อีกบทบาทหนึ่งที่ภาคภูมิใจในชีวิต คือการได้สอนนักศึกษาแพทย์ ในเรื่องศัลยศาสตร์

1. Wound Healing
สรีระวิทยาและกลไกการหายของบาดแผล
นายแพทย์ ชูชัย ศรชา นิพบ. วว. ศัลยศาสตร์ทั่วไป
chuchai.s@nhso.go.th chuchai.sn@gmail.com

2. INTRODUCTION
Wound healing is a vague term that often confuses
and diverts the clinician from focusing on a specific
diagnosis.
Over the ages, many agents have been placed on
wounds to improve healing.

3. To date nothing has been identified that
can accelerate healing in a normal
individual.
• Over the ages, many agents have been
placed on wounds to improve healing.
• Many hinder the healing process.
• A surgeon’s goal in wound management
is to create an environment where the
healing process can proceed optimally.

4. Normal Wound-healing Process
Phase Cellular and Bio-physiologic Events
Hemostasis 1.vascular constriction
2.platelet aggregation, degranulation, and fibrin
formation (thrombus)
Inflammation 1.neutrophil infiltration
2.monocyte infiltration and differentiation to
macrophage
3.lymphocyte infiltration
Proliferation 1.re-epithelialization
2.angiogenesis
3.collagen synthesis
4.ECM formation
Remodeling 1.collagen remodeling
2.vascular maturation and regression
ECM, extracellular matrix.
ที่มา J Dent Res. Mar 2010; 89(3): 219–229.

5. Wound Healing Events
Approximate times of the different phases of wound healing, with
faded intervals marking substantial variation, depending mainly on
wound size and healing conditions, but image does not include
major impairments that cause chronic wounds.

6. Wounding
• Blood vessels are disrupted, resulting in
bleeding. Hemostasis is the first goal achieved
in the healing process.
• Cellular damage occurs, this initiates an
inflammatory response.
• The inflammatory response triggers events that
have implications for the entire healing
process.
• Step one then is hemostasis, resulting in Fibrin.

7. Wound Healing
1. Vascular and inflammatory
phase
2. Re epithelization
3. Granulation tissue formation
4. Fibroplasia and matrix
formation
5. Wound contraction
6. Neo vascularization
7. Matrix and collagen
remodelling

8. PART I
NORMAL WOUND
HEALING
E.G. CLEAN CUT WOUND

9. EARLY EVENTS

10. Steps
i. diapedesis
ii. hemostatic clot – formed by
plateletes
iii. fibrin clot formation –
formed by fibroblasts
Plateletes – 1st cells to produce
essential cytokines which
modulates most of the
subsequent steps in wound
healing

11. Early Events
The early phase, which begins
immediately following skin
injury, involves cascading
molecular and cellular
events leading to
hemostasis and formation
of an early, makeshift
extracellular matrix—
providing structural support
for cellular attachment and
subsequent cellular
proliferation.

12. Hemostasis : Vascular
• Initial vasoconstriction (5-10
min) then vasodilation
(persistent)
• Exposure of sub endothelial
von Willebrand / factor VII,
and fibrillar collagen –
platelet plug
• Hageman factor (XII) –
initiation of clotting cascade
and fibrin clot formation

13. Hemostasis : Fibrin
• Fibrin and fibronectin form a lattice
that provides scaffold for migration
of inflammatory, endothelial, and
mesenchymal cells.
• Fibronectin is produced by
fibroblasts, has a dozen or so
binding sites.
• Binds cytokines
• Its breakdown products stimulate
angiogenesis.

14. Hemostasis : Clotting Cascade
Intrinsic Pathway
Surface Contact
F XI F XIa
F IX F IXa
Platelet Factor 3
Factor F X
Collagen
FXII activator
F XII F XIIa
Ca2+
Ca2+
Extrinsic Pathway
Tissue/Cell Defect
F VIIa F VII
Ca2+
F III (Tissue
Thromboplastin)
Ca2+ Factor F X
Ca2+
Fibrin Fibrinogen
monomers
Fibrin
polymers
Crosslinked
Fibrin Meshwork
F XIIIa F XIII
F Va F V
F VIII F VIIIa
Prothrombin I
Factor F Xa
Ca2+ Thrombin

15. Inflammation : Signs
• Erythema
• Edema
• Pain
• Heat
Inflammation – migration of leukocytes into the wound. 1st 24
hours, polymorphonucleocytes followed by macrophages.

