Surgery Basics Flashcards

1
Q

WOUND HEALING steps(5)

A

Hemostasis
Inflammation
Proliferation
Maturation
Remodeling

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2
Q

wound healing

Hemostasis

A

Disruption in tissue integrity
Division of blood vessels

Exposure of extracellular matrix to platelets
-Platelet activation
-Degranulation
-Coagulation activation

Fibrin clot

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3
Q

wound healing

Inflammation

A

Platelet degranulation releases wound active substances
Platelet Derived Growth Factor (PDGF)
Transforming Growth Factor- 𝛃 (TGFb)
Platelet activating factor
Fibronectin
Serotonin

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4
Q

wound healing

Inflammation/ Neutrophils

A

Fibrin clot serves as matrix for PMNs and monocytes

Neutrophils

24-48 hours
Chemotactic factors
TNF-𝛼 – angiogenesis and collagen synthesis
Collagenase – matrix and ground substance degradation

Phagocytosis of bacteria and debris

Does not directly promote healing
Inflammatory response
Cleaning
Environment for Macrophages
Environment for vessels and collagen

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5
Q

wound healing

inflammation/Macrophages

A

Fibrin clot serves as matrix for PMNs and monocytes

Macrophages
48 – 96 hours
Remain through-out process until wound healing complete
Wound debridement and phagocytosis
Cytokine and growth factors
-Cell Proliferation
-Matrix synthesis
-Angiogenesis

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6
Q

wound healing

inflammation/ T-lymphocytes

A

1 week post injury
Bridge transition from inflammatory to proliferation
Modulation of the wound environment

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7
Q

wound healing

proliferation

A

Days 4-12
Establish tissue continuity

Fibroblast – recruited by platelet-derived growth factor (PDGF)
Proliferate in wound
Activated by cytokines (from macrophages)

Endothelial cells
Migration from venules
Promote angiogenesis

Matrix (collagen) synthesis
Dependent on oxygen, vascularization, vitamin, cofactors, sterility
Collagen deposition
-Type I – extracellular skin matrix
-Type III – repair of skin

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8
Q

wound healing

Maturation

A

Reorganization of previously synthesized collagen

Re-establishment of extracellular matrix
-Fibronectin and Type III collagen deposition
-Then Proteoglycans and GAGs deposition
-Finally, type I collagen deposition in the matrix

Tensile strength depends on ratios of collagen types and quality

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9
Q

wound healing

remodeling

A

Constant turnover of collagen
-Synthesis, lysis and deposition
-Shift of types to type I

Final tensile strength
-Cross-linking of fibril
-6 weeks – 6 months
-Less strength than uninjured tissue
-75-80% strength

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10
Q
A
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11
Q

wound healing

epithelialization

A

Final step in tissue integrity
Proliferation and migration of adjacent epithelial cells

Begins day 1
Thickening of epidermal wound edge
Migration across matrix surface
Keratinize after cross-bridging complete

48 hours for reapproximated incised wounds
Days to weeks for larger wounds

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12
Q

WOUND CONTRACTION

A

Secondary intention only

Myofibroblast
Migrate to wound day 6
Contract to decrease wound size

Fibroblast
Initial contraction in days 1-6

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13
Q

WOUND CLASSIFICATION

acute vs chronic

A

Acute wound
Recent wound (< 4 weeks duration)

Chronic wound
Any acute wound not healed by 4 weeks

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14
Q

TYPES OF WOUND HEALING

primary/secondary/tertiary

A

Primary Intention
Closure using suture/material
Clean wounds

Secondary Intention
Healing through tissue granulation
Tissue loss; contamination

Tertiary Intention
Delayed primary closure
Combination of primary and secondary intention

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15
Q

Causes of delayed healing

A

Advanced age?
Or is it confounded based on co-morbidity
Smoking
Hypoxia, hypoperfusion- Optimal collagen synthesis requires oxygen as a cofactor
Steroids, chemo drugs
Diabetes Mellitus; metabolic disorders
Obesity; nutrition
Infection

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16
Q

delay in healing

Diabetes Mellitus

A

Impaired inflammation, angiogenesis, collagen synthesis
Vascular related disease
Hypoxia, hypoperfusion
Decreased growth factor production
Impaired leukocyte function

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17
Q

delay iin healing

obesity

A

Obesity
Independent factor for delayed wound healing
Proinflammatory nature of adipose tissue
Adipokines, cytokines

Related to comorbid conditions
Diabetes mellitus
Vascular disease

Increased tension on repaired surgical wounds
Risk of dehiscence: failure of wound healing

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18
Q

delay in healing

Nutrition

A

Protein deficiency – impaired collagen synthesis

Caloric deficiency – decreased granulation and matrix formation

Usually requires long-standing impairment
But easily improved with intensive, short-term treatment

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19
Q

delay in healing

vitamin deficiencies

A

Vitamin A deficiency – impairs wound healing
Decreases inflammatory stage
Impaired collagen synthesis
Treatment with Vitamin stimulates both aspects

Vitamin C deficiency – increased wound infections
Neutrophil impairment

Zinc deficiency – enzymatic cofactor

20
Q

delay in healing

Infection/inflammation

A

5-10% overall infection rate (SSI)
Bacteria:
Staphylococcus
Coag-negative Streptococcus
Enterococci
E. Coli
Degree of contamination or colonization is predictive

21
Q

WOUND INFECTIONS(3)

A

Superficial Incisional
Deep incisional
Organ/space wound infections

22
Q

WOUND INFECTIONS

Superficial Incisional

A

75% of all wound infections
Skin and subcutaneous tissue only
Erythematous and edematous skin
Tenderness
Low grade fever
Leukocytosis (often mild)
Incisional pain
Wound culture
Cotton-tipped application
May require suture/staple removal

