3 Wound healing and tissue repair ABNORMAL WOUND HEALING ABNORMAL WOUND HEALING Various factors can adversely a ff ect wound healing ( Summary box 3.1 ). Some wounds fail to heal in a timely and orderly manner, resulting in chronic non-healing wounds, signifi cant morbidity and poor cosmesis. On the other hand, Summary box 3.1 Local and systemic factors infl uencing wound healing /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF , described these nodes in 1878. Local Skin tension Hypoxia and ischaemia Vascular insuf /f_i ciency Lymphoedema Contamination Infection Presence of foreign bodies Radiotherapy Systemic Advancing age Obesity Malnutrition . Then, Smoking Diseases (e.g. diabetes mellitus, connective tissue diseases) Immunocompromised (e.g. acquired immunode /f_i ciency syndrome) Medications (e.g. steroids, immunosuppressants, chemotherapy) inflammation can result in excessive scar tissue, for example hypertrophic and keloid scars. These abnormal scars contain excess collagen, which is arranged in a disorganised pattern in keloid scars as opposed to a parallel pattern in hypertrophic scars. Hypertrophic scars do not extend beyond the boundary of the original incision or wound and eventually regress. They are more common in areas of increased tension, wounds crossing tension lines , deep dermal burns and wounds left to heal by secondary intention (longer than 3 weeks). Keloid scars extend beyond the boundaries of the original incision or wound ( Figure 3.5 ), do not spontaneously regress and are di ffi cult to treat. The aetiology is unknown but genetic predisposition is implicated. They often occur as a result of relatively minor trauma and mainly in those with dar ker skin pigmentation. ABNORMAL WOUND HEALING Various factors can adversely a ff ect wound healing ( Summary box 3.1 ). Some wounds fail to heal in a timely and orderly manner, resulting in chronic non-healing wounds, signifi cant morbidity and poor cosmesis. On the other hand, Summary box 3.1 Local and systemic factors infl uencing wound healing /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF , described these nodes in 1878. Local Skin tension Hypoxia and ischaemia Vascular insuf /f_i ciency Lymphoedema Contamination Infection Presence of foreign bodies Radiotherapy Systemic Advancing age Obesity Malnutrition . Then, Smoking Diseases (e.g. diabetes mellitus, connective tissue diseases) Immunocompromised (e.g. acquired immunode /f_i ciency syndrome) Medications (e.g. steroids, immunosuppressants, chemotherapy) inflammation can result in excessive scar tissue, for example hypertrophic and keloid scars. These abnormal scars contain excess collagen, which is arranged in a disorganised pattern in keloid scars as opposed to a parallel pattern in hypertrophic scars. Hypertrophic scars do not extend beyond the boundary of the original incision or wound and eventually regress. They are more common in areas of increased tension, wounds crossing tension lines , deep dermal burns and wounds left to heal by secondary intention (longer than 3 weeks). Keloid scars extend beyond the boundaries of the original incision or wound ( Figure 3.5 ), do not spontaneously regress and are di ffi cult to treat. The aetiology is unknown but genetic predisposition is implicated. They often occur as a result of relatively minor trauma and mainly in those with dar ker skin pigmentation. ABNORMAL WOUND HEALING Various factors can adversely a ff ect wound healing ( Summary box 3.1 ). Some wounds fail to heal in a timely and orderly manner, resulting in chronic non-healing wounds, signifi cant morbidity and poor cosmesis. On the other hand, Summary box 3.1 Local and systemic factors infl uencing wound healing /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF , described these nodes in 1878. Local Skin tension Hypoxia and ischaemia Vascular insuf /f_i ciency Lymphoedema Contamination Infection Presence of foreign bodies Radiotherapy Systemic Advancing age Obesity Malnutrition . Then, Smoking Diseases (e.g. diabetes mellitus, connective tissue diseases) Immunocompromised (e.g. acquired immunode /f_i ciency syndrome) Medications (e.g. steroids, immunosuppressants, chemotherapy) inflammation can result in excessive scar tissue, for example hypertrophic and keloid scars. These abnormal scars contain excess collagen, which is arranged in a disorganised pattern in keloid scars as opposed to a parallel pattern in hypertrophic scars. Hypertrophic scars do not extend beyond the boundary of the original incision or wound and eventually regress. They are more common in areas of increased tension, wounds crossing tension lines , deep dermal burns and wounds left to heal by secondary intention (longer than 3 weeks). Keloid scars extend beyond the boundaries of the original incision or wound ( Figure 3.5 ), do not spontaneously regress and are di ffi cult to treat. The aetiology is unknown but genetic predisposition is implicated. They often occur as a result of relatively minor trauma and mainly in those with dar ker skin pigmentation. ACUTE WOUNDS Bites ACUTE WOUNDS Bites Most bites involve either puncture wounds or avulsions. Wounds over the metacarpophalangeal joint should be treated as a human bite following a punch to the mouth until proven Victor-Auguste-François Morel-Lavallée , 1811–1865, surgeon who first described this lesion in 1863. Summary box 3.4 Reconstruction options for wound closure /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF otherwise. Joint infections are a surgical emergency as they can result in articular cartilage destruction. They present as hot, swollen and tender joints with a limited range of motion. Figure 3.11 Degloving buttock injury. Primary closure Full-thickness skin graft Secondary closure Dermal matrices 78 : Tertiary (delayed primary) Local, regional or pedicled closure /f_l ap NPWT Tissue expansion Split-thickness skin graft Free /f_l ap ACUTE WOUNDS Bites Most bites involve either puncture wounds or avulsions. Wounds over the metacarpophalangeal joint should be treated as a human bite following a punch to the mouth until proven Victor-Auguste-François Morel-Lavallée , 1811–1865, surgeon who first described this lesion in 1863. Summary box 3.4 Reconstruction options for wound closure /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF otherwise. Joint infections are a surgical emergency as they can result in articular cartilage destruction. They present as hot, swollen and tender joints with a limited range of motion. Figure 3.11 Degloving buttock injury. Primary closure Full-thickness skin graft Secondary closure Dermal matrices 78 : Tertiary (delayed primary) Local, regional or pedicled closure /f_l ap NPWT Tissue expansion Split-thickness skin graft Free /f_l ap ACUTE WOUNDS Bites Most bites involve either puncture wounds or avulsions. Wounds over the metacarpophalangeal joint should be treated as a human bite following a punch to the mouth until proven Victor-Auguste-François Morel-Lavallée , 1811–1865, surgeon who first described this lesion in 1863. Summary box 3.4 Reconstruction options for wound closure /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF otherwise. Joint infections are a surgical emergency as they can result in articular cartilage destruction. They present as hot, swollen and tender joints with a limited range of motion. Figure 3.11 Degloving buttock injury. Primary closure Full-thickness skin graft Secondary closure Dermal matrices 78 : Tertiary (delayed primary) Local, regional or pedicled closure /f_l ap NPWT Tissue expansion Split-thickness skin graft Free /f_l ap Acute compartment syndrome Acute compartment syndrome Acute compartment syndrome occurs when there is increased interstitial pressure within a closed osteofascial compartment, which results in microvascular compromise. It is a surgical emergency as delayed treatment may lead to irreversible muscle ischaemia and signifi cant long-term morbidity . Compartment syndrome most commonly occurs after lower limb fractures, both open and closed (see Chapter 32 ). It also occurs in the upper limb, buttock and abdomen. Other causes include soft-tissue trauma, arterial injuries, burns and prolonged compression. It is characterised by pain out of pro - portion to the injury , particularly with passive movement of the a ff ected compartment muscles. Paraesthesia is another early sign. Absent pulses are uncommon and suggest the possibility of vascular injur y . Compartment syndrome is generally a clinical diagnosis. It can be di ffi cult to diagnose in the presence of impaired con - sciousness, in c hildren and in patients with regional nerve blocks. Monitoring intracompartment pressures (ICPs) can sometimes help to guide management. A pressure of ≤ 30 /uni00A0 mmHg between the diastolic pressure and ICP has been recommended as the threshold for fasciotomy . Fasciotomy involves incising the skin and deep fascia with long axial incisions ( Figure 3.13 ). If the compartment pressure - was high, the muscle will then be seen bulging out through the fasciotomy opening. The lower limb is reliably decompressed via two incisions. A medial longitudinal incision 1–2 /uni00A0 cm poste - ). rior to the medial border of the tibia decompresses the super - fi cial and deep posterior compartments. A lateral longitudinal incision 2 /uni00A0 cm lateral to the anterior tibial border decompresses the peroneal and anterior compartments. Late diagnosis of compartment syndrome is a management dilemma as a late fasciotomy may r esult in rhabdomyolysis, infection, need for amputation and even death. et 21 (1): Acute compartment syndrome Acute compartment syndrome occurs when there is increased interstitial pressure within a closed osteofascial compartment, which results in microvascular compromise. It is a surgical emergency as delayed treatment may lead to irreversible muscle ischaemia and signifi cant long-term morbidity . Compartment syndrome most commonly occurs after lower limb fractures, both open and closed (see Chapter 32 ). It also occurs in the upper limb, buttock and abdomen. Other causes include soft-tissue trauma, arterial injuries, burns and prolonged compression. It is characterised by pain out of pro - portion to the injury , particularly with passive movement of the a ff ected compartment muscles. Paraesthesia is another early sign. Absent pulses are uncommon and suggest the possibility of vascular injur y . Compartment syndrome is generally a clinical diagnosis. It can be di ffi cult to diagnose in the presence of impaired con - sciousness, in c hildren and in patients with regional nerve blocks. Monitoring intracompartment pressures (ICPs) can sometimes help to guide management. A pressure of ≤ 30 /uni00A0 mmHg between the diastolic pressure and ICP has been recommended as the threshold for fasciotomy . Fasciotomy involves incising the skin and deep fascia with long axial incisions ( Figure 3.13 ). If the compartment pressure - was high, the muscle will then be seen bulging out through the fasciotomy opening. The lower limb is reliably decompressed via two incisions. A medial longitudinal incision 1–2 /uni00A0 cm poste - ). rior to the medial border of the tibia decompresses the super - fi cial and deep posterior compartments. A lateral longitudinal incision 2 /uni00A0 cm lateral to the anterior tibial border decompresses the peroneal and anterior compartments. Late diagnosis of compartment syndrome is a management dilemma as a late fasciotomy may r esult in rhabdomyolysis, infection, need for amputation and even death. et 21 (1): Acute compartment syndrome Acute compartment syndrome occurs when there is increased interstitial pressure within a closed osteofascial compartment, which results in microvascular compromise. It is a surgical emergency as delayed treatment may lead to irreversible muscle ischaemia and signifi cant long-term morbidity . Compartment syndrome most commonly occurs after lower limb fractures, both open and closed (see Chapter 32 ). It also occurs in the upper limb, buttock and abdomen. Other causes include soft-tissue trauma, arterial injuries, burns and prolonged compression. It is characterised by pain out of pro - portion to the injury , particularly with passive movement of the a ff ected compartment muscles. Paraesthesia is another early sign. Absent pulses are uncommon and suggest the possibility of vascular injur y . Compartment syndrome is generally a clinical diagnosis. It can be di ffi cult to diagnose in the presence of impaired con - sciousness, in c hildren and in patients with regional nerve blocks. Monitoring intracompartment pressures (ICPs) can sometimes help to guide management. A pressure of ≤ 30 /uni00A0 mmHg between the diastolic pressure and ICP has been recommended as the threshold for fasciotomy . Fasciotomy involves incising the skin and deep fascia with long axial incisions ( Figure 3.13 ). If the compartment pressure - was high, the muscle will then be seen bulging out through the fasciotomy opening. The lower limb is reliably decompressed via two incisions. A medial longitudinal incision 1–2 /uni00A0 cm poste - ). rior to the medial border of the tibia decompresses the super - fi cial and deep posterior compartments. A lateral longitudinal incision 2 /uni00A0 cm lateral to the anterior tibial border decompresses the peroneal and anterior compartments. Late diagnosis of compartment syndrome is a management dilemma as a late fasciotomy may r esult in rhabdomyolysis, infection, need for amputation and even death. et 21 (1): CHRONIC WOUNDS CHRONIC WOUNDS These wounds fail to progress through the normal stages of wound healing in a timely manner. They are often characterised by a prolonged inflammatory phase and persistent infections. The management of chronic wounds therefore often involves Jean-Nicholas Marjolin , 1780–1850, surgeon, Paris, France, described the development of carcinomatous ulcers in scars in 1828. - debridement ( Table 3.4 ), control of infection and inflamma - tion and appropriately selected dressings to correct moisture imbalances. Chronic wounds can be categorised into vascular ulcers (venous or arterial), diabetic ulcers and pressure ulcers. - Figure 3.15 Pressure ulcer. CHRONIC WOUNDS These wounds fail to progress through the normal stages of wound healing in a timely manner. They are often characterised by a prolonged inflammatory phase and persistent infections. The management of chronic wounds therefore often involves Jean-Nicholas Marjolin , 1780–1850, surgeon, Paris, France, described the development of carcinomatous ulcers in scars in 1828. - debridement ( Table 3.4 ), control of infection and inflamma - tion and appropriately selected dressings to correct moisture imbalances. Chronic wounds can be categorised into vascular ulcers (venous or arterial), diabetic ulcers and pressure ulcers. - Figure 3.15 Pressure ulcer. CHRONIC WOUNDS These wounds fail to progress through the normal stages of wound healing in a timely manner. They are often characterised by a prolonged inflammatory phase and persistent infections. The management of chronic wounds therefore often involves Jean-Nicholas Marjolin , 1780–1850, surgeon, Paris, France, described the development of carcinomatous ulcers in scars in 1828. - debridement ( Table 3.4 ), control of infection and inflamma - tion and appropriately selected dressings to correct moisture imbalances. Chronic wounds can be categorised into vascular ulcers (venous or arterial), diabetic ulcers and pressure ulcers. - Figure 3.15 Pressure ulcer. CLASSIFICATION OF WOUNDS CLASSIFICATION OF WOUNDS Wounds are diverse and there is no standard classification system that incorporates all relevant aspects for di ff erent clinical contexts. A wide variety of classifications ( Summary box 3.3 are used and descriptors from more than one system are required to accurately describe a given wound. A widely accepted wound classification was first introduced 1 to describe the in 1964 by the US National Research Council degree of bacterial load or contamination of surgical wounds ). at the time of surgery . It was subsequently adapted by the 2 US Centers for Disease Prevention and Control to classify wounds as clean, clean–contaminated, contaminated and dirty ( Table 3.1 ). Although the simplicity of this classification has led to its widespread use, the definitions are not entirely clear 3,4 and low interobserver reliability has been reported. Various grading and scoring systems exist for specific condi - tions such as pressure ulcers and diabetic ulcers. The National Nosocomial Infections Surveillance (NNIS) score is commonly used to predict surgical site infections (SSIs). It was established in recognition of the e ff ectiveness of infection surveillance in 5 reducing SSIs. The NNIS score stratifies surgical wound infec - tion rates by risk factors. This risk index score ranges from 0 (lowest SSI risk) to 3 (highest SSI risk) with a point allocated for the presence of each of the following risk factors: ) Figure 3.5 Multiple keloid scars. TABLE 3.1 US Centers for Disease Prevention and 2 Control surgical wound classi /f_i cation. Class I Uninfected operative wounds No in /f_l ammation is encountered Clean Respiratory, alimentary, genital or uninfected urinary tracts are not entered Primarily closed and, if necessary, drained using a closed system Respiratory, alimentary, genital or urinary Class II tracts are entered under controlled conditions Clean– and without unusual contamination contaminated No evidence of infection or major break in technique is encountered Class III Open, fresh, accidental wounds Operations with major br eaks in sterile Contaminated technique (e.g. open cardiac massage) or gross spillage fr om the gastrointestinal tract Incisions in which acute, non-purulent in /f_l ammation is encountered Class IV Old traumatic wounds with retained devitalised tissue and those that involve Dirty existing clinical infection or perforated viscera /uni25CF American Society of Anesthesiologists score ≥ 3; /uni25CF operative time longer than the expected duration for simi lar procedures (>75th percentile). Summary box 3.3 Synopsis of wound classification systems /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Aetiology Complexity Clean, surgical Simple Shearing or degloving Complex Crush Signi /f_i cant soft-tissue loss Blast Open fracture or joint Burn (thermal, electrical, chemical, radiation, Visceral involvement mechanical) Complicated Cold injury Infection Avulsion or traction Necrosis Low