16. Inflammation : Physiological Changes
• Immediately after injury, intense
vasoconstriction leads to blanching, a process
mediated by epinephrine, NE, and
prostaglandins released by injured cells.
• Vasoconstriction reversed after 10 min, by
vasodilatation.
• Now redness and warmth.
• Vasodilatation mediated by histamine, linins,
prostaglandins.

17. • Platelets
– derived growth factor (PDGF), proteases and
vasoactive substances such as serotonin and
histamine
• Polymorphonuclear leukocytes
• Macrophages (replace PMNs after 5 days)
• Fibroblasts (recruited by chemotactic factors
released by the above cells)

18. Inflammation : Physiological Changes
• As microvenules dilate, gaps form between the
endothelial cells , resulting in vascular
permeability. Plasma leaks out into
extravascular space.
• Leukocytes now migrate into the wound by
diapedesis, adhere to endothelial cells, to
wounded tissues.
• Alteration in pH from breakdown products of
tissue and bacteria, along with swelling causes
the pain.

19. Inflammation : Physiological Changes
• Neutrophils, macrophages and lymphocytes come
into wound.
• Neutrophils first on scene, engulf and clean up.
Macrophages then eat them or they die releasing O2
radicals and destructive enzymes into wound.
• Monocytes migrate into extravascular space and turn
into macrophages.
• Macrophages very important in normal wound
healing.

20. Inflammation : Physiological Changes
• Macrophages eat bacteria, dead tissue, secrete
matrix metallo proteinases that break down
damaged matrix.
• Macrophages source of cytokines that stimulate
fibroblast proliferation, collagen production.
• Lymphocytes produce factors like FGF, EGF, IL-2.
• At 48-72 hrs, macrophages outnumber neuts.
• By days 5-7 few remain.

21. INTERMEDIATE EVENTS

22. Intermediate Events
As in the other phases of wound healing, steps in
the proliferative phase do not occur in a series but
rather partially overlap in time.
•About two or three days after the wound
occurs, fibroblasts begin to enter the wound site, marking
the onset of the proliferative phase even before the
inflammatory phase has ended.

23. Proliferation
• Mesenchymal cell
chemotaxis
• Mesenchymal cell
proliferation
• Angiogenesis
• Epithelialization
Fibroplasia – increases wound strength, hence tissue integrity is
restored. Within 10 hours after injury, there is increased wound
collagen synthesis. Within 5-7 days, collagen has peaked and will
decline gradually.

24. Proliferation
• Fibroblasts are the major mesenchymal cells
involved in wound healing, although smooth
muscle cells are also involved.
• Normally reside in dermis, damaged by
wounding.
• Macrophage products are chemotactic for
fibroblasts. PDGF, EGF, TGF, IL-1, lymphocytes
are as well.

25. Proliferation
Angiogenesis reconstructs vasculature in areas damaged by
wounding, stimulated by high lactate levels, acidic pH, decreased O2
tension in tissues.
• Cytokines directly stimulate the endothelial cell
migration and proliferation required for angiogenesis.
Many are produced by Macs.
• Fibroblast growth factor : FGF-1 is most potent
angiogenic stimulant identified. Heparin important as
cofactor, Transforming growth factor : TGF-alpha, beta,
prostaglandins also stimulate.

26. Epithelialization
The formation of granulation tissue
in an open wound allows the re
epithelialization phase to take
place, as epithelial cells migrate
across the new tissue to form a
barrier between the wound and
the environment.
They advance in a sheet across the
wound site and proliferate at its
edges, ceasing movement when
they meet in the middle.

27. Epithelialization
• The process of epithelial renewal
after injury.
• Particularly important in partial
thickness injuries, but plays a role
in all healing.
• Partial thickness wounds have
epidermis and dermis damaged,
with some dermis preserved.
• Epithelial cells involved in healing
come from wound edges and
sweat glands, sebaceous glands in
the more central portion of
wound.

