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Surgery > wounds > Flashcards

wounds Flashcards

1
Q

3 stages/phases of physiologic process of wound healing

A
  1. inflammatory or substrate
  2. proliferative
  3. maturation or remodeling
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2
Q

what basic physiologic process is common to all wounds

A

inflammation

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3
Q

cardinal signs of inflammation

A

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

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4
Q

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

A

phagocytes, fibroblasts, and endothelial cells

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5
Q

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

A

first 1-2hrs

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6
Q

what are the first cells that enter the wound

A

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

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7
Q

what happens when platelets contact the damaged collagen

A

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

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8
Q

what do cytokines and growth factors do

A

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

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9
Q

arachidonic acid

A

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

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10
Q

when do the phases of wound healing begin

A

only when the wound is covered by epithelium

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11
Q

other names for substrate phase

A

inflammatory phase, lag phase, or exudative phase

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12
Q

main cells involved in substrate phase

A

polymorphonuclear leukocytes (PMNs), platelets, and macrophages

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13
Q

how long do PMNs remain the predominant cell during substrate phase

A

48hr

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14
Q

what is a crucial part of normal wound healing

A

macrophages

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15
Q

when do monocytes reach max numbers during substrate phase

A

enter wound after PMN and reach max # 24hrs later

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16
Q

main cell involved in wound debridement

A

macrophages (what monocytes become)

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17
Q

tissue matrix metalloproteinases (TMMPs)

A

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

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18
Q

interleukin 1 (IL 1)

A

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

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19
Q

during primary wound healing, when does the substrate phase occur

A

occurs over approx 4day period

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20
Q

what does the wound like look like during substrate phase

A

edematous and erythematous

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21
Q

substrate phase during secondary or tertiary intention

A

continues indefinitely until wound surface is closed by ectodermal elements

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22
Q

characterized by the production of collagen in the wound

A

proliferative phase

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23
Q

appearance of the wound during proliferative phase

A

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

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24
Q

primary cell of proliferative phase

A

fibroblast which produces collagen

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25
Q

absence of ascorbic acid during proliferative phase leads to

A

wound breakdown

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26
Q

scurvy

A

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

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27
Q

characterized by the maturation of collagen by intermolecular cross linking

A

maturation phase “remodeling”

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28
Q

wound appearance during maturation phase

A

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

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29
Q

how long does wound maturation in an adult take

A

9-12m

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30
Q

what are considered acute wounds

A

surgical incisions; wounds sustained as result from acute trauma

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31
Q

examples of chronic wounds

A

chronic venous stasis ulcers, pressure sores, diabetic foot wounds

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32
Q

what happens during chronic wound healing

A

normal wound healing process is frustrated or arrested for some reason

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33
Q

mc method to close acute wound

A

primarily close the wound resulting in healing by primary intention

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34
Q

what does healing by primary intention encompass

A

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

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35
Q

advantages of primary intention closure

A

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

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36
Q

disadvantage of primary intention closure

A

risk of wound infection

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37
Q

secondary intention

A

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)

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38
Q

tx of secondary intention

A

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

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39
Q

what happens when the moist sponge dries out with secondary intention

A

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

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40
Q

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

A

granulation tissue: friable reddish granules of tiny capillary buds

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41
Q

how does healing occur during secondary intention

A

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

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42
Q

what draws the edges of the wound together during secondary intention

A

myofibroblasts at the edge of the wound exert a centripetal force

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43
Q

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

A

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

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44
Q

disadvantages of secondary intention

A

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

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45
Q

adv of secondary intention

A

wound infection is virtually impossible

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46
Q

tertiary intention “delayed primary closure”

A

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

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47
Q

why is delayed primary closure successful

A

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

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48
Q

adv of delayed primary closure

A

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

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49
Q

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

A

skin grafting

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50
Q

what do split thickness skin grafts consist of

A

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

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51
Q

what do the perforations “fishnet” allow a graft to do

A

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

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52
Q

process of imbibition

A

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

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53
Q

how does a donor site for skin graft heal

A

epithelialization because it is not a full thickness defect

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54
Q

avulsion or crush wounds need to be derided until

A

all nonviable tissue is removed

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55
Q

what should be done to grossly contaminated wounds

A

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

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56
Q

why must bleeding of a wound be controlled

A

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

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57
Q

how does radiation affect local wound healing

A

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

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58
Q

what does an infx do to a wound

A

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

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59
Q

what can help reduce wound contamination

A

cleansing agents (simplest is soap and water)