or high energy Haematoma Bite Gas gangrene Depth Compartment syndrome Epidermal Dermal (super /f_i cial or Chronic deep) Vascular ulcers (venous or arterial) Full thickness Contamination Pressure ulcers Clean Diabetic ulcers Clean–contaminated Contaminated Dirty Implant or non-implant CLASSIFICATION OF WOUNDS Wounds are diverse and there is no standard classification system that incorporates all relevant aspects for di ff erent clinical contexts. A wide variety of classifications ( Summary box 3.3 are used and descriptors from more than one system are required to accurately describe a given wound. A widely accepted wound classification was first introduced 1 to describe the in 1964 by the US National Research Council degree of bacterial load or contamination of surgical wounds ). at the time of surgery . It was subsequently adapted by the 2 US Centers for Disease Prevention and Control to classify wounds as clean, clean–contaminated, contaminated and dirty ( Table 3.1 ). Although the simplicity of this classification has led to its widespread use, the definitions are not entirely clear 3,4 and low interobserver reliability has been reported. Various grading and scoring systems exist for specific condi - tions such as pressure ulcers and diabetic ulcers. The National Nosocomial Infections Surveillance (NNIS) score is commonly used to predict surgical site infections (SSIs). It was established in recognition of the e ff ectiveness of infection surveillance in 5 reducing SSIs. The NNIS score stratifies surgical wound infec - tion rates by risk factors. This risk index score ranges from 0 (lowest SSI risk) to 3 (highest SSI risk) with a point allocated for the presence of each of the following risk factors: ) Figure 3.5 Multiple keloid scars. TABLE 3.1 US Centers for Disease Prevention and 2 Control surgical wound classi /f_i cation. Class I Uninfected operative wounds No in /f_l ammation is encountered Clean Respiratory, alimentary, genital or uninfected urinary tracts are not entered Primarily closed and, if necessary, drained using a closed system Respiratory, alimentary, genital or urinary Class II tracts are entered under controlled conditions Clean– and without unusual contamination contaminated No evidence of infection or major break in technique is encountered Class III Open, fresh, accidental wounds Operations with major br eaks in sterile Contaminated technique (e.g. open cardiac massage) or gross spillage fr om the gastrointestinal tract Incisions in which acute, non-purulent in /f_l ammation is encountered Class IV Old traumatic wounds with retained devitalised tissue and those that involve Dirty existing clinical infection or perforated viscera /uni25CF American Society of Anesthesiologists score ≥ 3; /uni25CF operative time longer than the expected duration for simi lar procedures (>75th percentile). Summary box 3.3 Synopsis of wound classification systems /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Aetiology Complexity Clean, surgical Simple Shearing or degloving Complex Crush Signi /f_i cant soft-tissue loss Blast Open fracture or joint Burn (thermal, electrical, chemical, radiation, Visceral involvement mechanical) Complicated Cold injury Infection Avulsion or traction Necrosis Low or high energy Haematoma Bite Gas gangrene Depth Compartment syndrome Epidermal Dermal (super /f_i cial or Chronic deep) Vascular ulcers (venous or arterial) Full thickness Contamination Pressure ulcers Clean Diabetic ulcers Clean–contaminated Contaminated Dirty Implant or non-implant CLASSIFICATION OF WOUNDS Wounds are diverse and there is no standard classification system that incorporates all relevant aspects for di ff erent clinical contexts. A wide variety of classifications ( Summary box 3.3 are used and descriptors from more than one system are required to accurately describe a given wound. A widely accepted wound classification was first introduced 1 to describe the in 1964 by the US National Research Council degree of bacterial load or contamination of surgical wounds ). at the time of surgery . It was subsequently adapted by the 2 US Centers for Disease Prevention and Control to classify wounds as clean, clean–contaminated, contaminated and dirty ( Table 3.1 ). Although the simplicity of this classification has led to its widespread use, the definitions are not entirely clear 3,4 and low interobserver reliability has been reported. Various grading and scoring systems exist for specific condi - tions such as pressure ulcers and diabetic ulcers. The National Nosocomial Infections Surveillance (NNIS) score is commonly used to predict surgical site infections (SSIs). It was established in recognition of the e ff ectiveness of infection surveillance in 5 reducing SSIs. The NNIS score stratifies surgical wound infec - tion rates by risk factors. This risk index score ranges from 0 (lowest SSI risk) to 3 (highest SSI risk) with a point allocated for the presence of each of the following risk factors: ) Figure 3.5 Multiple keloid scars. TABLE 3.1 US Centers for Disease Prevention and 2 Control surgical wound classi /f_i cation. Class I Uninfected operative wounds No in /f_l ammation is encountered Clean Respiratory, alimentary, genital or uninfected urinary tracts are not entered Primarily closed and, if necessary, drained using a closed system Respiratory, alimentary, genital or urinary Class II tracts are entered under controlled conditions Clean– and without unusual contamination contaminated No evidence of infection or major break in technique is encountered Class III Open, fresh, accidental wounds Operations with major br eaks in sterile Contaminated technique (e.g. open cardiac massage) or gross spillage fr om the gastrointestinal tract Incisions in which acute, non-purulent in /f_l ammation is encountered Class IV Old traumatic wounds with retained devitalised tissue and those that involve Dirty existing clinical infection or perforated viscera /uni25CF American Society of Anesthesiologists score ≥ 3; /uni25CF operative time longer than the expected duration for simi lar procedures (>75th percentile). Summary box 3.3 Synopsis of wound classification systems /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Aetiology Complexity Clean, surgical Simple Shearing or degloving Complex Crush Signi /f_i cant soft-tissue loss Blast Open fracture or joint Burn (thermal, electrical, chemical, radiation, Visceral involvement mechanical) Complicated Cold injury Infection Avulsion or traction Necrosis Low or high energy Haematoma Bite Gas gangrene Depth Compartment syndrome Epidermal Dermal (super /f_i cial or Chronic deep) Vascular ulcers (venous or arterial) Full thickness Contamination Pressure ulcers Clean Diabetic ulcers Clean–contaminated Contaminated Dirty Implant or non-implant Contractures Contractures Scar contractures can cause severe functional, psychological and aesthetic problems ( Figure 3.19 ). Contractures across joints may restrict the range of movement, leading to deformity , - impairment and disability . Contractures may also result from the di ff erential growth pattern between scar and surrounding tissues. - Surgical contracture r elease and reconstruction can be an e ff ective treatment option. A key principle is the replacement of scar tissue with healthy tissue. A wide range of r econstruc - tions are described ( Summary box 3.4 ) and typically involve 14 skin grafts or flaps (more information can be found in Part 6 ). - Local flaps suc h as Z-plasty ( Figure 3.20 ) and its variants can be used to lengthen and transpose the scar. Many other local flaps have been described, including Y–V , V–Y and W-plasty . Free flaps may be required for resurfacing sever e contractures. In general, flaps are preferable to skin grafts because of - graft contracture. When skin grafts are used, full thickness is preferred to split thickness as they have a better texture and contract less during healing. (red/raised) (dark/raised) Intralesional corticosteroids Silicone gel/sheeting + a intralesional corticosteroids 5-FU + intralesional corticosteroids b Fractional or pulsed-dye laser therapy Patient counselling regarding reccurence rate and expectations Surgical excision with adjuvant • Silicone gel or sheeting or intralesional corticosteroids or both • Radiotherapy • Alternative therapies (bleomycin, mitomycin C, imiquimod) Figure 3.18 Management algorithm for keloids. Light grey indicates initial management strategies; dark grey indicates secondary man a agement options. Cryotherapy may be used in conjunction with intralesional corticosteroids, depending on physician experience and b comfort with its application. Ablative fractional lasers are the pre ferred initial laser therapy option for patients with minor keloids. 5-FU, 5- /f_l uorouracil. (Redrawn with permission from Gold MH, McGuire M, Mustoe TA et al . Updated international clinical recommendations on scar management: part 2–algorithms for scar prevention and treat ment. Dermatol Surg 2014; 40 (8): 825–31.) Contractures Scar contractures can cause severe functional, psychological and aesthetic problems ( Figure 3.19 ). Contractures across joints may restrict the range of movement, leading to deformity , - impairment and disability . Contractures may also result from the di ff erential growth pattern between scar and surrounding tissues. - Surgical contracture r elease and reconstruction can be an e ff ective treatment option. A key principle is the replacement of scar tissue with healthy tissue. A wide range of r econstruc - tions are described ( Summary box 3.4 ) and typically involve 14 skin grafts or flaps (more information can be found in Part 6 ). - Local flaps suc h as Z-plasty ( Figure 3.20 ) and its variants can be used to lengthen and transpose the scar. Many other local flaps have been described, including Y–V , V–Y and W-plasty . Free flaps may be required for resurfacing sever e contractures. In general, flaps are preferable to skin grafts because of - graft contracture. When skin grafts are used, full thickness is preferred to split thickness as they have a better texture and contract less during healing. (red/raised) (dark/raised) Intralesional corticosteroids Silicone gel/sheeting + a intralesional corticosteroids 5-FU + intralesional corticosteroids b Fractional or pulsed-dye laser therapy Patient counselling regarding reccurence rate and expectations Surgical excision with adjuvant • Silicone gel or sheeting or intralesional corticosteroids or both • Radiotherapy • Alternative therapies (bleomycin, mitomycin C, imiquimod) Figure 3.18 Management algorithm for keloids. Light grey indicates initial management strategies; dark grey indicates secondary man a agement options. Cryotherapy may be used in conjunction with intralesional corticosteroids, depending on physician experience and b comfort with its application. Ablative fractional lasers are the pre ferred initial laser therapy option for patients with minor keloids. 5-FU, 5- /f_l uorouracil. (Redrawn with permission from Gold MH, McGuire M, Mustoe TA et al . Updated international clinical recommendations on scar management: part 2–algorithms for scar prevention and treat ment. Dermatol Surg 2014; 40 (8): 825–31.) Contractures Scar contractures can cause severe functional, psychological and aesthetic problems ( Figure 3.19 ). Contractures across joints may restrict the range of movement, leading to deformity , - impairment and disability . Contractures may also result from the di ff erential growth pattern between scar and surrounding tissues. - Surgical contracture r elease and reconstruction can be an e ff ective treatment option. A key principle is the replacement of scar tissue with healthy tissue. A wide range of r econstruc - tions are described ( Summary box 3.4 ) and typically involve 14 skin grafts or flaps (more information can be found in Part 6 ). - Local flaps suc h as Z-plasty ( Figure 3.20 ) and its variants can be used to lengthen and transpose the scar. Many other local flaps have been described, including Y–V , V–Y and W-plasty . Free flaps may be required for resurfacing sever e contractures. In general, flaps are preferable to skin grafts because of - graft contracture. When skin grafts are used, full thickness is preferred to split thickness as they have a better texture and contract less during healing. (red/raised) (dark/raised) Intralesional corticosteroids Silicone gel/sheeting + a intralesional corticosteroids 5-FU + intralesional corticosteroids b Fractional or pulsed-dye laser therapy Patient counselling regarding reccurence rate and expectations Surgical excision with adjuvant • Silicone gel or sheeting or intralesional corticosteroids or both • Radiotherapy • Alternative therapies (bleomycin, mitomycin C, imiquimod) Figure 3.18 Management algorithm for keloids. Light grey indicates initial management strategies; dark grey indicates secondary man a agement options. Cryotherapy may be used in conjunction with intralesional corticosteroids, depending on physician experience and b comfort with its application. Ablative fractional lasers are the pre ferred initial laser therapy option for patients with minor keloids. 5-FU, 5- /f_l uorouracil. (Redrawn with permission from Gold MH, McGuire M, Mustoe TA et al . Updated international clinical recommendations on scar management: part 2–algorithms for scar prevention and treat ment. Dermatol Surg 2014; 40 (8): 825–31.) Degloving Degloving Degloving is the avulsion of skin and subcutaneous fat from the underlying fascia, muscle or bone. A degloving injury may be open or closed. An example of an open degloving is a finger avulsion injury with loss of skin ( Figure 3.10 ). Closed degloving injuries result from shearing forces, which may occur with motor vehicle collisions. The extent of these injuries is often underappreciated and much of the skin perforating may be non-viable ( Figure 3.11 ). Disruption of vascular and lymphatic vessels may result in a characteristic - haemolymphatic collection between the fascial planes called a Morel-Lavallée lesion ( Figure 3.12 ). Although these lesions ver the greater tro - were originally described as occurring o chanter the term is also used now for similar lesions in other anatomical locations. Assessing the viability of degloved tissue can be di ffi cult and may therefore require more than one surgical exploration ore definitive reconstruction. Non-viable and debridement bef ed staining and thrombosis of subcutane - skin may show fix ous veins. Most surgeons serially excise the degloved skin until punctate dermal bleeding is seen from viable tissue. Intrave - non-viable tissue, but nous fluorescein may also help delineate it requires specialist equipment and there is a small risk of anaphylaxis. More recently , the use of indocyanine green fl u orescence has been reported. A useful classifi cation system to help guide management describes four patterns of degloving ( Summary box 3.5 severe multiplanar degloving. Summary box 3.5 9 Classifi cation of degloving injuries in limb trauma Subcutaneous fat Superficial fascia Deep fascia Muscle Bone Figure 3.12 Mechanism of injury for Morel-Lavallée lesions. Cross-sectional illustrations of the layers of tissue from the skin to the bone demonstrate how a shearing force can cause the comparatively mobile subcutaneous tissues to move relative to the comparatively /f_i xed underlying deep fascia, causing shearing of perforating arteries (red), veins (blue) and lymphatics (green) and ultimately leading to the formation of a haemolymphatic collection in this potential space. (Adapted with permission from Bonilla-Yoon I, Masih S, Patel DB al . The Mor el-Lavallée lesion: pathophysiology, clinical presentation, imaging features, and treatment options. Emerg Radiol 2014; 35–43.) Figure 3.13 Fasciotomy of the leg. 1 Limited degloving with abrasion or avulsion 2 Non-circumferential degloving 3 Circumferential single plane degloving 4 Circumferential multiplanar degloving Degloving Degloving is the avulsion of skin and subcutaneous fat from the underlying fascia, muscle or bone. A degloving injury may be open or closed. An example of an open degloving is a finger avulsion injury with loss of skin ( Figure 3.10 ). Closed degloving injuries result from shearing forces, which may occur with motor vehicle collisions. The extent of these injuries is often underappreciated and much of the skin perforating may be non-viable ( Figure 3.11 ). Disruption of vascular and lymphatic vessels may result in a characteristic - haemolymphatic collection between the fascial planes called a Morel-Lavallée lesion ( Figure 3.12 ). Although these lesions ver the greater tro - were originally described as occurring o chanter the term is also used now for similar lesions in other anatomical locations. Assessing the viability of degloved tissue can be di ffi cult and may therefore require more than one surgical exploration ore definitive reconstruction. Non-viable and debridement bef ed staining and thrombosis of subcutane - skin may show fix ous veins. Most surgeons serially excise the degloved skin until punctate dermal bleeding is seen from viable tissue. Intrave - non-viable tissue, but nous fluorescein may also help delineate it requires specialist equipment and there is a small risk of anaphylaxis. More recently , the use of indocyanine green fl u orescence has been reported. A useful classifi cation system to help guide management describes four patterns of degloving ( Summary box 3.5 severe multiplanar degloving. Summary box 3.5 9 Classifi cation of degloving injuries in limb trauma Subcutaneous fat Superficial fascia Deep fascia Muscle Bone Figure 3.12 Mechanism of injury for Morel-Lavallée lesions. Cross-sectional illustrations of the layers of tissue from the skin to the bone demonstrate how a shearing force can cause the comparatively mobile subcutaneous tissues to move relative to the comparatively /f_i xed underlying deep fascia, causing shearing of perforating arteries (red), veins (blue) and lymphatics (green) and ultimately leading to the formation of a haemolymphatic collection in this potential space. (Adapted with permission from Bonilla-Yoon I, Masih S, Patel DB al . The Mor el-Lavallée lesion: pathophysiology, clinical presentation, imaging features, and treatment options. Emerg Radiol 2014; 35–43.) Figure 3.13 Fasciotomy of the leg. 1 Limited degloving with abrasion or avulsion 2 Non-circumferential degloving 3 Circumferential single plane degloving 4 Circumferential multiplanar