28. Re epithelization
• Migration (wound edges, hair follicles,
adnexa)
• Proliferation (48-72 hours)
• Sutured wounds have a layer of keratinocytes
within 24-48 hours

29. Skin Anatomy
• Epidermis is composed of multiple layers of
epithelial cells superficial to the dermis.
• The first layer above the dermis is the basal
layer, which is composed of basaloid cells.
• The cells become more elongated as you go
to superficial stratum corneum.
• Stratum corneum is mostly keratin and dead
tissue.

30. Layers of Skin

31. Clean incision wound
Epithelialization
• In contrast in an incisional wound, cellular
migration occurs over a short distance.
• Incisional wounds are re-epithelialized in 24-
48h.
• The sequence of events here are cellular
detachment, migration, proliferation,
differentiation.

32. Epithelialization
• First 24h, basal cell layer thickens, then elongate,
detach from basement membrane (BM) and migrate
to wound as a monolayer across denuded area.
• Generation of a provisional BM which includes
fibronectin, collagens type 1 and 5.
• Basal cells at edge of wound divide 48-72 h after
injury.
• Epithelial cells proliferation contributes new cells to
the monolayer. Contact inhibition when edges come
together.

33. LATE WOUND HEALING EVENTS

34. Late Wound Healing Events
RE MODELING
Cytokines –provides communication for cell to cell interaction.
Roles include:
1. Regulation of Fibrosis
2. Healing of wounds and skin grafts.
3. Vascularization
4. Bone and Tendon Strengthening
5. Control of Malignancy

35. Collagen
• Synthesized by fibroblasts beginning 3-5 days after
injury.
• Rate increases rapidly, and continues at a rapid rate
for 2-4 weeks in most wounds.
• As more collagen is synthesized, it gradually replaces
fibrin as the primary matrix in the wound.
• After 4 weeks, synthesis declines, balancing
destruction by collagenase.

37. Keratinocytes
• Fibronectin
– Cross links to fibrin – matrix/scaffold for keratinocyte adhesion and
migration
– Functions as an early component of the extracellular matrix.
– Binds to collagen and interacts with matrix glycosaminoglycans.
– Has chemotactic properties for macrophages, fibroblasts and endothelial
and epidermal cells.
– Promotes opsonization and phagocytosis.
– Forms a component of the fibronexus.
– Forms scaffolding for collagen deposition
• Collagenases and neutral proteases – debridement
• Plasminogen activator – clot dissolution
• Type V collagen
• Requires moisture for epithelial migration

38. Granulation
• Highly vascular network of
glycoproteins, collagen and
glycosaminoglycans
• Fibroblasts
– collagen
– Elastin
– Fibronectin
– Sulfated and non-sulfated
Glycosaminoglycans
– Proteases
• Inflammatory cells

39. Fibroplasia
• Fibroblasts
• Mainly Type III collagen first
• Replaced by type I and II collagen
• Hydroxylation of proline and lysine
– Iron, copper, vitamin C
– Cross linkage

40. Collagen
• Synthesized by fibroblasts beginning 3-5 days after
injury.
• Rate increases rapidly, and continues at a rapid rate
for 2-4 weeks in most wounds.
• As more collagen is synthesized, it gradually replaces
fibrin as the primary matrix in the wound.
• After 4 weeks, synthesis declines, balancing
destruction by collagenase.

42. Collagen
• Age, tension, pressure and stress affect rate of
collagen synthesis.
• TGF-b stimulates it, glucocorticoids inhibit it.
• 28 types identified. Type 1(80-90%) most common,
found in all tissue. The primary collagen in a healed
wound.
• Type 3(10-20%) seen in early phases of wound
healing. Type V smooth muscle, Types 2,11 cartilage,
Type 4 in BM.

43. Collagen
• Three polypeptide chains, right handed
helix.
• Most polypeptide chains used in collagen
assembly are alpha chains.

45. Collagen
• Every third AA residue is Glycine.
• Another critical component is hydroxylation of lysine
and proline within the chains. Hydroxyproline is
necessary for this. Requires Vit C, ferrous iron, and
alpha ketoglutarate as co-enzymes.
• Steroids suppress much of this, resulting in
underhydroxylated collagen, which is incapable of
making strong cross-links leading to easy breakdown.

