2-3 wound healing Flashcards
what is wound healing
mechanism whereby the body attempts to restore the integrity of the injured part.
what is Sanatio per Primum
which kinds of wounds heal this way
primary intention healing
- wounds with smooth edges in close proximity
- NO infection or without scar necrosis
- surgical wounds that are surgically treated and sutured
- in 6-8 days a gentle linear scar is formed
- stitches removed in 7-10 days
- this is called First intention closure
- Wound edges opposed. Normal healing. Minimal scars
- skin graft placement, or flap closure
Complications of Sana per Primum
- dehiscencte- reopening of the wound
- bleeding from the wound
- suppuration - redness - infiltrate - purulent collection
what is Sana per Secundum
describe it’s characterisics
why is there a formation of large granulations
explain the procedure
wound healing by Secondary Intention
characteristics
- for larger wounds with edges that are far apart
- wounds infected with necrotic tissue and thus closure is C.I
procedure
- Wound is left open to heal by granulation, contraction and epithelialisation to seal it from the base upwards
- covered to prevent drying of wound and promote healing
- Increased inflammation and proliferation compraed to first intension results in a larger scar and less functioning tissue upon healing
what is San Sub crustam
when is it employed
tertiary intention (also called delayed primary intention) used in superficial wounds
procedure
- Wound initially left open
- Edges later opposed when healing conditions are favourable
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what are the 3 phases of wound healing and when do they occur
- inflammatory/migratory/destructive phase: 0-3 days
- proliferation phase: day 3 - 3 weeks
- maturation phase: 6 weeks-1-2 years
describe the inflammatory phase
what is the initial structural support in this phase
- after onset of the trauma bleeding occurs and damaged epithelial tissue relases cytokines & vasoactive amines (hps)
- such as histamine, prostaglandins and ,serotonin
- this is followed by vasoconstriction and thrombus formation to limit blood loss.
- Platelets stick to the damaged endothelial lining of vessels, releasing adenosine diphosphate (ADP), which causes thrombocytic aggregation to fill the wound.
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When bleeding stops, the platelets then release cytokines from their alpha granules.
- plateletderived growth factor (PDGF), platelet factor IV and transforming growth factor beta (TGFβ).
- cytokines attract inflammatory cells such as polymorphonuclear lymphocytes aka neutrophils and macrophages.
- Platelets also release HSP vasoactive amines to increase vascular permeability, thereby aiding infiltration of these inflammatory cells.
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Macrophages have 2 functions
- remove dead tissue and micro-organisms
- regulating fibroblast activity in the proliferative phase
The initial framework for structural support of cells is provided by fibrin produced by fibrinogen.
describe the proliferative phase
what is the wound tissue formed at the end of this stage that is also the main mechanism in secondary intention (sana per secundum
what is the nature and type of collagen in this phase and how does it affect the strength of the wound
- The proliferative phase lasts from the third day to the third week
- macrophages regulate this phase by doing the following
- release growth factors to regulate fibroblast activity
- fribroblasts make collagen using vitamin C and ground substance (glycosaminoglycans and proteoglycans),
- release GF’s for (angioneogenesis)
- release GF’s thgat stim epithelial mitosis for the sake of re-epithelialisation of the wound surface. .
- release growth factors to regulate fibroblast activity
- The wound tissue formed in the early part of this phase is called granulation tissue.
- there is an increase in the tensile strength of the wound due to increased collagen, which is at first deposited in a random fashion and consists of type III collagen.
describe the remodelling phase
- The remodelling phase is characterised by maturation of collagen:
- __type I replacing type III until a ratio of 4:1 is achieved).
