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OS and Pain Management 2 > Wound Repair > Flashcards

Wound Repair Flashcards

1
Q

Anytime you perform SURGERY you create a WOUND
* Leaves underlying tissue vulnerable to —
* ~ — million surgeries per year in the US
* Wound healing remains problematic →why and what can we do to lessen this?

A

infection
50

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2
Q

CAUSES OF INJURY
physical (7)

A

compromised blood flow
crushing
desiccation
incision
irradiation
overcooling
overheating

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3
Q

CAUSES OF INJURY
chemical (5)

A

agents with unphysiologic pH
agents with unphysiologic tonicity
proteases
vasoconstrictors
thrombogenic agents

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4
Q

EPITHELIALIZATION
* Noted with —
* Renewal of epithelium occurs within — after injury
* Occurs faster with — substrate over wound

A

abrasions
hours
moisten

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5
Q

Renewal of epithelium occurs within hours after injury
(2)

A
  • Completion occurs at 24 – 48 hours
  • Free edge of epithelium migrate until it contacts the opposite edge
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6
Q
  • Free edge of epithelium migrate until it contacts the opposite edge
    (2)
A
  • Signal is terminated in CONTACT INHIBITION
  • Occurs over wound bed but under scabbing/superficial blood clot
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7
Q
  • Occurs faster with moisten substrate over wound
  • Epithelium does cross over
A

desiccated surface

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8
Q

PHASES OF WOUND HEALING
* Inflammatory phase
* Day
* Fibroplastic phase
* Days
* Maturation/remodeling phase
*

A

1-6
4- 3 weeks
3 weeks – 1 year

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9
Q

INFLAMMATORY PHASE: DAYS 1- 5ISH
Also called LAG PHASE:
(4)

A
  • No increase in wound strength
  • Due to little collagen deposition
  • FIBRIN principle material holding wound together
  • Has little tensile strength
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10
Q

2 phases of the Inflammatory Phase

A
  • Vascular
  • Cellular
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11
Q

VASCULAR PHASE
* Vasoconstriction of disrupted vessels
(2)

A
  • Coagulation (platelets and fibrin)
  • Clot formation 5-10 minutes
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12
Q

Vasodilation
(3)

A
  • Increases permeability to site to allow healing factors and cells to
    reach injury site
  • Mediated by histamine and prostaglandins (E1 and E2) from WBCs
  • Causes EDEMA (leak of cells and fluid to site of injury)
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13
Q

CELLULAR PHASE
* PMN (neutrophils) arrive within 24 hrs of injury
(4)

A
  • Margination:
  • Diapedesis:
  • Degranulation:
  • Macrophages continue clearance of debris
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14
Q
  • Margination:
A
  • PMNs stick to side of blood vessels
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15
Q
  • Diapedesis:
A
  • PMNs migrate through vessel walls
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16
Q
  • Degranulation:
A
  • PMNS releasing lysosomal enzymes to destroy bacteria/foreign
    materials/necrotic tissue
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17
Q

FIBROPLASTIC PHASE: DAY 4 – 3 WEEKS
* — are the dominant cell

A

Fibroblasts

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18
Q

Fibroblasts are the dominant cell
* Deposits

A

ground substance and TROPOCOLLAGEN over fibrin lattice
* Ground substance contains mucopolysaccharides →cement collagen fibers together

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19
Q

Fibroblasts are the dominant cell
* Secretes

A

FIBRONECTIN

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20
Q

FIBRONECTIN
(3)

A
  • Stabilize fibrin
  • Assists in recognizing foreign material
  • Chemotactic factor to aid recruitment of fibroblasts and macrophages
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21
Q

FIBROPLASTIC PHASE: DAY 4 – 3 WEEKS
* Angiogenesis occurs:
(2)

A
  • Increase vascularity (from wound edges inward)
  • Causes raised and red color of wound
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22
Q

FIBROPLASTIC PHASE: DAY 4 – 3 WEEKS
Superfluous fibrin strands removed by —

A

plasmin

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23
Q

FIBROPLASTIC PHASE: DAY 4 – 3 WEEKS
* Excessive collagen deposited in haphazard manner
(2)

A
  • Increases tensile strength (~ 5-7 days after injury →timing for suture removal)
  • 70%-80% tensile strength compared to uninjured tissue
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24
Q

REMODELING PHASE: 3 WEEKS TO 1 YEAR/INDEFINITE
* Increase in collagen ORGANIZATION AND STRENGTH
(3)