46. Wound Contraction
• Contraction is a key phase of wound healing. If
contraction continues for too long, it can lead to
disfigurement and loss of function.
• Fibroblasts, stimulated by growth factors,
differentiate into myofibroblasts. Myofibroblasts,
which are similar to smooth muscle cells, are
responsible for contraction. Myofibroblasts
contain the same kind of actin as that found
in smooth muscle cells.

47. Contraction
• Myofibroblasts
• Fibronexus (Singer)
– Connections between intracellular actin
microfilaments and extracellular
collagen, fibronectin, and between
myofibroblasts
– Transmits force along entire network
– Centripetal contraction

48. Wound Contraction
• Begins approximately 4-5 days after wounding.
• Represents centripetal movement of the
wound edge towards the center of the wound.
• Maximal contraction occurs for 12-15 days,
although it will continue longer if wound
remains open.

49. Wound Contraction
• The wound edges move toward
each other at an average rate of
0.6 to .75 mm/day.
• Wound contraction depends on
laxity of tissues, so a buttocks
wound will contract faster than
a wound on the scalp or
pretibial area.
• Wound shape also a factor,
square is faster than circular.

50. Wound Contraction
• Contraction of a wound across a joint can
cause contracture.
• Appears in 2nd degree burns or skin loss

51. Wound Contraction
• Can be limited by skin grafts, full better than
split thickness.
• The earlier the graft the less contraction.
• Splints temporarily slow contraction.

52. TERMINAL WOUND HEALING
EVENT

53. Neovascularization
• Fibronectin
• Macrophage derived angiogenic factor
• Endothelial migration

54. Wound Remodeling
• Increased tensile strength
• Decreased bulk, and
erythema
• Replacement of fibronectin
by collagen
• Dehydration
– Promotes further crosslinkage
of collagen
– Reorientation of collagen to
parallel skin collagen.

55. Remodeling
• After 21 days, net accumulation of collagen
becomes stable. Bursting strength is only 15%
of normal at this point. Remodeling
dramatically increases this.
• 3-6 weeks after wounding greatest rate of
increase, so at 6 weeks you are at 80% to 90%
of eventual strength and at 6mos 90% of skin
breaking strength.

56. Remodeling
• The number of intra and intermolecular cross-links
between collagen fibers increases dramatically.
• A major contributor to the increase in wound
breaking strength.
• Quantity of Type 3 collagen decreases replaced by
Type 1 collagen
• Remodeling continues for 12 mos, so scar revision
should not be done prematurely.

57. HEALING AT DIFFERENT PART OF
BODY

58. Healing at Different Part of Body
Skin graft
• donor site
• Split (partial) thickness skin graft
• Full thickness skin graft
Skin Flap
• Local flap
• Distance flap
Contraction : the process whereby there is
spontaneous closure of full thickness skin
wounds

59. Healing at Different Part of Body
• Tendon – composed mainly of type I
collagen with significant amounts of
proteoglycan. After disruption tendon and
sheath have to be sutured.
– Connective Tissue Matrix Deposition : the process
whereby fibroblasts are recruited to the site of
injury and produce a new connective tissue
matrix. The cross-linked collagen provides the
strength and integrity to all tissue.

60. Healing at Different Part of Body
Bone
• Soft callus formation
• Mineralized as cartilage
• Replaced by osteoid or bone – beginning of
remodeling

61. Healing at Different Part of Body
Gastrointestinal Tract : Bowel anastomotic
strength develops more rapidly than that of the
skin.
Major complications of intestinal anastomoses are
a. leak
b. disruption
The submucosa provide the major strength in
anastmotic closure because it contains the majority
of the fibrous connective tissue.
Contraction : constriction of tubular organs such as
the CBD or esophagus.