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60
Q

what should be done to wound contains streptococci

A

should not be closed

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61
Q

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

A

clostridium tetani

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62
Q

local factors that affect wound healing

A

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

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63
Q

systemic factors that affect wound healing

A

nutrition, DM, medications, chronic illness, smoking

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64
Q

why do patients need adequate nutrition for wound healing

A

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

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65
Q

what is critical to the proper formation of collagen

A

folic acid

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66
Q

what is required for absorption of vit DAKE

A

adequate fat intake

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67
Q

what is vit K essential for

A

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

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68
Q

what does a dec in clotting factors lead to

A

hematoma formation and altered wound healing

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69
Q

what role does vit A play in wound healing

A

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

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70
Q

what are magnesium and zinc required for

A

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

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71
Q

what affect does uncontrolled DM have on wound healing

A

uncontrolled hyperglycemia, impairs wound healing, and alters collagen formation

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72
Q

what does hyperglycemia inhibit

A

fibroblast and endothelial cell proliferation within the wound

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73
Q

what do steroids do to wound healing

A

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

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74
Q

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

A

predispose to infx, protein def, and malnutrition

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75
Q

affect of smoking on wound healing

A

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

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76
Q

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

A

amides: xylocaine, bupivacaine, mepivacaine, and prilocaine

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77
Q

besides amides another local anesthetic class used for wounds

A

esters: procaine, chloroprocaine, tetracaine, and cocaine

can’t be used if sensitivity to p-aminobenzoic acid “PABA”

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78
Q

how do local anesthetics work

A

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.

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79
Q

order of loss in nerve function

A

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

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80
Q

what determines the duration of action of local anesthetics

A

solubility, protein binding, and pH and vascularity of tissues

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81
Q

example of a vasoconstrictor

A

mc is epinephrine

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82
Q

toxic limit of xylocaine

A

7mg/kg given in 1 hr

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

(50mL is toxic level for 70kg person)

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83
Q

major side effects of local anesthetics

A

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

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84
Q

local anesthetics containing vasoconstrictors should not be used

A

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

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85
Q

dose, OA, DA xylocaine

A

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

onset (1-5m)

duration (60/90min)

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86
Q

dose, onset, duration bupivacaine

A

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

onset (5-10m)

duration (12/18hr)

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87
Q

dose, onset, duration procaine

A

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

onset (1-2m)

duration (60m)

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88
Q

dose, onset, duration chloroprocaine

A

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

onset (6-12m)

duration (60/90m)

89
Q

clean wound

A

relatively new (

90
Q

how are clean wounds classified

A

presentation and method of injury

91
Q

steps clean wound care

A
  1. sterile prep and draping
  2. admin of local anesthetic
  3. hemostasis
  4. irrigation and debridement
  5. closure in layers
  6. dressing and bandage
92
Q

how should wound edges be approximated

A

without tension; no overlap

93
Q

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

A

avulsion injury

94
Q

care of avulsion injury

A

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

95
Q

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

A

abrasion

96
Q

care of an abrasion

A

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

97
Q

care of puncture wound

A

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

98
Q

loss of significant amounts of tissue that may initially appear viable

A

crush injury

99
Q

care of crush injury

A

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

100
Q

suture size for skin on torso and extremities

A

3-0 or 4-0

101
Q

suture size for face and neck

A

5-0 or 6-0

102
Q

suture size for deeper tissue

A

2-0 to 4-0

103
Q

nylon suture

A

“nurolon”, synthetic, mono/polyfilament, nonabsorbable, used for skin

104
Q

polyester

A

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

105
Q

silk suture

A

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

106
Q

catgut suture

A

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

107
Q

chromic catgut

A

“chromic”, natural, monofilament, abs, 14d tensile, used below skin

108
Q

polyglycolic acid

A

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

109
Q

polypropylene

A

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

110
Q

polyglyconate

A

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

111
Q

polydloxanone

A

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

112
Q

pollglecaprone

A

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

113
Q

poly suture

A

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

114
Q

stainless steel suture

A

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

115
Q

why should there be no tension of wound edges

A

lead to necrosis of skin

116
Q

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

A

7-10d

117
Q

how long should sutures of face and neck be left in

A

4d

118
Q

what suture should be used on the skin and why

A

monofilament non abs because it is less reactive

119
Q

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

A

fascia for muscle and dermis for skin

120
Q

why is a dressing placed over the closed wound

A

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

121
Q

exceptions to primary closure of these contaminated wounds

A

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

122
Q

monofilament skin sutures are used to reduce the possibility of

A

wound infection

123
Q

when should f/u be with delay closure

A

within 48 hr to detect early signs of clinical infection

124
Q

examples of clean wound

A

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

125
Q

ex of clean contaminated wounds

A

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

126
Q

ex contaminated wounds

A

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

127
Q

ex dirty wounds

A

infx within tissue, abscess

128
Q

when is a wound considered infected

A

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

129
Q

most important technique to dec bacterial count

A

debridement then frequent cleaning

130
Q

dressing changes should be limited to

A

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

131
Q

use of systemic abx in infected wound

A

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

132
Q

topical abx for wound infx

A

mafenide acetate, silver sulfadiazine (not used on face)