23
Q

WOUND INFECTIONS

Deep Incisional

A

Adjacent to the fascia
More pronounced incisional changes
Fever
Leukocytosis
Possible wound dehiscence
Wound culture
Pack wound open, drainage

24
Q

WOUND INFECTIONS

Necrotizing fasciitis

A

Deep incisional infection
Invasive, spreading infection
Vascular necrosis and skin necrosis
Septic thrombosis of vessels
Toxic appearing with high fever
Dehydration
Tachycardia
Rapidly progressing
Mixed flora (most often)
Excision and debridement

25
Q

WOUND INFECTIONS

Organ/Space wound infections

A

Infection within an organ, cavity or confined deep space
Abdominal, thoracic, pelvic

26
Q

CHRONIC WOUNDS

general

A

> 4 weeks healing time
Delayed or absent progression through the ‘normal’ healing process

Includes ‘skin ulcers’
Diabetic
Venous
Ischemic

Ischemic ulcers
Arterial
Venous

Diabetic ulcer
Decubitus ulcers

27
Q

PRESSURE ULCERS

general

A

‘Decubitus’ or ‘Pressure’ ulcers

Localized area of tissue necrosis that develops when soft tissue is compressed
Between a bony prominence and external surface
2-9% incidence in cute care
2-23% in long-term care

Excessive pressure causes capillary collapse

28
Q

Pressure ulcer

Staging

A

Staging
I – non-blanching erythema of intact skin
II – Partial thickness skin loss involving dermis/epidermis
III – Full-thickness skin loss but not through fascia
IV- Full-thickness skin loss with extensive involvement of bone, muscle, tissue
Unstageable- unable to assess due to wound slough, eschar or other obscuring factor

29
Q
A
30
Q

pressure ulcers

Preventive techniques

A

Frequent skin assessment

Repositioning
-Slide boards
-Avoid shearing

Pressure reduction, removal, and distribution
Air mattress, sitting up, foam supports, skin barriers

Elimination of moisture
Attention to incontinence
Wound drainage

31
Q

pressure ulcers

Tx

A

Treatment: multidisciplinary team approach
Address host issues (nutrition, diabetes, ischemia)
Debride necrotic tissue

Maintain a favorable wound environment
Moist
Clean – dressing changes
Sterile

Relief of pressure
Hyperbaric oxygen *
Flap rotation *
Skin grafting*

32
Q

EXCESS HEALING

Hypertrophic scars

A

Overabundance of fibroplasia in dermal healing
Rise above skin level
Stay within confines of original wound

33
Q

Excess healing

Keloids

A

Overabundance of fibroplasia in dermal healing
Rise above skin level
Extend beyond confines of original wound
15x more likely in darker-pigmented ethnicities

34
Q

PERITONEAL ADHESIONS

general

A

Fibrous band of tissue that forms between organs
Either normally separated and are now attached OR
Between organs and abdominal wall
Increased risk with infection
Trauma
Bowel injury

Can lead to obstruction, ischemia, or pain

35
Q

peritoneal adhesions

prevention/ tx

A

“lysis of adhesions”
Exploratory laparotomy
Incision of fibrous bands

Prevention
Decrease trauma, retraction, infection
Film or gel placed between organs or between organs and wall

36
Q

WOUND CLOSURE

surgical

A

Suture
Staples
Glue - dermabond
Secondary intention/wound vacuum
Muscle/Tissue flaps
To cover extensive losses
Skin grafting - autologous
Skin allografts
Porcine
Cadaveric

37
Q

WOUND CLOSURE

Suture

A

Choose smallest required for approximation
Minimize suture related inflammation

Fascia:
Non-absorbable
Slowly absorbable

Skin:
Braided absorbable
Careful skin re-approximation

38
Q

Suture -nonabsorbable

Silk
Used for

A

Silk suture
Inert animal protein
Favorable handling characteristics
Requires only 3 knots
Does not braid or break easily
Slowly loses strength over time
Multifilament
Mechanical immune barriers
Used for “tying off” vessels and structures
Promotes minimal scarring

39
Q

SUTURE: NONABSORBABLE

Nylon

A

Ethilon, Dermalon)
Smooth, non-reactive
Permanent
Good for vascular anastomoses to graft
Difficult to tie (4 good throws)
Skin closure (plastics) but requires removal

40
Q

SUTURE: NONABSORBABLE

Prolene

A

Monofilament
Easier to tie but more reactive than Nylon
Permanent
Vascular surgery

41
Q

SUTURE: ABSORBABLE

Vicryl

A

Synthetic, braided multifilament
Absorbable at predictive rate
Less reaction
GI, GU, GYN tissue
Fascia

42
Q

SUTURE: ABSORBABLE

PDS

A

Synthetic, monofilament
Absorbable at predictive rate
Retain strength longer than nylon
Fascia

43
Q

SUTURE: ABSORBABLE

Chromic (Catgut, surgical gut)

A

Absorbable, multifilament
Variable rate of absorption
Stronger inflammatory reaction
Loses strength quickly
Mucosa to mucosa

44
Q

SUTURE: ABSORBABLE

Monocryl

A

Monofilament
Absorbable (2-3 weeks)
Good for dermal, subcuticular wounds

45
Q

SUTURE

Steel

A

Permanent
Bone closure
Contaminated wounds
May need to be removed later
Hard to tie
Large “knots” can be felt and may cause pain

46
Q
A
47
Q
A