62. Part II
DISTURBANCES IN WOUND
HEALING

63. Factors Affecting Wound Healing
Local Factors Systemic Factors
•Oxygenation
•Infection
•Foreign body
•Venous
sufficiency
•Age and gender
•Sex hormones
•Stress
•Ischemia
•Diseases: diabetes, keloids, fibrosis, hereditary
healing disorders, jaundice, uremia
•Obesity
•Medications: glucocorticoid steroids, non-steroidal
anti-inflammatory drugs, chemotherapy
•Alcoholism and smoking
•Immunocompromised conditions: cancer,
radiation therapy, AIDS
•Nutrition

64. รายละเอียดของ Local Factors
• Infection versus contamination
• Infection is when number or virulence of
bacteria exceed the ability of local defenses to
control them.
• 100,000 organisms per gram of tissue.
• Foreign bodies, hematomas promote infection,
impaired circulation, radiation.

65. รายละเอียดของ Systemic Factors
• Smoking stimulates vasoconstriction.
• Increases platelet adhesiveness
• Limits O2 carrying capacity
• Endothelial changes
• Diminished amount of collagen deposition.

66. รายละเอียดของ Systemic Factors
• Radiation damages the DNA of cells in exposed areas.
• Fibroblasts that migrate into radiated tissues are
abnormal.
• Collagen is synthesized to an abnormal degree in
irradiated tissue causing fibrosis.
• Blood vessels become occluded.
• Damage to hair and sweat glands
• Vitamin A has been used to counteract this.

67. รายละเอียดของ Systemic Factors
• Malnutrition
• Cancer
• Old Age
• Diabetes- impaired neutrophil chemotaxis,
phagocytosis.
• Steroids and immunosuppression suppresses
macrophage migration, fibroblast proliferation,
collagen accumulation, and angiogenesis.
Reversed by Vitamin A 25,000u per day.

68. เมื่อแผลไม่หายหรือหายช้า
Consider the negative effects of
1. Endocrine diseases (eg, diabetes,
hypothyroidism)
2. Hematologic conditions (eg, anemia,
polycythemia, myeloproliferative disorders)
3. Cardiopulmonary problems (eg, chronic
obstructive pulmonary disease , congestive
heart failure)

69. เมื่อแผลไม่หายหรือหายช้า
Consider the negative effects of
6. GI problems that cause malnutrition and
vitamin deficiencies
7. Obesity
8. Peripheral vascular pathology (eg,
atherosclerotic disease, chronic venous
insufficiency, lymphedema)

71. Part III
SET BALANCE

72. Hypertrophic Scars and Keloids
• Excessive healing results in a
raised, thickened scar, with
both functional and cosmetic
complications.
• If it stays within margins of
wound it is hypertrophic.
Keloids extend beyond the
confines of the original injury.
• Dark skinned, ages of 2-40.
Wound in the presternal or
deltoid area, wounds that
cross langerhans lines.

73. Growth Factors
• Epidermal growth factor
• Macrophage derived growth
factor (MDGF)
• Platelet derived growth factor
(PDGF)
• Thrombin
• Insulin
• Lymphokines

74. Plasminogen activator inhibitor
• Found to be elevated in
Keloid scars
• PAI-1 -/- “knockout” mice
show accelerated wound
healing after cutaneous
injury
• PAI-1 seems to regulate
fibrinolytic and proteolytic
activity during the
replacement of fibrin by
collagen.
• PAI-1 is upregulated in
cultured fibroblasts in a
hypoxic environment

75. Metalloproteinases & Tissue Inhibitor of
Metalloproteinases
• Regulatory role in fibroblasia and scarring
– Found in high concentrations in fetal wounds
– MMP/TIMP is higher in “scarless” fetal wounds
– TGF-beta decreased the MMP/TIMP ratio by
increasing TIMP
– May promote more rapid epithelization

76. TGF Beta-1
• Higher concentrations and
exaggerated response in
keloid fibroblasts
• When added to fetal
wounds – thicker scars
made.

78. Hypertrophic Scars and Keloids
• Excessive healing results in a
raised, thickened scar, with both
functional and cosmetic
complications.
• If it stays within margins of wound
it is hypertrophic. Keloids extend
beyond the confines of the
original injury.
• Dark skinned, ages of 2-40.
Wound in the presternal or
deltoid area, wounds that cross
langerhans lines.

