Surgery Basics Flashcards
WOUND HEALING steps(5)
Hemostasis
Inflammation
Proliferation
Maturation
Remodeling
wound healing
Hemostasis
Disruption in tissue integrity
Division of blood vessels
Exposure of extracellular matrix to platelets
-Platelet activation
-Degranulation
-Coagulation activation
Fibrin clot
wound healing
Inflammation
Platelet degranulation releases wound active substances
Platelet Derived Growth Factor (PDGF)
Transforming Growth Factor- π (TGFb)
Platelet activating factor
Fibronectin
Serotonin
wound healing
Inflammation/ Neutrophils
Fibrin clot serves as matrix for PMNs and monocytes
Neutrophils
24-48 hours
Chemotactic factors
TNF-πΌ β angiogenesis and collagen synthesis
Collagenase β 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
wound healing
inflammation/Macrophages
Fibrin clot serves as matrix for PMNs and monocytes
Macrophages
48 β 96 hours
Remain through-out process until wound healing complete
Wound debridement and phagocytosis
Cytokine and growth factors
-Cell Proliferation
-Matrix synthesis
-Angiogenesis
wound healing
inflammation/ T-lymphocytes
1 week post injury
Bridge transition from inflammatory to proliferation
Modulation of the wound environment
wound healing
proliferation
Days 4-12
Establish tissue continuity
Fibroblast β 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 β extracellular skin matrix
-Type III β repair of skin
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
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 β 6 months
-Less strength than uninjured tissue
-75-80% strength
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
WOUND CONTRACTION
Secondary intention only
Myofibroblast
Migrate to wound day 6
Contract to decrease wound size
Fibroblast
Initial contraction in days 1-6
WOUND CLASSIFICATION
acute vs chronic
Acute wound
Recent wound (< 4 weeks duration)
Chronic wound
Any acute wound not healed by 4 weeks
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
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
delay in healing
Diabetes Mellitus
Impaired inflammation, angiogenesis, collagen synthesis
Vascular related disease
Hypoxia, hypoperfusion
Decreased growth factor production
Impaired leukocyte function
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
delay in healing
Nutrition
Protein deficiency β impaired collagen synthesis
Caloric deficiency β decreased granulation and matrix formation
Usually requires long-standing impairment
But easily improved with intensive, short-term treatment
delay in healing
vitamin deficiencies
Vitamin A deficiency β impairs wound healing
Decreases inflammatory stage
Impaired collagen synthesis
Treatment with Vitamin stimulates both aspects
Vitamin C deficiency β increased wound infections
Neutrophil impairment
Zinc deficiency β 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 βnormalβ healing process
Includes βskin ulcersβ
Diabetic
Venous
Ischemic
Ischemic ulcers
Arterial
Venous
Diabetic ulcer
Decubitus ulcers
PRESSURE ULCERS
general
βDecubitusβ or βPressureβ 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 β non-blanching erythema of intact skin
II β Partial thickness skin loss involving dermis/epidermis
III β 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 β 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
βlysis of adhesionsβ
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 βtying offβ 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 βknotsβ can be felt and may cause pain
