result with autograft.*

*Dindo classification of surgical complications.*

limbs (**Figure 9**) and who were treated at Hospital Alemán in the city of Buenos Aires. All of them were females with ages ranging from 19 to 73 years (median: 32 years). All of their lesions belonged to Group 4 of Benaim's severity classification and ranked as full-thickness burns in Benaim's depth classification [18]. The affected body surface was calculated based on the rule of nines described by Pulaski and Tennison in 1949 [19] (**Figure 10**) with the following results: 8% in the 19-year-old patient, 24% in the 22-year-old, 28% in the 43-year-old, and 8% in the 73-year-old (**Table 4**).

In all cases, escharectomy was performed on fascia within the first 48 h of the accident. Immediately afterward, the wounds were covered with cadaver skin from the tissue bank. Over the next 5–9 days, epidermolysis was observed (i.e., spontaneous removal of the epidermis), as well as vascularization and arrest of the homologous dermis on the receptor bed. In the second stage, the artificial skin was placed on the built-in vascularized homologous dermis. Once the artificial skin had been placed, we waited for 21 days before removing the silicone layer and completing the third and last surgical stage with the placement of a 1/4-thick autograft, obtained with an electric dermatome, over the heterologous vascularized neodermis. **Figure 11** illustrates the procedure we followed and the results we obtained.

We used a grid of manual design to evaluate the arrest of the cadaver and artificial skin (expressed in percentages). The arrest of the cadaver skin was of 95% and the placement of the heterologous matrix with an ultrathin autograft was of 94%. The average hospital time was 46 days. No major complications were present, but only minimal difficulties belonging to grades 3b, 4, and 5 of the Dindo and Clavien table [20] (**Table 7**). After a year of follow-up, we observed that favorable functional results had been obtained in highly complex articular areas such as ankles or knees due to the contribution of homologous and heterologous matrixes that provided adequate scaffolding. With respect to the esthetic results, no depression of the covered surfaces was observed with respect to the adjacent normal dermal tissue. Furthermore, there was no evidence of pathological scarring (such as keloids or hypertrophic scars).

#### **4. Conclusions**

The goal of any healing process is not only that the scar does not bring about functional disruptions, but also that it is as inconspicuous as possible. Patients of both cosmetic and reconstructive surgery expect scars that do not stand out from the normal surrounding skin, yet there is no consensus among medical practitioners as to which healing methods can achieve both functional and esthetic goals most effectively. In this chapter, we have accounted for two studies carried out at Hospital Alemán in the city of Buenos Aires, the promising results of which may help practitioners arrive at a standard for treating scars resulting from cosmetic and reconstructive surgery.

Regarding postcosmetic surgery scars, we have tested the progress of the scars of 32 patients, each having two postsurgical scars that were treated with two different creams. The results of our research show that performing a topical treatment with a cream that contains silver sulfadiazine, vitamin A, and lidocaine from the onset of the treatment decreases the size of the wound more quickly, improves the quality of the scar and the patient's perception of it. These findings contrast with the less positive outcome of the scars treated with a moisturizing cream without active ingredients [23]. Thus, we conclude that using creams with active ingredients should be promoted as a common practice.

In turn, in our study related to reconstructive surgery, we followed the progress of four patients whose massive skin loss was treated with a combination of artificial and cadaveric dermal substitutes. Using modern biotechnology to reconstruct damaged structures and to provide a new extracellular matrix constitutes the greatest breakthrough in reconstructive surgery of recent times. The development of homografts and artificial skin has allowed professionals to accelerate healing by covering wounds transitorily or permanently. At the same time, they work as a barrier against infections, help maintain the hydroelectrolytic balance [24], and improve esthetic and functional results. As we explained in the previous section, the quality of the scar and the properties of the neodermis depend on the use of an appropriate extracellular matrix [25].