degloving Degloving Degloving is the avulsion of skin and subcutaneous fat from the underlying fascia, muscle or bone. A degloving injury may be open or closed. An example of an open degloving is a finger avulsion injury with loss of skin ( Figure 3.10 ). Closed degloving injuries result from shearing forces, which may occur with motor vehicle collisions. The extent of these injuries is often underappreciated and much of the skin perforating may be non-viable ( Figure 3.11 ). Disruption of vascular and lymphatic vessels may result in a characteristic - haemolymphatic collection between the fascial planes called a Morel-Lavallée lesion ( Figure 3.12 ). Although these lesions ver the greater tro - were originally described as occurring o chanter the term is also used now for similar lesions in other anatomical locations. Assessing the viability of degloved tissue can be di ffi cult and may therefore require more than one surgical exploration ore definitive reconstruction. Non-viable and debridement bef ed staining and thrombosis of subcutane - skin may show fix ous veins. Most surgeons serially excise the degloved skin until punctate dermal bleeding is seen from viable tissue. Intrave - non-viable tissue, but nous fluorescein may also help delineate it requires specialist equipment and there is a small risk of anaphylaxis. More recently , the use of indocyanine green fl u orescence has been reported. A useful classifi cation system to help guide management describes four patterns of degloving ( Summary box 3.5 severe multiplanar degloving. Summary box 3.5 9 Classifi cation of degloving injuries in limb trauma Subcutaneous fat Superficial fascia Deep fascia Muscle Bone Figure 3.12 Mechanism of injury for Morel-Lavallée lesions. Cross-sectional illustrations of the layers of tissue from the skin to the bone demonstrate how a shearing force can cause the comparatively mobile subcutaneous tissues to move relative to the comparatively /f_i xed underlying deep fascia, causing shearing of perforating arteries (red), veins (blue) and lymphatics (green) and ultimately leading to the formation of a haemolymphatic collection in this potential space. (Adapted with permission from Bonilla-Yoon I, Masih S, Patel DB al . The Mor el-Lavallée lesion: pathophysiology, clinical presentation, imaging features, and treatment options. Emerg Radiol 2014; 35–43.) Figure 3.13 Fasciotomy of the leg. 1 Limited degloving with abrasion or avulsion 2 Non-circumferential degloving 3 Circumferential single plane degloving 4 Circumferential multiplanar degloving Haemostasis Haemostasis Disruption of the vascular endothelium following injury causes vasoconstriction and exposure of the subendothelial extracel lular matrix. This encourages platelets to adhere, activate and aggregate, resulting in a platelet plug, which also helps limit further blood loss. Platelet adhesion results in their activa tion and release of granules. Alpha granules contain hundreds of proteins, includ ing cytokines and growth factor s; for example, transforming growth factor beta, platelet-derived growth factor, fibroblast growth factor, e pidermal growth factor and vascular endo thelial growth factor. These are involved in the deposition of extracellular matrix, chemotaxis, epithelialisation and the for - mation of new blood vessels (angiogenesis). Platelet aggregation occurs once platelets become activated. At the same time, tissue factor at the site of injury initiates the coagulation cascade ( Figure 3.2 ), resulting in the formation of thrombin. Thr ombin performs various functions, including fibrin generation, which helps to stabilise the platelet plug and form a sca ff old for infiltrating cells . The principles of wound management • The principles of scar management • Haemostasis Disruption of the vascular endothelium following injury causes vasoconstriction and exposure of the subendothelial extracel lular matrix. This encourages platelets to adhere, activate and aggregate, resulting in a platelet plug, which also helps limit further blood loss. Platelet adhesion results in their activa tion and release of granules. Alpha granules contain hundreds of proteins, includ ing cytokines and growth factor s; for example, transforming growth factor beta, platelet-derived growth factor, fibroblast growth factor, e pidermal growth factor and vascular endo thelial growth factor. These are involved in the deposition of extracellular matrix, chemotaxis, epithelialisation and the for - mation of new blood vessels (angiogenesis). Platelet aggregation occurs once platelets become activated. At the same time, tissue factor at the site of injury initiates the coagulation cascade ( Figure 3.2 ), resulting in the formation of thrombin. Thr ombin performs various functions, including fibrin generation, which helps to stabilise the platelet plug and form a sca ff old for infiltrating cells . The principles of wound management • The principles of scar management • Haemostasis Disruption of the vascular endothelium following injury causes vasoconstriction and exposure of the subendothelial extracel lular matrix. This encourages platelets to adhere, activate and aggregate, resulting in a platelet plug, which also helps limit further blood loss. Platelet adhesion results in their activa tion and release of granules. Alpha granules contain hundreds of proteins, includ ing cytokines and growth factor s; for example, transforming growth factor beta, platelet-derived growth factor, fibroblast growth factor, e pidermal growth factor and vascular endo thelial growth factor. These are involved in the deposition of extracellular matrix, chemotaxis, epithelialisation and the for - mation of new blood vessels (angiogenesis). Platelet aggregation occurs once platelets become activated. At the same time, tissue factor at the site of injury initiates the coagulation cascade ( Figure 3.2 ), resulting in the formation of thrombin. Thr ombin performs various functions, including fibrin generation, which helps to stabilise the platelet plug and form a sca ff old for infiltrating cells . The principles of wound management • The principles of scar management • Introduction INTRODUCTION Wound healing is a complex and dynamic biological process. In human adults, the normal response to injury across all organ systems typically results in fibrosis and scar formation. Fibrotic healing causes tissue dysfunction and its potential impact on patients is often underappreciated. This contrasts with early gestation when fetal tissues can remarkably heal without fibrosis. Regenerative medicine is therefore an exciting field of research. A better understanding of the mechanisms involved can potentially help reduce the global burden of disease asso ciated with wound healing. This chapter describes the patho physiology of wound healing, the types of healing and how to classify wounds. Clinical judgement is crucial in managing wounds. A framework is provided to better understand the key principles of wound and scar management. Inflammation Inflammation In the early inflammatory phase (days 1–2), platelet activation causes an influx of inflammatory cells led by polymorpho - nuclear leukocytes, particularly neutrophils. The latter are important for minimising bacterial contamination of the wound. Platelets and the local injured tissue also release vasoactive amines such as histamine and serotonin, which increase vascular permeability , thereby aiding infiltration of inflammatory cells. During the late inflammatory phase (days 2–3) monocytes appear in the wound and di ff erentiate into macrophages. Macrophages play a vital role in wound healing. They func - tion as phagocytic cells and release proteolytic enzymes to help debride the wound. T hey are also the primary producer of cytokines and growth factors promoting fibroblast proliferation and angiogenesis. Historically , this phase has been described by rubor (red - ness), tumor (swelling), calor (heat) and dolor (pain). - Inflammation In the early inflammatory phase (days 1–2), platelet activation causes an influx of inflammatory cells led by polymorpho - nuclear leukocytes, particularly neutrophils. The latter are important for minimising bacterial contamination of the wound. Platelets and the local injured tissue also release vasoactive amines such as histamine and serotonin, which increase vascular permeability , thereby aiding infiltration of inflammatory cells. During the late inflammatory phase (days 2–3) monocytes appear in the wound and di ff erentiate into macrophages. Macrophages play a vital role in wound healing. They func - tion as phagocytic cells and release proteolytic enzymes to help debride the wound. T hey are also the primary producer of cytokines and growth factors promoting fibroblast proliferation and angiogenesis. Historically , this phase has been described by rubor (red - ness), tumor (swelling), calor (heat) and dolor (pain). - Inflammation In the early inflammatory phase (days 1–2), platelet activation causes an influx of inflammatory cells led by polymorpho - nuclear leukocytes, particularly neutrophils. The latter are important for minimising bacterial contamination of the wound. Platelets and the local injured tissue also release vasoactive amines such as histamine and serotonin, which increase vascular permeability , thereby aiding infiltration of inflammatory cells. During the late inflammatory phase (days 2–3) monocytes appear in the wound and di ff erentiate into macrophages. Macrophages play a vital role in wound healing. They func - tion as phagocytic cells and release proteolytic enzymes to help debride the wound. T hey are also the primary producer of cytokines and growth factors promoting fibroblast proliferation and angiogenesis. Historically , this phase has been described by rubor (red - ness), tumor (swelling), calor (heat) and dolor (pain). - Learning objectives Learning objectives To understand: Normal wound healing and how it can be adversely • affected Types of healing and how to classify wounds • Learning objectives To understand: Normal wound healing and how it can be adversely • affected Types of healing and how to classify wounds • Learning objectives To understand: Normal wound healing and how it can be adversely • affected Types of healing and how to classify wounds • Leg ulcers Leg ulcers 12 In developed countries, the most common chronic wounds It are leg ulcers. An ulcer can be defined as a break in the epithelial continuity . A prolonged inflammatory phase leads to overgrowth of granulation tissue and attempts to heal by scarring leave a fibrotic margin. Necrotic tissue, often at the - ulcer centre, is called slough. The more common aetiologies are listed in Summary box 3.7 . A chronic ulcer that is unresponsive to dressings and simple treatments should be biopsied to rule out neoplastic change, a squamous cell carcinoma known as a Marjolin’s ulcer being the most common. E ff ective treatment of any leg ulcer depends on treating the underlying cause , and diagnosis is therefore vital. Arterial and venous circulation should be assessed, as should sensation throughout the lower limb. Surgical treatment is only indicated if non-operative treatment has failed. Summary box 3.7 Aetiology of leg ulcers /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Vascular (venous, arterial, mixed) Trauma (bites, self-in /f_l icted, burns) Infection (bacterial, fungal, mycobacterial, syphilis) Metabolic disorders (diabetes mellitus, gout, calciphylaxis) Autoimmune disorders (vasculitis, systemic sclerosis, rheumatoid arthritis) Neoplastic (squamous cell carcinoma, basal cell carcinoma) Leg ulcers 12 In developed countries, the most common chronic wounds It are leg ulcers. An ulcer can be defined as a break in the epithelial continuity . A prolonged inflammatory phase leads to overgrowth of granulation tissue and attempts to heal by scarring leave a fibrotic margin. Necrotic tissue, often at the - ulcer centre, is called slough. The more common aetiologies are listed in Summary box 3.7 . A chronic ulcer that is unresponsive to dressings and simple treatments should be biopsied to rule out neoplastic change, a squamous cell carcinoma known as a Marjolin’s ulcer being the most common. E ff ective treatment of any leg ulcer depends on treating the underlying cause , and diagnosis is therefore vital. Arterial and venous circulation should be assessed, as should sensation throughout the lower limb. Surgical treatment is only indicated if non-operative treatment has failed. Summary box 3.7 Aetiology of leg ulcers /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Vascular (venous, arterial, mixed) Trauma (bites, self-in /f_l icted, burns) Infection (bacterial, fungal, mycobacterial, syphilis) Metabolic disorders (diabetes mellitus, gout, calciphylaxis) Autoimmune disorders (vasculitis, systemic sclerosis, rheumatoid arthritis) Neoplastic (squamous cell carcinoma, basal cell carcinoma) Leg ulcers 12 In developed countries, the most common chronic wounds It are leg ulcers. An ulcer can be defined as a break in the epithelial continuity . A prolonged inflammatory phase leads to overgrowth of granulation tissue and attempts to heal by scarring leave a fibrotic margin. Necrotic tissue, often at the - ulcer centre, is called slough. The more common aetiologies are listed in Summary box 3.7 . A chronic ulcer that is unresponsive to dressings and simple treatments should be biopsied to rule out neoplastic change, a squamous cell carcinoma known as a Marjolin’s ulcer being the most common. E ff ective treatment of any leg ulcer depends on treating the underlying cause , and diagnosis is therefore vital. Arterial and venous circulation should be assessed, as should sensation throughout the lower limb. Surgical treatment is only indicated if non-operative treatment has failed. Summary box 3.7 Aetiology of leg ulcers /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Vascular (venous, arterial, mixed) Trauma (bites, self-in /f_l icted, burns) Infection (bacterial, fungal, mycobacterial, syphilis) Metabolic disorders (diabetes mellitus, gout, calciphylaxis) Autoimmune disorders (vasculitis, systemic sclerosis, rheumatoid arthritis) Neoplastic (squamous cell carcinoma, basal cell carcinoma) NORMAL HEALING IN OTHER SPECIFIC TISSUES Bone NORMAL HEALING IN OTHER SPECIFIC TISSUES Bone Bone healing occurs in similar phases to those for skin but with some di ff erences ( Figure 3.3 ). Most fractures heal by callus formation, which involves intramembranous and endo - chondral ossifi cation. This is known as indirect or secondar y bone healing and typically occurs in non-operative fracture management. A haematoma forms at the fracture site and - there is an infl ammatory response. T he fracture haematoma is gradually replaced by a soft callus. This fibrocartilage callus then undergoes endochondral ossifi cation to form hard callus, which is woven bone helping to stabilise the fracture. Intramembranous ossifi cation also occurs directly adjacent to the distal and proximal fracture ends. Hard callus formation is Plasma kallikrein Pre-kallikrein HK Intrinsic pathway HK of coagulation FXII FXIIa (contact system) 2+ Ca FXIa FXI 2+ Ca FIX FIXa FVIIIa FVIII 2+ Ca FXa FX FVa FV Ca FII (Prothrombin) Common pathway of coagulation Figure 3.2 Schematic representation of the coagulation cascade and the /f_i brinolytic system. The coagulation cascade (blue arrows) can be activated during haemostasis via the intrinsic pathway (contact system; red arrows) or the extrinsic pathway (black arrows), which ultimately converge on the common pathway of coagulation. Both pathways lead to the activation of factor X and subsequently of thrombin, which is required for the conversion of /f_i brinogen into /f_i brin and for activation of factor XIII. The /f_i brin clot is cross-linked and stabilised by factor XIII. Fibrinolysis (green arrows) is activated at the same time as the coagulation system but operates more slowly and is important for the regulation of haemostasis. During /f_i brinolysis, plasminogen is converted into plasmin, which degrades the /f_i brin network. Coagulation by ‘F’ followed by a roman numeral; an additional ‘a’ denotes the activated form. HK, high-molecular-weight kininogen; tP activator; uPA, urokinase plasminogen activator. (Adapted with permission from Loof TG, Deicke C, Medina E. The role of coagulation/ /f_i brino lysis during Streptococcus pyogenes infection. Front Cell Infect Microbiol (a) Medullary cavity Fibrocartilage Haematoma Soft callus New blood vessel Periosteum Compact bone Figure 3.3 Common stages of bone healing. (a) callus formation. (c) Hard callus formation from osteoblasts forming woven bone. osteoblasts facilitating the conversion of woven bone into lamellar bone shape. (Adapted with permission from Li J, Kacena MA, Stocum DL. Fracture healing. In: Burr DB, Allen MR (eds). applied bone biology , 2nd edn. London: Academic Press, 2019: 235–53.) Extrinsic pathway of coagulation Tissue factor FVIIa FVII Fibrinolysis uPA,tPA Plasminogen Plasmin Fibrinogen 2+ FIIa Fibrin (Thrombin) Cross-linked Fibrin fibrin clot degradation products FXIIIa FXIII factors are indicated A, tissue plasminogen 2014; 4 : 128. 2014. http://creativecommons.org/licenses/by/4.0/) (b) (c) (d) Spongy bone Bony callus At the fracture site, haematoma formation and in /f_l ammation lead to (b) soft (d) Remodelling proceeds with osteoclasts and and eventually recreating the appropriate anatomical Basic and by lamellar bone. Primary bone healing is a direct bone union process involv ing intramembranous ossifi cation without callus formation. It does not commonly occur in the natural process of healing since it requires fracture ends to be directly apposed and rigidly fi xed with absolute stability . If a gap exists, then secondary healing may lead to delay ed union, non-union or malunion. Primary healing is therefore the aim of open reduction and internal fi xation surgery . (See also Chapter 32 ) . Augustus Volney Waller , 1816–1870, general practitioner of Kensington, London, UK (1842–1851), subsequently worked as a physiologist in Bonn, Germany; Paris, France; Birmingham, UK; and Geneva, Switzerland. Louis Antoine Ranvier , 1835–1922, physician and histologist who was a professor in the College of France, Paris, France Peripheral nerve degeneration and regeneration are - summarised in Figure 3.4 . Distal to nerve injury (neurotmesis), Wallerian degeneration occurs. Proximally , the nerve su ff ers degeneration as far as the nearest node of Ranvier. The regenerating nerve fi bres are attracted to their receptors by neur otropism, which is mediated by growth factors, hormones and the extracellular matrix. Injury of the perineurium and inflammation can lead to neuroma formation, where the disorganised nerve regeneration leads to a painful lump. (a) Normal nerve (b) Wallerian degeneration (c) Phagocytosis and reconstruction (d) Axonal regeneration and remyelination Myelin debris Schwann cell Macrophage Figure 3.4 Schematic diagram illustrating the process of degeneration and regeneration after peripheral nerve injury. When normal nerves (a) suffer a physical injury, the portion of the lesion site and its distal stump undergo destruction and break down to produce myelin debris. This degenerative process is called Wallerian degeneration (b) Schwann cells (SCs) recruit macrophages to scavenge degenerated myelin fragments (c) . Meanwhile, SCs proliferate and migrate alone to the basal lamina to form bands of Büngner, which guide the axon to reinnervate towards the corresponding target (d) . (Adapted from Li R, Li DH, Zhang HY et al . Growth factor-based therapeutic strate gies and their underlying signaling mechanisms for peripheral nerve regeneration. Acta Pharmacol Sin 2020; 41 : 1289–300. 