7. TETANUS
• Tetanus is an important endemic infection in India with an annual incidence of 100 per 1,00,000 population in most cases following a street accident. The signs and symptoms are a manifestation of the effects of the endotoxin of cl.tetani.
• All wounds must be thoroughly cleaned with removal of all organic and inorganic debris
• Immunisation against tetanus is done using:
a) Human Anti tetanus globulin (ATG)
b) Tetanus Toxoid Vaccine
• In fully immunised patients with a booseter dose within the past 5 years, no further immunisation is required. Fully immunized patients but with more than 5 years since last booster only require a booster toxoid dose-0.5ml 1/m at the time of injury. These patients with dirty, heavily contaminated wounds also require a dose - 250-500 IU 1/m of ATG at the time of injury
• Patients with no immunization/incomplete immunisation should receive full course of immunisation. Such patients with contaminated, penetrating or injuries more than 6 hours old should also receive one dose of ATG
8. Wound dehiscence or breakdown occurs most often in postoperative abdominal incisions usually in the first week when the tensile strength is low and especially when tension increases due to abdominal distention or coughing.It may also occur due to already mentioned factors influencing wound healing (Section 4).
Other factors responsible are:
• Obesity
• Corticosteroid therapy
• Abdominal distension (ileus)
• Advanced age
9. SCARS
Most wounds continue to remodel for more than a year.However, some scars are not accpetable.
9.1 Hypertrophic scars are composed of dense fibrous tissue due to excessive collagen synthesis and have
a) Tense swollen appearance
b) Reddish colour
c) Itching - tenderness and hypertrophy
d) No tendency to spread to adjoining tissue
They do not enlarge beyond six months after injury.
Fig 1.8
9.2 KELOIDS
These scars invade adjoining tissue and enlarge even after 6 months. Treatment of these scars is difficult (discussed in chapter 10.
May require local cortisone or radiotherapy to control their spread and other symptoms.
Any questions be sent to drmmkapur@gmail.com
Tuesday, April 27, 2010
WOUNDS NONHEALING
CAUSES
Chronic or nonhealing wounds are open wounds that fail to epithelialize and close up in a reasonable amount of time. These wounds present as clinically unhealed ulcers without evidence of further healing. These wounds can be broadly classified as: Pressure sores, lower extremity ulcers, and radiation skin injury.
Pressure sores
Pressure sores develop over a subcutaneous point, usually in a bed ridden patient. These are frequently called “decubitus ulcers” or “bed sores”. The sacrum ischium, and greater trochanter are the most common location affected.
Pressure necrosis results from the amount or pressure on the tissue trapped between the bone and the bed and duration of continuous pressure. Microcirculation is when the tissue pressure is greater than 25 30 mmHg. this blocks capillary perfusion pressure. Necrosis can occur with as little as 2 hours of sustained pressure at this level.
Skin is more resistant to pressure necrosis than the underlying fat and muscle, which explains the common finding of a small area of skin ulceration overlying a large are of subcutaneous fat and muscle necrosis.
To begin treatment of these patients, efforts should be made to control the factors leading to increased pressure.
Paralyzed patients require periodic rotation and air mattress or other type of low pressure beds.
In other cases behavior and contractures may need to be addressed.
Tight fitting casrs should be removed and replaced by those with no excess pressure.
Other contributing factors should be identified and controlled, such as malnutrition infection and diabetes control. Necrotic tissue requires debridement.
With avoidance of pressure over the involved area, most pressure sores heal. However they beal with scar formation which is less resistant to trauma than intract skin. Thus a higher incidence or recurrence exists atter spontaneous closure of these wounds than if they are closed surgically with flaps of normal skin and muscle over the bony prominence.
Lower extremity ulcer
Leg ulcer generally arise either different vascular diseases. Arterial or venous insufficiency. Most (80% - 90%) result form venous valvular disese (venous in sufficiency)
Increased venous pressure in the dependent lower extremity lead to localize edema and tissue necrosis. Tissue edema is though to be a manor inhibitor of repair at the ulcer site, but the exact mechanism is not known. Oxygen delivery and diffusion are likely impaired. Postcapillary obstruction leads to an increased perfusion pressure and hypoxia. Protein and red blood cell extravasation occurs which further limits diffusion and oxygen delivery.
Arterial insufficiency to the lower extremity greatly impairs healing. Minor trauma resulting form scratches and abrasion that would otherwise heal quickly in a normal patient, can progress into large wounds and ultimately narcotizing, infection can cause death. Clinical sign of adequate arterial inflow is the simple presence of an pulse if a single is present in the foot then most wounds will heal.
A non healing wound in a ischaemic extremity is generally regarded as an indication for revascluration of the extremity.
External beam radiation through skin to treat deep pathology has both acute and chronic effects on skin. Acutely, a self limiting erythema may develop that spontaneously resolves.
Its late effects can be a more significant injury to fibroblasts, keratinocytes, and endothelial cells. DNA damage to these cells propagates over time and impairs the ability of these cells to divide successfully. Ultimately, a skin ulcer may occur spontaneously, but usually it occurs after repeated mild trauma such as abrasions.
If a surgical incision needs to be placed through an area of irradiated skin, then that incision is not likely to heal. Currently the only treatment modalities for these wounds are hyperbar oxygen therapy or coverage with vascularized tissue flaps
Any questions be sent to drmmkapur@gmail.com
Chronic or nonhealing wounds are open wounds that fail to epithelialize and close up in a reasonable amount of time. These wounds present as clinically unhealed ulcers without evidence of further healing. These wounds can be broadly classified as: Pressure sores, lower extremity ulcers, and radiation skin injury.
Pressure sores
Pressure sores develop over a subcutaneous point, usually in a bed ridden patient. These are frequently called “decubitus ulcers” or “bed sores”. The sacrum ischium, and greater trochanter are the most common location affected.