As part of our research, we assessed the progress of the four patients' scars, focusing on such characteristics as color, thickness, volume, and pain, as well as on the restoration of function at affected sites. We noted positive outcomes in all evaluated parameters, which points at the advantages entailed in implementing this technique. Moreover, the number of hypertrophic scars was lower than the average. Our method fulfilled the ultimate goal of tissue engineering, namely, to restore damaged or lost tissue in traumatic wounds that result in a functional barrier, providing, at the same time, for rapid closure to prevent dehydration and bacterial infection. As attested by our results, the advantages of combining both dermal substitutes include better functional and esthetic outcomes, pain relief, and enhancement of the overall quality of the scar.

All in all, the results of both studies are indicative of the direction that modern scar treatment can take in order to achieve the desired goals in both cosmetic and reconstructive surgery. In the case of the former, achieving an esthetically pleasing scar has long been recognized as a fundamental requirement of a successful intervention. Here, the most optimal results can be achieved if wound treatment and care are initiated early. However, the esthetic factor should not be limited to this type of procedures. Our work on reconstructive surgery centers around the concept that such surgery should not only merely aim at "rebuilding" but also at obtaining the best functional and esthetic outcome with the least possible number of interventions. Recent advances in biotechnology offer us effective skin substitutes, which can be combined so as to achieve a better evolution of the wounds. [26] Such improved esthetic and functional results in posttraumatic reconstructive surgery ensure an ad integrum recovery of the affected areas, which, ultimately, enhances the quality of patients' lives.

**81**

**Author details**

Gustavo E. Prezzavento

provided the original work is properly cited.

Hospital Alemán, Buenos Aires, Argentina

*Scars: A New Point of View in Plastic Surgery DOI: http://dx.doi.org/10.5772/intechopen.84127*

© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

\*Address all correspondence to: prezzavento.gustavo@gmail.com

*Scars: A New Point of View in Plastic Surgery DOI: http://dx.doi.org/10.5772/intechopen.84127*

*Scars*

**4. Conclusions**

should be promoted as a common practice.

appropriate extracellular matrix [25].

The goal of any healing process is not only that the scar does not bring about functional disruptions, but also that it is as inconspicuous as possible. Patients of both cosmetic and reconstructive surgery expect scars that do not stand out from the normal surrounding skin, yet there is no consensus among medical practitioners as to which healing methods can achieve both functional and esthetic goals most effectively. In this chapter, we have accounted for two studies carried out at Hospital Alemán in the city of Buenos Aires, the promising results of which may help practitioners arrive at a standard for treating scars resulting from cosmetic and reconstructive surgery.

Regarding postcosmetic surgery scars, we have tested the progress of the scars of 32 patients, each having two postsurgical scars that were treated with two different creams. The results of our research show that performing a topical treatment with a cream that contains silver sulfadiazine, vitamin A, and lidocaine from the onset of the treatment decreases the size of the wound more quickly, improves the quality of the scar and the patient's perception of it. These findings contrast with the less positive outcome of the scars treated with a moisturizing cream without active ingredients [23]. Thus, we conclude that using creams with active ingredients

In turn, in our study related to reconstructive surgery, we followed the progress of four patients whose massive skin loss was treated with a combination of artificial and cadaveric dermal substitutes. Using modern biotechnology to reconstruct damaged structures and to provide a new extracellular matrix constitutes the greatest breakthrough in reconstructive surgery of recent times. The development of homografts and artificial skin has allowed professionals to accelerate healing by covering wounds transitorily or permanently. At the same time, they work as a barrier against infections, help maintain the hydroelectrolytic balance [24], and improve esthetic and functional results. As we explained in the previous section, the quality of the scar and the properties of the neodermis depend on the use of an

