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Flashcards in wounds Deck (219):

3 stages/phases of physiologic process of wound healing

1. inflammatory or substrate

2. proliferative

3. maturation or remodeling


what basic physiologic process is common to all wounds



cardinal signs of inflammation

redness (rubor), heat (valor), swelling (tumor), pain (dolor), and loss of function


trauma activates a cascade of chemoattractants (PDGFs and C5A) and mitogens that recruit

phagocytes, fibroblasts, and endothelial cells


when does the initial event of clotting blood and recruitment of cells occur after injury

first 1-2hrs


what are the first cells that enter the wound

platelets which come into contact w damaged collagen at time of injury


what happens when platelets contact the damaged collagen

platelets degranulate and release alpha granules that contain multiple growth factors, including PDGF and transforming growth factor beta (TGF beta)


what do cytokines and growth factors do

cytokines are soluble proteins that are secreted by a cell and influence activities of other cells; growth factors are proteins that bind to cell receptors and initiate cellular proliferation and differentiation


arachidonic acid

contained in walls of cells and released when cell is injured; degradation of arachidonic acid into derivatives of prostaglandins and thromboxanes causes a number of responses assoc w inflammatory response, including vasodilation, swelling, and pain


when do the phases of wound healing begin

only when the wound is covered by epithelium


other names for substrate phase

inflammatory phase, lag phase, or exudative phase


main cells involved in substrate phase

polymorphonuclear leukocytes (PMNs), platelets, and macrophages


how long do PMNs remain the predominant cell during substrate phase



what is a crucial part of normal wound healing



when do monocytes reach max numbers during substrate phase

enter wound after PMN and reach max # 24hrs later


main cell involved in wound debridement

macrophages (what monocytes become)


tissue matrix metalloproteinases (TMMPs)

after injury stimulated and help degrade surrounding matrix proteins such as collagen and necrotic cellular macromolecules


interleukin 1 (IL 1)

important growth factor in regulation of many processes in the inflammatory response; induce fever, promote hemostasis by interacting with endothelial cells, enhance fibroblast proliferation, and active T cells


during primary wound healing, when does the substrate phase occur

occurs over approx 4day period


what does the wound like look like during substrate phase

edematous and erythematous


substrate phase during secondary or tertiary intention

continues indefinitely until wound surface is closed by ectodermal elements


characterized by the production of collagen in the wound

proliferative phase


appearance of the wound during proliferative phase

less edematous and inflamed; wound scar may be raised, red, and hard


primary cell of proliferative phase

fibroblast which produces collagen


absence of ascorbic acid during proliferative phase leads to

wound breakdown



caused by vit C deficiency, characterized by impaired wound healing, cutaneous sores, and hemorrhagic gingivitis


characterized by the maturation of collagen by intermolecular cross linking

maturation phase "remodeling"


wound appearance during maturation phase

wound scar gradually flattens and becomes less prominent and more pale and supple


how long does wound maturation in an adult take



what are considered acute wounds

surgical incisions; wounds sustained as result from acute trauma


examples of chronic wounds

chronic venous stasis ulcers, pressure sores, diabetic foot wounds


what happens during chronic wound healing

normal wound healing process is frustrated or arrested for some reason


mc method to close acute wound

primarily close the wound resulting in healing by primary intention


what does healing by primary intention encompass

surgical incisions and lacerations that are closed w sutures, staples, adhesives or any technique by which the surgeon intentionally approximates the epidermal edges of a wound; tissue transfer techniques and flaps


advantages of primary intention closure

easiest for patient to manage wound, rapid return of function of wounded part, and final cosmetic result is superior


disadvantage of primary intention closure

risk of wound infection


secondary intention

leave the wound open to heal; usually full thickness wounds, sub cut abscess after i&d, or likelihood of wound infection is too great (open appe for perf appe)


tx of secondary intention

"wet to dry" dressings wherein a gauze sponge is moistened w saline and used to pack the wound, covered w dry dressing


what happens when the moist sponge dries out with secondary intention

removed and changed once or twice a day, gentle debridement of the wound is achieved


what will form at the base of the wound with secondary intention

granulation tissue: friable reddish granules of tiny capillary buds


how does healing occur during secondary intention

primarily by wound contraction since epithelial cells can't migrate across granulation tissue