Pressure necrosis results from the amount or pressure on the tissue trapped between the bone and the bed and duration of continuous pressure. Microcirculation is when the tissue pressure is greater than 25 30 mmHg. this blocks capillary perfusion pressure. Necrosis can occur with as little as 2 hours of sustained pressure at this level.
Skin is more resistant to pressure necrosis than the underlying fat and muscle, which explains the common finding of a small area of skin ulceration overlying a large are of subcutaneous fat and muscle necrosis.
To begin treatment of these patients, efforts should be made to control the factors leading to increased pressure.
Paralyzed patients require periodic rotation and air mattress or other type of low pressure beds.
In other cases behavior and contractures may need to be addressed.
Tight fitting casrs should be removed and replaced by those with no excess pressure.
Other contributing factors should be identified and controlled, such as malnutrition infection and diabetes control. Necrotic tissue requires debridement.
With avoidance of pressure over the involved area, most pressure sores heal. However they beal with scar formation which is less resistant to trauma than intract skin. Thus a higher incidence or recurrence exists atter spontaneous closure of these wounds than if they are closed surgically with flaps of normal skin and muscle over the bony prominence.
Lower extremity ulcer
Leg ulcer generally arise either different vascular diseases. Arterial or venous insufficiency. Most (80% - 90%) result form venous valvular disese (venous in sufficiency)
Increased venous pressure in the dependent lower extremity lead to localize edema and tissue necrosis. Tissue edema is though to be a manor inhibitor of repair at the ulcer site, but the exact mechanism is not known. Oxygen delivery and diffusion are likely impaired. Postcapillary obstruction leads to an increased perfusion pressure and hypoxia. Protein and red blood cell extravasation occurs which further limits diffusion and oxygen delivery.
Arterial insufficiency to the lower extremity greatly impairs healing. Minor trauma resulting form scratches and abrasion that would otherwise heal quickly in a normal patient, can progress into large wounds and ultimately narcotizing, infection can cause death. Clinical sign of adequate arterial inflow is the simple presence of an pulse if a single is present in the foot then most wounds will heal.
A non healing wound in a ischaemic extremity is generally regarded as an indication for revascluration of the extremity.
External beam radiation through skin to treat deep pathology has both acute and chronic effects on skin. Acutely, a self limiting erythema may develop that spontaneously resolves.
Its late effects can be a more significant injury to fibroblasts, keratinocytes, and endothelial cells. DNA damage to these cells propagates over time and impairs the ability of these cells to divide successfully. Ultimately, a skin ulcer may occur spontaneously, but usually it occurs after repeated mild trauma such as abrasions.
If a surgical incision needs to be placed through an area of irradiated skin, then that incision is not likely to heal. Currently the only treatment modalities for these wounds are hyperbar oxygen therapy or coverage with vascularized tissue flaps
Any questions be sent to drmmkapur@gmail.com
WOUND MANAGEMENT
5. SURGICAL CLASSIFICATION OF WOUND
5.1. Clean wounds: These include surgical wounds which are acquired under relatively sterile conditions and do not involve entry into the
• GI tract
• Respiratory and
• Urinary tracts
5.2 Clean contaminated wounds: These occur when the above tracts are opened under sterile conditions.
5.3 Contaminated wounds : Contaminated wounds are all wounds outside the O.T. i.e.
• Street, industrial and domestic accidents.
• War injuries would also fall into this category.
5.4. Infected wounds: Infected wounds are one of the above wounds which may present with signs of infection or are contaminated and left untreated for more than 6-8 hours.
6. MANAGEMENT OF WOUNDS
6.1 Primary wound closure: All clean, clean contaminated and contaminated wounds qualify for this treatment. However, the contaminated wounds presenting within six hours would require cleaning and debridement under sterile conditions and suturing. Antibiotics may need to be given for both clean contaminated and contaminated wounds.In most cases the wound will heal by primary intent. However:
Fig 1.6 a & b
• Inspect under good light for assessment of contamination injury to structures. Decide if decontamination and repair require local regional or general anaesthesia.
• Small wounds require local anaesthesia. In casualty theatere the wounds is cleaned with 1% cetrimide and irrigated with sterile saline.
• The devitalized tissue is removed the help of forceps and scalpel (debridment) The deep layers are repaired using catgut suture and skin edge with silk or nylon (primary suture)
6.2. Delayed primary suture: In contaminated wounds when doubt exists due to delay in presentation:
• The wound is cleaned with cetrimide 1% and H2O2 and debrided by removing the devitalised tissue and cutting the skin edges to get a linear scar.
• The wound is not sutured but dressed and if no infection is seen in 24-48 hours later the wound is sutured at that time.
• In cases of gross contamination and infections the wound is cleaned and debrided as before,but left open packed with gauge soaked in antiseptic. Antibiotics are given after frequent dressings for a few days, a DELAYED PRIMARY SUTURE can be performed for closure of wound.
Fig 1.7
6.3. Secondary suture: This method is suitable for those wounds that show infection. These are cleaned and dressed after removing dead tissue and the patient kept on appropriate antibiotics. When pink healthy granulation appears the skin edges can be freed from the granulation and sutured. This is referred to as healing by secondary intent by production of granulation tissue.
6.4 Skin grafting: In some wounds the skin loss may be large as in burns. Initial treatment is with regular dressings and on appearance of granulation, splits thickness skin graft is obtained from a healthy donor site of the patient and transferred to the wound site. The skin graft survives on top of the granulations and fills in the skin gap.
Any questions be sent to drmmkapur@gmail.com
5.1. Clean wounds: These include surgical wounds which are acquired under relatively sterile conditions and do not involve entry into the
• GI tract
• Respiratory and
• Urinary tracts
5.2 Clean contaminated wounds: These occur when the above tracts are opened under sterile conditions.
5.3 Contaminated wounds : Contaminated wounds are all wounds outside the O.T. i.e.
• Street, industrial and domestic accidents.
• War injuries would also fall into this category.