As part of our research, we assessed the progress of the four patients' scars, focusing on such characteristics as color, thickness, volume, and pain, as well as on the restoration of function at affected sites. We noted positive outcomes in all evaluated parameters, which points at the advantages entailed in implementing this technique. Moreover, the number of hypertrophic scars was lower than the average. Our method fulfilled the ultimate goal of tissue engineering, namely, to restore damaged or lost tissue in traumatic wounds that result in a functional barrier, providing, at the same time, for rapid closure to prevent dehydration and bacterial infection. As attested by our results, the advantages of combining both dermal substitutes include better functional and esthetic outcomes, pain relief, and enhancement of the overall quality of the scar. All in all, the results of both studies are indicative of the direction that modern scar treatment can take in order to achieve the desired goals in both cosmetic and reconstructive surgery. In the case of the former, achieving an esthetically pleasing scar has long been recognized as a fundamental requirement of a successful intervention. Here, the most optimal results can be achieved if wound treatment and care are initiated early. However, the esthetic factor should not be limited to this type of procedures. Our work on reconstructive surgery centers around the concept that such surgery should not only merely aim at "rebuilding" but also at obtaining the best functional and esthetic outcome with the least possible number of interventions. Recent advances in biotechnology offer us effective skin substitutes, which can be combined so as to achieve a better evolution of the wounds. [26] Such improved esthetic and functional results in posttraumatic reconstructive surgery ensure an ad integrum recovery of the

affected areas, which, ultimately, enhances the quality of patients' lives.

**80**

#### **Author details**

Gustavo E. Prezzavento Hospital Alemán, Buenos Aires, Argentina

\*Address all correspondence to: prezzavento.gustavo@gmail.com

© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

### **References**

[1] Glat PM, Longaker MT. Wound healing. In: Aston SJ, Beasley RW, Thorne CH, editors. Grabb and Smith's Plastic Surgery. 5th ed. Philadelphia: Lippencott; 1997. pp. 3-12

[2] Mordon S, Trelles MA. Advantages of laser assisted scar healing (LASH). Cirugía Plástica Ibero-Latinoamericana. 2011;**37**(4):387-392

[3] Andrades P, Benitez S, Prado A. Guidelines for the treatment of kelloids and hipertrophic scars. Revista Chilena de Cirugía, Santiago de Chile, Chile. 2006;**58**(2):78-88

[4] Sullivan T, Smith J, Kermode J, et al. Rating the burn scar. The Journal of Burn Care & Rehabilitation. 1990;**11**:256-260

[5] Draaijers L, Tempelman F, Botman Y, et al. The patient and observer scar assessment scale: A reliable and feasible tool for scar evaluation. Plastic and Reconstructive Surgery. 2004;**113**:1960-1965

[6] Hunt TK. Vitamin A and wound healing. Journal of the American Academy of Dermatology. 1986;**15**:817-821

[7] Robson MC. Wound infection. A failure of wound healing caused by an imbalance of bacteria. The Surgical Clinics of North America. 1997;**77**:637-650

[8] Parsons D, Bowler PG, Myles V, et al. Silver antimicrobial dressings in wound management: A comparison of antibacterial, physical, and chemical characteristics. Wounds. 2005;**17**:222-232

[9] Leclerc T, Thepenier PJ, Bey E, Peltzer J, Trouillas M, Duhamel P, et al. Cell therapy of burns. Cell Proliferation. 2011;**44**:48-54

[10] Lee KH. Tissue-engineered human living skin substitutes: Development

and clinical application. Yonsei Medical Journal. 2000;**41**:774-779

[11] Andreadis ST, Hamoen KE, Yarmush ML, Morgan JR. Keratinocyte growth factor induces hyperproliferation and delays differentiation in a skin equivalent model system. The FASEB Journal. 2001;**15**:898-906

[12] Leventhal D, Furr M, Reiter D. Treatment of keloids and hypertrophic scars. Archives of Facial Plastic Surgery. 2006;**8**:362-368

[13] May SR, De Clement FA. Skin banking methodology; an eva- luation of package format, cooling and warming rates, storage,efficiency. Cryobiology. 1970;**17**:33