what draws the edges of the wound together during secondary intention

myofibroblasts at the edge of the wound exert a centripetal force


wound contraction occurs to greater extent where compared to not as pronounced areas such as

greater where surrounding tissues are redundant (abdomen and buttock) and not pronounced (scalp or pretibial where skin is taut)


disadvantages of secondary intention

daily dressing changes are required until the wound is healed and final result is a cicatrix that may be unsightly


adv of secondary intention

wound infection is virtually impossible


tertiary intention "delayed primary closure"

wound is initially managed as a secondary intention wound, that is, left open with dressing changes. After a matter of about 5 days or so, when the wound is clean and granulation tissue is abundant, the wound edges are actively approximated


why is delayed primary closure successful

granulation tissue which is not sterile, is extremely vascular and as such is highly resistant to infection


adv of delayed primary closure

final cosmetic result, rapid return to function, reduce risk of infection


for large surface area full thickness wound that can't be closed primarily, an alt to the lengthy application of secondary intention is

skin grafting


what do split thickness skin grafts consist of

epidermis and a portion of the underlying dermis and are harvested using a dermatome


what do the perforations "fishnet" allow a graft to do

expand to cover an irregularly shaped wound and also prevent pooling of blood or serum under the graft which would prevent take


process of imbibition

first 48hr, grafted skin derives nutrients by passive absorption from recipient bed; then graftbecomes revascularized and adherent to the bed, and the wound closes as a result of a combination of contraction and epithelialization


how does a donor site for skin graft heal

epithelialization because it is not a full thickness defect


avulsion or crush wounds need to be derided until

all nonviable tissue is removed


what should be done to grossly contaminated wounds

cleaned as completely as possible to remove particulate matter (foreign bodies) and should be irrigated copiously


why must bleeding of a wound be controlled

prevent hematoma formation which is an excellent medium for bacterial growth, separates wound edges which prevent proper contact of tissues necessary for healing


how does radiation affect local wound healing

causes vasculitis, which leads to local hypoxia and ischemia; they impede healing by reducing amount of nutrients and oxygen that are available at the wound site


what does an infx do to a wound

dec rate of healing, affects proper granulation tissue formation, dec oxygen delivery, and depletes wound for needed nutrients


what can help reduce wound contamination

cleansing agents (simplest is soap and water)


what should be done to wound contains streptococci

should not be closed


there is a potential for what with devitalized tissue of a wound

clostridium tetani


local factors that affect wound healing

debridement nonviable tissue; foreign bodies; hematoma (bleeding), radiation, infection


systemic factors that affect wound healing

nutrition, DM, medications, chronic illness, smoking


why do patients need adequate nutrition for wound healing

support protein synthesis, collagen formation, and metabolic energy for wound healing


what is critical to the proper formation of collagen

folic acid


what is required for absorption of vit DAKE

adequate fat intake


what is vit K essential for

carboxylation of glutamate in synthesis of clotting factors 2,7,9,10


what does a dec in clotting factors lead to

hematoma formation and altered wound healing


what role does vit A play in wound healing

inc inflammatory response, inc collagen synthesis, and inc influx of macrophages into a wound


what are magnesium and zinc required for

magnesium for protein synthesis and zinc is cofactor for RNA and DNA polymerase


what affect does uncontrolled DM have on wound healing

uncontrolled hyperglycemia, impairs wound healing, and alters collagen formation


what does hyperglycemia inhibit

fibroblast and endothelial cell proliferation within the wound


what do steroids do to wound healing

blunt inflammatory response, dec available vit A in wound, and alter deposition and remodeling of collagen


what will chronic illness (immune def, cancer, uremia, liver ds, jaundice) do to wound healing

predispose to infx, protein def, and malnutrition


affect of smoking on wound healing

dec oxygen carrying capacity of hemoglobin, dec collagen formation within a wound; hypoxia results in dec in oxygen delivery to a wound and retards healing


which class of local anesthetics is mc used for deriding or suturing and examples

amides: xylocaine, bupivacaine, mepivacaine, and prilocaine


besides amides another local anesthetic class used for wounds

esters: procaine, chloroprocaine, tetracaine, and cocaine

(can't be used if sensitivity to p-aminobenzoic acid "PABA")


how do local anesthetics work

reversibly inhibit the conduction of nerve impulses by decreasing the membrane permeability to sodium, which decreases the rate of depolarization and leads to an increase in the excitability threshold of the nerve and inhibition of the nerve impulse.