2020. http:// creativecommons.org/licenses/by/4.0/) NORMAL HEALING IN OTHER SPECIFIC TISSUES Bone Bone healing occurs in similar phases to those for skin but with some di ff erences ( Figure 3.3 ). Most fractures heal by callus formation, which involves intramembranous and endo - chondral ossifi cation. This is known as indirect or secondar y bone healing and typically occurs in non-operative fracture management. A haematoma forms at the fracture site and - there is an infl ammatory response. T he fracture haematoma is gradually replaced by a soft callus. This fibrocartilage callus then undergoes endochondral ossifi cation to form hard callus, which is woven bone helping to stabilise the fracture. Intramembranous ossifi cation also occurs directly adjacent to the distal and proximal fracture ends. Hard callus formation is Plasma kallikrein Pre-kallikrein HK Intrinsic pathway HK of coagulation FXII FXIIa (contact system) 2+ Ca FXIa FXI 2+ Ca FIX FIXa FVIIIa FVIII 2+ Ca FXa FX FVa FV Ca FII (Prothrombin) Common pathway of coagulation Figure 3.2 Schematic representation of the coagulation cascade and the /f_i brinolytic system. The coagulation cascade (blue arrows) can be activated during haemostasis via the intrinsic pathway (contact system; red arrows) or the extrinsic pathway (black arrows), which ultimately converge on the common pathway of coagulation. Both pathways lead to the activation of factor X and subsequently of thrombin, which is required for the conversion of /f_i brinogen into /f_i brin and for activation of factor XIII. The /f_i brin clot is cross-linked and stabilised by factor XIII. Fibrinolysis (green arrows) is activated at the same time as the coagulation system but operates more slowly and is important for the regulation of haemostasis. During /f_i brinolysis, plasminogen is converted into plasmin, which degrades the /f_i brin network. Coagulation by ‘F’ followed by a roman numeral; an additional ‘a’ denotes the activated form. HK, high-molecular-weight kininogen; tP activator; uPA, urokinase plasminogen activator. (Adapted with permission from Loof TG, Deicke C, Medina E. The role of coagulation/ /f_i brino lysis during Streptococcus pyogenes infection. Front Cell Infect Microbiol (a) Medullary cavity Fibrocartilage Haematoma Soft callus New blood vessel Periosteum Compact bone Figure 3.3 Common stages of bone healing. (a) callus formation. (c) Hard callus formation from osteoblasts forming woven bone. osteoblasts facilitating the conversion of woven bone into lamellar bone shape. (Adapted with permission from Li J, Kacena MA, Stocum DL. Fracture healing. In: Burr DB, Allen MR (eds). applied bone biology , 2nd edn. London: Academic Press, 2019: 235–53.) Extrinsic pathway of coagulation Tissue factor FVIIa FVII Fibrinolysis uPA,tPA Plasminogen Plasmin Fibrinogen 2+ FIIa Fibrin (Thrombin) Cross-linked Fibrin fibrin clot degradation products FXIIIa FXIII factors are indicated A, tissue plasminogen 2014; 4 : 128. 2014. http://creativecommons.org/licenses/by/4.0/) (b) (c) (d) Spongy bone Bony callus At the fracture site, haematoma formation and in /f_l ammation lead to (b) soft (d) Remodelling proceeds with osteoclasts and and eventually recreating the appropriate anatomical Basic and by lamellar bone. Primary bone healing is a direct bone union process involv ing intramembranous ossifi cation without callus formation. It does not commonly occur in the natural process of healing since it requires fracture ends to be directly apposed and rigidly fi xed with absolute stability . If a gap exists, then secondary healing may lead to delay ed union, non-union or malunion. Primary healing is therefore the aim of open reduction and internal fi xation surgery . (See also Chapter 32 ) . Augustus Volney Waller , 1816–1870, general practitioner of Kensington, London, UK (1842–1851), subsequently worked as a physiologist in Bonn, Germany; Paris, France; Birmingham, UK; and Geneva, Switzerland. Louis Antoine Ranvier , 1835–1922, physician and histologist who was a professor in the College of France, Paris, France Peripheral nerve degeneration and regeneration are - summarised in Figure 3.4 . Distal to nerve injury (neurotmesis), Wallerian degeneration occurs. Proximally , the nerve su ff ers degeneration as far as the nearest node of Ranvier. The regenerating nerve fi bres are attracted to their receptors by neur otropism, which is mediated by growth factors, hormones and the extracellular matrix. Injury of the perineurium and inflammation can lead to neuroma formation, where the disorganised nerve regeneration leads to a painful lump. (a) Normal nerve (b) Wallerian degeneration (c) Phagocytosis and reconstruction (d) Axonal regeneration and remyelination Myelin debris Schwann cell Macrophage Figure 3.4 Schematic diagram illustrating the process of degeneration and regeneration after peripheral nerve injury. When normal nerves (a) suffer a physical injury, the portion of the lesion site and its distal stump undergo destruction and break down to produce myelin debris. This degenerative process is called Wallerian degeneration (b) Schwann cells (SCs) recruit macrophages to scavenge degenerated myelin fragments (c) . Meanwhile, SCs proliferate and migrate alone to the basal lamina to form bands of Büngner, which guide the axon to reinnervate towards the corresponding target (d) . (Adapted from Li R, Li DH, Zhang HY et al . Growth factor-based therapeutic strate gies and their underlying signaling mechanisms for peripheral nerve regeneration. Acta Pharmacol Sin 2020; 41 : 1289–300. 2020. http:// creativecommons.org/licenses/by/4.0/) NORMAL HEALING IN OTHER SPECIFIC TISSUES Bone Bone healing occurs in similar phases to those for skin but with some di ff erences ( Figure 3.3 ). Most fractures heal by callus formation, which involves intramembranous and endo - chondral ossifi cation. This is known as indirect or secondar y bone healing and typically occurs in non-operative fracture management. A haematoma forms at the fracture site and - there is an infl ammatory response. T he fracture haematoma is gradually replaced by a soft callus. This fibrocartilage callus then undergoes endochondral ossifi cation to form hard callus, which is woven bone helping to stabilise the fracture. Intramembranous ossifi cation also occurs directly adjacent to the distal and proximal fracture ends. Hard callus formation is Plasma kallikrein Pre-kallikrein HK Intrinsic pathway HK of coagulation FXII FXIIa (contact system) 2+ Ca FXIa FXI 2+ Ca FIX FIXa FVIIIa FVIII 2+ Ca FXa FX FVa FV Ca FII (Prothrombin) Common pathway of coagulation Figure 3.2 Schematic representation of the coagulation cascade and the /f_i brinolytic system. The coagulation cascade (blue arrows) can be activated during haemostasis via the intrinsic pathway (contact system; red arrows) or the extrinsic pathway (black arrows), which ultimately converge on the common pathway of coagulation. Both pathways lead to the activation of factor X and subsequently of thrombin, which is required for the conversion of /f_i brinogen into /f_i brin and for activation of factor XIII. The /f_i brin clot is cross-linked and stabilised by factor XIII. Fibrinolysis (green arrows) is activated at the same time as the coagulation system but operates more slowly and is important for the regulation of haemostasis. During /f_i brinolysis, plasminogen is converted into plasmin, which degrades the /f_i brin network. Coagulation by ‘F’ followed by a roman numeral; an additional ‘a’ denotes the activated form. HK, high-molecular-weight kininogen; tP activator; uPA, urokinase plasminogen activator. (Adapted with permission from Loof TG, Deicke C, Medina E. The role of coagulation/ /f_i brino lysis during Streptococcus pyogenes infection. Front Cell Infect Microbiol (a) Medullary cavity Fibrocartilage Haematoma Soft callus New blood vessel Periosteum Compact bone Figure 3.3 Common stages of bone healing. (a) callus formation. (c) Hard callus formation from osteoblasts forming woven bone. osteoblasts facilitating the conversion of woven bone into lamellar bone shape. (Adapted with permission from Li J, Kacena MA, Stocum DL. Fracture healing. In: Burr DB, Allen MR (eds). applied bone biology , 2nd edn. London: Academic Press, 2019: 235–53.) Extrinsic pathway of coagulation Tissue factor FVIIa FVII Fibrinolysis uPA,tPA Plasminogen Plasmin Fibrinogen 2+ FIIa Fibrin (Thrombin) Cross-linked Fibrin fibrin clot degradation products FXIIIa FXIII factors are indicated A, tissue plasminogen 2014; 4 : 128. 2014. http://creativecommons.org/licenses/by/4.0/) (b) (c) (d) Spongy bone Bony callus At the fracture site, haematoma formation and in /f_l ammation lead to (b) soft (d) Remodelling proceeds with osteoclasts and and eventually recreating the appropriate anatomical Basic and by lamellar bone. Primary bone healing is a direct bone union process involv ing intramembranous ossifi cation without callus formation. It does not commonly occur in the natural process of healing since it requires fracture ends to be directly apposed and rigidly fi xed with absolute stability . If a gap exists, then secondary healing may lead to delay ed union, non-union or malunion. Primary healing is therefore the aim of open reduction and internal fi xation surgery . (See also Chapter 32 ) . Augustus Volney Waller , 1816–1870, general practitioner of Kensington, London, UK (1842–1851), subsequently worked as a physiologist in Bonn, Germany; Paris, France; Birmingham, UK; and Geneva, Switzerland. Louis Antoine Ranvier , 1835–1922, physician and histologist who was a professor in the College of France, Paris, France Peripheral nerve degeneration and regeneration are - summarised in Figure 3.4 . Distal to nerve injury (neurotmesis), Wallerian degeneration occurs. Proximally , the nerve su ff ers degeneration as far as the nearest node of Ranvier. The regenerating nerve fi bres are attracted to their receptors by neur otropism, which is mediated by growth factors, hormones and the extracellular matrix. Injury of the perineurium and inflammation can lead to neuroma formation, where the disorganised nerve regeneration leads to a painful lump. (a) Normal nerve (b) Wallerian degeneration (c) Phagocytosis and reconstruction (d) Axonal regeneration and remyelination Myelin debris Schwann cell Macrophage Figure 3.4 Schematic diagram illustrating the process of degeneration and regeneration after peripheral nerve injury. When normal nerves (a) suffer a physical injury, the portion of the lesion site and its distal stump undergo destruction and break down to produce myelin debris. This degenerative process is called Wallerian degeneration (b) Schwann cells (SCs) recruit macrophages to scavenge degenerated myelin fragments (c) . Meanwhile, SCs proliferate and migrate alone to the basal lamina to form bands of Büngner, which guide the axon to reinnervate towards the corresponding target (d) . (Adapted from Li R, Li DH, Zhang HY et al . Growth factor-based therapeutic strate gies and their underlying signaling mechanisms for peripheral nerve regeneration. Acta Pharmacol Sin 2020; 41 : 1289–300. 2020. http:// creativecommons.org/licenses/by/4.0/) NORMAL WOUND HEALING IN SKIN NORMAL WOUND HEALING IN SKIN Classically , wound healing has been arbitrarily described in three overlapping but distinct stages, including inflammation, proliferation and remodelling ( Figure 3.1 ). An additional stage, haemostasis, is often described as the immediate phase occurring before inflammation. NORMAL WOUND HEALING IN SKIN Classically , wound healing has been arbitrarily described in three overlapping but distinct stages, including inflammation, proliferation and remodelling ( Figure 3.1 ). An additional stage, haemostasis, is often described as the immediate phase occurring before inflammation. NORMAL WOUND HEALING IN SKIN Classically , wound healing has been arbitrarily described in three overlapping but distinct stages, including inflammation, proliferation and remodelling ( Figure 3.1 ). An additional stage, haemostasis, is often described as the immediate phase occurring before inflammation. Necrotising fasciitis Necrotising fasciitis This is a severe, rapidly progressing infection of the soft tissue and fascia associated with signifi cant morbidity and mortality ( Figure 3.14 ). Reported mortality rates vary widely but a Danish nationwide cohort study including over 1500 patients found 30-day and 1-year mortality rates of up to 26% and 10 40%, respectively . The infection is commonly polymicrobial but monomicrobial presentation with Streptococcus pyogenes (group A streptococcus) is also frequent. Examples of other organisms include Staphylococcus aureus , Escherichia coli , Pseudo monas , Clostridium and Bacteroides . There is usually a history of trauma or surgery with wound contamination. Diabetes mellitus is the most common comor bidity , although up to 30% of patients may not have any 10,11 comorbidities. Clinical features are shown in Summary box 3.6 . A scoring system to aid clinical decision making has been developed, but its performance remains questionable. remains primarily a clinical diagnosis and surgical treatment should not be delayed if suspicion is high. Treatment consists of appropriate intravenous antibiotics with urgent radical surgical debridement. A second look opera tion is usually planned in 24–48 hours depending on clinical response. Multiple debridements may be required. Summary box 3.6 Signs and symptoms of necrotising fasciitis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Figure 3.14 Necrotising fasciitis of the anterior abdominal wall. Local Unusual pain Erythema, oedema, warmth Crepitus Blisters, bullae Greyish drainage (‘dishwater pus’) Fixed staining Necrosis, gangrene Systemic Fever, tachycardia, tachypnoea Shock Coagulopathy Multiorgan failure Necrotising fasciitis This is a severe, rapidly progressing infection of the soft tissue and fascia associated with signifi cant morbidity and mortality ( Figure 3.14 ). Reported mortality rates vary widely but a Danish nationwide cohort study including over 1500 patients found 30-day and 1-year mortality rates of up to 26% and 10 40%, respectively . The infection is commonly polymicrobial but monomicrobial presentation with Streptococcus pyogenes (group A streptococcus) is also frequent. Examples of other organisms include Staphylococcus aureus , Escherichia coli , Pseudo monas , Clostridium and Bacteroides . There is usually a history of trauma or surgery with wound contamination. Diabetes mellitus is the most common comor bidity , although up to 30% of patients may not have any 10,11 comorbidities. Clinical features are shown in Summary box 3.6 . A scoring system to aid clinical decision making has been developed, but its performance remains questionable. remains primarily a clinical diagnosis and surgical treatment should not be delayed if suspicion is high. Treatment consists of appropriate intravenous antibiotics with urgent radical surgical debridement. A second look opera tion is usually planned in 24–48 hours depending on clinical response. Multiple debridements may be required. Summary box 3.6 Signs and symptoms of necrotising fasciitis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Figure 3.14 Necrotising fasciitis of the anterior abdominal wall. Local Unusual pain Erythema, oedema, warmth Crepitus Blisters, bullae Greyish drainage (‘dishwater pus’) Fixed staining Necrosis, gangrene Systemic Fever, tachycardia, tachypnoea Shock Coagulopathy Multiorgan failure Necrotising fasciitis This is a severe, rapidly progressing infection of the soft tissue and fascia associated with signifi cant morbidity and mortality ( Figure 3.14 ). Reported mortality rates vary widely but a Danish nationwide cohort study including over 1500 patients found 30-day and 1-year mortality rates of up to 26% and 10 40%, respectively . The infection is commonly polymicrobial but monomicrobial presentation with Streptococcus pyogenes (group A streptococcus) is also frequent. Examples of other organisms include Staphylococcus aureus , Escherichia coli , Pseudo monas , Clostridium and Bacteroides . There is usually a history of trauma or surgery with wound contamination. Diabetes mellitus is the most common comor bidity , although up to 30% of patients may not have any 10,11 comorbidities. Clinical features are shown in Summary box 3.6 . A scoring system to aid clinical decision making has been developed, but its performance remains questionable. remains primarily a clinical diagnosis and surgical treatment should not be delayed if suspicion is high. Treatment consists of appropriate intravenous antibiotics with urgent radical surgical debridement. A second look opera tion is usually planned in 24–48 hours depending on clinical response. Multiple debridements may be required. Summary box 3.6 Signs and symptoms of necrotising fasciitis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Figure 3.14 Necrotising fasciitis of the anterior abdominal wall. Local Unusual pain Erythema, oedema, warmth Crepitus Blisters, bullae Greyish drainage (‘dishwater pus’) Fixed staining Necrosis, gangrene Systemic Fever, tachycardia, tachypnoea Shock Coagulopathy Multiorgan failure Post exposure management for Tetanus Prone Wounds Post exposure management for Tetanus Prone Wounds underappreciated and is not as simple as is often perceived. The end points of surgical debridement can sometimes be di ffi cult to determine. Healthy subcutaneous fat is yellow and soft. Muscle viability is judged by its colour, capacity to bleed and contractility . Contaminated, complex and complicated wounds often requir e more than one surgical debridement before definitive repair and closure; for example, blast injuries and necrotising fasciitis (see Part 4 ). Other types of debridement are summarised in Table 3.4 . All wounds should be irrigated at the first available oppor- tunity to reduce bacterial contamination. This also allows bet - ter visualisation for wound assessment. W arm normal saline Immunisation Status Clean wound Those aged 11 years and over , who have received 1 with an adequate priming course of tetanus vaccine the last dose within 10 years None required Children aged 5-10 years who have received priming course and pre-school booster Children under 5 years who have received an adequate priming course Received adequate priming course of tetanus 3 vaccine but last dose more than 10 years ago None required Children aged 5-10 years who have received an adequate priming course but no pre-school booster (Includes UK born after 1961 with history of accepting vaccinations) Immediate Not received adequate priming course 3 of tetanus vaccine reinforcing (Includes uncertain immunisation status and/or born before 1961) dose of vaccine 1 Clean wounds are de /f_i ned as wounds less than six 3 At least three doses of tetanus vaccine at Patients who are severely hours old, non-penetrating with negligible tissue appropriate intervals. This de /f_i nition of “adequate immunosuppressed may not be adequately damage. course” is for risk assessment of tetanus-prone protected against tetanus, despite having wounds only. The full UK schedule is /f_i ve doses been fully immunised and additional booster 2 If TIG is not available, HNIG may be used as an of tetanus containing vaccine. alternative. Figure 3.6 Postexposure management for tetanus-prone wounds. (Redrawn with permission from https://www.gov.uk/government/publica tions/tetanus-prone-wounds-posters. © Crown copyright 2019. 