[14] Takami Y, Matsuda T, et al. Dispas/detergent treated dermal matrix as a dermal substitute. Burns. 1996;**22**:182-290

[15] Moerman E et al. The temporary use of allograft for complicated wounds in plastic surgery. Burns. 2002;**28**(Suppl. 1): S13-S15

[16] Sanger C, Molnar JA, Newman CE, et al. Poster 37: Immediate skin grafting of an engineered dermal substitute. Plastic and Reconstructive Surgery. 2005;**116**(35). American Society of Plastic Surgery, Plastic Surgery 2005. Chicago, IL. 24-28 Sept

[17] Janis JE, Kwon R, et al. The new reconstructive ladder: Modifications to the traditional model. Plastic and Reconstructive Surgery. 2011;**127**(Suppl. 1)

[18] Benaim F. Enfoque global del tratamiento de las quemaduras. In: Coiffman F editors. Cirugía plástica recosntructiva y estética. Barcelona, España: Editorial Masson-Salvat; 1994. pp. 443-4961

**83**

*Scars: A New Point of View in Plastic Surgery DOI: http://dx.doi.org/10.5772/intechopen.84127*

[19] Knaysi GA, Crikelair GF, et al. The rule of nine's; its history and accuracy. Plastic and Reconstructive Surgery.

[20] Dindo D, Demartines N, et al. Classification of surgical complications: A new proposal with evaluation in a cohort of 6336 patients and results of a survey. Annals of Surgery.

[21] Jones GE, Nelson EA. Skin grafting for venous leg ulcers (review). The Cochrane collaboration; 2007

[22] Pham C, Greenwood J, et al. Bioengineered skin substitutes for the management of burns: A systematic review. Burns. 2007;**33**:946-957

[23] Prezzavento GE, Racca L, Bottai H. Scarring: An evaluation of two topical treatments commonly used in post-aesthetic surgery scar. Cir. plást. iberolatinoam. 2017;**43**(3):255-263

[24] Eisenbud D, Huang NF, et al. Skin substitutes and wound healing: Current status and challenges. Wounds.

[25] Kagan RJ, Robb EC, Plessinger RT. Human skin banking. Clinics in Laboratory Medicine. 2005;**25**:587-605

[26] Prezzavento G. Skin substitutes. Can these be combined? (review). Journal of Embryology & Stem Cell

Research. 2018;**2**(1):000104

2004;**16**(1):2-17

1968;**41**:560-563

2004;**240**:205-213

*Scars: A New Point of View in Plastic Surgery DOI: http://dx.doi.org/10.5772/intechopen.84127*

[19] Knaysi GA, Crikelair GF, et al. The rule of nine's; its history and accuracy. Plastic and Reconstructive Surgery. 1968;**41**:560-563

[20] Dindo D, Demartines N, et al. Classification of surgical complications: A new proposal with evaluation in a cohort of 6336 patients and results of a survey. Annals of Surgery. 2004;**240**:205-213

[21] Jones GE, Nelson EA. Skin grafting for venous leg ulcers (review). The Cochrane collaboration; 2007

[22] Pham C, Greenwood J, et al. Bioengineered skin substitutes for the management of burns: A systematic review. Burns. 2007;**33**:946-957

[23] Prezzavento GE, Racca L, Bottai H. Scarring: An evaluation of two topical treatments commonly used in post-aesthetic surgery scar. Cir. plást. iberolatinoam. 2017;**43**(3):255-263

[24] Eisenbud D, Huang NF, et al. Skin substitutes and wound healing: Current status and challenges. Wounds. 2004;**16**(1):2-17

[25] Kagan RJ, Robb EC, Plessinger RT. Human skin banking. Clinics in Laboratory Medicine. 2005;**25**:587-605

[26] Prezzavento G. Skin substitutes. Can these be combined? (review). Journal of Embryology & Stem Cell Research. 2018;**2**(1):000104