order of loss in nerve function

pain, temp, touch, proprioception, and skeletal muscle tone


what determines the duration of action of local anesthetics

solubility, protein binding, and pH and vascularity of tissues


example of a vasoconstrictor

mc is epinephrine


toxic limit of xylocaine

7mg/kg given in 1 hr

(1mL of 1% contains 10mg of drug)

(50mL is toxic level for 70kg person)


major side effects of local anesthetics

CNS (tinnitus, blurred vision, tremors, and depression) and cardiovascular (myocardial depression, atrioventricular block, dec cardiac output)


local anesthetics containing vasoconstrictors should not be used

in tissues supplied by end arteries (nose, digits, penis, ear) because necrosis can occur


dose, OA, DA xylocaine

max (4.5mg/kg-350mg), max w epi (7mg/kg-500mg);

onset (1-5m)

duration (60/90min)


dose, onset, duration bupivacaine

max(2.5mg/kg-175mg), max w epi (3.5mg/kg-225mg);

onset (5-10m)

duration (12/18hr)


dose, onset, duration procaine

max (350mg); max w epi (600mg)

onset (1-2m)

duration (60m)


dose, onset, duration chloroprocaine

max (11mg/kg-800mg), max w epi (14mg/kg-1000mg)

onset (6-12m)

duration (60/90m)


clean wound

relatively new (


how are clean wounds classified

presentation and method of injury


steps clean wound care

1. sterile prep and draping
2. admin of local anesthetic
3. hemostasis
4. irrigation and debridement
5. closure in layers
6. dressing and bandage


how should wound edges be approximated

without tension; no overlap


skin violated by shearing forces and underlying tissue has been undermined and elevated, creating a flap or total loss of skin

avulsion injury


care of avulsion injury

cleaning, debridement of necrotic tissue, and closure if appropriate w suturing the flap of tissue down w absorbable suture and then close wound edges; pressure dressing to dec fluid collection


superficial loss of epithelial elements, w portions of the dermis and deeper structures remaining intact



care of an abrasion

usually only cleansing of the wound is required because remaining epithelial cells regenerate and migrate to close the wound; layer of petroleum jelly or abx ointment to prevent desiccation


care of puncture wound

usually not closed; assess damage to underlying vital structures and exam for foreign body (+/- radiographs); carefully followed clinically


loss of significant amounts of tissue that may initially appear viable

crush injury


care of crush injury

nonviable tissue must be debrided and wound closed w either skin graft or myocutaneous flap


suture size for skin on torso and extremities

3-0 or 4-0


suture size for face and neck

5-0 or 6-0


suture size for deeper tissue

2-0 to 4-0


nylon suture

"nurolon", synthetic, mono/polyfilament, nonabsorbable, used for skin



"dacron, tevdek, ethlbond", synthetic, polyfilament, nonabs, used for skin, mucosal areas, fascia


silk suture

natural, polyfilament, permanent, 2yr tensile, used for below skin


catgut suture

natural, monofilament, abs, 7d tensile, used for below skin


chromic catgut

"chromic", natural, monofilament, abs, 14d tensile, used below skin


polyglycolic acid

"vycrll, dexon", synthetic, polyfilament, abs, 14-30d tensile, used below skin



"prolene", synthetic, monofilament, perm, used for skin, fascia, vascular, tendon, bone



"maxon", synthetic, monofilament, abs, 30-60d tensile, used below skin, fascia, bowel, ducts



"PDS", synthetic, monofilament, abs, 60d tensile, used below skin, fascia, bowel, ducts



"monocryl", synthetic, monofilament, abs, 30-50d, used subcuticular skin closure


poly suture

"panacryl", synthetic, polyfilament, abs, 90d tensile, used for bone, tendon, fascia


stainless steel suture

mono/polyfilament, no nabs used for bone, fascia and skin


why should there be no tension of wound edges

lead to necrosis of skin


how long should sutures of the skin of torso and extremities be left in



how long should sutures of face and neck be left in



what suture should be used on the skin and why

monofilament non abs because it is less reactive


for closure of muscle and skin, what provides the greatest strength for the suture to be placed in

fascia for muscle and dermis for skin


why is a dressing placed over the closed wound

protection, immobilize area, compress area evenly, absorb secretions, and aesthetically acceptable