133
Q

what type of dressings dec bacterial level

A

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

134
Q

wounds that are slow to heal as classified as

A

chronic

135
Q

examples of chronic wounds

A

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

136
Q

what phase of healing are chronic wounds stopped in

A

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

137
Q

chronic wounds have elevated levels of

A

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

138
Q

why do chronic wounds develop

A

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

139
Q

4 types of chronic wounds generally seen in practice

A

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

140
Q

common sites for pressure ulcers

A

heel, sacrum, and ischial tuberosities

141
Q

grade 1 pressure ulcer

A

non blanching erythematous area on intact skin

142
Q

grade 2 pressure ulcer

A

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

143
Q

grade 3 pressure ulcer

A

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

144
Q

grade 4 pressure ulcer

A

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

145
Q

pelvic pressure ulcers can become severely infected from

A

fecal soiling

146
Q

mc local care pelvic ulcers

A

saline moistened gauze w twice daily changing

147
Q

negative pressure wound vacuum device (wound VAC)

A

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

148
Q

mc chronic wounds in adults

A

venous stasis ulcers

149
Q

venous ulcers

A

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

150
Q

path behind venous ulcer

A

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

151
Q

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

A

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

152
Q

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

A

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

153
Q

tx venous ulcers

A

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)

154
Q

arterial ulcers involve

A

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

155
Q

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

A

arterial ds

156
Q

what pulses are usually absent in relation to arterial ulcers

A

pedal

157
Q

what ulcers/wounds usually cause limb loss from infection

A

arterial

158
Q

tx arterial wounds

A

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

159
Q

Charcot’s foot

A

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

160
Q

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

A

excessive weight bearing on surfaces at risk for pressure ulcers

161
Q

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

A

diabetic ulcer

162
Q

tx diabetic ulcer

A

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

163
Q

adv care for chronic wounds

A
  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)
164
Q

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

A

negative pressure; used if no infx and undergone debridement

165
Q

negative pressure is contraindicated in

A

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

166
Q

prevent loss of moisture and desiccation

A

topical foams and occlusive bandages

167
Q

topical broad spectrum antimicrobial preps

A

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

168
Q

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.

A

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.

169
Q

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.

A

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

170
Q

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.

A

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.

171
Q

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

A

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

172
Q

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.

A

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.

173
Q

what is undermining

A

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

174
Q

4 c’s of viable tissue

A

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

175
Q

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

A

prolene (blue)

176
Q

2 ways to cauterize

A

electrical or silver nitrate

177
Q

major categories of dressings

A

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

178
Q

when can surgical wound dressing be removed

A

when skin seals 48hrs after closure

179
Q

difference between dry and exudative wounds in terms of moisture

A

dry conserve and exudative remove

180
Q

abx ointments

A

neosporin, bacitracin, muciprocin, gentimycin

181
Q

antimicrobials: silver containing

A

silvadene, silvasorb

182
Q

antimicrobials: iodine containing

A

iodosorb, iodoflex

183
Q

antimicrobials: sulfa containing

A

sulfamylon

184
Q

disinfectants

A

dakin’s solution: contains Na hypochlorite (bleach)

185
Q

types of biologically active dressings

A

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

186
Q

regranax

A

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

187
Q

cellulose containing biologically active dressings

A

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

188
Q

collagen biologic active dressing

A

stimulates fibroblasts

189
Q

living cell biologic active dressings

A

apligraf and dermagraft; have growth factor factories

190
Q

neg pressure wound therapy biologic active dressings

A

VAC system and blue sky

191
Q

indications for skin graft

A

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

192
Q

types of skin grafts

A

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

193
Q

mc bacteria found in postop wound infx

A

staph aureus; e coli; enterococcus

194
Q

bacteria cause fever and infx within first 24hr postop

A

streptococcus and clostridium (bronze brown weeping tender wound)

195
Q

pt factors influence dev of infx

A

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

196
Q

dressings serve to

A

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

197
Q

when does an uncomplicated surgical wound dressing need to be changed

A

5-7d if clean and dry

198
Q

a well closed incision should be sealed with epithelium when

A

24-48hr

199
Q

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

A

pain, odor, exudate, excessive bleeding

200
Q

when can standard skin suture be removed

A

when incision is closed, depends on location and age

kid(3-5d)
adult abd (7-10d)
eld ant knee (2-3w)

201
Q

when should steri strips be removed

A

don’t until they peel off

202
Q

when should staples be removed

A

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

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

203
Q

abrasion

A

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

204
Q

incision

A

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

205
Q

laceration

A

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

206
Q

puncture

A

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

207
Q

perforation

A

wound w entrance and exit

208
Q

avulsion

A

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

209
Q

jane inflammation stage

A

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

210
Q

jane collagen synthesis phase (proliferative phase)

A

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

211
Q

jane epithelialization phase

A

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

212
Q

scar maturation

A

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

213
Q

jane primary intention

A

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

214
Q

jane secondary intention

A

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

215
Q

jane tertiary intention

A

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

216
Q

wound disruption complications

A

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

217
Q

keloids

A

excessive deposition of collagen creating heaped up scars; AA

218
Q

hyper granulation tissue (proud flesh)

A

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

219
Q

langer’s lines

A

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

Surgery (21 decks)

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