Response and Wound Healing Flashcards
(43 cards)
What are the signs and symptoms of vasovagal syncope?
Loss of consciousness
Warm sweaty extremities
Fast pulse
How to manage VVS?
Head down posture
What are the phases of physiological response to trauma and their respective lengths?
Ebb, flow, recovery
Hours, days, weeks
What is the ebb phase of trauma response?
Hypovolemic shock
Priority is to maintain life/homeostasis by reducing cardiac output, oxygen consumption, BP, and therefore tissue perfusion
Body temperature drops
Metabolic rate drops
What is the flow phase of trauma response?
Increase in catecholamines, glucocorticoids, glucagon and release of cytokines and lipid mediators
Acute phase protein production
Basically catabolism causing hypermetabolism, breakdown of skeletal muscle protein, lipid stores, glycogen stores, insulin resistance
What is the significance of the flow phase?
Prolonged metabolic stress without provision of adequate calories and protein leads to impaired body functions and ultimately malnutrition due to the catabolic phase
What are the 4 categories of wounds?
Clean
Clean/contaminated
Contaminated
Infected
What is a clean wound
Operative incisional wound following nonpenetrative (blunt) trauma
What is a clean/contaminated wound
Uninfected wound with no inflammation but respiratory, GI, genital and/or urinary tract has been entered
What is a contaminated wound
Open, traumatic wound or surgical wound involving a major break in sterile technique showing evidence of inflammation
What is an infected wound
Old, traumatic wounds containing dead tissue and wounds with evidence of clinical infection like purulent discharge
What are the categories of wound closure
Primary intention (all layers close quickly and cleanly)
Secondary intention (deep layers close but superficial layers left to heal from inside out)
Tertiary intention (delayed primary closure)
What causes inflammation in wounds?
Damaged endothelial cells release cytokines to increase integrand expression in circulating lymphocytes
Histamine, serotonin and kinins cause vessel contraction, decreases blood loss, and causes chemotaxis of neutrophils (most abundant cell in initial 24h)
What is proliferative phase of wound healing?
After neutrophils have removed cellular debris and released cytokines to attract macrophages
Lasts for up to 3 weeks
Fibroblasts migrate into wound and secrete collagen type III
Angiogenesis occurs by 48h
Macrophage remodelling and secretion
Greatest increase in wound strength
What is maturation phase of wound healing
Final phase, from 3rd week to 9-12 months
Collagen III is converted to collagen I, tensile strength increases up to 80% of normal tissue
What type of healing occurs in extraction wounds?
Secondary intention
- Wound edges separated
- Gap between them cannot be bridged directly
- Extensive loss of epithelium
- Severe wound contamination or
- Significant subepithelial tissue damage
Immediately after extraction:
Blood fills extraction site
Intrinsic and extrinsic clotting cascade pathways activated
Fibrin meshwork forms containing entrapped RBCs, sealing off torn BV and reducing wound size
First 24-48h after extraction:
Clot organisation
Engorgement and dilation of BV in PDL remnants
Leukocytic migration
Formation of fibrin layer
V impt as if blood clot disintegrates healing may be greatly delayed and may be extremely painful
First week after extraction:
Clot forms temporary scaffold for inflammatory cell migration
Epithelium at periphery grows over surface of clot
Inflammatory stage - WBCs enter socket to remove bacteria and debris like bone fragments
Fibroplasia - ingrowth of fibroblasts and capillaries
Epithelial migration down socket wall until it contacts epithelium from the other side of the socket or encounters the bed of granulation tissues under the clot, over which it can migrate
Osteoclasts accumulate along crestal bone
Second week after extraction:
Large amount of granulation tissue fills socket
Osteoid deposition along alveolar bone lining socket, in smaller sockets epithelium may already be fully intact
Trabeculae of osteoid extends into clot from alveolus, and osteoclastic resorption of cortical margin of alveolar socket is more distinct
These processes continue into week 3 and 4, along with completion of epithelialization of most sockets
Third week after extraction
Filled with granulation tissue with poorly calcified bone at wound perimeter
Surface completely reepithelialized with minimal or no scar formation
Active bone remodeling by deposition and resorption continues for several more weeks
Histological phases of the healing continuum
Inflammatory
Proliferative
Remodeling
Inflammatory phase of the healing continuum
Initial transient vasoconstriction followed by vasodilation
Initiation: tissue trauma and bleeding activates factor XII (Hageman factor) initiating healing cascade effectors such as complements, plasminogen, kinins and clotting systems
Aggregation of circulating platelets at injury sites, adhering together and the exposed vascular subendothelial collagen to form a primary platelet plug within a fibrin matrix, achieving hemostasis
Clot serves as a reservoir of cytokines and growth factors that are released as activated platelets degranulate (interleukins, TGF-8, PDGF, VEGF) to regulate subsequent healing
Adjacent epithelium begins to migrate
Undifferentiated mesenchymal cells begin to transform into fibroblasts
Proliferative phase of the healing continuum
Cytokines and growth factors of inflammatory phase stimulate proliferative phase
Starts as early as 2nd day and lasts up to 3 weeks
Formation of pink granulation tissue, with establishment of local microcirculation to supply oxygen and nutrients for elevated metabolic needs of regenerating tissues
Epithelial thickness increases, collagen fibers haphazardly laid down by fibroblasts, building capillaries establish contact with their counterparts from other sites in wound