exceptions to primary closure of these contaminated wounds

high bacterial inoculum (human bite, farm injury), long time lapse since initial injury, suspected or known presence of species, and severe crush injury; all these should have delayed closure


monofilament skin sutures are used to reduce the possibility of

wound infection


when should f/u be with delay closure

within 48 hr to detect early signs of clinical infection


examples of clean wound

Atraumatic, no gastrointestinal (Gl) or genitourinary system (GU) or respiratory track (R) involvement


ex of clean contaminated wounds

Minor sterile breaks, entrance into Gl, GU, or R tract without significant contamination


ex contaminated wounds

Entrance into Gl, GU, or R tract with spillage of contents, traumatic wounds with soil and particulate matter


ex dirty wounds

infx within tissue, abscess


when is a wound considered infected

level of contamination is >10^5 organisms/gram of tissue


most important technique to dec bacterial count

debridement then frequent cleaning


dressing changes should be limited to

BID to prevent adversely affecting the progression of healing within an open wound


use of systemic abx in infected wound

little use in local bacterial control because don't penetrate granulating wound bed


topical abx for wound infx

mafenide acetate, silver sulfadiazine (not used on face)


what type of dressings dec bacterial level

biologic (allograft, amniotic membrane):successful adherence predicts success


wounds that are slow to heal as classified as



examples of chronic wounds

diabetic foot ulcers, venous stasis ulcers, and open wounds that have failed to close


what phase of healing are chronic wounds stopped in

inflammatory; poor granulation tissue formation, altered cell cycles, and biochemical imbalances


chronic wounds have elevated levels of

inflammatory cytokines and TMMPs- presence of both inhibits or slows natural progression of healing


why do chronic wounds develop

when normal healing mechanisms are not capable of repairing the tissue injury. They are a consequence of the equilibrium between the systemic and local factors favoring healing and those that oppose it being tilted toward chronicity


4 types of chronic wounds generally seen in practice

pressure ulcers, venous stasis ulcers, arterial insuff ulcers, and diabetic neuropathic ulcers


common sites for pressure ulcers

heel, sacrum, and ischial tuberosities


grade 1 pressure ulcer

non blanching erythematous area on intact skin


grade 2 pressure ulcer

Partial-thickness skin loss with the involvement of the epidermis and/or the dermis. This is usually superficial and can appear as a blister or abrasion


grade 3 pressure ulcer

full thickness skin loss w necrosis of subcutaneous tissue that can extend to fascia


grade 4 pressure ulcer

full thickness skin loss w necrosis; destruction can involve muscle, bone, and tendons


pelvic pressure ulcers can become severely infected from

fecal soiling


mc local care pelvic ulcers

saline moistened gauze w twice daily changing


negative pressure wound vacuum device (wound VAC)

porous sponge packed into the wound connected to negative pressure applied by the VAC that stimulates more rapid closure of the wound while simultaneously promoting drainage and creating a moist wound environment favorable for ingrowth of granulation tissue


mc chronic wounds in adults

venous stasis ulcers


venous ulcers

superficial wounds in anteromedial aspect of leg "gaiter zone" not involving he foot


path behind venous ulcer

consequence of venous htn transmitted to microcirculation of the skin; leading to anatomic changes in capillaries that slowly enlarge and become tortuous


w venous ulcers red cells break down in the tissue causing deposition of hemosiderin pigment leading to

hyperpigmentation and edema (dermatofibrosis) of the leg above the ankle


why do pt w chronic venous insuff who dev a wound have impaired healing

dec skin perfusion as consequence of elevated venous pressures in capillaries and dec delivery of oxygen and glucose to tissue from edema and protein deposition in interstitium; tendency of wounds to weep fluid copiously w maceration of surrounding normal tissues and further skin damage


tx venous ulcers

compression (paste bandages-Unna boots, or multiple dry bandage layers-charing cross or dry boots); debridement of necrotic tissue, systemic abx if infx, elevate limb; weekly/biweekly compression bandages w topical meds (usually heals in several months)


arterial ulcers involve

toes (mummified, black, "dry gangrene") or have suppuration w oozing (wet gangrene); but any part of foot, ankle, or leg can dev ulcer


presence of black, infarcted skin or multiple wounds raise suspicion for

arterial ds


what pulses are usually absent in relation to arterial ulcers



what ulcers/wounds usually cause limb loss from infection



tx arterial wounds

arterial interventions to improve tissue perfusion; local care w wet to dry gauze or abx ointments


