HEMOSTASIS AND BLEEDING DISORDERS
In health blood in the Blood vessels stays in the
fluid state.
This is essential for delivery of oxygen and nutrients
**Blood composition and Formation
The Blood is made up of two components:
- The plasma and
- The cellular elements floating in it.
The plasma represents the fluid fraction and accounts for 55% of the total blood volume; plasma volume is estimated to be roughly 7% to 8% of the total body weight.
The plasma reaches the tissues and provides nutrients and soluble ions, and carries proteins (such as albumin, complement immunoglobulin, and enzymes) to the cells and tissues.
-The cellular component represents 45% of the blood volume and is divided into three major cell type erythrocytes, leukocytes, and megakaryocytes.
-Each of these cells can be traced back to a single pluripotent stem cell.
-Erythrocytes (Red Blood Cells) function is to carry oxygen to body tissues.
-Leukocytes (White Blood Cells) are a variety of more specialized cells, whose function involves host defense and immunity. The last major cell type is the megakaryocyte. -Platelets and endothelial cells are derived from this cell line and are essential for the mechanisms of hemostasis.
-The process of blood formation is called hematopoiesis. Hematopoiesis is an ongoing, lifelong process in the bone marrow in the adult.
-The production of blood cells starts in the yolk sac of the embryo and continues throughout the first trimester.
-Extramedullary hematopoiesis (outside the bone marrow) begins during the third gestational month in the fetal liver.
-The spleen, kidneys, thymus, and lymph nodes are responsible for a minor role in hematopoiesis during fetal development.
-After birth, the lymph nodes assume a primary function in the proliferation and differentiation of leukocytes and lymphocytes, while the bone marrow takes over as the major source of blood cell production.
-Similarly, the liver and spleen assume important role in the reticuloendothelial system for the destruction and turnover (apoptosis) of aged and dysfunctional cells.
Red Blood Cell
The normal red blood cell is a biconcave disk approximately to 7.5ยต in diameter. It is the major component of the cellular compartment of the blood, with a circulating life of about 100 to 120 days.
The primary role of RBC is to deliver oxygen to the tissues for metabolism and carry dissolved carbon dioxide to the lungs for release into the air. The red cell depends on the hemoglobin molecule to for transport of these gases.
The number of erythrocytes in the blood ranges form 3.8 to 5.9 million cells per micro liter of blood, with a hemoglobin concentration ranging form 17 to 17g/dl and a hematocrit of 35% to 52%.
This normal range is broad for it cover men and women young and old, and with people living at altitude. Induced erythropeiesis, leading to the expansion of red cell mass, occurs in response to hypoxia, blood loss, and a variety of hormones and disease states.
The most potent stimulator of erythropoiesis is erythropoietin.
Erythropoietin is a hormone produced by the kidney in response to hypoxia. This hormone stimulates the pluripotent stem cells in the bone marrow to become mature.
The bone marrow is capable of increasing the production of red cells by 5 to 10 times normal under the influence of erythropoietin. However, because of the limiting factor of iron in diet the increase is only two to three times normal.
In patients with chronic renal failure or after a nephrectomy, the ability to generate a erythropoietin response is slower.**
Any questions be sent to drmmkapur@gmail.com
Monday, May 3, 2010
Tuesday, April 27, 2010
WOUND COMPLICATIONS
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
• 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
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
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