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Phase 1 > Ch. 75, 76, & 81 Wounds and Burns > Flashcards

Ch. 75, 76, & 81 Wounds and Burns Flashcards

1
Q

How is the vascular supply of the subcutaneous tissue divided?
Three divisions

A

superficial aka subpapillary plexus
middle aka cutaneous plexus
deep aka subdermal/subcutaneous plexus

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2
Q

what is a cutaneous angiosome

A

a given region of skin is supplied by a regional artery and vein is a cutaneous angiosome
Cats and dogs have different kinds of angiosomes - cats have a smaller number but wider distribution of cutaneous perforating vessels than dogs

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3
Q

How strong is wounded skin at 14 days after surgery

A

only 5-10% of its unwounded strength
and only 25% by 3-4 weeks
several months later it maxes out at 70-80%

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4
Q

How do cat wounds heal compared to dogs?

A

Cats have lower cutaneous perfusion immediately following surgery than dogs
Cat open wounds heal more by contraction whereas dogs heal more by fibroblasts and epithelialization

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5
Q

How should larger defects be closed in regards to tension lines as a general guideline

A

large defects should be created and closed PARALLEL to tension lines

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6
Q

How far will char penetrate when skin is incised by radiowaves vs CO2 laser vs monopolar

A

radiowave - 0.171 mm
CO2 laser - 0.215 mm
monopolar - 0.255 mm

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7
Q

Is the wound strength stronger or weaker with a blade vs cautery?`

A

Incisions made by sharp dissection with a scalpel blade had TWICE the wound strength at 10-12 days post incision
Scalpel incisions produced less drainage than laser and electrocautery incisions and had faster and stronger healing

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8
Q

Why should you primarily close traumatic wounds within 3-6 hours?

A

within 3-6 hours, bacteria within a minimally contaminated wound can multiply to 10^5 per gram of tissue or ml of exudate and that increases the risk of infection dramatically

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9
Q

What are the theoretical ways that low level laser therapy aids in wound healing

A

enhance leukocyte infiltration
increase growth factors, macrophage activity, neovascularization, and fibroblast and keratinocyte proliferation
promote early epithelialization

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10
Q

What is an abrasion

A

partial thickness epithelial injury usually from blunt trauma or shearing
minimal bleeding occurs and they heal rapidly by re epithelialization

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11
Q

What is a puncture wound

A

penetration of an object into the tissues and is characterized by a small skin opening with deep tissue contamination and damage
may include bite wounds, gunshot injuries, wounds cause by penetration of foreign bodies

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12
Q

What is a laceration

A

sharply incised skin edges and may extend into deep tissue such as muscle and tendons
usually minimal peripheral trauma to wound edges

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13
Q

What is a degloving injury

A

extensive loss of skin and underlying tissue
immediate or delayed exposure of the wound bed
a physiologic degloving is where the skin surface is intact but avulsed from the underlying SQ tissues and blood supply - delayed necrosis will occur

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14
Q

what is a thermal burn

A

the result of close proximity or direct application of heat to the skin
fire, cage dryers, heating pads, electrical cords, heat lamps, hot liquids, and malicious incidents
extent of the wound is difficult to predict because of delayed microvascular damage

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15
Q

what is a decubital ulcer

A

the result of compression of the skin and soft tissues between the bony prominence and a hard surface, resulting in skin loss over a bony protuberance

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16
Q

What is a more relevant conceptualization of the effect of the microbial burden on a wound than the usual greater than 10^5 CFU/gram of tissue or ml of exudate

A

(number of microorganisms x virulence)/host resistance

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17
Q

What is primary wound closure

A

first intention healing

wound edges are apposed

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18
Q

what is delayed primary wound closure

A

appositional closure but within 3-5 days after wounding (PRIOR to granulation bed forming)

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19
Q

what is secondary wound closure

A

appositional closure AFTER 3-5 days when there is granulation tissue
may also be called third intension healing which is dumb

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20
Q

what is second intention healing

A

healing by contraction and epithelialization

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21
Q

true or false

there is no difference in risk for infection with tap water vs sterile saline irrigation of a wound

A

true! no difference in people anyway in a prospective or a systemic review
there is no difference in development of wound infection with use of tap water vs distilled vs boiled

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22
Q

What constitutes as low pressure irrigation?

A

less than 5 PSI

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23
Q

what constitutes high pressure irrigation?