79. Hypertrophic Scars and Keloids
• Keloids more familial
• Hypertrophic scars
develop soon after
injury, keloids up to a
year later.
Hypertrophic scars more likely to
cause contracture over joint
surface.

80. Hypertrophic Scars and Keloids
Keloids Treatment
i. Triamcinolone
ii. Excision – high recurrence rate

82. Part IV
Wound Closure

83. Types of Wound Closure
Primary intention
1. Primary Closure
approximate disrupted tissues by sutures,
staples, or tapes. With time there will be
a. synthesis
b. deposition
c. cross-linking of collagen to
provide the tissue with strength.

84. Types of Wound Closure
Secondary intention
2. Delayed Primary Closure – also called
tertiary closure.
Wound closure is delayed for several days to
prevent wound infection where there is:
a. bacterial contamination
b. foreign bodies
c. extensive tissue trauma
* Cleaning of the wound is done daily using NSS

85. Primary intention
Examples: well-repaired lacerations, well reduced bone fractures,
healing after flap surgery
• involves epidermis and dermis
without total penetration of dermis
healing by process of epithelialization
• When wound edges are brought
together so that they are adjacent to
each other (re-approximated)

86. Primary intention
Examples: well-repaired lacerations, well reduced bone fractures,
healing after flap surgery
• Minimizes scarring
• Most surgical wounds heal by
primary intention healing
• Wound closure is performed with
sutures (stitches), staples, or
adhesive tape

87. Secondary intention
Examples: gingivectomy, gingivoplasty, tooth extraction sockets,
poorly reduced fractures.
• The wound is allowed to granulate
• Surgeon may pack the wound with
a gauze or use a drainage system
• Granulation results in a broader
scar

88. Secondary intention
Examples: hepatectomy, loss skin open wound, burn
• Healing process can be slow due to
presence of drainage from infection
• Wound care must be performed daily
to encourage wound debris removal
to allow for granulation tissue
formation

89. Types of Wound Closure
Delayed primary closure or secondary suture
3. Spontaneous Closure
- wound closes by contraction of the
wound edges.

90. Tertiary intention
(Delayed primary closure or secondary suture)
Examples: healing of wounds by use of tissue grafts.
• The wound is initially cleaned, debrided and
observed, typically 4 or 5 days before closure.
• The wound is purposely left open

91. Tertiary intention
• If the wound edges are not re approximated
immediately, delayed primary wound healing
transpires.
• This type of healing may be desired in the case of
contaminated wounds. By the fourth day, phagocytosis
of contaminated tissues is well underway, and the
processes of epithelization, collagen deposition, and
maturation are occurring.

92. Tertiary intention
• Foreign materials are walled off by macrophages that
may metamorphose into epithelioid cells, which are
encircled by mononuclear leukocytes, forming
granulomas.
• Usually the wound is closed surgically at this
juncture, and if the "cleansing" of the wound is
incomplete, chronic inflammation can ensue,
resulting in prominent scarring.

93. PART V
WOUND CARE

94. Basic Elements of Wound Care
• Cleanse Debris from the Wound
• Possible Debridement
• Absorb Excess Exudate
• Promote Granulation and Epithelialization
When Appropriate
• Possibly Treat Infections
• Minimize Discomfort

95. Prevention
• Inspect skin
• Moisture control
• Proper positioning and transfer techniques
• Nutrition
• Avoid pressure on heels and bony prominences
• Use of positioning devices

96. Risk Assessment
• Nutritional status
• Alteration in sensation
• Co-morbid conditions
• Medications that delay healing
• Decreased blood flow

97. Assessment & Monitor
• Location
• Stage and Size
• Periwound
• Undermining
• Tunneling
• Exudate
• Color of wound bed
• Necrotic Tissue
• Granulation Tissue
• Effectiveness of
Treatment

98. Types of Wounds
• Surgical Wounds
• Pressure Ulcers
• Arterial Insufficiency
• Diabetic Ulcers
• Venous Insufficiency
• Tumors

99. Wet or Dry Dressings
• Causes Injury to New Tissue Growth
• Is Painful
• Predisposes Wound to Infection
• Becomes a Foreign Body
• Delays Healing Time

100. Frequency
• Goal is to minimize the
frequency of dressing
change
• Daily dressing changes
increase chances of
infection and disrupts the
healing of tissue
Decrease Frequency
of Dressing Changes

101. General treatment of non healing wounds
• Successful treatment of difficult wounds
requires assessment of the entire patient and
not just the wound.
• Systemic problems often impair wound
healing; conversely, non healing wounds may
herald systemic pathology.