A
  • Collagen oriented in direction to better resist tension
  • Type III collagen replaced by Type I
  • Excess collagen removed →scar softens
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25
Q

Wound strength never reaches above

A

80% - 85% of
uninjured tissue
* Peak tensile strength at 60 days

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26
Q

REMODELING PHASE: 3 WEEKS TO 1 YEAR/INDEFINITE
* Wound erythema decreases as
* Wound contraction occurs by

A

vascularity decreases to site
migration of wound edges
toward each other

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27
Q

FACTORS THAT IMPAIR WOUND HEALING
* Foreign material
(4)

A
  • Dirt, wood, glass, suture, bacteria
  • “Non-self” material causes chronic inflammation
  • Decreases fibroplasia
  • Bacteria proliferation causing infection
  • Destroys host tissue with bacteria byproducts
  • Non-bacteria causes a harbor for bacteria
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28
Q

FACTORS THAT IMPAIR WOUND HEALING
Necrotic tissue

A
  • Free bony fragment in extraction site is classic example
  • Barrier to ingrowth of reparative cells
  • Serves as a protected niche for bacteria
  • Hematoma formation:
  • Nidus for bacteria, as well as food source for bacteria
  • Blood clot is small and functional, hematoma is large and of no use
29
Q

FACTORS THAT IMPAIR WOUND HEALING
* Ischemia
(2)

A
  • Decreased blood supply, resulting in poor oxygen delivery to needed site
  • Increases wound infection by halting delivery of PMNs, WBCs, antibodies, ABX
30
Q
  • Ischemia
  • Results from:
    (4)
A
  • Poorly designed flaps
  • Tight sutures
  • Internal pressure from edema/hematoma
  • Hypotension during surgery
31
Q

FACTORS THAT IMPAIR WOUND HEALING
* Tension
(2)

A
  • Wounds closed under tension will cause ischemia at
    margins with eventual opening (dehiscence)
  • If suture removed too early, the wound under tension will
    reopen and heal with excessive scar formation
32
Q

HYPERTROPHY
(5)

A
  • Overgrowth of tissue within border of
    wound edges
  • Any race
  • Common in pediatrics
  • Regresses with time
  • Common on flexor surfaces
33
Q

KELOID
(5)

A
  • Overgrowth beyond border of wound
    edges
  • Common in darker skin/hereditary
  • Rare in pediatrics
  • Grows for years
  • Common on upper body, head/neck
34
Q

KELOID/HYPERTROPHY TREATMENT
* Similar strategy for both findings
* — significantly more difficult to eradicate
* Triple therapy:

A

Keloid

  • Surgical excision
  • Corticosteroid injection
  • 40 mg/cc injection intralesional
  • 2-3 times per month for 6 months
  • Silicone pressure dressing
  • Worn 12-24 hours per day
  • For 2-3 months
35
Q

WOUND HEALING
(3)

A
  • Primary intention
  • Secondary intention
  • Tertiary intention
  • Delayed primary healing
36
Q

PRIMARY INTENTION
(5)

A
  • Edges of wound returned to anatomic position
  • Wound edges directly next to each other
  • Little loss of tissue
  • Minimal scar
  • Closure stabilized and accomplished with
    sutures/staples/adhesives
37
Q

PRIMARY INTENTION
ex (2)

A
  • Lacerations
  • Well reduced bone fractures
38
Q

SECONDARY INTENTION
(4)

A
  • Wound is allowed to granulate in
  • May be packed by surgeon with gauze or drain
  • Granulation results in broad scar
  • Slower healing process
39
Q

SECONDARY INTENTION
ex (3)

A
  • Gingivectomy
  • Tooth extraction
  • Poorly reduced fracture
40
Q

TERTIARY INTENTION

A
  • Delayed primary closure
  • Related to contaminated wounds
  • Wound cleaned, debrided and observed
  • Closure attempted after 4-5 days
  • Purposely left open to observe for any signs and
    symptoms of infection or further tissue necrosis
  • Skin grafting or flaps can be used to cover these type of
    wounds
41
Q

Primary intention
Epithelial migration
Amount of collagen
Contracture
Speed of healing
Remodeling necessary
Loss of function

A

none
minimal
minimal
rapid
little
little

42
Q

Secondary intention
Epithelial migration
Amount of collagen
Contracture
Speed of healing
Remodeling necessary
Loss of function

A

considerable
large
considerable
delayed
considerable
potentially great

43
Q

HEALING OF EXTRACTION SOCKETS
* Most cases healing is by

A

SECONDARY INTENTION

44
Q

Immediately after extraction:
(3)

