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Inf & Wound Healing

Chapter 13-Infection & Wound Healing

QuestionAnswer
What is inflammatory response and what is the goal? Reaction to cell injury. Goal: remove necrotic debris and make suitable for healing
What is an infection? Organism-bacteria, protozoa, fungus--invades tissues
What is intensity of response? The degree of response depends on degree of injury; immune suppression decreased = decreased response
Types of inflammatory response systems? Vascular Response & Cellular Response
Vascular Response (what the arteries will do?) Arteries initially dilate, to allow chemoreceptors into area=redness & warmth
Cellular Response (what do the different cells do?)Neutrophils Neutrophils: 1st line of defense, immature WBC "shift to the left", arrive in 6-12 hours, only around 24-48 hrs. Puss=accumulation of dead neurtrophils
Cellular Response (what do the different cells do?)Monocytes 2nd WBC to arrive, arrive in 3-7 days, transform into macrophages to eat debris
Lymphocytes 3rd WBC to arrive, involved in humoral and cell-mediated immunity--how vaccines work
Chemical Mediators: Complement System, Protaglandins, Leukotrienes Complement system: chemical reaction, multiple enzymes react in sequence that cause more inflammation to occur. Get appropriate cells to area to clean it out and allow healing to occur
Prostaglandins Produced by injured cells; cause vasodilation and sensitive pain receptors (why we hurt)
Leukotrienes active in anaphylactic reaction, cause smooth muscle contraction of bronchi, increase capillary permeability--get bronchial restriction and pulmonary edema
Clinical manifestations: 1) local response, 2) systemic response, 3)Fever local response: redness, pain, swelling systemic: incr WBC, fever, malaise Fever: triggered by protaglandins & cytokines; response to chem agts being sent out; incr temp creates a "bad" envir; treat fever >101.5; lower fever part of immune resp
Inflammation Acute: comes on & resolves in 2-3 wks; temp, no long damage Chronic: weeks to months to yrs; Lupus pts, RA pts
Nursing Management: vitals, fever, meds, RICE Sympts of inflam response: initial bp incr, systemic sepsis decrease bp; temp incr,hr incr, RR incr Fever: not damaging until >104; treat for comf., 105.8=brain damage; "rate" of incline-rapid incrs=seizures Meds:tylenol, ibuprofen, aspirin
Two types of healing: regeneration & repair Regeneration: replacement of lost or damaged cells w/same cell type Repair: replacement of damaged cells w/ connective tissue-leads to scar tissue
Primary repair-wound edges well approximated (i.e. surgical incision) Primary Repair: Initial-neutrophils, platelets form clots,meshwork Granulation-start of new tissue; bright red Fibroblasts-immature connective tissue cells; secrete collegen and form scar tissue Maturation&scar-can last 7 days to years
Secondary repair-wound is open healing from sides in & bottom up; must keep wound bed clean
Tertiary repair-delayed primary repair wound too swollen to close, surgically come back to put together
Complications of scars Hypertrophic Scars & Keloids Contracture Dehiscence Excess granulation tissue Adhesions
Hypertrophic Scars & Keloids Hypertrophic: over abundance of collegen--red-raised scars, excessive scar formation Keloids: protusion of scar tissue; huge over growth, expands beyond boundary of wound; pt. may complain of pain & tenderness,hereditary, more common in dark skin people
Contracture Connective tissue doesn't skin to expand; burns of injuries over joints--must keep moving to keep mobility, always have in functional position
Dehiscence wound opens Risk factors: infection, diabetes, obesity, too much pressure on wound/surgical site (split w/pillow)
Excess granulation tissue "proud flesh" granulation tissue that protrudes above surface of wound--surgically removable, will not grow back
Adhesions most common area=abdominal cavity; attaches to greater omentum & organs Scar tissue in abd cavity, can cause small bowel obstruction
Wounds: need to make note of closure device sutures (7-10 days), staples (head, abdomen, hips), glue (open heart), retention sutures (trying to bring edges together)
Wound colors Red: Good!!granulation tissue, pink, a little bleeding, wet wound Yellow: needs to be debrided for wound to heal; wet-to-dry & pack to pull of slough Black: eschar tissue, surgically removed, debride in order for healing to occur
nutrition management high protein, high calorie, Vit. A,B,C,D NG tube first option for feeding--want to use "gut" first; TPN next
Infection prevention use cleanest technique possible (aseptic tech,) watch MD order Culture-ID microorganism (ideal before 1st dose of antibiotic) Sensitivity-IDs most effective antibiotic
Patient teaching note change in drainage, wound color, adequate rest, good nutrition
What causes Pressure Ulcers? Pressure, friction, sheering forces, moisture, length on side *pressure ulcers heal by secondary intention; significant PU can take months to years to heal
How many Stages of PUs? Suspected deep tissue injury, Stages I-IV & unstagable
Suspected Deep Tissue injury purple of maroon localized are of discolored intact skin or blood filled blister due to damage of underlying soft tissue from pressure and/or sheer. Area may be preceded by tissue that is painful, firm, mushy, boggy, warm or cool as compared to adj tissue
Stage I intact skin w/nonblanchable redness of local area usually over bony prominence. Area may be painful, firm, soft, warm or cooler than adjac. skin
Stage II partial-thickness loss of dermis manifesting as a shallow, open ulcer with a red-pink wound bed w/out slough. May look like serum-filled blister
Stage III full-thickness tissue loss. subcut fat may be visible, but bone, tendon and muscle are not exposed. Slough may be present. May include undermining and tunneling
Stage IV full-thickness tissue loss w/exposed bone, tendon or muscle. Slough and eschar may be present. Often includes undermining and tunneling
Unstageable full-thickness tissue loss in which base of ulcer is covered by slough (yellow, tan, gray, green or brown) and/or eschar in the wound bed
Created by: divelmama