A

5-8 PSI

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24
Q

How can you consistently get about 7-8 PSI on an irrigation system

A

attach a 16-22 G needle to an IV fluid bag set and then place the fluid bag under 300 mmHg with a pressure bag and cuff

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25
Q

Topical wound dressings for open wounds: Hypertonic saline dressing
Stage of wound healing:
Indications:

A

Topical wound dressings for open wounds: Hypertonic saline dressing
Stage of wound healing: inflammatory, early repair, infected wound in aany stage
Indications: it is 20% saline and hypertonicity is antimicrobial and will facilitate autolytic debridement

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26
Q

Topical wound dressings for open wounds: honey
Stage of wound healing:
Indications:

A

Topical wound dressings for open wounds: honey
Stage of wound healing: inflammatory, early repair
Indications: antibacterial, enhances autolytic debridement, reduces edema and inflammation, enhances granulation tissue and epithelialization

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27
Q

Topical wound dressings for open wounds: sugar
Stage of wound healing:
Indications:

A

Topical wound dressings for open wounds: sugar
Stage of wound healing: inflammatory, early repair
Indications: hyperosmotic, questionable antimicrobial effect

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28
Q

Topical wound dressings for open wounds: enzymatic agents like collagenase
Stage of wound healing:
Indications:

A

Topical wound dressings for open wounds: enzymatic agents like collagenase
Stage of wound healing: inflammatory, debridement, early repair
Indications: enzymatic debridement, adjunct to surgical debridement, may be useful in poor granulation tissue in chronic wounds

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29
Q

Topical wound dressings for open wounds: maggots
Stage of wound healing:
Indications:

A

Topical wound dressings for open wounds: maggots
Stage of wound healing: inflammatory, debridement, early repair
Indications: maggots secrete digestive enzymes to dissolve necrotic tissue and may be useful when surgical debridement is prohibitive

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30
Q

Topical wound dressings for open wounds: topical antibiotic ointment
Stage of wound healing:
Indications:

A

Topical wound dressings for open wounds: topical antibiotic ointment
Stage of wound healing: inflammatory
Indications: reduces surface microbial burden

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31
Q

Topical wound dressings for open wounds: silver
Stage of wound healing:
Indications:

A

Topical wound dressings for open wounds: silver
Stage of wound healing: inflammatory, early repair, infected wound in any stage
Indications: infected wounds

Incorportaion of silver into hydrophilic dressings are more effective than silver alone - may have synergistic effect with alginate and together they will have improved binding affinity for elastase, matric metalloproteinase 2, TNF alpha, IL 8… however may be cytotoxic so use only for infected wounds

32
Q

Topical wound dressings for open wounds: hydrogel
Stage of wound healing:
Indications:

A

Topical wound dressings for open wounds: hydrogel
Stage of wound healing: inflammatory, repair
Indications: provides exogenous moisture, good for wounds with minimal to no exudate like abrasions, keeps wound surface moist and promotes epithelialization

33
Q

Topical wound dressings for open wounds: hydrocolloid or synthetic hydrophilic
Stage of wound healing:
Indications:

A

Topical wound dressings for open wounds: hydrocolloid or synthetic hydrophilic
Stage of wound healing: inflammatory, repair
Indications: wounds with moderate or copious exudates, absorbs exudate and keeps wound surface moist, enhances autolytic debridement, promotes granulation tissue formation

34
Q

Topical wound dressings for open wounds: alginate
Stage of wound healing:
Indications:

A

Topical wound dressings for open wounds: alginate
Stage of wound healing: inflammatory, repair
Indications: wounds with moderate or copious exudates, absorbs exudates and keeps wound surface moist, enhances autolytic debridement, promotes granulation tissue formation

35
Q

Topical wound dressings for open wounds: bioscaffolds
Stage of wound healing:
Indications:

A

Topical wound dressings for open wounds: bioscaffolds
Stage of wound healing: repair, chronic indolent wounds
Indications: semiocclusive dressing, provides scaffold for development of extracellular matrix, they stimulate matrix deposition, angiogenesis and epithelialization because of their collagenous and growth factor content
ex. porcine small intestinal submucosa

36
Q

Topical wound dressings for open wounds: chitosan
Stage of wound healing:
Indications:

A

Topical wound dressings for open wounds: chitosan
Stage of wound healing: repair
Indications: linear copolymer of linked beta glucosamine and N acetyl D glucosamine derived from chitin rich crab shell