5.4. Infected wounds: Infected wounds are one of the above wounds which may present with signs of infection or are contaminated and left untreated for more than 6-8 hours.
6. MANAGEMENT OF WOUNDS
6.1 Primary wound closure: All clean, clean contaminated and contaminated wounds qualify for this treatment. However, the contaminated wounds presenting within six hours would require cleaning and debridement under sterile conditions and suturing. Antibiotics may need to be given for both clean contaminated and contaminated wounds.In most cases the wound will heal by primary intent. However:
Fig 1.6 a & b
• Inspect under good light for assessment of contamination injury to structures. Decide if decontamination and repair require local regional or general anaesthesia.
• Small wounds require local anaesthesia. In casualty theatere the wounds is cleaned with 1% cetrimide and irrigated with sterile saline.
• The devitalized tissue is removed the help of forceps and scalpel (debridment) The deep layers are repaired using catgut suture and skin edge with silk or nylon (primary suture)
6.2. Delayed primary suture: In contaminated wounds when doubt exists due to delay in presentation:
• The wound is cleaned with cetrimide 1% and H2O2 and debrided by removing the devitalised tissue and cutting the skin edges to get a linear scar.
• The wound is not sutured but dressed and if no infection is seen in 24-48 hours later the wound is sutured at that time.
• In cases of gross contamination and infections the wound is cleaned and debrided as before,but left open packed with gauge soaked in antiseptic. Antibiotics are given after frequent dressings for a few days, a DELAYED PRIMARY SUTURE can be performed for closure of wound.
Fig 1.7
6.3. Secondary suture: This method is suitable for those wounds that show infection. These are cleaned and dressed after removing dead tissue and the patient kept on appropriate antibiotics. When pink healthy granulation appears the skin edges can be freed from the granulation and sutured. This is referred to as healing by secondary intent by production of granulation tissue.
6.4 Skin grafting: In some wounds the skin loss may be large as in burns. Initial treatment is with regular dressings and on appearance of granulation, splits thickness skin graft is obtained from a healthy donor site of the patient and transferred to the wound site. The skin graft survives on top of the granulations and fills in the skin gap.
Any questions be sent to drmmkapur@gmail.com
WOUND HEALING 5
3. LOCAL GROWTH FACTORS
These are released by many activated cells in a healing wound. These factors stimulate cell proliferation, migration and synthesis of required products. Among the cytokines is TGFB that helps all phase of healing. Topical application of TGFB acclerates wound healing.
Angiogenesis is simulated by acid and basic fibroblast growth factors (aFGF + bFGF). Epithelialisation is stimulated by epithelial growth factor (EGF) and keratinocyte growth factor (KGF).
4. CLINICAL FACTORS EFFECTING WOUND HEALING
Age: The younger the patient the more rapid the healing
Nutrition: Malnutrition impedes the healing process. The prime nutritional factors are protein,
Vitamin C for the synthesis of ground substance
Vitamin A for epithelisation
Vitamin D for bone formation
Vascularity: Highly vascular areas like face and scalp heal better than less vascular areas like the pretibial region.
This is because the level of oxygen available for the healing process is less, thus tight sutures, tight bandaging and hypotension can impede healing.
Local sepsis: This is the most common factor delaying healing of wounds in practice.
Diabetes: Wound healing is affected by diabetes. (Poor blood flow, high cortisol levels , high infections the mechanism is not understood).
Control of blood sugar restores the normal healing
Cortico: Steroid therapy impairs inflamation steroids epithelialisation and collagen synthesis
Radiation : Both have a significant effect on dividing cells chemotherapy and these effect fibroblasts and keratinocytes.
Thus both of these shoud be avoided for 5-7 days post-operatively.
Any questions be sent to drmmkapur@gmail.com
These are released by many activated cells in a healing wound. These factors stimulate cell proliferation, migration and synthesis of required products. Among the cytokines is TGFB that helps all phase of healing. Topical application of TGFB acclerates wound healing.
Angiogenesis is simulated by acid and basic fibroblast growth factors (aFGF + bFGF). Epithelialisation is stimulated by epithelial growth factor (EGF) and keratinocyte growth factor (KGF).
4. CLINICAL FACTORS EFFECTING WOUND HEALING
Age: The younger the patient the more rapid the healing
Nutrition: Malnutrition impedes the healing process. The prime nutritional factors are protein,
Vitamin C for the synthesis of ground substance
Vitamin A for epithelisation
Vitamin D for bone formation
Vascularity: Highly vascular areas like face and scalp heal better than less vascular areas like the pretibial region.
This is because the level of oxygen available for the healing process is less, thus tight sutures, tight bandaging and hypotension can impede healing.
Local sepsis: This is the most common factor delaying healing of wounds in practice.
Diabetes: Wound healing is affected by diabetes. (Poor blood flow, high cortisol levels , high infections the mechanism is not understood).
Control of blood sugar restores the normal healing
Cortico: Steroid therapy impairs inflamation steroids epithelialisation and collagen synthesis
Radiation : Both have a significant effect on dividing cells chemotherapy and these effect fibroblasts and keratinocytes.
Thus both of these shoud be avoided for 5-7 days post-operatively.
Any questions be sent to drmmkapur@gmail.com
Sunday, April 25, 2010
WOUNDS 4
Healing 4
2.2.3 PROLIFERATIVE PHASE (FIBROPLASIA) Within 10 hours, if no infection, occurs, fibroblasts begin to migrate and lay down collagen. In the Incremental phase the fibroblasts continue to produce larger quantity of collagen and the tensile strength of the healing wound increases. More fibroblasts appear perhaps from the primitive mesodermal stem cells and this further increases the quantity of collagen produced by the endoplasmic reticulum of the fibroblasts and forms cross banded fibrils; fibroblasts also manufacture mucopolysaccharide ground substance. This helps the alignment and approximation of the collagen.