2019TET02 10K OCT 2019 (APS). TABLE 3.4 Types of debridement. Excision of non-viable tissue using surgical Surgical instruments such as a scalpel, curette, scissors or rongeur until healthy bleeding occurs at the wound edges Non-selective debridement such as using irrigation, Mechanical wet-to-dry dressings and hydrotherapy. Both non viable and viable tissue may be removed Using dressings such as hydrocolloids or Autolytic transparent /f_i lms to retain moisture and allow wound enzymes to selectively liquefy non-viable tissue Chemically liquefy necrotic tissue with enzymes Enzymatic using topical agents such as collagenase or papain– urea Medical-grade larvae of Lucilia sericata r elease Biological proteolytic and antimicr obial substances to remove necr otic tissue. They also directly promote wound healing Immediate treatment Later treatment 1 Tetanus prone High risk tetanus prone None required None required Further doses as required to complete the recommended Immediate One dose of Immediate reinforcing schedule (to reinforcing human tetanus 2 dose of vaccine ensure future dose of immunoglobulin immunity) in a different site vaccine Immediate One dose of Immediate One dose of reinforcing human tetanus reinforcing human tetanus 2 2 dose of immunoglobulin dose of immunoglobulin in a different site vaccine in a different site vaccine doses or treatment may be required. Figure 3.7 Meshing a split-thickness skin graft. (Reproduced with per- mission of MA Healthcare Limited from Hili S, Wong KY , Stephens /uni00A0 P . Pretibial lacerations. Br J Hosp Med 2017; 78 : C162–6.) such as water and antiseptic solutions. Irrigation can also be performed with a soft brush or sponge to clear particulate mat ter prior to preoperative application of skin antiseptic prepa ration. Wounds should be explored to determine the extent of injury , including any damage to underlying neurovascular structures, tendons, joints and bones. Careful tissue handling and meticulous technique are important throughout. Repair of all damaged structures may be attempted once the wounds are clean. Repair of nerves and vessels should be performed under magnification using loupes or a microscope. Skin closure should always be without tension. Direct clo sure is not always possible and other reconstruction methods should be considered. Historically , the reconstructive ladder 8 and its variants such as the reconstructive elevator have been used as a framework to consider the simplest means to achieve wound closure for the desired goal. Advances in technology and surgical techniques have led to ongoing adjustments of these frameworks. Although these frameworks do not guide the useful reminder of the options available ( Summary box 3.4 ). - A skin graft has no inherent b lood supply and is dependent - on a well-vascularised recipient site for survival and wound healing. Split-thickness skin grafts ( Figur e 3.7 ) consist of the epidermis and a small portion of dermis whereas full-thickness skin grafts consist of the epidermis and the majority of the dermis. A flap contains tissue with its intrinsic blood supply that is transferred from one part of the body (donor) to another (recipient). The blood supply of the flap therefore does not rely on the recipient site like a skin graft. A free flap contains - tissue with its vascular pedicle that is surgically detached and transferred from its original location to a distant recipient site ( Figure 3.8 ). A microscope is used to perform microvascular anastomoses to connect the blood vessels in the free flap to blood vessels close to the recipient site. Since its development in the 1990s, negative-pressure wound therapy (NPWT) is now widely used. It is not a replace - ment for definitive wound closure but is a useful adjunct (a) (b) Figure 3.8 Left mastectomy (a, b) and delayed left breast reconstruction with a deep inferior epigastric artery perforator free /f_l ap and nipple reconstruction (c) (d) (c, d) (©Addenbrookes Hospital). ( Figure 3.9 ). Negative pressure helps draw the wound edges together, remove exudate, reduce oedema and promote gran ulation tissue formation. NPWT is not recommended in the setting of exposed vessels, malignancy , untreated osteomyelitis, necrotic tissue or non-enteric and unexplored fistulae. Figure 3.9 Negative-pressure wound therapy for a lower limb wound. (Reproduced with permission of MA Healthcare Limited from Hili S, Wong KY , Stephens P . Pretibial lacerations. Br J Hosp Med 2017; C162–6.) Figure 3.10 Degloving injury of the right little and ring /f_i ngers. Post exposure management for Tetanus Prone Wounds underappreciated and is not as simple as is often perceived. The end points of surgical debridement can sometimes be di ffi cult to determine. Healthy subcutaneous fat is yellow and soft. Muscle viability is judged by its colour, capacity to bleed and contractility . Contaminated, complex and complicated wounds often requir e more than one surgical debridement before definitive repair and closure; for example, blast injuries and necrotising fasciitis (see Part 4 ). Other types of debridement are summarised in Table 3.4 . All wounds should be irrigated at the first available oppor- tunity to reduce bacterial contamination. This also allows bet - ter visualisation for wound assessment. W arm normal saline Immunisation Status Clean wound Those aged 11 years and over , who have received 1 with an adequate priming course of tetanus vaccine the last dose within 10 years None required Children aged 5-10 years who have received priming course and pre-school booster Children under 5 years who have received an adequate priming course Received adequate priming course of tetanus 3 vaccine but last dose more than 10 years ago None required Children aged 5-10 years who have received an adequate priming course but no pre-school booster (Includes UK born after 1961 with history of accepting vaccinations) Immediate Not received adequate priming course 3 of tetanus vaccine reinforcing (Includes uncertain immunisation status and/or born before 1961) dose of vaccine 1 Clean wounds are de /f_i ned as wounds less than six 3 At least three doses of tetanus vaccine at Patients who are severely hours old, non-penetrating with negligible tissue appropriate intervals. This de /f_i nition of “adequate immunosuppressed may not be adequately damage. course” is for risk assessment of tetanus-prone protected against tetanus, despite having wounds only. The full UK schedule is /f_i ve doses been fully immunised and additional booster 2 If TIG is not available, HNIG may be used as an of tetanus containing vaccine. alternative. Figure 3.6 Postexposure management for tetanus-prone wounds. (Redrawn with permission from https://www.gov.uk/government/publica tions/tetanus-prone-wounds-posters. © Crown copyright 2019. 2019TET02 10K OCT 2019 (APS). TABLE 3.4 Types of debridement. Excision of non-viable tissue using surgical Surgical instruments such as a scalpel, curette, scissors or rongeur until healthy bleeding occurs at the wound edges Non-selective debridement such as using irrigation, Mechanical wet-to-dry dressings and hydrotherapy. Both non viable and viable tissue may be removed Using dressings such as hydrocolloids or Autolytic transparent /f_i lms to retain moisture and allow wound enzymes to selectively liquefy non-viable tissue Chemically liquefy necrotic tissue with enzymes Enzymatic using topical agents such as collagenase or papain– urea Medical-grade larvae of Lucilia sericata r elease Biological proteolytic and antimicr obial substances to remove necr otic tissue. They also directly promote wound healing Immediate treatment Later treatment 1 Tetanus prone High risk tetanus prone None required None required Further doses as required to complete the recommended Immediate One dose of Immediate reinforcing schedule (to reinforcing human tetanus 2 dose of vaccine ensure future dose of immunoglobulin immunity) in a different site vaccine Immediate One dose of Immediate One dose of reinforcing human tetanus reinforcing human tetanus 2 2 dose of immunoglobulin dose of immunoglobulin in a different site vaccine in a different site vaccine doses or treatment may be required. Figure 3.7 Meshing a split-thickness skin graft. (Reproduced with per- mission of MA Healthcare Limited from Hili S, Wong KY , Stephens /uni00A0 P . Pretibial lacerations. Br J Hosp Med 2017; 78 : C162–6.) such as water and antiseptic solutions. Irrigation can also be performed with a soft brush or sponge to clear particulate mat ter prior to preoperative application of skin antiseptic prepa ration. Wounds should be explored to determine the extent of injury , including any damage to underlying neurovascular structures, tendons, joints and bones. Careful tissue handling and meticulous technique are important throughout. Repair of all damaged structures may be attempted once the wounds are clean. Repair of nerves and vessels should be performed under magnification using loupes or a microscope. Skin closure should always be without tension. Direct clo sure is not always possible and other reconstruction methods should be considered. Historically , the reconstructive ladder 8 and its variants such as the reconstructive elevator have been used as a framework to consider the simplest means to achieve wound closure for the desired goal. Advances in technology and surgical techniques have led to ongoing adjustments of these frameworks. Although these frameworks do not guide the useful reminder of the options available ( Summary box 3.4 ). - A skin graft has no inherent b lood supply and is dependent - on a well-vascularised recipient site for survival and wound healing. Split-thickness skin grafts ( Figur e 3.7 ) consist of the epidermis and a small portion of dermis whereas full-thickness skin grafts consist of the epidermis and the majority of the dermis. A flap contains tissue with its intrinsic blood supply that is transferred from one part of the body (donor) to another (recipient). The blood supply of the flap therefore does not rely on the recipient site like a skin graft. A free flap contains - tissue with its vascular pedicle that is surgically detached and transferred from its original location to a distant recipient site ( Figure 3.8 ). A microscope is used to perform microvascular anastomoses to connect the blood vessels in the free flap to blood vessels close to the recipient site. Since its development in the 1990s, negative-pressure wound therapy (NPWT) is now widely used. It is not a replace - ment for definitive wound closure but is a useful adjunct (a) (b) Figure 3.8 Left mastectomy (a, b) and delayed left breast reconstruction with a deep inferior epigastric artery perforator free /f_l ap and nipple reconstruction (c) (d) (c, d) (©Addenbrookes Hospital). ( Figure 3.9 ). Negative pressure helps draw the wound edges together, remove exudate, reduce oedema and promote gran ulation tissue formation. NPWT is not recommended in the setting of exposed vessels, malignancy , untreated osteomyelitis, necrotic tissue or non-enteric and unexplored fistulae. Figure 3.9 Negative-pressure wound therapy for a lower limb wound. (Reproduced with permission of MA Healthcare Limited from Hili S, Wong KY , Stephens P . Pretibial lacerations. Br J Hosp Med 2017; C162–6.) Figure 3.10 Degloving injury of the right little and ring /f_i ngers. Post exposure management for Tetanus Prone Wounds underappreciated and is not as simple as is often perceived. The end points of surgical debridement can sometimes be di ffi cult to determine. Healthy subcutaneous fat is yellow and soft. Muscle viability is judged by its colour, capacity to bleed and contractility . Contaminated, complex and complicated wounds often requir e more than one surgical debridement before definitive repair and closure; for example, blast injuries and necrotising fasciitis (see Part 4 ). Other types of debridement are summarised in Table 3.4 . All wounds should be irrigated at the first available oppor- tunity to reduce bacterial contamination. This also allows bet - ter visualisation for wound assessment. W arm normal saline Immunisation Status Clean wound Those aged 11 years and over , who have received 1 with an adequate priming course of tetanus vaccine the last dose within 10 years None required Children aged 5-10 years who have received priming course and pre-school booster Children under 5 years who have received an adequate priming course Received adequate priming course of tetanus 3 vaccine but last dose more than 10 years ago None required Children aged 5-10 years who have received an adequate priming course but no pre-school booster (Includes UK born after 1961 with history of accepting vaccinations) Immediate Not received adequate priming course 3 of tetanus vaccine reinforcing (Includes uncertain immunisation status and/or born before 1961) dose of vaccine 1 Clean wounds are de /f_i ned as wounds less than six 3 At least three doses of tetanus vaccine at Patients who are severely hours old, non-penetrating with negligible tissue appropriate intervals. This de /f_i nition of “adequate immunosuppressed may not be adequately damage. course” is for risk assessment of tetanus-prone protected against tetanus, despite having wounds only. The full UK schedule is /f_i ve doses been fully immunised and additional booster 2 If TIG is not available, HNIG may be used as an of tetanus containing vaccine. alternative. Figure 3.6 Postexposure management for tetanus-prone wounds. (Redrawn with permission from https://www.gov.uk/government/publica tions/tetanus-prone-wounds-posters. © Crown copyright 2019. 