Surgery Basics Flashcards by Leslie Mancini

WOUND HEALING steps(5)

Hemostasis
Inflammation
Proliferation
Maturation
Remodeling

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wound healing

Hemostasis

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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wound healing

Inflammation

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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wound healing

Inflammation/ Neutrophils

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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wound healing

inflammation/Macrophages

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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wound healing

inflammation/ T-lymphocytes

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

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wound healing

proliferation

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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wound healing

Maturation

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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wound healing

remodeling

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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wound healing

epithelialization

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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WOUND CONTRACTION

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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WOUND CLASSIFICATION

acute vs chronic

Acute wound
Recent wound (< 4 weeks duration)

Chronic wound
Any acute wound not healed by 4 weeks

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TYPES OF WOUND HEALING

primary/secondary/tertiary

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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Causes of delayed healing

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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delay in healing

Diabetes Mellitus

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

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delay iin healing

obesity

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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delay in healing

Nutrition

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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delay in healing

vitamin deficiencies

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

delay in healing

Infection/inflammation

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

WOUND INFECTIONS(3)

Superficial Incisional
Deep incisional
Organ/space wound infections

WOUND INFECTIONS

Superficial Incisional

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

WOUND INFECTIONS

Deep Incisional

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

WOUND INFECTIONS

Necrotizing fasciitis

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

# WOUND INFECTIONS Organ/Space wound infections

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

# CHRONIC WOUNDS general

>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

# PRESSURE ULCERS general

‘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

# Pressure ulcer Staging

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

# pressure ulcers Preventive techniques

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

# pressure ulcers Tx

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*

# EXCESS HEALING Hypertrophic scars

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

# Excess healing Keloids

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

# PERITONEAL ADHESIONS general

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

# peritoneal adhesions prevention/ tx

“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

# WOUND CLOSURE surgical

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

# WOUND CLOSURE Suture

Choose smallest required for approximation Minimize suture related inflammation Fascia: Non-absorbable Slowly absorbable Skin: Braided absorbable Careful skin re-approximation

# Suture -nonabsorbable Silk Used for

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

# SUTURE: NONABSORBABLE Nylon

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

# SUTURE: NONABSORBABLE Prolene

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

# SUTURE: ABSORBABLE Vicryl

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

# SUTURE: ABSORBABLE PDS

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

# SUTURE: ABSORBABLE Chromic (Catgut, surgical gut)

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

# SUTURE: ABSORBABLE Monocryl

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

# SUTURE Steel

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