Within 2 to 3 days, the inflammatory cell population begins to change to one of monocyte predominance. These mono cytes are attracted and infiltrate the wound site. These monocytes differentiate into macrophages, and in conjunction with resident macrophages, join the repair process. Macrophages not only continue to phagocytose tissue and bacterial debris, but also secrete multiple growth factors. These peptide growth factors activate and attract local endothelial cells, fibroblasts, and keratinocytes to begin their respective repair functions. More than 20 different cytokines and growth factors are known to be secreted by macrophages, the primary cells responsible for regulating repair.
Ell Proliferation (FIBROPLASIA )
*The proliferating phase starts with this deposition of febrin and fibrinogen matrix and the activation and production of local fibroblasts (fibroplasial). At the beginning fibrin fibrinogen matrix is populated with platelets and macrophages. These macrophages and the local extra cellular matrix (ECM) release growth factors that initiate fibroblast activation.
Fibroblasts migrate into the wound using the newly deposited fibrin and fibronectin matrix as a scaffold.
Local fibroblasts become activated and increase protein synthesis in preparation for cell division.
As fibroblasts proliferate, they become the prominent cell type in 3 to 5 days in clean, non infected wounds, After cell division and proliferation, fibroblast begin synthesis and secretion of extra cellular matrix products. The initial wound matrix is temporary and is composed of fibrin and the glycosaminoglycan (GAG), hyaluronic acid. Because of its large water of hydration, hyaluronic acid provides and matrix that helps cell migration.
As fibroblasts enter and populate the wound, they use hyaluronidase to digest the provisional hyaluronic acid-rich matrix, and larger, gulfated GAGs deposited in addition collagens are deposited here and there by fibroblasts onto the fibroneetin and GAG scaffold.
Collagen types I and III are the major fibrillar collagens comprising the extracellular matrix and are the major structural proteins both in unwounded and wounded skin.
There are now at least 19 different types of collagens described, each of which shares the right handed triple helix as the bias structural unit. Most collagen types are synthesized by fibroblasts, however, it is now known that some types are synthesized by epidermal cells.*
2.2.4 EPETHELIALISATION: The keratinocytes in the skin at the site of injury show activity. The epidermis thickens, the basal cells enlarge and move over to cover the wound defect. The fixed basal cell divide and the new cells cover the defect. Adhesion glycoproteins (fibronectin) provide direction and tracks for these cells till the cover is complete.
*Within hours after injury, morphological changes can be seen in karatinocytes at the wound margin.
In skin wounds the epidermis thickens, and marginal basal cells enlarge and migrate over the wound defect.
Wound closure is provided by fixed basal cells in a zone near the edge of the wound. Their daughter cells flatten and migrate over the wound matrix as a sheet. Cells adhesion glycoprotcins, such as tenascin and fibrocction provide the “railroad tracks” to facilitate epithelial cell migration over the wound matrix. Following the restablishment of the epithelial layer, jeratinocytes and fibriblasts secrete laminin and type IV collagen to form the basement membrance. The kertinocytes then become columnar and divide as the layering of the epidermis is established, thus reforming a barrier to further contamination and moisture loss of the wound.
The ultimate pattern of collagen is scar is one of densely packed fibers and not the reticular pattern found in unwounded dermis.*
2.2.5 REMODELLING: The extracellular matrix is a network of protein and polysaccharides. Collagen is the main component of this matrix.
Fibroblasts also contain myofibrilis which help to pull the wound edges together.This wound contraction further adds to the tensile strength.
*During remodeling, wounds gradually becomes stronger with time. Wound tensile strength increases rapidly form 1 to 8 weeks post wounding. Thereafter, tensile strength increases at a slower pace and has been documented to increase up to 1 year after wounding in animal studies. However, the tensile strength of wounded skin at best only reaches approximately 80% that of unwounded skin. The final result of tissue repair is scar, which is brittle, less elastic than normal skin, and does not contain any skin appendages such as hair follicles or sweat glands.*
2.2.6 CLINICAL WOUND HEALING OPEN WOUNDS: At the end of 4 weeks an uncomplicated wound has reached
• 50% of its final strength
• 75% at the end of 8 weeks and
• Nearly 95% after 6 months
• A dialogue will emerge if questions are received.I will respond to them
drmmkapur@yahoo.com
The information in large print is sufficient for your undergraduate course. The sections between astrix* knowledge is required for the higher postgraduate courses.
2.2.3 PROLIFERATIVE PHASE (FIBROPLASIA) Within 10 hours, if no infection, occurs, fibroblasts begin to migrate and lay down collagen. In the Incremental phase the fibroblasts continue to produce larger quantity of collagen and the tensile strength of the healing wound increases. More fibroblasts appear perhaps from the primitive mesodermal stem cells and this further increases the quantity of collagen produced by the endoplasmic reticulum of the fibroblasts and forms cross banded fibrils; fibroblasts also manufacture mucopolysaccharide ground substance. This helps the alignment and approximation of the collagen.
Within 2 to 3 days, the inflammatory cell population begins to change to one of monocyte predominance. These mono cytes are attracted and infiltrate the wound site. These monocytes differentiate into macrophages, and in conjunction with resident macrophages, join the repair process. Macrophages not only continue to phagocytose tissue and bacterial debris, but also secrete multiple growth factors. These peptide growth factors activate and attract local endothelial cells, fibroblasts, and keratinocytes to begin their respective repair functions. More than 20 different cytokines and growth factors are known to be secreted by macrophages, the primary cells responsible for regulating repair.
Ell Proliferation (FIBROPLASIA )
*The proliferating phase starts with this deposition of febrin and fibrinogen matrix and the activation and production of local fibroblasts (fibroplasial). At the beginning fibrin fibrinogen matrix is populated with platelets and macrophages. These macrophages and the local extra cellular matrix (ECM) release growth factors that initiate fibroblast activation.
Fibroblasts migrate into the wound using the newly deposited fibrin and fibronectin matrix as a scaffold.