Charcot's foot

collapse of mid foot w plantar subluxation of ruined bones (diabetic ulcer)


what do Charcot's foot and clawing of the toes with the change in bony architecture lead to (diabetic ulcer)

excessive weight bearing on surfaces at risk for pressure ulcers


fibrotic granulated bed surrounded by hypertrophic skin (callus) which identifies the exposure to excess pressure usually metatarsal head, heel , dorsal surface of toe

diabetic ulcer


tx diabetic ulcer

control infx; surgical debridement if penetrate into bone or joint; special shoe to alleviate pressure; +/- arterial surgery


adv care for chronic wounds

1. Intermittent negative pressure devices

2. Topical foams and occlusive bandages to promote a moist wound environment

3. Topical application of growth factors and collagen preparations to promote healing

4. Topical use of broad-spectrum antimicrobial compounds to decrease the bacterial burden of the wound

5. Topical enzyme preparations

6. Use of engineered living skin substitutes

7. Hyperbaric oxygen therapy (Lawrence 141)


promotes new tissue growth, removes edema fluid, reduces TMMPs, and assists in contraction of wound

negative pressure; used if no infx and undergone debridement


negative pressure is contraindicated in

cancer growth, untx osteomyelitis, active bleeding, or necrotic tissue


prevent loss of moisture and desiccation

topical foams and occlusive bandages


topical broad spectrum antimicrobial preps

1% silver nitrate solution, silvadene cream, cadexomer iodine; gentamicin and metronidazole ointment; dilute acetic acid suppress pseudomonas


A 42-year-old woman is seen in clinic 2 weeks after undergoing left partial mastectomy and sentinel lymph node biopsy for stage 1 breast cancer. Whole breast radiation Is recommended. She is concerned about the effects of radiation on her Incision. Which of the following statements is least accurate regarding radiation effects and wound healing?

A. Rapidly dividing cells are the least affected by radiation therapy.

B. Radiation effects on fibroblasts should be negligible.

C. Radiation causes increased amounts of collagen deposition.

D. Long-term effects of radiation are often reversible after 24 months.

E. Wound healing is impaired postradiation secondary to venous injury.

Answer: D

The effects of external beam radiation often cause local tissue damage and Impaired wound healing. Given the sensitivity of radiation to the various phases of the cell cycle, rapidly dividing cells are the most sensitive to radiation. Two major manifestations of impaired wound healing secondary to radiation are the result of direct injury to fibroblasts, leading to a lack of collagen, and endothelial cell injury resulting in inefficient wound healing. The effects of radiation are permanent and irreversible cell damage, as manifested by progressive fibrosis and obliterate endarteritis.


A 28-year-old ultimate fighter is seen in clinic 2 weeks after undergoing splenectomy for a ruptured spleen sustained during a prize fight. He is feeling well with minimal incisional pain. There Is a midline laparotomy Incision that appears to be healing well without evidence of infection or other problems. He wants to know when his incision will be healed enough for him to return to professional fighting. Regarding the tensile strength of his wound,

A. it will increase steadily over the first 6 weeks and achieve maximal strength by 12 weeks.

B. it will achieve maximal tensile strength at the point of maximal collagen deposition.

C. it will take a full year for the wound to regain the same tensile strength as preoperatively.

D. wound tensile strength reaches 90% at 26 weeks and this is its plateau.

E. collagen deposition reaches a maximum level in the first 6 weeks and is quickly degraded thereafter.

Answer: D

Collagen secretion is initiated by fibroblasts in the first 24 to 72 hours after injury. Peak collagen production begins by 1 week postinjury. By 3 weeks after injury, collagen synthesis and collagen deposition/degradation achieve a steady state. After 3 weeks, wound tensile strength remains


A 52-year-old man is in the operating room undergoing an emergent laparotomy because of a perforated ulcer. There is free intraperitoneal perforation and approximately 2 L of murky green fluid with obvious vegetable matter is suctioned from the peritoneal cavity. A Graham patch is performed to close the perforation. The abdomen is irrigated with normal saline and suctioned until all return is clear of green fluid and vegetable matter. After closing the fascia the next most appropriate step would be

A. interrupted skin closure.

B. closure of skin with a skin closure polymer (i.e., Dermabond).

C. wound left open and wound care until clean and granulating and then delayed closure.

D. closure of skin with staples.

E. subcuticular suture skin closure.

Answer: C

This is a contaminated surgical field. Wound infection in this setting can be as high as 15% of wounds, regardless of irrigating until clear. Allowing the wound to stay open with wound care until robust granulation is occurring and the wound bed is clean reduces this risk once the delayed closure is done. If the wound granulates but continues to have a high bacterial load, it can be allowed to heal by secondary intention.