2019TET02 10K OCT 2019 (APS). TABLE 3.4 Types of debridement. Excision of non-viable tissue using surgical Surgical instruments such as a scalpel, curette, scissors or rongeur until healthy bleeding occurs at the wound edges Non-selective debridement such as using irrigation, Mechanical wet-to-dry dressings and hydrotherapy. Both non viable and viable tissue may be removed Using dressings such as hydrocolloids or Autolytic transparent /f_i lms to retain moisture and allow wound enzymes to selectively liquefy non-viable tissue Chemically liquefy necrotic tissue with enzymes Enzymatic using topical agents such as collagenase or papain– urea Medical-grade larvae of Lucilia sericata r elease Biological proteolytic and antimicr obial substances to remove necr otic tissue. They also directly promote wound healing Immediate treatment Later treatment 1 Tetanus prone High risk tetanus prone None required None required Further doses as required to complete the recommended Immediate One dose of Immediate reinforcing schedule (to reinforcing human tetanus 2 dose of vaccine ensure future dose of immunoglobulin immunity) in a different site vaccine Immediate One dose of Immediate One dose of reinforcing human tetanus reinforcing human tetanus 2 2 dose of immunoglobulin dose of immunoglobulin in a different site vaccine in a different site vaccine doses or treatment may be required. Figure 3.7 Meshing a split-thickness skin graft. (Reproduced with per- mission of MA Healthcare Limited from Hili S, Wong KY , Stephens /uni00A0 P . Pretibial lacerations. Br J Hosp Med 2017; 78 : C162–6.) such as water and antiseptic solutions. Irrigation can also be performed with a soft brush or sponge to clear particulate mat ter prior to preoperative application of skin antiseptic prepa ration. Wounds should be explored to determine the extent of injury , including any damage to underlying neurovascular structures, tendons, joints and bones. Careful tissue handling and meticulous technique are important throughout. Repair of all damaged structures may be attempted once the wounds are clean. Repair of nerves and vessels should be performed under magnification using loupes or a microscope. Skin closure should always be without tension. Direct clo sure is not always possible and other reconstruction methods should be considered. Historically , the reconstructive ladder 8 and its variants such as the reconstructive elevator have been used as a framework to consider the simplest means to achieve wound closure for the desired goal. Advances in technology and surgical techniques have led to ongoing adjustments of these frameworks. Although these frameworks do not guide the useful reminder of the options available ( Summary box 3.4 ). - A skin graft has no inherent b lood supply and is dependent - on a well-vascularised recipient site for survival and wound healing. Split-thickness skin grafts ( Figur e 3.7 ) consist of the epidermis and a small portion of dermis whereas full-thickness skin grafts consist of the epidermis and the majority of the dermis. A flap contains tissue with its intrinsic blood supply that is transferred from one part of the body (donor) to another (recipient). The blood supply of the flap therefore does not rely on the recipient site like a skin graft. A free flap contains - tissue with its vascular pedicle that is surgically detached and transferred from its original location to a distant recipient site ( Figure 3.8 ). A microscope is used to perform microvascular anastomoses to connect the blood vessels in the free flap to blood vessels close to the recipient site. Since its development in the 1990s, negative-pressure wound therapy (NPWT) is now widely used. It is not a replace - ment for definitive wound closure but is a useful adjunct (a) (b) Figure 3.8 Left mastectomy (a, b) and delayed left breast reconstruction with a deep inferior epigastric artery perforator free /f_l ap and nipple reconstruction (c) (d) (c, d) (©Addenbrookes Hospital). ( Figure 3.9 ). Negative pressure helps draw the wound edges together, remove exudate, reduce oedema and promote gran ulation tissue formation. NPWT is not recommended in the setting of exposed vessels, malignancy , untreated osteomyelitis, necrotic tissue or non-enteric and unexplored fistulae. Figure 3.9 Negative-pressure wound therapy for a lower limb wound. (Reproduced with permission of MA Healthcare Limited from Hili S, Wong KY , Stephens P . Pretibial lacerations. Br J Hosp Med 2017; C162–6.) Figure 3.10 Degloving injury of the right little and ring /f_i ngers. Pressure ulcers Pressure ulcers Pressure ulcers occur over a bony prominence or under a medical or other device ( Figure 3.15 ) . A number of similar classifications exist. The US National Pressure Injury Advisory injury’ in its staging system ( Table 3.5 ) to provide a more accurate description of injuries to both intact and ulcerated 13 skin. Pressure injuries should be regarded as preventable. There is a higher incidence in those who are severely ill, those who have impaired mobility or those with a significant loss of sensa tion. The most common sites are listed in Summary box 3.8 Summary box 3.8 Common sites for pressure injuries and ulcers /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Prevention starts with assessing risk using a validated score to support clinical judgement such as the Braden scale, Waterlow score or Norton risk assessment scale. Patients at risk of developing pressure injuries should have a skin assessment, regular repositioning every 2–4 hours and the use of pressure- redistributing devices as appropriate. Patients should receive education on self-care and risk factors need to be addressed, such as providing nutritional support for any deficiencies. The treatment of pressure ulcers should focus on patient optimisation especially any aspects of poor nutrition and ongoing poorly managed medical problems to address any risk factors. Preventative measures are used and debridement ma y be appropriate ( Table 3.4 ). Dressings should be chosen to create an optimum wound-healing environment and appropri ate antibiotics given if there are signs of infection. Surgery is not first-line treatment and is only considered when the above measures have been fully implemented. Patients must also be well motivated and able to fully comply with postoperativ ventative measures. Surgical management of pressure sores follows some of the same principles described for wound management in Table 3.2 Barbara Braden , contemporary , developed the Braden scale with Nancy Bergstrom in 1987. Judy Waterlow , contemporary , developed the Waterlow score in 1985. Doreen Norton , 1922–2007, nur se, developed the Norton risk assessment scale in 1962. are likely to fail. In suitable patients, successful reconstruction options include the use of large fasciocutaneous or m usculocu - taneous flaps. If possible, use a flap that can be advanced fur - ther if there is recur rence and that does not interfere with the planning of neighbouring flaps that may be used in the future. - . TABLE 3.5 US National Pressure Injury Advisory Panel 13 staging of pressure injuries. Stage Description 1 Non-blanchable erythema of intact skin 2 Partial-thickness skin loss with exposed dermis 3 Full-thickness skin loss 4 Full-thickness skin and tissue loss Obscured full-thickness skin and tissue Unstageable full- loss thickness pressure injury Deep tissue pressure Persistent non-blanchable, deep red, injury maroon or purple discoloration Ischium Heel Greater trochanter Malleolus Sacrum Occiput Pressure ulcers Pressure ulcers occur over a bony prominence or under a medical or other device ( Figure 3.15 ) . A number of similar classifications exist. The US National Pressure Injury Advisory injury’ in its staging system ( Table 3.5 ) to provide a more accurate description of injuries to both intact and ulcerated 13 skin. Pressure injuries should be regarded as preventable. There is a higher incidence in those who are severely ill, those who have impaired mobility or those with a significant loss of sensa tion. The most common sites are listed in Summary box 3.8 Summary box 3.8 Common sites for pressure injuries and ulcers /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Prevention starts with assessing risk using a validated score to support clinical judgement such as the Braden scale, Waterlow score or Norton risk assessment scale. Patients at risk of developing pressure injuries should have a skin assessment, regular repositioning every 2–4 hours and the use of pressure- redistributing devices as appropriate. Patients should receive education on self-care and risk factors need to be addressed, such as providing nutritional support for any deficiencies. The treatment of pressure ulcers should focus on patient optimisation especially any aspects of poor nutrition and ongoing poorly managed medical problems to address any risk factors. Preventative measures are used and debridement ma y be appropriate ( Table 3.4 ). Dressings should be chosen to create an optimum wound-healing environment and appropri ate antibiotics given if there are signs of infection. Surgery is not first-line treatment and is only considered when the above measures have been fully implemented. Patients must also be well motivated and able to fully comply with postoperativ ventative measures. Surgical management of pressure sores follows some of the same principles described for wound management in Table 3.2 Barbara Braden , contemporary , developed the Braden scale with Nancy Bergstrom in 1987. Judy Waterlow , contemporary , developed the Waterlow score in 1985. Doreen Norton , 1922–2007, nur se, developed the Norton risk assessment scale in 1962. are likely to fail. In suitable patients, successful reconstruction options include the use of large fasciocutaneous or m usculocu - taneous flaps. If possible, use a flap that can be advanced fur - ther if there is recur rence and that does not interfere with the planning of neighbouring flaps that may be used in the future. - . TABLE 3.5 US National Pressure Injury Advisory Panel 13 staging of pressure injuries. Stage Description 1 Non-blanchable erythema of intact skin 2 Partial-thickness skin loss with exposed dermis 3 Full-thickness skin loss 4 Full-thickness skin and tissue loss Obscured full-thickness skin and tissue Unstageable full- loss thickness pressure injury Deep tissue pressure Persistent non-blanchable, deep red, injury maroon or purple discoloration Ischium Heel Greater trochanter Malleolus Sacrum Occiput Pressure ulcers Pressure ulcers occur over a bony prominence or under a medical or other device ( Figure 3.15 ) . A number of similar classifications exist. The US National Pressure Injury Advisory injury’ in its staging system ( Table 3.5 ) to provide a more accurate description of injuries to both intact and ulcerated 13 skin. Pressure injuries should be regarded as preventable. There is a higher incidence in those who are severely ill, those who have impaired mobility or those with a significant loss of sensa tion. The most common sites are listed in Summary box 3.8 Summary box 3.8 Common sites for pressure injuries and ulcers /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Prevention starts with assessing risk using a validated score to support clinical judgement such as the Braden scale, Waterlow score or Norton risk assessment scale. Patients at risk of developing pressure injuries should have a skin assessment, regular repositioning every 2–4 hours and the use of pressure- redistributing devices as appropriate. Patients should receive education on self-care and risk factors need to be addressed, such as providing nutritional support for any deficiencies. The treatment of pressure ulcers should focus on patient optimisation especially any aspects of poor nutrition and ongoing poorly managed medical problems to address any risk factors. Preventative measures are used and debridement ma y be appropriate ( Table 3.4 ). Dressings should be chosen to create an optimum wound-healing environment and appropri ate antibiotics given if there are signs of infection. Surgery is not first-line treatment and is only considered when the above measures have been fully implemented. Patients must also be well motivated and able to fully comply with postoperativ ventative measures. Surgical management of pressure sores follows some of the same principles described for wound management in Table 3.2 Barbara Braden , contemporary , developed the Braden scale with Nancy Bergstrom in 1987. Judy Waterlow , contemporary , developed the Waterlow score in 1985. Doreen Norton , 1922–2007, nur se, developed the Norton risk assessment scale in 1962. are likely to fail. In suitable patients, successful reconstruction options include the use of large fasciocutaneous or m usculocu - taneous flaps. If possible, use a flap that can be advanced fur - ther if there is recur rence and that does not interfere with the planning of neighbouring flaps that may be used in the future. - . TABLE 3.5 US National Pressure Injury Advisory Panel 13 staging of pressure injuries. Stage Description 1 Non-blanchable erythema of intact skin 2 Partial-thickness skin loss with exposed dermis 3 Full-thickness skin loss 4 Full-thickness skin and tissue loss Obscured full-thickness skin and tissue Unstageable full- loss thickness pressure injury Deep tissue pressure Persistent non-blanchable, deep red, injury maroon or purple discoloration Ischium Heel Greater trochanter Malleolus Sacrum Occiput Principles Principles Clinical judgement is crucial in managing wounds. Some general principles of wound management are summarised in Table 3.2 . Antibiotic prophylaxis is needed for clean–contam - inated, contaminated and dirty wounds. It may also be used in clean wounds when there is a high risk of infection or when the sequelae of infection are potentially disastrous. Tetanus prophylaxis should be given based on the type of wound ( T able 3.3 ) and immunisation status ( Figure 3.6 ). ). - /uni25CF - /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - Debridement is essential to remove any devitalised tissue and foreign material from the wound. Non-viable tissue - must be excised until healthy bleeding occurs at the wound edges. The importance of thorough debridement is often TABLE 3.2 Principles of wound management. Preparation Antibiotic prophylaxis Tetanus prophylaxis Adequate analgesia/anaesthesia Wound irrigation Wound Early debridement and irrigation Exploration Repair structures Haemostasis Closure Skin closure without tension Consider reconstruction options Suture choice Consider drains Optimal dressings Follow-up Removal of sutures/splints Physiotherapy Monitoring for complications Scar management 7 TABLE 3.3 Tetanus-prone wounds. Tetanus-prone wounds High-risk tetanus-prone wounds Any tetanus-prone wound with: Puncture-type injuries in a contaminated environment Heavy contamination, e.g. soil or manure Bites Compound fractures Wound requiring surgery with >6-hour delay Containing foreign bodies Wounds or burns with Extensive devitalised tissue systemic sepsis Adapted from https://www.gov.uk/government/publications/tetanus prone-wounds-posters. Principles Clinical judgement is crucial in managing wounds. Some general principles of wound management are summarised in Table 3.2 . Antibiotic prophylaxis is needed for clean–contam - inated, contaminated and dirty wounds. It may also be used in clean wounds when there is a high risk of infection or when the sequelae of infection are potentially disastrous. Tetanus prophylaxis should be given based on the type of wound ( T able 3.3 ) and immunisation status ( Figure 3.6 ). ). - /uni25CF - /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - Debridement is essential to remove any devitalised tissue and foreign material from the wound. Non-viable tissue - must be excised until healthy bleeding occurs at the wound edges. The importance of thorough debridement is often TABLE 3.2 Principles of wound management. Preparation Antibiotic prophylaxis Tetanus prophylaxis Adequate analgesia/anaesthesia Wound irrigation Wound Early debridement and irrigation Exploration Repair structures Haemostasis Closure Skin closure without tension Consider reconstruction options Suture choice Consider drains Optimal dressings Follow-up Removal of sutures/splints Physiotherapy Monitoring for complications Scar management 7 TABLE 3.3 Tetanus-prone wounds. Tetanus-prone wounds High-risk tetanus-prone wounds Any tetanus-prone wound with: Puncture-type injuries in a contaminated environment Heavy contamination, e.g. soil or manure Bites Compound fractures Wound requiring surgery with >6-hour delay Containing foreign bodies Wounds or burns with Extensive devitalised tissue systemic sepsis Adapted from https://www.gov.uk/government/publications/tetanus prone-wounds-posters. Principles Clinical judgement is crucial in managing wounds. Some general principles of wound management are summarised in Table 3.2 . Antibiotic prophylaxis is needed for clean–contam - inated, contaminated and dirty wounds. It may also be used in clean wounds when there is a high risk of infection or when the sequelae of infection are potentially disastrous. Tetanus prophylaxis should be given based on the type of wound ( T able 3.3 ) and immunisation status ( Figure 3.6 ). ). - /uni25CF - /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - Debridement is essential to remove any devitalised tissue and foreign material from the wound. Non-viable tissue - must be excised until healthy bleeding occurs at the wound edges. The importance of thorough debridement is often TABLE 3.2 Principles of wound management. Preparation Antibiotic prophylaxis Tetanus prophylaxis Adequate analgesia/anaesthesia Wound irrigation Wound Early debridement and irrigation Exploration Repair structures Haemostasis Closure Skin closure without tension Consider reconstruction options Suture choice Consider drains Optimal dressings Follow-up Removal of sutures/splints Physiotherapy Monitoring for complications Scar management 7 TABLE 3.3 Tetanus-prone wounds. Tetanus-prone wounds High-risk tetanus-prone wounds Any tetanus-prone wound with: Puncture-type injuries in a contaminated environment Heavy contamination, e.g. soil or manure Bites Compound fractures Wound requiring surgery with >6-hour delay Containing foreign bodies Wounds or burns with Extensive devitalised tissue systemic sepsis Adapted from https://www.gov.uk/government/publications/tetanus prone-wounds-posters. Proliferation Proliferation The proliferative phase starts around day 3 and lasts for 2–4 weeks. It consists mainly of fibroblast activity with the production of ground substance (glycosaminoglycans and - proteoglycans), collagen, angiogenesis and re-epithelialisation of the wound. The wound tissue formed in the early part of this phase is - called granulation tissue. It has a pink and granular appear - ance. In the later part of this phase, there is an increase in the tensile strength of the wound as a result of increased colla gen synthesised by fi broblasts. Some fi broblasts di ff erentiate into myofi broblasts, which are contractile cells. These play an important role in contraction to bring the edges of the wound together . (a) Epithelial cell Sebaceous gland Fibrin clot Sweat duct gland Platelet Neutrophil Fibroblast Eschar (b) Macrophage New blood vessel Granulation tissue Monocyte Figure 3.1 Classic stages of wound healing. (a) In /f_l ammation. G, Werner S, Barrandon Y et al . Wound repair and regeneration. Proliferation The proliferative phase starts around day 3 and lasts for 2–4 weeks. It consists mainly of fibroblast activity with the production of ground substance (glycosaminoglycans and - proteoglycans), collagen, angiogenesis and re-epithelialisation of the wound. The wound tissue formed in the early part of this phase is - called granulation tissue. It has a pink and granular appear - ance. In the later part of this phase, there is an increase in the tensile strength of the wound as a result of increased colla gen synthesised by fi broblasts. Some fi broblasts di ff erentiate into myofi broblasts, which are contractile cells. These play an important role in contraction to bring the edges of the wound together . (a) Epithelial cell Sebaceous gland Fibrin clot Sweat duct gland Platelet Neutrophil Fibroblast Eschar (b) Macrophage New blood vessel Granulation tissue Monocyte Figure 3.1 Classic stages of wound healing. (a) In /f_l ammation. G, Werner S, Barrandon Y et al . Wound repair and regeneration. Proliferation The proliferative phase starts around day 3 and lasts for 2–4 weeks. It consists mainly of fibroblast activity with the production of ground substance (glycosaminoglycans and - proteoglycans), collagen, angiogenesis and re-epithelialisation of the wound. The wound tissue formed in the early part of this phase is - called granulation tissue. It has a pink and granular appear - ance. In the later part of this phase, there is an increase in the tensile strength of the wound as a result of increased colla gen synthesised by fi broblasts. Some fi broblasts di ff erentiate into myofi broblasts, which are contractile cells. These play an important role in contraction to bring the edges of the wound together . (a) Epithelial cell Sebaceous gland Fibrin clot Sweat duct gland Platelet Neutrophil Fibroblast Eschar (b) Macrophage New blood vessel Granulation tissue Monocyte Figure 3.1 Classic stages of wound healing. (a) In /f_l ammation. G, Werner S, Barrandon Y et al . Wound repair and regeneration. REFERENCES REFERENCES 1 Berard F , Gandon J. Postoperative wound infections: the influence of ultraviolet irradiation of the operating room and various other factors. Ann Surg 1964; 160 (Suppl): 1–192. 