Local fibroblasts become activated and increase protein synthesis in preparation for cell division.
As fibroblasts proliferate, they become the prominent cell type in 3 to 5 days in clean, non infected wounds, After cell division and proliferation, fibroblast begin synthesis and secretion of extra cellular matrix products. The initial wound matrix is temporary and is composed of fibrin and the glycosaminoglycan (GAG), hyaluronic acid. Because of its large water of hydration, hyaluronic acid provides and matrix that helps cell migration.
As fibroblasts enter and populate the wound, they use hyaluronidase to digest the provisional hyaluronic acid-rich matrix, and larger, gulfated GAGs deposited in addition collagens are deposited here and there by fibroblasts onto the fibroneetin and GAG scaffold.
Collagen types I and III are the major fibrillar collagens comprising the extracellular matrix and are the major structural proteins both in unwounded and wounded skin.
There are now at least 19 different types of collagens described, each of which shares the right handed triple helix as the bias structural unit. Most collagen types are synthesized by fibroblasts, however, it is now known that some types are synthesized by epidermal cells.*
2.2.4 EPETHELIALISATION: The keratinocytes in the skin at the site of injury show activity. The epidermis thickens, the basal cells enlarge and move over to cover the wound defect. The fixed basal cell divide and the new cells cover the defect. Adhesion glycoproteins (fibronectin) provide direction and tracks for these cells till the cover is complete.
*Within hours after injury, morphological changes can be seen in karatinocytes at the wound margin.
In skin wounds the epidermis thickens, and marginal basal cells enlarge and migrate over the wound defect.
Wound closure is provided by fixed basal cells in a zone near the edge of the wound. Their daughter cells flatten and migrate over the wound matrix as a sheet. Cells adhesion glycoprotcins, such as tenascin and fibrocction provide the “railroad tracks” to facilitate epithelial cell migration over the wound matrix. Following the restablishment of the epithelial layer, jeratinocytes and fibriblasts secrete laminin and type IV collagen to form the basement membrance. The kertinocytes then become columnar and divide as the layering of the epidermis is established, thus reforming a barrier to further contamination and moisture loss of the wound.
The ultimate pattern of collagen is scar is one of densely packed fibers and not the reticular pattern found in unwounded dermis.*
2.2.5 REMODELLING: The extracellular matrix is a network of protein and polysaccharides. Collagen is the main component of this matrix.
Fibroblasts also contain myofibrilis which help to pull the wound edges together.This wound contraction further adds to the tensile strength.
*During remodeling, wounds gradually becomes stronger with time. Wound tensile strength increases rapidly form 1 to 8 weeks post wounding. Thereafter, tensile strength increases at a slower pace and has been documented to increase up to 1 year after wounding in animal studies. However, the tensile strength of wounded skin at best only reaches approximately 80% that of unwounded skin. The final result of tissue repair is scar, which is brittle, less elastic than normal skin, and does not contain any skin appendages such as hair follicles or sweat glands.*
2.2.6 CLINICAL WOUND HEALING OPEN WOUNDS: At the end of 4 weeks an uncomplicated wound has reached
• 50% of its final strength
• 75% at the end of 8 weeks and
• Nearly 95% after 6 months
• A dialogue will emerge if questions are received.I will respond to them
drmmkapur@yahoo.com
The information in large print is sufficient for your undergraduate course. The sections between astrix* knowledge is required for the higher postgraduate courses.
WOUNDS 3
Healing 3
2.2 WOUND HEALING IN PRACTICE
Wound healing is best studied in a clean sutured surgical wound. The features of wound healing are common to all clean wounds in any tissue. The healing phases follow one another and also overlap.
2.2.1 Hemostasis Phase (Coagulation) starts immediately with release of bradykinins serotonin and histamine (Mast cells) causing Vasoconstriction and diapedesis (migration) of cells.
Fig 1.5
Platelets release clotting factors leading to production of fibrin. They also produce cytokinins the wound hormone.
2.2.2 INFLAMMATION PHASE: It is also referred to as Lag phase. This phase starts soon after injury and displays all the features described under inflammation. The exudate is partly reabsorbed and dead tissue removed by phagocytosis.
2.2.2.1 GRANULATION: This is the pink irregular surfaced tissue seen in all wounds that have no skin cover.
It is full of fibroblasts derived from cells around the wound.
Within this there is also a network of capillary endothelial growth.
These fibroblast grow into and onto the fibrin and fibronectin matrix already present as a result of the coagulation process setup during the inflamation phase.
The granulation is infiltrated with macrophages.
The fibroblasts use hyaluronidase to digest the matrix and lay down collagen.
*Granulation tissue is present in all wounds healing by secondary intention. This tissue is clinically characterized by the most like red appearance (i.e. “proud flash”) which is because of the rich bed of new capillary networks (neoangiogenesis) that have formed form endothelial cell division and migration. The directed growth of vascular endothelial cells is stimulated by platelet and activated macrophage and fibroblast products. One example is vascular endothelial growth factors, which is secreted by macrophages and acts to induce migration and proliferation of endothelial cells.
Cranulation tissue is a dense population of blood vessels, macrophages, and fiboblasts embedded within a loose provisional matrix of fibronection, hyaluronic acid and collagen.
The presence of granulation tissue is used as clinical indictor that the wound is ready for skin graft treatment. Wounds that benefit from skin grafts are of sufficient size such that the healing time would be decreased. The high degree of vascularity enables granulation tissue to readily accept and support skin grafts.*
Contraction
Open wounds partially healed by contraction this is minimal in closed surgical incioions. Open wound occurs after trauma, burns and when previously closed wounds are re-opened because of infection.
In practice wound contraction can be in excess, and can lead to contractures which results in decreased function. This is seen most often contracture near joints
Your comments and questions will result in a dialogue drmmkapur@gmail.com
2.2 WOUND HEALING IN PRACTICE
Wound healing is best studied in a clean sutured surgical wound. The features of wound healing are common to all clean wounds in any tissue. The healing phases follow one another and also overlap.