- There is a realignment of collagen fibres along the lines of tension,
- decreased wound vascularity
- wound contraction due tofibroblast and myofibroblast activity.
list the 2 types of factors that affect wound healing
Local:
- site of the wound
- structures involved in the wound
- mechanism of the wounding -
- Crush -Incision -Crush avulsion
Systemic
- malnutrition
- vit c required for collagen synthesis
- diseases- DB mellitus
- medications - steroids
- immune deficiencies
- smoking
- explosions causing contamination from other ppl’s tissues
what are the 4 types of wounds
describe thr caharacteristics of each
which wounds are related to the genitourinary tract, billiary tract and viscera
• Clean
- Non-traumatic, uninfected operative wound
- No break in sterile technique
- Respiratory, alimentary or genitourinary tract not entered
• Clean-Contaminated
- Gastrointestinal or respiratory tract entered without significant spillage
- Oropharynx, vagina,
- non-infected genitourinary or biliary tract entered
- Minor break in sterile technique
• Contaminated
- Soft tissue lacerations, open fractures, penetrating wounds and other trauma
- Major break in sterile technique
- Traumatic wound
- Gross spillage from GI tract
- Entrance into genitourinary or biliary tracts in presence of infected urine or bile
• Dirty
- Wounds that are heavily contaminated
- Wounds that are clinically infected pre-op e.g. -Abscess -Perforated viscera
- Old traumatic wound with retained devitalized tissue or foreign body
• Clean wound characteristics
- Non-traumatic, uninfected operative wound
- No break in sterile technique
- Respiratory, alimentary or genitourinary tract not entered
Clean-Contaminated
- Gastrointestinal or respiratory tract entered without significant spillage
- Oropharynx, vagina,
-non-infected genitourinary or biliary tract entered
• Contaminated
- Soft tissue lacerations, open fractures, penetrating wounds and other trauma
- Major break in sterile technique
- Traumatic wound
- Gross spillage from GI tract
- Entrance into genitourinary or biliary tracts in presence of infected urine or bile
• Dirty
- Wounds that are heavily contaminated
- Wounds that are clinically infected pre-op e.g. -Abscess -Perforated viscera
- Old traumatic wound with retained devitalized tissue or foreign body
list the steps required in the management of the ACUTE wound
CEDD MRS
- Cleansing⇒Exploration⇒Diagnosis and Debridement( saline>knife)
- Repair of structures and Replacement of any lost tissues
- Skin cover/ skin closure without tenstion
- Meticulous handling at every stage
Management of the bleeding wound
- Elevate and apply pressure
- torniqutte in limb damage
- avoid clamping vessels ⇒ nerve damage⇒ losst anastomosing abilty
- torniqutte in limb damage
- analgesia to allow adequate dg
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how to determine muscle viablilty in a acute wound
colour
bleeding pattern
contractility
number 1 most important factor in preventing infection of the wound
host resistance to infection
describe scars
- how long it tgakes to mature
- appearance of mature vs immature
- comparison to normal skin tissue
- The immature is at first pink, hard, raised and often itchy.
- disorganised collagen fibres become aligned along stress lines with their strength being in their weave rather than in their amount
- The external appearance of the scar becomes paler, while the scar becomes softer, flattens and its itchiness diminishes.
- Most of these changes occur over the first 3 months but a scar will continue to mature for 1–2 years.
- Tensile strength will continue to increase but will never reach that of normal skin.
what are the 3 types of scars
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Atrophic scar
- pale, flat and stretched in appearance
- Etio: back and areas of tension.
- stre: easily traumatised as the epidermis and dermis are thinned.
- Hypertrophic scar
- app: excessive scar tissue that does not extend beyond the boundary of the original incision or wound
- Etio:1) prolonged inflammatory phase2) unfavourable scar siting (i.e. across the lines of skin tension e.g. facial expression
- Keloid.
- app: excessive scar tissue that extends beyond the boundaries of the original incision or wound.
- etio: unknown, but it is associated with elevated levels of growth factor, deeply pigmented skin, an inherited
histological dx between keloid and hypertrophic scar
- excess collagen with hypervascularity in both but keloids> hypertrophic
- keloids have more type B collagen. with random orientation
- keloids have myofibroblasts but hypertrophic does not
- hypertrophic has scant mucin- keloids are very mucinous
- Hypertrophic scars improve spontaneously with time, where as keloids do not.
how to treat hypertrophic/ keloid scars
- pressure
- silicone gel sheets
- excision and steroid injection to stop inflammation
- excision and post operative radiation (beam/ brachytherapy)
- intralesional excision-> keloids only
- laser
- vitamin e massage but not proven