2 Garner JS. CDC guideline for prevention of surgical wound infec tions, 1985. Infect Control 1986; 7 (3): 193–200. 3 Levy SM, Holzmann-Pazgal G, Lally KP et al . Quality check of a quality measure: surgical wound classification discrepancies impact risk-stratified surgical site infection rates in pediatric appendicitis. Am Coll Surg 2013; 217 (6): 969–73. 4 Onyekwelu I, Yakkanti R, Protzer L et al. Surgical wound classifica tion and surgical site infections in the orthopaedic patient. J Am Acad Orthop Surg Glob Res Rev 2017; 1 (3): e022. 5 Haley RW , Culver DH, White JW et al. The e ffi cacy of infection sur veillance and control programs in preventing nosocomial infections in US hospitals. Am J Epidemiol 1985; 121 : 182–205. 6 Eccles S, Handley B, Khan U et al . Standards for the management of open fractures . Oxford: Oxford University Press, 2020. 7 Public Health England. Post exposure management for tetanus prone wounds 2019. Available from https://www .gov .uk/government/publications/ tetanus-prone-wounds-posters (accessed 29 January 2021) 8 Gottlieb LJ, Krieger LM. From the reconstructive ladder to the reconstructive elevator. Plast Reconstr Surg 1994; 93 (7): 1503–4. 9 Arnez ZM, Khan U, Tyler MP . Classification of soft-tissue degloving in limb trauma. J Plast Reconstr Aesthet Surg 2010; 63 (11): 1865–9. 10 Hedetoft M, Madsen MB, Madsen LB et al . Incidence, comorbid - ity and mortality in patients with necrotising soft-tissue infections, 2005–2018: a Danish nationwide register-based cohort study . BMJ Open 2020; 10 : e041302. 11 Madsen MB, Skrede S, Perner A et al . Patient’s characteristics and outcomes in necrotising soft-tissue infections: results from a Scan - dinavian, multicentre, prospective cohort study . Intensive Care Med . - 2019; 45 (9): 1241–51. 12 Fernando SM, Tran A, Cheng W et al . Necrotizing Soft tissue infec - tion: diagnostic accuracy of physical examination, imaging, and LRINEC score: a systematic review and meta-analysis. Ann Surg J 2019; 269 (1): 58–65. 13 Edsberg LE, Black JM, Goldberg M et al. Revised National Pressure - Ulcer Advisory Panel pressure injury staging system: revised pressure injury staging system. J Wound Ostomy Continence Nurs 2016; 43 (6): 585–97. - 14 Monstrey S, Middelkoop E, Vranckx JJ et al. Updated scar manage - ment practical guidelines: non-invasive and invasive measures. J Plast Reconstr Aesthet Surg 2014; 67 (8): 1017–25. 15 Gold MH, McGuire M, Mustoe TA et al . Updated international clin - ical recommendations on scar management: part 2—algorithms for , scar prevention and treatment. Dermatol Surg 2014; 40 (8): 825–31. a Figure 3.19 Midline neck contracture from a chainsaw injury. Figure 3.20 Multiple Z-plasty release of /f_i nger contracture. REFERENCES 1 Berard F , Gandon J. Postoperative wound infections: the influence of ultraviolet irradiation of the operating room and various other factors. Ann Surg 1964; 160 (Suppl): 1–192. 2 Garner JS. CDC guideline for prevention of surgical wound infec tions, 1985. Infect Control 1986; 7 (3): 193–200. 3 Levy SM, Holzmann-Pazgal G, Lally KP et al . Quality check of a quality measure: surgical wound classification discrepancies impact risk-stratified surgical site infection rates in pediatric appendicitis. Am Coll Surg 2013; 217 (6): 969–73. 4 Onyekwelu I, Yakkanti R, Protzer L et al. Surgical wound classifica tion and surgical site infections in the orthopaedic patient. J Am Acad Orthop Surg Glob Res Rev 2017; 1 (3): e022. 5 Haley RW , Culver DH, White JW et al. The e ffi cacy of infection sur veillance and control programs in preventing nosocomial infections in US hospitals. Am J Epidemiol 1985; 121 : 182–205. 6 Eccles S, Handley B, Khan U et al . Standards for the management of open fractures . Oxford: Oxford University Press, 2020. 7 Public Health England. Post exposure management for tetanus prone wounds 2019. Available from https://www .gov .uk/government/publications/ tetanus-prone-wounds-posters (accessed 29 January 2021) 8 Gottlieb LJ, Krieger LM. From the reconstructive ladder to the reconstructive elevator. Plast Reconstr Surg 1994; 93 (7): 1503–4. 9 Arnez ZM, Khan U, Tyler MP . Classification of soft-tissue degloving in limb trauma. J Plast Reconstr Aesthet Surg 2010; 63 (11): 1865–9. 10 Hedetoft M, Madsen MB, Madsen LB et al . Incidence, comorbid - ity and mortality in patients with necrotising soft-tissue infections, 2005–2018: a Danish nationwide register-based cohort study . BMJ Open 2020; 10 : e041302. 11 Madsen MB, Skrede S, Perner A et al . Patient’s characteristics and outcomes in necrotising soft-tissue infections: results from a Scan - dinavian, multicentre, prospective cohort study . Intensive Care Med . - 2019; 45 (9): 1241–51. 12 Fernando SM, Tran A, Cheng W et al . Necrotizing Soft tissue infec - tion: diagnostic accuracy of physical examination, imaging, and LRINEC score: a systematic review and meta-analysis. Ann Surg J 2019; 269 (1): 58–65. 13 Edsberg LE, Black JM, Goldberg M et al. Revised National Pressure - Ulcer Advisory Panel pressure injury staging system: revised pressure injury staging system. J Wound Ostomy Continence Nurs 2016; 43 (6): 585–97. - 14 Monstrey S, Middelkoop E, Vranckx JJ et al. Updated scar manage - ment practical guidelines: non-invasive and invasive measures. J Plast Reconstr Aesthet Surg 2014; 67 (8): 1017–25. 15 Gold MH, McGuire M, Mustoe TA et al . Updated international clin - ical recommendations on scar management: part 2—algorithms for , scar prevention and treatment. Dermatol Surg 2014; 40 (8): 825–31. a Figure 3.19 Midline neck contracture from a chainsaw injury. Figure 3.20 Multiple Z-plasty release of /f_i nger contracture. REFERENCES 1 Berard F , Gandon J. Postoperative wound infections: the influence of ultraviolet irradiation of the operating room and various other factors. Ann Surg 1964; 160 (Suppl): 1–192. 2 Garner JS. CDC guideline for prevention of surgical wound infec tions, 1985. Infect Control 1986; 7 (3): 193–200. 3 Levy SM, Holzmann-Pazgal G, Lally KP et al . Quality check of a quality measure: surgical wound classification discrepancies impact risk-stratified surgical site infection rates in pediatric appendicitis. Am Coll Surg 2013; 217 (6): 969–73. 4 Onyekwelu I, Yakkanti R, Protzer L et al. Surgical wound classifica tion and surgical site infections in the orthopaedic patient. J Am Acad Orthop Surg Glob Res Rev 2017; 1 (3): e022. 5 Haley RW , Culver DH, White JW et al. The e ffi cacy of infection sur veillance and control programs in preventing nosocomial infections in US hospitals. Am J Epidemiol 1985; 121 : 182–205. 6 Eccles S, Handley B, Khan U et al . Standards for the management of open fractures . Oxford: Oxford University Press, 2020. 7 Public Health England. Post exposure management for tetanus prone wounds 2019. Available from https://www .gov .uk/government/publications/ tetanus-prone-wounds-posters (accessed 29 January 2021) 8 Gottlieb LJ, Krieger LM. From the reconstructive ladder to the reconstructive elevator. Plast Reconstr Surg 1994; 93 (7): 1503–4. 9 Arnez ZM, Khan U, Tyler MP . Classification of soft-tissue degloving in limb trauma. J Plast Reconstr Aesthet Surg 2010; 63 (11): 1865–9. 10 Hedetoft M, Madsen MB, Madsen LB et al . Incidence, comorbid - ity and mortality in patients with necrotising soft-tissue infections, 2005–2018: a Danish nationwide register-based cohort study . BMJ Open 2020; 10 : e041302. 11 Madsen MB, Skrede S, Perner A et al . Patient’s characteristics and outcomes in necrotising soft-tissue infections: results from a Scan - dinavian, multicentre, prospective cohort study . Intensive Care Med . - 2019; 45 (9): 1241–51. 12 Fernando SM, Tran A, Cheng W et al . Necrotizing Soft tissue infec - tion: diagnostic accuracy of physical examination, imaging, and LRINEC score: a systematic review and meta-analysis. Ann Surg J 2019; 269 (1): 58–65. 13 Edsberg LE, Black JM, Goldberg M et al. Revised National Pressure - Ulcer Advisory Panel pressure injury staging system: revised pressure injury staging system. J Wound Ostomy Continence Nurs 2016; 43 (6): 585–97. - 14 Monstrey S, Middelkoop E, Vranckx JJ et al. Updated scar manage - ment practical guidelines: non-invasive and invasive measures. J Plast Reconstr Aesthet Surg 2014; 67 (8): 1017–25. 15 Gold MH, McGuire M, Mustoe TA et al . Updated international clin - ical recommendations on scar management: part 2—algorithms for , scar prevention and treatment. Dermatol Surg 2014; 40 (8): 825–31. a Figure 3.19 Midline neck contracture from a chainsaw injury. Figure 3.20 Multiple Z-plasty release of /f_i nger contracture. Remodelling Remodelling The remodelling phase begins 2–3 weeks after injury and lasts for a year or more. This phase is characterised by maturation of collagen. Type III collagen, which is prevalent during prolif eration, is replaced by stronger type I collagen until the normal skin ratio of 4:1 type I to type III collagen is re-established. The collagen becomes more cross-linked and uniformly aligned. This ma turation of collagen leads to increased tensile strength in the wound, which is maximal 12 weeks post injury and represents approximately 80% of the uninjured skin strength. - Hair Bacteria Epidermis Oxygen Dermis Subcutaneous layer Collagen Capillary (c) Collagen (b) Proliferation. (c) Remodelling. (Adapted by permission from Springer: Gurtner Nature 2008; 453 : 314–21. 2008). Remodelling The remodelling phase begins 2–3 weeks after injury and lasts for a year or more. This phase is characterised by maturation of collagen. Type III collagen, which is prevalent during prolif eration, is replaced by stronger type I collagen until the normal skin ratio of 4:1 type I to type III collagen is re-established. The collagen becomes more cross-linked and uniformly aligned. This ma turation of collagen leads to increased tensile strength in the wound, which is maximal 12 weeks post injury and represents approximately 80% of the uninjured skin strength. - Hair Bacteria Epidermis Oxygen Dermis Subcutaneous layer Collagen Capillary (c) Collagen (b) Proliferation. (c) Remodelling. (Adapted by permission from Springer: Gurtner Nature 2008; 453 : 314–21. 2008). Remodelling The remodelling phase begins 2–3 weeks after injury and lasts for a year or more. This phase is characterised by maturation of collagen. Type III collagen, which is prevalent during prolif eration, is replaced by stronger type I collagen until the normal skin ratio of 4:1 type I to type III collagen is re-established. The collagen becomes more cross-linked and uniformly aligned. This ma turation of collagen leads to increased tensile strength in the wound, which is maximal 12 weeks post injury and represents approximately 80% of the uninjured skin strength. - Hair Bacteria Epidermis Oxygen Dermis Subcutaneous layer Collagen Capillary (c) Collagen (b) Proliferation. (c) Remodelling. (Adapted by permission from Springer: Gurtner Nature 2008; 453 : 314–21. 2008). SCAR MANAGEMENT Principles SCAR MANAGEMENT Principles The remodelling and maturation phase of wound healing results in scar formation. The immature scar is at first pink, hard, raised and often itchy . As the collagen matures, the scar becomes almost acellular as the fibroblasts and blood vessels reduce. The external appearance of the scar becomes paler, while the scar becomes softer, flattens and its itchiness dimin - ishes. Most of these changes occur over the first 3 months but a scar will continue to mature over 1–2 years, and sometimes more. Tensile strength will continue to increase but would not be expected to ex ceed around 80% that of normal skin. There is well-established evidence for managing scars with pressure/compression therapy , silicone sheets and gels, 14 intralesional corticosteroid injection and surgery . Other treatment modalities include massage therapy , psychologi - cal counselling, laser therapy , radiotherapy , cryosurgery and intralesional injection of other products. Prevention of adverse scar formation is better than treat - ment, so it is important to correctly manage wounds ( Table 3.2 ). Optimal surgical management starts with careful planning, tissue handling and meticulous technique. For example, plac - ing incisions along relaxed skin tension lesions where possi - ble, and avoiding straight-line incisions across flexion creases. Early debridement reduces the risk of infection and allows for earlier /uni00A0 wound closure. Dirt-ingrained (tattooed) scars ar e usu - ally preventable by proper initial scrubbing and cleansing of the wound ( Figure 3.16 ). It is important to recognise normal - e pre - . Figure 3.16 Dirt-ingrained scar. anatomical landmarks to avoid misaligned scars, such as at the lip vermilion border where even a 1-mm discrepancy is noticeable at a distance. Skin closure should be without tension and allow for postoperative oedema typically associated with injury and healing. Wounds should be sutured in layers unless they are very small. Deep dermal absorbable sutures hold the skin edges together to allow subsequent subcuticular or skin sutures. Large and deep wounds also require closure of the fascial layer, for example Scarpa’s fascia in the abdomen. Sub cuticular suturing avoids skin suture marks. If skin sutures are used, suture marks may be minimised by using monofilament sutures that are removed in a timely fashion depending on ana tomical location. For example, sutures are typically removed by 5 days in the face versus 10–14 days in the lower limb. Following wound closure, scar prevention measures include tension relief, taping , hydration and ultraviolet protection. Silicone sheeting or gel is widely accepted as the first-line pro phylactic and treatment option for hypertrophic and keloid scars. The management of hypertrophic and keloid scars is di ffi cult and international recommendations from 2014 are 15 summarised in Figur es 3.17 and 3.18 . Later scar treatment includes intralesional cortico steroid injections, typically using triamcinolone acetonide 10–40 /uni00A0 mg/mL every 4–6 weeks until the scar has flattened. Antonio Scarpa , 1747–1832, Professor of Anatomy , Pavia, Italy . Revisional scar surgery may be appropriate . For example, for correcting alignment of scars. (red, slightly raised) (red/raised, itchy) Silicone gel or sheeting Apply prevention algorithim (i.e. silicone gel or sheeting, hypoallergenic paper tape or onion extract cream) corticosteroid injection (repeat monthly) PDL If persists for >1 month, treat as a linear hypertrophic scar Pressure therapy a PDL or fractional laser therapy Surgical excision + postoperative silicone gel or sheeting Figure 3.17 Management algorithm for hypertrophic scars. Light grey indicates initial management strategies; dark grey indicates secondary a b management options. Preferred initial option. 2.5–20 mg/mL (face); 20–40 mg/mL (body). include bleomycin, mitomycin C, laser therapy and cryotherapy. e stabilisation. Combination and alternative therapies include massage, physical therapy, corticosteroids, tension-relieving surgical interven tion, excision, grafting or /f_l ap coverage, hydrocolloid dressings, antihistamines and laser therapy. 5-FU, 5- /f_l uorouracil; PDL, pulsed-dye laser. (Redrawn with permission from Gold MH, McGuire M, Mustoe TA part 2–algorithms for scar prevention and treatment. Dermatol Surg hypertrophic (red/raised) Admission to a specialty d burn unit (2 months) Intralesional Silicone gel or sheeting, b pressure garments and/or onion extract cream a or fractional Fractional laser therapy laser therapy Combination or alternative e therapies Severe scars Surgical excision + corticosteroids 5-FU + corticosteroids c or alternative therapies c Alternative therapy options for severe lesions d Scar prevention and treatment should not begin before epithelium and wound et al . Updated international clinical recommendations on scar management: 2014; 40 (8): 825–31.) SCAR MANAGEMENT Principles The remodelling and maturation phase of wound healing results in scar formation. The immature scar is at first pink, hard, raised and often itchy . As the collagen matures, the scar becomes almost acellular as the fibroblasts and blood vessels reduce. The external appearance of the scar becomes paler, while the scar becomes softer, flattens and its itchiness dimin - ishes. Most of these changes occur over the first 3 months but a scar will continue to mature over 1–2 years, and sometimes more. Tensile strength will continue to increase but would not be expected to ex ceed around 80% that of normal skin. There is well-established evidence for managing scars with pressure/compression therapy , silicone sheets and gels, 14 intralesional corticosteroid injection and surgery . Other treatment modalities include massage therapy , psychologi - cal counselling, laser therapy , radiotherapy , cryosurgery and intralesional injection of other products. Prevention of adverse scar formation is better than treat - ment, so it is important to correctly manage wounds ( Table 3.2 ). Optimal surgical management starts with careful planning, tissue handling and meticulous technique. For example, plac - ing incisions along relaxed skin tension lesions where possi - ble, and avoiding straight-line incisions across flexion creases. Early debridement reduces the risk of infection and allows for earlier /uni00A0 wound closure. Dirt-ingrained (tattooed) scars ar e usu - ally preventable by proper initial scrubbing and cleansing of the wound ( Figure 3.16 ). It is important to recognise normal - e pre - . Figure 3.16 Dirt-ingrained scar. anatomical landmarks to avoid misaligned scars, such as at the lip vermilion border where even a 1-mm discrepancy is noticeable at a distance. Skin closure should be without tension and allow for postoperative oedema typically associated with injury and healing. Wounds should be sutured in layers unless they are very small. Deep dermal absorbable sutures hold the skin edges together to allow subsequent subcuticular or skin sutures. Large and deep wounds also require closure of the fascial layer, for example Scarpa’s fascia in the abdomen. Sub cuticular suturing avoids skin suture marks. If skin sutures are used, suture marks may be minimised by using monofilament sutures that are removed in a timely fashion depending on ana tomical location. For example, sutures are typically removed by 5 days in the face versus 10–14 days in the lower limb. Following wound closure, scar prevention measures include tension relief, taping , hydration and ultraviolet protection. Silicone sheeting or gel is widely accepted as the first-line pro phylactic and treatment option for hypertrophic and keloid scars. The management of hypertrophic and keloid scars is di ffi cult and international recommendations from 2014 are 15 summarised in Figur es 3.17 and 3.18 . Later scar treatment includes intralesional cortico steroid injections, typically using triamcinolone acetonide 10–40 /uni00A0 mg/mL every 4–6 weeks until the scar has flattened. Antonio Scarpa , 1747–1832, Professor of Anatomy , Pavia, Italy . Revisional scar surgery may be appropriate . For example, for correcting alignment of scars. (red, slightly raised) (red/raised, itchy) Silicone gel or sheeting Apply prevention algorithim (i.e. silicone gel or sheeting, hypoallergenic paper tape or onion extract cream) corticosteroid injection (repeat monthly) PDL If persists for >1 month, treat as a linear hypertrophic scar Pressure therapy a PDL or fractional laser therapy Surgical excision + postoperative silicone gel or sheeting Figure 3.17 Management algorithm for hypertrophic scars. Light grey indicates initial management strategies; dark grey indicates secondary a b management options. Preferred initial option. 