2.2.1 Hemostasis Phase (Coagulation) starts immediately with release of bradykinins serotonin and histamine (Mast cells) causing Vasoconstriction and diapedesis (migration) of cells.
Fig 1.5
Platelets release clotting factors leading to production of fibrin. They also produce cytokinins the wound hormone.
2.2.2 INFLAMMATION PHASE: It is also referred to as Lag phase. This phase starts soon after injury and displays all the features described under inflammation. The exudate is partly reabsorbed and dead tissue removed by phagocytosis.
2.2.2.1 GRANULATION: This is the pink irregular surfaced tissue seen in all wounds that have no skin cover.
It is full of fibroblasts derived from cells around the wound.
Within this there is also a network of capillary endothelial growth.
These fibroblast grow into and onto the fibrin and fibronectin matrix already present as a result of the coagulation process setup during the inflamation phase.
The granulation is infiltrated with macrophages.
The fibroblasts use hyaluronidase to digest the matrix and lay down collagen.
*Granulation tissue is present in all wounds healing by secondary intention. This tissue is clinically characterized by the most like red appearance (i.e. “proud flash”) which is because of the rich bed of new capillary networks (neoangiogenesis) that have formed form endothelial cell division and migration. The directed growth of vascular endothelial cells is stimulated by platelet and activated macrophage and fibroblast products. One example is vascular endothelial growth factors, which is secreted by macrophages and acts to induce migration and proliferation of endothelial cells.
Cranulation tissue is a dense population of blood vessels, macrophages, and fiboblasts embedded within a loose provisional matrix of fibronection, hyaluronic acid and collagen.
The presence of granulation tissue is used as clinical indictor that the wound is ready for skin graft treatment. Wounds that benefit from skin grafts are of sufficient size such that the healing time would be decreased. The high degree of vascularity enables granulation tissue to readily accept and support skin grafts.*
Contraction
Open wounds partially healed by contraction this is minimal in closed surgical incioions. Open wound occurs after trauma, burns and when previously closed wounds are re-opened because of infection.
In practice wound contraction can be in excess, and can lead to contractures which results in decreased function. This is seen most often contracture near joints
Your comments and questions will result in a dialogue drmmkapur@gmail.com
WOUNDS 2
HEALING 2
1.2 CLINICAL FEATURES
Acute inflammation due to any cause is manifest by:
• Rubor: Redness due to the dilated vessels
• Calor: Local heat due to excess blood flow
• Edema: Swelling due to inflammatory exudate
• Dolor: Pain due to the exudate and specific pain factors
• Functio-laesor: loss of function
The inflammatory process may:
1.2.1 RESOLVE completely when the exudate is reabsorbed and the particulate necrosed cellular elements are phagocytosed.(removed by macrophages)
This is achieved when there is minimal injury, the injured part i.e. rested and the skin and deeper part are in continuity. This is referred to as healing by PRIMARY intent
1.2.2 SUPPURATION occurs following bacterial inflammation at the start of injury or when infection is superadded on the injured tissue at a later date. The pus formed is a combination of liquefied injured cells, W.B.C. and in addition dead and alive causative bacteria (thus the need of pus for culture).
1.2.3 ULCERATION occurs if the injury is close to the surface. Epithelium (skin, mucosa) is destroyed and this allows bacteria to infect the exposed deeper structures.
1.2.4 GANGRENE is diagnosed when there is change of colour and viability is lost of a large volume of tissue and, usually occurs due to injury to the blood supply of that part.
1.2.5 FIBROSIS is the end result in all varieties of above events except those that resolve. There is in all other cases, a loss of tissue which is replaced by fibrosis. There is thus a delay in return of function and in some cases there may be a permanent loss of a certain amount of function. This is healing by SECONDARY intent
1.3 MANAGEMENT
1.3.1 All inflamed parts require REST. Raising the part will reduce the pain by avoiding dependant edema. Compression dressing will also help. However, it must not be so tight as to impede arterial flow. ANALGESICS anti-inflammatory drugs and ANTIBIOTICS may be required.
1.3.2 If the patient shows swinging temperatures, throbbing pain in the part and in superficial inflammations, local edema, tense shinning overlying skin, local redness and fluctuation, an abscess must be suspected (aspirate to confirm). These patients will require drainage of the abscess under antibiotic cover using local or generalized anesthesia.
Hilton’s method of skin incision in the long axis of the limbs to avoid injury to vessel and nerves is used, the abscess is entered with a sinus forceps (Fig.1.2). The index finger is then introduced to break all the septa in the abscess cavity, which is now closed with a drain in the cavity or left open with a dressing pack. Frequent dressings will be required till the wound heals by SECONDARY intent.
Your comments and Questions are the starting point of a dialogue drmmkapur@gmail.com
1.2 CLINICAL FEATURES
Acute inflammation due to any cause is manifest by:
• Rubor: Redness due to the dilated vessels
• Calor: Local heat due to excess blood flow
• Edema: Swelling due to inflammatory exudate
• Dolor: Pain due to the exudate and specific pain factors
• Functio-laesor: loss of function
The inflammatory process may:
1.2.1 RESOLVE completely when the exudate is reabsorbed and the particulate necrosed cellular elements are phagocytosed.(removed by macrophages)
This is achieved when there is minimal injury, the injured part i.e. rested and the skin and deeper part are in continuity. This is referred to as healing by PRIMARY intent
1.2.2 SUPPURATION occurs following bacterial inflammation at the start of injury or when infection is superadded on the injured tissue at a later date. The pus formed is a combination of liquefied injured cells, W.B.C. and in addition dead and alive causative bacteria (thus the need of pus for culture).
1.2.3 ULCERATION occurs if the injury is close to the surface. Epithelium (skin, mucosa) is destroyed and this allows bacteria to infect the exposed deeper structures.