How does it work? enhances the function of inflammatory cells and increases granulation tissue through upregulation of TGF beta, PDGF, and IL 8

37
Q

Topical wound dressings for open wounds: growth factors
Stage of wound healing:
Indications:

A

Topical wound dressings for open wounds: growth factors
Stage of wound healing: repair
Indications: only if wound is deficient in or contains excessive target cell or mediator

ex. Becaplermin or PRP

38
Q

Topical wound dressings for open wounds: non adherent, semiocclusive
Stage of wound healing:
Indications:

A

Topical wound dressings for open wounds: non adherent, semiocclusive
Stage of wound healing: maturation
Indications: wound with intact surface. not for open wounds though because it will be non hydrophilic and drying

39
Q

What concentration of 1:40 does chlorhexidine 2% dilution produce?

A

0.05 to 0.1%

40
Q

What concentration of 1:100 or 1:1000 does povidone iodine 10% dilution produce?

A

0.1 to 0.01%

41
Q

How does the subcutaneous tissue influence epithelialization in the dog and cat

A

When subcutis was left in place, the percentage of epithelialization of experimental wounds at day 21 was 34% in cats and 89% in dogs. Without the subcutis though, it was 20% in cats and 61% in dogs

42
Q

What is the inhibin number in regards to honey

A

the amount of dilution to which the honey will retain its antibacterial properties and is measured at dilutions of 25, 20, 15, 10 and 5%

43
Q

What species of maggots is used for medical debridement and why

A

the green blow fly, Lucilia sericata, is used because these larvae will not damage heatlhy dermis or SQ tissue (but will damage epidermis)

44
Q

How may a bioscaffold be of particular use in a chronic wound over an acute?

A

Acute vs chronic wounds have imbalances of metalloproteinases

Collagen or collagen/oxidized regenerated cellulose bioscaffold dressings can act as competitive substrates for matrix metalloproteinase 2 and 9 and also bacterial collagenases

This will favor the wound toward inhibiting metalloproteinases so that the extracellular matrix can form

45
Q

What pore size is recommended for negative pressure wound therapy in an open wound

A

400 to 600 um

46
Q

How does NPWT increase oxygenation in a wound bed if it actually reduces the PaO2

A

Theory is that macrodeformations in the tissue due to differing forces at the surface and depths of the wound may change pressure gradients, flow, and then oxygenation which then could release growth factors like VEGF

47
Q

What is the NPWT pressure recommended by the Morykwas study

A

Negative! -125 mmHg

The study showed that this pressure increased blood flow to four times above baseline

48
Q

Another study suggested a different pressure for NPWT for less dense tissues to stimulate blood flow while minimizing marginal hypoperfusion - what pressure was that

A

-75 to -100 mmHg

49
Q

General recommend pressure for NPWT for gauze based vs foam based systems

A
  • 80 mmHg for gauze
  • 125 mmHg for foam

the biggest wound contraction is seen at pressures from 0 to -50 mmHg though

50
Q

What two cytokines are significantly higher with NPWT treatment over regular foam dressing?

A

VEGF
IL 8

but recent studies show that it may also upregulat IL 1beta too

51
Q

what NPWT pressure is reommended for placement over skin grafts

A

-65 to -75 mmHg

52
Q

Will intermittent or continuous NPWT have a greater effect on promotion of vascular proliferation within a wound

A

Intermittent apparently

53
Q

What are the four burn categories based on their energy source

A

thermal
chemical
electrical
radiation

54
Q

definition of a thermal burn

A

caused by tissue exposure to temperature extremes (high or low) that will cause cellular damage

55
Q

How is heat transferred in a thermal burn

A

conduction - direct contact with hot object
convection - airborne heat transfer
radiation - electromagnetic energy is converted to heat

56
Q

At what temperature will a cell membrane sodium pump fail

A

40-44 degrees celsius or 104 to 11 degrees F

57
Q

At what temperature will epidermal and dermal necrosis occur if the skin temp reaches it for 1 sec

A

epidermal necrosis will occur at 60 C/140 F for one sec

full thickness through the dermis will occur at 70 C/158 F for less than one sec

58
Q

How is an animal’s body divided with the rule of 9

A 
head and neck = 9
each forelimb = 9
each hindlimb = 18
dorsal trunk = 18
ventral trunk = 18
59
Q

How do you use the veterinary burn card

A

the card is the same dimensions as a credit card and is 45 cm^2
Measure the burn with the card and count how many cards cover the burn
weigh the patient and then convert the weight to surface area m^2 (like chemo dosing)
use this formula:

% total body surface area that is burned = ((# of cards) x 0.45)/m^2

60
Q

What are the three zones of a burn

A

zone of coagulation (or necrosis or destruction)
zone of stasis (reduced perfusion)
zone of hyperemia (primary area that will have inflammation)

61
Q

What is the role of nitric oxide in burns

A

it is upregulated within the area of thermal injury
acts as a vasodilator via direct effects on smooth muscle but also indirectly by stimulating other vasodilatory compounds like substance P

62
Q

what leads to post burn edema

A

increased perfusion to the area (courtesy of NO and substance P)
increased capillary permeability

63
Q

What is the majority of injury from smoke inhalation caused by?

A

two types - thermal and toxic
thermal is generally only the upper airways because the air is cooled fast enough in the trachea to not be too hot by the time it reaches the lungs
therefore, TOXIC is where most effects are from

64
Q

What are the toxic compounds that contribute to smoke inhalation damage

A

carbon monoxide
hydrogen cyanide from nitrogen contaning products (like Formica, wool)
inorganic acids
free hydroxyl and carbon radicals

65
Q

How is carbon monoxide toxic? three mechanisms

A
  1. preferentially binds to hemoglobin (making carboxyhemoglobin) which reduces RBC oxygen carrying capacity
  2. carboxyhemoglobin formation results in a LEFT shift of the oxyhemoglobin dissociation curve which makes it a higher affinity and reduces oxygen delivery to the tissues
  3. binding of carbon monoxide with myoglobin will reduce oxygen availability to muscle
66
Q

How is hydrogen cyanide toxic?

A

binds with mitochondrial cytochrome oxidase which disrupts electron transport chain and prevents cellular respiration

67
Q

How are hydrochloride and other diatomic halide acids toxic in smoke inhalation

A

irritating to respiratory mucous membranes, produce laryngospasm and bronchospasm

68
Q

What is the lung’s response to smoke inhalation

A

increased pulmonary vascular permeability
venoconstriction
rapid accumulation of fluid, mucus, neutrophils within the alveoli and airways (pulmonary edema)
atelectasis
decreased alveolar ventilation
deactivation of pulmonary surfactant
decreased lung compliance

All leading to ARDS

69
Q

how does thromboxane A2 play a role in pulmonary response to smoke

A

TxA2 is also made by pulmonary macrophages and gets released in smoke inhalation
they lead to an increase in pulmonary transvascular flux and vascular resistance secondary to marked pulmonary venoconstriction

70
Q

Why do burn patients get hypovolemic

A

combo of extreme systemic extravasation and evaporation

71
Q

Why does the body’s blood become hyperviscous in burn patients

A

profound hypovolemia in concert with erythrocyte deformability
this effect is then worsened by systemic vasoconstriction and it leads to tissue hypoxia and metabolic acidosis

72
Q

What effects do large burns have on myocardial function

A

direct effects!
decreased left ventricular contractility because of increased Ca2+ in cardiac myocytes due to oxidative injury (calcium leaks) and cytosolic sodium accumulation in myocytes

73
Q

How is the GI system affected in burn patients

A

barrier function is compromised
increased apototic rate of gut mucosal cells with no increased in mucosal proliferation
decreased motility
oxidative stress in hepatocytes and upregulation of acute phase proteins while albumin production decreases

74
Q

Why do burn patients become anemic

A

first, they have RBCs trapped in the wound, about 10% of RBC mass but that doesnt account for all of the anemia

Within 1 hour of a burn, the concentration of free hemoglobin in the plasma increases and that signals intravascular hemolysis which then occurs because of membrane damage that increases erythrocyte fragility and decreases erythrocyte deformability

The body will make more erythropoetin released but it usually isnt enough because of decreased iron availbility. For whatever reason though, the book does say that supplemental exogenous erythropoetin will help

75
Q

What are the metabolic effects of a burn

A

increase in body temp setting of the hypthalamus so the body wastes energy making the body tempertuare higher than usual
change in the utilization of predominantly fat in normal state to more protein catabolization in burn state
upregulation of gluconeogenesis and relative insulin resistance –> persistent hyperglycemia and catabolic state (“burn diabetes”)
Burn wounds have an increased rate of glucose uptake because of the high rate of anaerobic glycolysis by inflammatory and endothelial cells

Phase 1 (35 decks)

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