102. Successful treatment of wounds
• Characterize the wound
– chemotherapeutic drugs inhibit wound healing
• Ensure adequate oxygenation
• Ensure adequate nutrition
– (malnutrition affects wound healing by inhibiting
the immune response (opsonization)
– Address protein-calorie malnutrition and
deficiencies of vitamins and minerals e.g. Vitamin
C, E, Zinc)

103. Successful treatment of wounds
• Treat infection
– Bowel anastomotic strength develops more
rapidly than that of the skin. The submucosa
provide the major strength in anastmotic closure
because it contains the majority of the fibrous
connective tissue.
• Remove foreign bodies
• Irrigate, Provide a moist (not wet) wound bed

105. Part VI
SUTURE MATERIALS AND TECHNIQUES

106. The Ideal Suture Material
• Can be used in any tissue
• Easy to handle
• Good knot security
• Minimal tissue reaction

107. The Ideal Suture Material
• Unfriendly to bacteria
• Strong yet small
• Won’t tear through tissues
• Cheap

108. What’s It Used for?
• To bring tissue edges together and speed
wound healing (=tissue apposition)
• Orthopedic surgery to help stabilize joints
– Repair ligaments
• Ligate vessels or tissues

109. Types of Needles
• Eyed needles
– More Traumatic
– Only thread through
once
– Suture on a reel
– Tends to unthread
itself easily

110. Types of Needles
• Swaged-on needles
– Much less traumatic
– More expensive suture
material
– Sterile

111. Points of Needles
• Taper
– Atraumatic
– Internal organs

112. Points of Needles
Cutting
• Cutting edge on inside
of circle
• Skin
• Traumatic

113. Points of Needles
Reverse Cutting
• Cutting edge on outside of
circle
• Skin
• Less traumatic than
cutting

114. Cutting vs Reverse Cutting
• Cutting
• Reverse
cutting

115. Shapes of Needles
• 3/8 circle
• 1/2 circle
• Straight
• Specialty

116. Characteristics of Suture Material
• Absorbable VS. Non - absorbable
• Monofilament VS. Multifilament
• Natural or Synthetic

117. Absorbable Sutures
• Internal
• Intradermal/ subcuticular
• Rarely on skin

118. Non-absorbable Suture
• Primarily Skin
– Needs to be removed later
• Stainless steel = exception
– Can be used internally
• Ligature
• Orthopedics
– Can be left in place for long periods

120. Reading the Suture Label
Size
Needle
• Company
Order Code
Name
Also:
LENGTH
NEEDLE
SYMBOL
COLOR
Absorbable
or Non

121. Choosing
Absorbable Vs. Nonabsorbable
• How long you need it to
work
• Do you want to see the
animal again for suture
removal

122. Monofilament Vs. Multifilament
• memory easy to handle
• less tissue drag more tissue drag
• doesn’t wick wicks/ bacteria
• poor knot security good knot security
• - tissue reaction +tissue reaction

123. Natural Vs. Synthetic
• Natural:
– Gut
– Chromic Gut
– Silk
– Collagen
• All are absorbable

124. Gut/ Chromic Gut
• Made of submucosa of
small intestines
• Multifilament / Mono
filament
• Breaks down by
phagocytosis:
inflammatory reaction
common

125. Gut/ Chromic Gut
• Chromic: tanned, lasts
longer, less reactive
• Easy handling
• Plain: 3-5 days
• Chromic: 10-15 days
• Bacteria love this stuff!