1.2.4 GANGRENE is diagnosed when there is change of colour and viability is lost of a large volume of tissue and, usually occurs due to injury to the blood supply of that part.
1.2.5 FIBROSIS is the end result in all varieties of above events except those that resolve. There is in all other cases, a loss of tissue which is replaced by fibrosis. There is thus a delay in return of function and in some cases there may be a permanent loss of a certain amount of function. This is healing by SECONDARY intent
1.3 MANAGEMENT
1.3.1 All inflamed parts require REST. Raising the part will reduce the pain by avoiding dependant edema. Compression dressing will also help. However, it must not be so tight as to impede arterial flow. ANALGESICS anti-inflammatory drugs and ANTIBIOTICS may be required.
1.3.2 If the patient shows swinging temperatures, throbbing pain in the part and in superficial inflammations, local edema, tense shinning overlying skin, local redness and fluctuation, an abscess must be suspected (aspirate to confirm). These patients will require drainage of the abscess under antibiotic cover using local or generalized anesthesia.
Hilton’s method of skin incision in the long axis of the limbs to avoid injury to vessel and nerves is used, the abscess is entered with a sinus forceps (Fig.1.2). The index finger is then introduced to break all the septa in the abscess cavity, which is now closed with a drain in the cavity or left open with a dressing pack. Frequent dressings will be required till the wound heals by SECONDARY intent.
Your comments and Questions are the starting point of a dialogue drmmkapur@gmail.com
WOUND HEALING 1
1. WOUND HEALING Process
All living tissue responds to any injury with inflammation. This process is a part of the healing of the wound caused by physical injury and must be differentiated from infection caused by bacterial injury because the treatment differs.
Inflammation has similar characteristics in all modes of injury, which may be caused by:
• Physical trauma (including surgical trauma).
• Thermal: heat and cold
• Radiation, chemicals and
• Infection
The three overlapping time segments of the repair process are inflammation, proliferation, and remodeling. During the inflammatory phase homeostasis occurs and an acute inflammatory infiltrates are produced.
The proliferative phase has fibroplasia, granulation, contraction, and epithelizlization.
The final phase is remodeling which involves scar maturation.
Inflammation
Inflammation precedes the process of wound healing.
After tissue injury, the injured vessel immediately constrict and thromboplastic tissue products many from the sub endothelium, are released.
Platelets aggregates form the initial homeostatic(blood stopping) plug. The coagulation and complement cascades are initiated.
The intrinsic and extrinsic coagulation pathways lead to activation of prothrombin to thrombin, that converts fibrinogen to fibrin, this is subsequently polymerized into a stable clot.
As thrombus is formed, homeostasis in the wound is complete.
The aggregated platelets degranulate releasing powerful chemo attractants for inflammatory cells, activation factors for local fibroblasts and endothelial cells, and vasoconstrictors.
Platelet adhesiveness is achieved through integrin receptors such as GPIIIa
1.1
- The inflammatory response begins with local vaso-constriction
Platelets release granules providing
• Growth factor
• Adhesive glycoproteins
• Vasoactive serotonin
• Hydrolases
Fig 1.1
- The arterioles in the area of injury subsequently show dilation and increased blood flow.
- There is, in addition, opening of new capillaries resulting in congestion with excess blood and slowing of blood flow in the venous channels.
- The R.B.C. separate out and form a central core in the lumen of the capillaries.
- The W.B.Cs are displaced towards the walls (margination) of the capillaries and there is increased permeability due to serotenin with exudation of fluid into the surrounding tissue,
The chemical factors that initiate these events are histamine, serotonin, bradykinin, complement factors and prostaglandin’s.
- The W.B.C. (Neutrophils+ Monocytes) exit from the vessels by chemotaxisis and aggregate at the site of injury.
- The monocytes differentiate into macrophages and show phagocytosis.
*The repair process is initiated within minutes after on injury.
After the transient vasoconstriction induced by platelet factors local small vessels dilate caused by the effects of the coagulation and complement cascades.
Bradykinin is a potent vaso dilutor and a vascular permeability factor that is generated by activation of Hageman factor in the coagulation cascade.
The complement cascade generates the C3 and C5 anaphylatoxins, which directly increase blood vessel permeability and attract ncutrophils and monocytes to the wound area..
These complement components also stimulate the release of histamine and leukotrienes C4 and D4 form mast cells. The local endothelial cells then break cell to cell contact, which enhances the migration of inflammatory cells into the wound site.
White blood cells (first neutrophils, later monocytes) and plasma proteins leak form the blood vessel and enter the wound site. The early neutrophil infiltrate remove cellular debris, foreign bodies and bacteria. Activated complement fragments aid in bacterial killing through opsonization.
The primary role of the neutrophil is to sterilize the wound. The initial neutrophil infiltrate is decreased in clean surgical wounds when compared to contaminated or infected wounds.
The environment in the wound space is hypoxic, hypoglycemic and acidotic.*
The objective of all these events is protective. The final outcome is removal of the causative agents and the effects produced by these agents (necrotic tissue and cells) leading finally to repair.
The information in between astrix* is basic sciences data that will help those with a an interest postgraduate courses.
Send all questions to drmmkapur@gmail.com
All living tissue responds to any injury with inflammation. This process is a part of the healing of the wound caused by physical injury and must be differentiated from infection caused by bacterial injury because the treatment differs.
Inflammation has similar characteristics in all modes of injury, which may be caused by:
• Physical trauma (including surgical trauma).
• Thermal: heat and cold
• Radiation, chemicals and
• Infection
The three overlapping time segments of the repair process are inflammation, proliferation, and remodeling. During the inflammatory phase homeostasis occurs and an acute inflammatory infiltrates are produced.
The proliferative phase has fibroplasia, granulation, contraction, and epithelizlization.
The final phase is remodeling which involves scar maturation.
Inflammation
Inflammation precedes the process of wound healing.
