wounds Flashcards
3 stages/phases of physiologic process of wound healing
- inflammatory or substrate
- proliferative
- maturation or remodeling
what basic physiologic process is common to all wounds
inflammation
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
48hr
what is a crucial part of normal wound healing
macrophages
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
scurvy
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
9-12m
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
- sterile prep and draping
- admin of local anesthetic
- hemostasis
- irrigation and debridement
- closure in layers
- 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
abrasion
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
polyester
“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
polypropylene
“prolene”, synthetic, monofilament, perm, used for skin, fascia, vascular, tendon, bone
polyglyconate
“maxon”, synthetic, monofilament, abs, 30-60d tensile, used below skin, fascia, bowel, ducts
polydloxanone
“PDS”, synthetic, monofilament, abs, 60d tensile, used below skin, fascia, bowel, ducts
pollglecaprone
“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
7-10d
how long should sutures of face and neck be left in
4d
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
chronic
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
pedal
what ulcers/wounds usually cause limb loss from infection
arterial
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
- Intermittent negative pressure devices
- Topical foams and occlusive bandages to promote a moist wound environment
- Topical application of growth factors and collagen preparations to promote healing
- Topical use of broad-spectrum antimicrobial compounds to decrease the bacterial burden of the wound
- Topical enzyme preparations
- Use of engineered living skin substitutes
- 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
sulfamylon
disinfectants
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)
regranax
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
24-48hr
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
kid(3-5d)
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
abrasion
open wound; superficial wound of the epidermis which is scraped away; blood oozes from wound but bleeding seldom serious
incision
open wound; sharp, even cut w smooth edges; tend to bleed freely because blood vessels and tissue are severed
laceration
open wound; tear in skin characterized by uneven and ragged edges; bleed freely
puncture
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
perforation
wound w entrance and exit
avulsion
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)
keloids
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