A 55-year-old man is seen in clinic prior to undergoing elective repair of a large umbilical hernia. He is otherwise healthy and has had no previous surgery. He takes no medications. He does not smoke and does not drink alcohol. Except for a large reducible umbilical hernia, his physical exam is normal. Which micronutrient supplementation would not be beneficial to this patient to improve wound healing?

A. Vitamin C

B. Vitamin E

C. Vitamin K

D. Vitamin A

E. Zinc

Answer: C

Vitamins integral for wound healing are vitamin C and vitamin A. Vitamin C is required for the conversion of proline and lysine to hydroxyproline and hydroxylysine. Vitamin C deficiency or scurvy leads primarily to the failure of collagen synthesis. Vitamin E is an antioxidant, aids in immune function and fibroblast stimulation, and inhibits prostaglandin synthesis. Selenium is important for lymphocyte function and protects membranes from free radical damage. Zinc is possibly the most essential element for wound healing. Zinc deficiency leads to decreased fibroblast proliferation, decreased collagen synthesis, and likely decreased lymphocyte, cellular, and immunity. While vitamin A deficiency impairs wound healing, supplemental vitamin A benefits wound healing. Vitamin A enhances immune function, macrophage proliferation, collagen synthesis, and epithelial integrity. Supplemental vitamin A therapy can improve wound healing In patients receiving corticosteroids, cancer patients, diabetics, and patients undergoing chemotherapy. Vitamin Κ is involved in coagulation factor formation


A 25-year-old man is in the hospital recovering from open surgery for perforated appendicitis performed 5 days ago. Postoperatively his wound was left open with daily débridement and local dressing changes. Today, local anesthesia is applied and the wound is closed with a nylon suture at the bedside. This represents an example of

A. primary closure.

B. composite graft closure.

C. delayed primary closure.

D. healing by secondary intent.

E. local flap closure.

Answer: C

Surgical wounds can heal in several ways. An incised wound that is clean and suture closed is said to heal by primary intention. Primarily closed wounds are of a smaller volume in a clean surgical field. Often, because of bacterial common contamination or tissue loss, a wound will be left open to heal by granulation tissue formation. This is healing by secondary intent, and the wound must synthesize granulation tissue, contract at the wound periphery, and eventually cover the surface area with epithelial cells. Delayed primary closure represents a combination of the first two, consisting of the placement of sutures, allowing the wound to stay open for a few days, and then subsequent closure of the sutures. Delayed primary closure requires that the wound be free of excess bacteria. This is generally accomplished by good local wound care with irrigation and débridement if necessary during a postoperative interval. Wounds heal faster following delayed primary closure than by secondary intent.


what is undermining

process of separating the layers of the wound; helps relieve tension to make the wound easier to close


4 c's of viable tissue

color (redness), consistency (tissue contiguous and will approximate well), contractility (muscle should have intact contractile properties), capillary ooze


what type of suture do you use for brown or black hair

prolene (blue)


2 ways to cauterize

electrical or silver nitrate


major categories of dressings

gauze, (film & hydrocolloid conserve moisture) (foam & alginate absorb moisture)


when can surgical wound dressing be removed

when skin seals 48hrs after closure


difference between dry and exudative wounds in terms of moisture

dry conserve and exudative remove


abx ointments

neosporin, bacitracin, muciprocin, gentimycin


antimicrobials: silver containing

silvadene, silvasorb


antimicrobials: iodine containing

iodosorb, iodoflex


antimicrobials: sulfa containing




dakin's solution: contains Na hypochlorite (bleach)


types of biologically active dressings

regranax, cellulose containing, collagen, living cells (apligraf and derma graft), negative pressure wound therapy (NPWT)



biologically active dressing contains PDGF; platelet derived growth factor, regulate cell growth and division, angiogenesis from existing blood vessel tissue;