After tissue injury, the injured vessel immediately constrict and thromboplastic tissue products many from the sub endothelium, are released.
Platelets aggregates form the initial homeostatic(blood stopping) plug. The coagulation and complement cascades are initiated.
The intrinsic and extrinsic coagulation pathways lead to activation of prothrombin to thrombin, that converts fibrinogen to fibrin, this is subsequently polymerized into a stable clot.
As thrombus is formed, homeostasis in the wound is complete.
The aggregated platelets degranulate releasing powerful chemo attractants for inflammatory cells, activation factors for local fibroblasts and endothelial cells, and vasoconstrictors.
Platelet adhesiveness is achieved through integrin receptors such as GPIIIa
1.1
- The inflammatory response begins with local vaso-constriction
Platelets release granules providing
• Growth factor
• Adhesive glycoproteins
• Vasoactive serotonin
• Hydrolases
Fig 1.1
- The arterioles in the area of injury subsequently show dilation and increased blood flow.
- There is, in addition, opening of new capillaries resulting in congestion with excess blood and slowing of blood flow in the venous channels.
- The R.B.C. separate out and form a central core in the lumen of the capillaries.
- The W.B.Cs are displaced towards the walls (margination) of the capillaries and there is increased permeability due to serotenin with exudation of fluid into the surrounding tissue,
The chemical factors that initiate these events are histamine, serotonin, bradykinin, complement factors and prostaglandin’s.
- The W.B.C. (Neutrophils+ Monocytes) exit from the vessels by chemotaxisis and aggregate at the site of injury.
- The monocytes differentiate into macrophages and show phagocytosis.
*The repair process is initiated within minutes after on injury.
After the transient vasoconstriction induced by platelet factors local small vessels dilate caused by the effects of the coagulation and complement cascades.
Bradykinin is a potent vaso dilutor and a vascular permeability factor that is generated by activation of Hageman factor in the coagulation cascade.
The complement cascade generates the C3 and C5 anaphylatoxins, which directly increase blood vessel permeability and attract ncutrophils and monocytes to the wound area..
These complement components also stimulate the release of histamine and leukotrienes C4 and D4 form mast cells. The local endothelial cells then break cell to cell contact, which enhances the migration of inflammatory cells into the wound site.
White blood cells (first neutrophils, later monocytes) and plasma proteins leak form the blood vessel and enter the wound site. The early neutrophil infiltrate remove cellular debris, foreign bodies and bacteria. Activated complement fragments aid in bacterial killing through opsonization.
The primary role of the neutrophil is to sterilize the wound. The initial neutrophil infiltrate is decreased in clean surgical wounds when compared to contaminated or infected wounds.
The environment in the wound space is hypoxic, hypoglycemic and acidotic.*
The objective of all these events is protective. The final outcome is removal of the causative agents and the effects produced by these agents (necrotic tissue and cells) leading finally to repair.
The information in between astrix* is basic sciences data that will help those with a an interest postgraduate courses.
Send all questions to drmmkapur@gmail.com
FOCUS ON YOU
SURGSEMINAR 2
The subject headings list is vast (nearly 50) and each post needs to be short (3-500 words)
To achieve your sustained interest we will stay within your attention span.
The format of small group discourse is required to insure your participation in the dialogue.
The items have sub headings and hierarchal numberings preceding the sub headings
This will facilitate identification of issue and focus the discourse and help define meaningful dialogue.
Your feedback is my food for thought. It is nutrition to insure this effort has a future.
The subjects and their subheadings are essential in my way of thinking, Additions,
Curtailments or suggestions are welcome, and will receive consideration
drmmkapur@gmail.com
The subject headings list is vast (nearly 50) and each post needs to be short (3-500 words)
To achieve your sustained interest we will stay within your attention span.
The format of small group discourse is required to insure your participation in the dialogue.
The items have sub headings and hierarchal numberings preceding the sub headings
This will facilitate identification of issue and focus the discourse and help define meaningful dialogue.
Your feedback is my food for thought. It is nutrition to insure this effort has a future.
The subjects and their subheadings are essential in my way of thinking, Additions,
Curtailments or suggestions are welcome, and will receive consideration
drmmkapur@gmail.com
Monday, April 19, 2010
FOCUSED FOR YOU
SURGSEMINAR 1
You will benefit from the information transfer in these posts if you are
An undergraduate,
Aspiring post graduate, or
In general practice with a surgery OT.
A comprehensive textbook covering the entire range of issues related to the practice of surgery is of formidable size, with a price range out of the reach of most students.
The issues of size and price are also of concern for the Publishers, limiting the choice of
Texts available in print for the student, and the practice community
I have for this reason planned to make the text based on my updated lecture notes of my years as teacher at the AIIMS available on the internet thru this Blog.
I indeed hope a dialogue will emerge. The responses and comments will give us all a much needed feedback from students and with luck from Peers.
I hope in time to develop a CD and print version of this text incorporating feedback received.
The CD and Print version will have;
Illustrations.
Decision making flowcharts related to text information.
Summary boxed information for revision and recall
This effort is required for all do not have access to the internet.
drmmkapur@gmail.com
You will benefit from the information transfer in these posts if you are
An undergraduate,
Aspiring post graduate, or
In general practice with a surgery OT.
A comprehensive textbook covering the entire range of issues related to the practice of surgery is of formidable size, with a price range out of the reach of most students.
The issues of size and price are also of concern for the Publishers, limiting the choice of
Texts available in print for the student, and the practice community
I have for this reason planned to make the text based on my updated lecture notes of my years as teacher at the AIIMS available on the internet thru this Blog.
I indeed hope a dialogue will emerge. The responses and comments will give us all a much needed feedback from students and with luck from Peers.
I hope in time to develop a CD and print version of this text incorporating feedback received.
The CD and Print version will have;
Illustrations.
Decision making flowcharts related to text information.
Summary boxed information for revision and recall
This effort is required for all do not have access to the internet.
drmmkapur@gmail.com
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