126. Collagen and Silk
• Natural sutures
• VERY reactive,
absorbable
• Collagen : Ophthalmic
surgery only

127. Synthetic
Vicryl (Polyglactin 910)
• Braided, synthetic, absorbable
• Stronger than gut: retains strength 3 weeks
• Broken down by enzymes, not phagocytosis
• Break-down products inhibit bacterial growth
– Can use in contaminated wounds, unlike other
multifilaments

128. Synthetic
Dexon and PGA
• Polymer of glycolic acids
• Braided, synthetic, absorbable
• Broken down by enzymes
• Both PGA and dexon have increased tissue
drag, good knot security
• Both are stronger than gut

129. Synthetic
PDS (polydioxine)
• Monofilament (less drag,
worse knot security – lots
of “memory”)
• Synthetic, absorbable
• Very good tensile strength
(better than gut, vicryl,
dexon) which lasts months
• Absorbed completely by
182 days

130. Synthetic
Maxon (polyglyconate)
• Monofilament- memory
• Synthetic Absorbable
• Very little tissue drag
• Poor knot security
• Very strong

131. NONABSORBABLE SUTURES
• Natural or Synthetic
• Monofilament or multifilament

132. NYLON
• Synthetic
• Mono or Multifilament
• Memory
• Very little tissue
reaction
• Poor knot security

133. Polypropylene
• Prolene, Surgilene
• Monofilament, Synthetic
• Won’t lose tensile strength over time
• Good knot security
• Very little tissue reaction

134. Stainless Steel
• Monofilament
• Strongest !
• Great knot security
• Difficult handling
• Can cut through tissues
• Very little tissue reaction, won’t harbor
bacteria

135. Suture Sizes
• Sized #5-4-3-2-1-0-00-000-
0000…30-0
BIGGER
>>>>>>>>>>>>>>>>SMALLER
• 00 = 2-0, “two ought”
• SA : 0 through 3-0 (Optho
5-0 >>7-0)
• LA : 0 through 3

136. Suture Sizes (cont)
• Stainless Steel
– In gauges (like needles)
• Smaller gauge = bigger, stronger
• Larger gauge= smaller, finer
– 26 gauge = “ought”
– 28 gauge = 2-0

137. Skin Staples
• Very common in human medicine
• Expensive
• Very easy
• Very secure
• Very little tissue reaction
• Removal =
– Special tool required

138. Staples
• Rapid closure of wound
• Easy to apply
• Evert tissue when placed
properly

139. Tissue Adhesive
• Nexaband, Vetbond,
and others
• Little strength
• Should not be placed
between skin layers or
inside body

140. Steri-strips
• Sterile adhesive tapes
• Available in different
widths
• Frequently used with
subcuticular sutures
• Used following staple or
suture removal
• Can be used for delayed
closure

142. Suture Patterns

143. Knot Strength
• Generally 4 “throws” for >90% knot security
(nylon may need 5)
– Less “throws” = more likely to untie itself
• Stainless steel = exception again
– 2 “throws” = 99% knot security

144. Two-Hand Square Knot
• Easiest and most
reliable
• Used to tie most
suture materials

145. Instrument Tie
• Useful when one or
both ends of suture
material are short
• Commonly used
technique for
laceration repair

146. Wound Closure
• Basic suturing techniques:
– Simple sutures
– Mattress sutures
– Subcuticular sutures
• Goal: “approximate, not strangulate”

149. Simple Sutures
Simple interrupted stitch
– Single stitches, individually
knotted (keep all knots on
one side of wound)
– Used for uncomplicated
laceration repair and wound
closure

151. Simple Interrupted

152. Simple Continuous

153. Mattress Sutures
• Horizontal mattress stitch
– Provides added strength in
fascial closure; also used in
calloused skin (e.g. palms and
soles)
– Two-step stitch:
• Simple stitch made
• Needle reversed and 2nd
simple stitch made adjacent
to first (same size bite as first
stitch)

154. Mattress Sutures
Vertical mattress stitch
– Affords precise
approximation of skin edges
with eversion
– Two-step stitch:
• Simple stitch made – “far, far”
relative to wound edge (large
bite)
• Needle reversed and 2nd
simple stitch made inside first
– “near, near” (small bite)

156. Subcuticular Sutures
• Usually a running stitch,
but can be interrupted
• Intradermal horizontal
bites
• Allow suture to remain
for a longer period of
time without
development of
crosshatch scarring

157. Subcuticular

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