A
  • Remnants of periodontal ligament remain attached to the lamina dura
  • Gingival epithelial margin is separated at the crest
  • Coagulated blood seals socket
45
Q

HEALING OF EXTRACTION SOCKETS
* First week
(2)

A
  • Inflammatory phase
  • Fibroplasia begins
46
Q
  • Inflammatory phase
A
  • WBCs break down and digest bacteria and debris
47
Q
  • Fibroplasia begins
    (4)
A
  • Fibroblast proliferate forming granulation tissue
  • Neovascularization penetrates clot
  • Clinical correlation: Localized osteitis, “dry socket,” occurs if this
    phase fails
  • Epithelium begins to migrate down towards first granulation tissue
    it comes into contact with
48
Q

HEALING OF EXTRACTION SOCKETS
* Second week
(2)

A
  • Granulation tissue increase and matures
  • Small socket may close off at 14 days, molars by 3 weeks
49
Q
  • Third and Fourth week
    (2)
A
  • Almost all sockets will have epithelial closure by 21 days
  • Deposition of early bone (osteoid) within the socket
50
Q

HEALING OF EXTRACTION SOCKETS
* Four to six months
(3)

A
  • Continued resorption and recontouring of alveolus
  • Total resorption of lamina dura by 1 year
  • Clinical correlation:
  • What is time frame to wait before building a final prosthesis?
51
Q

BONE HEALING
* Where do osteogenic cells responsible for bone repair come from?
(3)

A
  • Periosteum
  • Endosteum
  • Circulating pluripotential mesenchymal cells
52
Q

Primary Intent
Bone separation
Fibrous matrix
Callus
Speed of re-ossification

A

< 1 mm
Little between or
subperiosteal
Little
Fast

53
Q

Secondary Intent
Bone separation
Fibrous matrix
Callus
Speed of re-ossification

A

> 1 mm
Large amounts extending past
bone ends
Large
Longer with replacement
process

54
Q

BONE HEALING
* Factors most important to proper bone healing
(2)

A
  • VASCULARITY
  • IMMOBILITY
55
Q
  • VASCULARITY
  • If low oxygenation →
  • If severe →
A

cartilage will form instead of bone
fibrous tissue may never calcify →fibrous union

56
Q
  • IMMOBILITY
    (2)
A
  • Intermaxillary fixation (IMF), bone plates, direct wires
  • Mobility prevents fibrous tissue from ossifying →fibrous union, non-union,
57
Q

NERVE REPAIR
* OMS considerations with (2) nerves

A

inferior alveolar or lingual

58
Q

Prognosis for return of sensory function is related to:
(3)

A
  • How bad was the damage (severed, crushed, stretched, pinched)
  • Condition of epineurium
  • Amount of separation between nerve ends
59
Q

NERVE REPAIR
* Two phases:
(2)

A
  • Degeneration
  • Regeneration
60
Q

Degeneration
(2)

A
  • Segmental demyelination
  • Wallerian Degeneration
61
Q
  • Segmental demyelination
    (2)
A
  • Myelin sheath dissolved in isolated segments (slows nerve conduction)
  • Symptoms: paresthesia, dysesthesia, hyperesthesia, hypoesthesia
62
Q
  • Wallerian Degeneration
    (2)
A
  • Axons and myelin sheath of nerve distal to site of interruption undergo disintegration in their
    entirety
  • Axons proximal to the site of interruption undergo some degeneration generally a few Nodes of
    Ranvier away
63
Q

Regeneration
(4)

A
  • Growth cone (growth of new nerve fibers from proximal nerve stump) starts growing down
    remnant Schwann cell tube
  • Progresses 1 mm per day
  • Continues until site innervated by the nerve is reached
  • New myelin sheaths may form as axons increase in diameter
64
Q

Abnormal nerve healing →

A

NEUROMA
* Mass of aimless nerve fibers
* Painful when disturbed (temperature, pressure, etc…)

65
Q

Paresthesia

A
  • Spontaneous and subjective altered sensation that IS NOT PAINFUL/UNCOMFORTABLE
66
Q

Dysesthesia

A
  • Spontaneous and subjective altered sensation that IS PAINFUL/UNCOMFORTABLE
67
Q
  • Hyperesthesia
A
  • Excessive sensitivity of a nerve to stimulation
68
Q
  • Hypoesthesia
A
  • Decreased sensitivity of a nerve to stimulation
69
Q
  • Anesthesia
A
  • No sensation when stimulated

OS and Pain Management 2 (10 decks)

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