used for diabetic foot ulcers


cellulose containing biologically active dressings

absorb enzymes, matrix metalloproteinases (MMPs); help slough out biofilms which consist of gelatinous matrix produced by bacteria that shields the microbes from the immune system; MMPs secreted by inflammatory cells surrounding biofilms digest (loosen) the attachments between the bacterial biofilms and wound bed; angiogenesis


collagen biologic active dressing

stimulates fibroblasts


living cell biologic active dressings

apligraf and dermagraft; have growth factor factories


neg pressure wound therapy biologic active dressings

VAC system and blue sky


indications for skin graft

infx caused lg amount skin loss; burns; cosmetic; skin cancer; surgeries that need it to heal; venous/pressure/diabetic ulcers that don't heal; very large wounds; unable to close wound properly


types of skin grafts

temporary (allograft, heterograft) or permanent (autograft-sheet or mesh)


mc bacteria found in postop wound infx

staph aureus; e coli; enterococcus


bacteria cause fever and infx within first 24hr postop

streptococcus and clostridium (bronze brown weeping tender wound)


pt factors influence dev of infx

urermia, hypovolmic shock, vascular occlusive states, adv age, distant area of infx


dressings serve to

protect wound from outside contamination and mechanical trauma, to absorb drainage, and sometimes to position or support wound


when does an uncomplicated surgical wound dressing need to be changed

5-7d if clean and dry


a well closed incision should be sealed with epithelium when



signs that the dressing should be removed and wound should be examined

pain, odor, exudate, excessive bleeding


when can standard skin suture be removed

when incision is closed, depends on location and age

adult abd (7-10d)
eld ant knee (2-3w)


when should steri strips be removed

don't until they peel off


when should staples be removed

earlier than sutures to prevent rail-road tracts; usually 5 day

can remove 1/2 at a time and other half 2 days later



open wound; superficial wound of the epidermis which is scraped away; blood oozes from wound but bleeding seldom serious



open wound; sharp, even cut w smooth edges; tend to bleed freely because blood vessels and tissue are severed



open wound; tear in skin characterized by uneven and ragged edges; bleed freely



open wound; penetration of sharp object thru skin and underlying structures; wound opening may be small but damage can involve deeper tissues;

predisposed to infx since no way out; check for fb



wound w entrance and exit



tearing, loose flap of skin which may be suspended from wound or lost entirely (finger tip)


jane inflammation stage

lasts 2-4d; starts w tissue injury; platelets activated in 1-2m to form clots and aid in hemostasis of wound; body responds w tissue release of substances like cytokines and chemotactic factors; leukocytes and macrophages start removing debris/bacteria/fb, edema dev


jane collagen synthesis phase (proliferative phase)

4th post injury day and cont 3-6w; pt needs enough Ca, platelets and tissue factor for phase to begging; prothrombin converts to thrombin helping fibrinogen convert to fibrin to stabilize clot;

wound edges appear red and raised w healing ridge formed by new collagen and new capillaries


jane epithelialization phase

begins 12hr post injury; epithelial cells migrate to cover the wound and prevent bacterial seeding; if wound has primary closure, epithelial cells seal the wound within 24-48hr; if left open takes much longer for epithelialization to occur because wound must granulate first


scar maturation

starts 3-6w post injury and can take 1yr to fully form; combo of collagen syn and breakdown; over the yr scar flattens, contracts and fades in color and considered healed


jane primary intention

most efficient/quickest/best cosmetic result; clean wounds; if wound repaired in time (12hr); wound edges approx w sutures/staples/steri strips/ tissue adhesive


jane secondary intention

wound heal on own; uses granulation and wound contracture; old/contaminated (infx) or open winds w tissue missing (avulsion,bites); longer healing; less risk infx; larger less cosmetic scar


jane tertiary intention

delayed primary closure; wound left open (after deb/clean) for 3-5d then closed; old/contam wounds or if unsure; faster and more cosmetic than secondary and less risk infx than primary


wound disruption complications

dehiscence (partial or complete separation of the skin edges); evisceration (extrusion of innards)



excessive deposition of collagen creating heaped up scars; AA


hyper granulation tissue (proud flesh)

exuberant granulation rising above the level of the surround skin, prevents epithelialization


langer's lines

tension lines within skin; incisions made along lines will scar less