**82**

2011;**44**:48-54

*Scars*

**References**

[1] Glat PM, Longaker MT. Wound healing. In: Aston SJ, Beasley RW, Thorne CH, editors. Grabb and Smith's Plastic Surgery. 5th ed. Philadelphia:

and clinical application. Yonsei Medical

[11] Andreadis ST, Hamoen KE, Yarmush ML, Morgan JR. Keratinocyte growth factor induces hyperproliferation and delays differentiation in a skin equivalent model system. The FASEB

Journal. 2000;**41**:774-779

Journal. 2001;**15**:898-906

1970;**17**:33

S13-S15

1996;**22**:182-290

Chicago, IL. 24-28 Sept

2011;**127**(Suppl. 1)

pp. 443-4961

[12] Leventhal D, Furr M, Reiter D. Treatment of keloids and

hypertrophic scars. Archives of Facial Plastic Surgery. 2006;**8**:362-368

[13] May SR, De Clement FA. Skin banking methodology; an eva- luation of package format, cooling and warming rates, storage,efficiency. Cryobiology.

[14] Takami Y, Matsuda T, et al. Dispas/detergent treated dermal matrix as a dermal substitute. Burns.

[15] Moerman E et al. The temporary use of allograft for complicated wounds in plastic surgery. Burns. 2002;**28**(Suppl. 1):

[16] Sanger C, Molnar JA, Newman CE, et al. Poster 37: Immediate skin grafting of an engineered dermal substitute. Plastic and Reconstructive Surgery. 2005;**116**(35). American Society of Plastic Surgery, Plastic Surgery 2005.

[17] Janis JE, Kwon R, et al. The new reconstructive ladder: Modifications to the traditional model. Plastic and Reconstructive Surgery.

[18] Benaim F. Enfoque global del tratamiento de las quemaduras. In: Coiffman F editors. Cirugía plástica recosntructiva y estética. Barcelona, España: Editorial Masson-Salvat; 1994.

[2] Mordon S, Trelles MA. Advantages of laser assisted scar healing (LASH). Cirugía Plástica Ibero-Latinoamericana.

[3] Andrades P, Benitez S, Prado A. Guidelines for the treatment of kelloids and hipertrophic scars. Revista Chilena de Cirugía, Santiago de Chile, Chile.

[4] Sullivan T, Smith J, Kermode J, et al. Rating the burn scar. The Journal

[5] Draaijers L, Tempelman F, Botman Y, et al. The patient and observer scar assessment scale: A reliable and feasible tool for scar evaluation. Plastic and Reconstructive Surgery.

[6] Hunt TK. Vitamin A and wound healing. Journal of the American Academy

[7] Robson MC. Wound infection. A failure of wound healing caused by an imbalance of bacteria. The Surgical Clinics of North America. 1997;**77**:637-650

[8] Parsons D, Bowler PG, Myles V, et al. Silver antimicrobial dressings in wound management: A comparison of antibacterial, physical, and chemical characteristics. Wounds. 2005;**17**:222-232

[9] Leclerc T, Thepenier PJ, Bey E, Peltzer J, Trouillas M, Duhamel P, et al. Cell therapy of burns. Cell Proliferation.

[10] Lee KH. Tissue-engineered human living skin substitutes: Development

of Dermatology. 1986;**15**:817-821

of Burn Care & Rehabilitation.

Lippencott; 1997. pp. 3-12

2011;**37**(4):387-392

2006;**58**(2):78-88

1990;**11**:256-260

2004;**113**:1960-1965

## *Edited by Anca Chiriac*

*SCARS* is an updated and comprehensive overview focused on the pathological scarring process. The chapters are written by international authors, researchers, and clinical practitioners with an interest in scars and united in a valuable study. The book aims at providing a guideline for the diagnosis and treatment of scars, as well as opening research paths for future developments.

Published in London, UK © 2019 IntechOpen © photominus / iStock

Scars

Scars

*Edited by Anca Chiriac*