2.5–20 mg/mL (face); 20–40 mg/mL (body). include bleomycin, mitomycin C, laser therapy and cryotherapy. e stabilisation. Combination and alternative therapies include massage, physical therapy, corticosteroids, tension-relieving surgical interven tion, excision, grafting or /f_l ap coverage, hydrocolloid dressings, antihistamines and laser therapy. 5-FU, 5- /f_l uorouracil; PDL, pulsed-dye laser. (Redrawn with permission from Gold MH, McGuire M, Mustoe TA part 2–algorithms for scar prevention and treatment. Dermatol Surg hypertrophic (red/raised) Admission to a specialty d burn unit (2 months) Intralesional Silicone gel or sheeting, b pressure garments and/or onion extract cream a or fractional Fractional laser therapy laser therapy Combination or alternative e therapies Severe scars Surgical excision + corticosteroids 5-FU + corticosteroids c or alternative therapies c Alternative therapy options for severe lesions d Scar prevention and treatment should not begin before epithelium and wound et al . Updated international clinical recommendations on scar management: 2014; 40 (8): 825–31.) SCAR MANAGEMENT Principles The remodelling and maturation phase of wound healing results in scar formation. The immature scar is at first pink, hard, raised and often itchy . As the collagen matures, the scar becomes almost acellular as the fibroblasts and blood vessels reduce. The external appearance of the scar becomes paler, while the scar becomes softer, flattens and its itchiness dimin - ishes. Most of these changes occur over the first 3 months but a scar will continue to mature over 1–2 years, and sometimes more. Tensile strength will continue to increase but would not be expected to ex ceed around 80% that of normal skin. There is well-established evidence for managing scars with pressure/compression therapy , silicone sheets and gels, 14 intralesional corticosteroid injection and surgery . Other treatment modalities include massage therapy , psychologi - cal counselling, laser therapy , radiotherapy , cryosurgery and intralesional injection of other products. Prevention of adverse scar formation is better than treat - ment, so it is important to correctly manage wounds ( Table 3.2 ). Optimal surgical management starts with careful planning, tissue handling and meticulous technique. For example, plac - ing incisions along relaxed skin tension lesions where possi - ble, and avoiding straight-line incisions across flexion creases. Early debridement reduces the risk of infection and allows for earlier /uni00A0 wound closure. Dirt-ingrained (tattooed) scars ar e usu - ally preventable by proper initial scrubbing and cleansing of the wound ( Figure 3.16 ). It is important to recognise normal - e pre - . Figure 3.16 Dirt-ingrained scar. anatomical landmarks to avoid misaligned scars, such as at the lip vermilion border where even a 1-mm discrepancy is noticeable at a distance. Skin closure should be without tension and allow for postoperative oedema typically associated with injury and healing. Wounds should be sutured in layers unless they are very small. Deep dermal absorbable sutures hold the skin edges together to allow subsequent subcuticular or skin sutures. Large and deep wounds also require closure of the fascial layer, for example Scarpa’s fascia in the abdomen. Sub cuticular suturing avoids skin suture marks. If skin sutures are used, suture marks may be minimised by using monofilament sutures that are removed in a timely fashion depending on ana tomical location. For example, sutures are typically removed by 5 days in the face versus 10–14 days in the lower limb. Following wound closure, scar prevention measures include tension relief, taping , hydration and ultraviolet protection. Silicone sheeting or gel is widely accepted as the first-line pro phylactic and treatment option for hypertrophic and keloid scars. The management of hypertrophic and keloid scars is di ffi cult and international recommendations from 2014 are 15 summarised in Figur es 3.17 and 3.18 . Later scar treatment includes intralesional cortico steroid injections, typically using triamcinolone acetonide 10–40 /uni00A0 mg/mL every 4–6 weeks until the scar has flattened. Antonio Scarpa , 1747–1832, Professor of Anatomy , Pavia, Italy . Revisional scar surgery may be appropriate . For example, for correcting alignment of scars. (red, slightly raised) (red/raised, itchy) Silicone gel or sheeting Apply prevention algorithim (i.e. silicone gel or sheeting, hypoallergenic paper tape or onion extract cream) corticosteroid injection (repeat monthly) PDL If persists for >1 month, treat as a linear hypertrophic scar Pressure therapy a PDL or fractional laser therapy Surgical excision + postoperative silicone gel or sheeting Figure 3.17 Management algorithm for hypertrophic scars. Light grey indicates initial management strategies; dark grey indicates secondary a b management options. Preferred initial option. 2.5–20 mg/mL (face); 20–40 mg/mL (body). include bleomycin, mitomycin C, laser therapy and cryotherapy. e stabilisation. Combination and alternative therapies include massage, physical therapy, corticosteroids, tension-relieving surgical interven tion, excision, grafting or /f_l ap coverage, hydrocolloid dressings, antihistamines and laser therapy. 5-FU, 5- /f_l uorouracil; PDL, pulsed-dye laser. (Redrawn with permission from Gold MH, McGuire M, Mustoe TA part 2–algorithms for scar prevention and treatment. Dermatol Surg hypertrophic (red/raised) Admission to a specialty d burn unit (2 months) Intralesional Silicone gel or sheeting, b pressure garments and/or onion extract cream a or fractional Fractional laser therapy laser therapy Combination or alternative e therapies Severe scars Surgical excision + corticosteroids 5-FU + corticosteroids c or alternative therapies c Alternative therapy options for severe lesions d Scar prevention and treatment should not begin before epithelium and wound et al . Updated international clinical recommendations on scar management: 2014; 40 (8): 825–31.) TYPES OF WOUND HEALING TYPES OF WOUND HEALING There are di ff erent types of healing ( Summary box 3.2 Primary healing is also known as healing by first intention. This occurs when there is direct approximation of the wound edges and is the aim of treatment. When there are no adverse influences, these wounds heal well and leave the best scar. Delayed primary healing occurs when the wound edges are not opposed immediately , which may be necessary in contaminated or untidy wounds. After debridement of non-viable tissue and when the wound is clean, the wound edges may be surgically approximated. This is also called healing by tertiary intention. Secondary healing or healing by secondary intention occurs in wounds that are left open and allowed to heal by granulation, contraction and re-epithelialisation. Summary box 3.2 Classification of wound closure and healing /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Primary Wound edges apposed Normal healing Minimal scar Secondary Wound left open Heals by granulation, contraction and re-epithelialisation Increased in /f_l ammation and proliferation Poor scar Tertiary (delayed primary) Wound initially left open Edges apposed later when healing conditions favourable TYPES OF WOUND HEALING There are di ff erent types of healing ( Summary box 3.2 Primary healing is also known as healing by first intention. This occurs when there is direct approximation of the wound edges and is the aim of treatment. When there are no adverse influences, these wounds heal well and leave the best scar. Delayed primary healing occurs when the wound edges are not opposed immediately , which may be necessary in contaminated or untidy wounds. After debridement of non-viable tissue and when the wound is clean, the wound edges may be surgically approximated. This is also called healing by tertiary intention. Secondary healing or healing by secondary intention occurs in wounds that are left open and allowed to heal by granulation, contraction and re-epithelialisation. Summary box 3.2 Classification of wound closure and healing /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Primary Wound edges apposed Normal healing Minimal scar Secondary Wound left open Heals by granulation, contraction and re-epithelialisation Increased in /f_l ammation and proliferation Poor scar Tertiary (delayed primary) Wound initially left open Edges apposed later when healing conditions favourable TYPES OF WOUND HEALING There are di ff erent types of healing ( Summary box 3.2 Primary healing is also known as healing by first intention. This occurs when there is direct approximation of the wound edges and is the aim of treatment. When there are no adverse influences, these wounds heal well and leave the best scar. Delayed primary healing occurs when the wound edges are not opposed immediately , which may be necessary in contaminated or untidy wounds. After debridement of non-viable tissue and when the wound is clean, the wound edges may be surgically approximated. This is also called healing by tertiary intention. Secondary healing or healing by secondary intention occurs in wounds that are left open and allowed to heal by granulation, contraction and re-epithelialisation. Summary box 3.2 Classification of wound closure and healing /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Primary Wound edges apposed Normal healing Minimal scar Secondary Wound left open Heals by granulation, contraction and re-epithelialisation Increased in /f_l ammation and proliferation Poor scar Tertiary (delayed primary) Wound initially left open Edges apposed later when healing conditions favourable Tendon Tendon Although repair follows the normal pattern of wound healing, there are two main mechanisms whereby nutrients, cells and new vessels reach the severed tendon. Intrinsic healing consists of vincular blood fl ow and synovial di ff usion. Extrinsic heal - ing depends on the formation of fi brous adhesions between the tendon and the tendon sheath. Early active mobilisation following tendon repairs prevents adhesions limiting the range of motion and therefore promotes the more desir ed intrinsic healing. At the same time, tendon repairs must be protected by splintage to avoid rupture. Tendon Although repair follows the normal pattern of wound healing, there are two main mechanisms whereby nutrients, cells and new vessels reach the severed tendon. Intrinsic healing consists of vincular blood fl ow and synovial di ff usion. Extrinsic heal - ing depends on the formation of fi brous adhesions between the tendon and the tendon sheath. Early active mobilisation following tendon repairs prevents adhesions limiting the range of motion and therefore promotes the more desir ed intrinsic healing. At the same time, tendon repairs must be protected by splintage to avoid rupture. Tendon Although repair follows the normal pattern of wound healing, there are two main mechanisms whereby nutrients, cells and new vessels reach the severed tendon. Intrinsic healing consists of vincular blood fl ow and synovial di ff usion. Extrinsic heal - ing depends on the formation of fi brous adhesions between the tendon and the tendon sheath. Early active mobilisation following tendon repairs prevents adhesions limiting the range of motion and therefore promotes the more desir ed intrinsic healing. At the same time, tendon repairs must be protected by splintage to avoid rupture. WOUND MANAGEMENT Assessment WOUND MANAGEMENT Assessment Wound management is guided by the timing and mechanism of injury as well as factors a ff ecting healing ( Summary box 3.1 It is also important to assess the patient’s ideas, concerns and expectations. Patient outcomes also rely on good postoperative compliance. Assess the patient using Advanced Trauma Life Support principles to first identify and treat life- and then limb-threat ening conditions. Some wounds require a multidisciplinary approach; for example, the in volvement of orthopaedic sur geons and plastic surgeons in managing complex open lower 6 limb fractures. Assess the site, size, geometry and nature of any wounds. Look for signs of contamination, infection, swelling and pul satile bleeding. Deformities may suggest underlying fractures or dislocations. Has there been skin loss or degloving? What structures are visible? Thorough irrigation of wounds will allow better visualisa tion. It is important to correlate the clinical examination with the mechanism of injury as seemingly innocuous wounds can lead to underestimation of tissue damage. For exam ple, high-pressure injection injuries of the hand can cause of amputation. The injected substances can track proximally into the forearm. Urgent surgical exploration and debridement - is required. Before palpation, ensure that the patient has adequate anal - gesia or a local anaesthetic block. When possible, it is important to assess motor and sensory function before any local anaes - thesia. Unless there are obvious muscle injuries, the purpose of testing specific muscle groups is to evalua te potential nerve or tendon injuries. Imaging is useful to e xclude foreign bodies, fractures or dislocations where appropriate. WOUND MANAGEMENT Assessment Wound management is guided by the timing and mechanism of injury as well as factors a ff ecting healing ( Summary box 3.1 It is also important to assess the patient’s ideas, concerns and expectations. Patient outcomes also rely on good postoperative compliance. Assess the patient using Advanced Trauma Life Support principles to first identify and treat life- and then limb-threat ening conditions. Some wounds require a multidisciplinary approach; for example, the in volvement of orthopaedic sur geons and plastic surgeons in managing complex open lower 6 limb fractures. Assess the site, size, geometry and nature of any wounds. Look for signs of contamination, infection, swelling and pul satile bleeding. Deformities may suggest underlying fractures or dislocations. Has there been skin loss or degloving? What structures are visible? Thorough irrigation of wounds will allow better visualisa tion. It is important to correlate the clinical examination with the mechanism of injury as seemingly innocuous wounds can lead to underestimation of tissue damage. For exam ple, high-pressure injection injuries of the hand can cause of amputation. The injected substances can track proximally into the forearm. Urgent surgical exploration and debridement - is required. Before palpation, ensure that the patient has adequate anal - gesia or a local anaesthetic block. When possible, it is important to assess motor and sensory function before any local anaes - thesia. Unless there are obvious muscle injuries, the purpose of testing specific muscle groups is to evalua te potential nerve or tendon injuries. Imaging is useful to e xclude foreign bodies, fractures or dislocations where appropriate. WOUND MANAGEMENT Assessment Wound management is guided by the timing and mechanism of injury as well as factors a ff ecting healing ( Summary box 3.1 It is also important to assess the patient’s ideas, concerns and expectations. Patient outcomes also rely on good postoperative compliance. Assess the patient using Advanced Trauma Life Support principles to first identify and treat life- and then limb-threat ening conditions. Some wounds require a multidisciplinary approach; for example, the in volvement of orthopaedic sur geons and plastic surgeons in managing complex open lower 6 limb fractures. Assess the site, size, geometry and nature of any wounds. Look for signs of contamination, infection, swelling and pul satile bleeding. Deformities may suggest underlying fractures or dislocations. Has there been skin loss or degloving? What structures are visible? Thorough irrigation of wounds will allow better visualisa tion. It is important to correlate the clinical examination with the mechanism of injury as seemingly innocuous wounds can lead to underestimation of tissue damage. For exam ple, high-pressure injection injuries of the hand can cause of amputation. The injected substances can track proximally into the forearm. Urgent surgical exploration and debridement - is required. Before palpation, ensure that the patient has adequate anal - gesia or a local anaesthetic block. When possible, it is important to assess motor and sensory function before any local anaes - thesia. Unless there are obvious muscle injuries, the purpose of testing specific muscle groups is to evalua te potential nerve or tendon injuries. Imaging is useful to e xclude foreign bodies, fractures or dislocations where appropriate.