The Surgical Wound
Cormac Joyce
November 6th 2008
Surgery
It is the branch of medicine concerned with diseases and conditions which require or are amenable to operative procedures
It is derived from Greek “cheirourgia”o “cheir” = the hando “ergon” = work
Surgery
It is often said that it is “controlled trauma”Carried out in a sterile environmentUnder aseptic conditions
Surgery
Many protocols are put in place to prevent infections in surgical wounds
o Hand washingo Gowns and gloveso Painting and drapingo Drainso Antibioticso Laminar flow theatreso Sterile instrumentso Sterile dressings
Mask does not come with beard attached!!
Operating Theatre
Surgery
But wound infections can occur despite these measures causing:
• Death
• Morbidity
• Longer hospital stays
• Cosmetically displeasing wounds
Wound Infection
Wound Infection
Wound Dehiscence
Healthy Wound
Surgery
Surgical wound infections are common Comprising 12% of nosocomial infections
The rate of infection depends on the type of surgery undertaken
Operation Types
The risk of a wound infection depends on the operation
For that reason, operations are classified into distinct types
o Cleano Clean-Contaminatedo Contaminatedo Dirty
Class I :Clean wounds
Elective operations (non emergency)Non traumatic injuryGood surgical techniqueRespiratory, gastrointestinal, biliary and
genitourinary tracts not breachedRisk of infection < 2%Eg: mastectomy, hernia repair
Class II: Clean - Contaminated
Urgent or emergency case that is otherwise clean
GI, GU or respiratory tracts entered electively, no spillage or unusual contamination
Minor break in sterile technique occurredEndogenous flora involvedRisk of infection: <10 %Eg: appendicectomy, bowel resection
Class III: Contaminated
Non-purulent inflammationGross spillage from GIT, entry into GU or
biliary tract in the presence of infected bile/urine.
Major break in techniquePenetrating trauma < 4hrs oldChronic open woundsRisk of infection: 20%Eg: GSW, rectal surgery
Class IV : Dirty
Purulent inflammation (abscess)Pre-operative perforation of GI, GU, biliary
or respiratory tractPenetrating trauma > 4 hrsExisting acute bacterial infection or a
perforated viscera is encountered (clean tissue is transected to gain access to pus).
Risk of infection: 40%
Signs of Infection
The cardinal points of acute inflammation
I. Calor
II.Rubor
III.Dolor
IV.Tumour
V.Functio Laesa
? Wound infection
Signs of Infection
Patient may be systemically unwell↑ TempTachycardicHypotensionWound breakdownWound dischargeWarm peripheriesSeptic shock
Prevention
Aseptic techniqueGood techniqueProphylactic antibiotics where appropriateMicrobiology inputClean operating theatreElective surgeryGood post op care
Wound Healing
Wound healing is a complex and dynamic process of restoring cellular structures and tissue layers
There are 3 distinct phasesThere are various categories of wound
healingthe ultimate outcome of any healing
process is repair of a tissue defect
Wound Healing
The types of wound healing:o 1° healingo Delayed 1° healingo 2° healingo (Epithelialisation)Even though different categories exist, the
interactions of cellular and extracellular constituents are similar.
Primary wound healing
Also known as “healing by primary intention”
Think of a typical surgical wound: the wound eges are approximated
Minimal number of cellular constituents dieResults in a small line of scar tissueMinimizes the need for granulation tissue so
scarring is minimized
Primary wound healing
Primary Intention
Keloid Scar
The importance of good…
TechniqueChoice of sutureChoice of needleTrainingInstrumentsAntibioticsAftercare
Delayed Primary healing
Occurs if wound egdes are not approximated immediately
May be desired in contaminated woundsBy day 4: phagocytosis of contaminated tissues
has occurred Usually wound is closed surgically at this stage If contamination is present still : chronic
inflammation ensues leading to prominent scar eventually
Delayed Primary healing
Delayed Primary healing
Secondary Healing
Also called healing by secondary intentionA full thickness wound is allowed to heal
by itself: there is no approximation of wound edges
Large amounts of granulation tissue formed
Wound eventually very contractedTakes much longer to heal
Secondary Intention Healing
Fungal sinusitis
Secondary Intention Healing
Post Op
Secondary Intention Healing
2 weeks post op – healing by 2° intention
Epithelialization
Epithelization is the process by which epithelial cells migrate and replicate via mitosis and traverse the wound
Occurs by one of 2 mechanismsCommon in the healing of ulcers and
erosions
Epithelialization: Mechanisms
Mechanism 1If basement membrane is intact ie some
dermis or dermal appendages remainEpithelialization occurs by epithelial cells
migrating upwards
Epithelialization: Mechanisms
Mechanism 2Occurs in a deeper woundA single layer of epithelial cells advance
from the wound edges to cover the woundThey then stratify so wound cover is
complete
Normal Wound Healing
There are 3 phases
I. Inflammatory phase: Days 0-4
II. Proliferative phase : Days 5-21
III. Remodelling phase: Days 22-60
Wound Healing
It can also be classified in 4 stages:
I. Haemostasis
II. Inflammation
III. Granulation
IV. Remodelling
Haemostasis
Injury causes local bleedingVasoconstriction is mediated by :
o Adrenaline
o Thrombaxane A2
o Prostaglandin 2α
Haemostasis
Platelets then adhere to damaged endothelium and discharge ADP
o Which promotes thrombocyte clumping and “dams” the wound
Inflammation is initiated by cytokine release from platelets
Haemostasis
α-granules from platelets release:Platelet Derived Growth Factor (PDGF)Platelet factor IVTransforming Growth Factor βThrombocyte dense bodies release:HistamineSerotonin
Haemostasis
PDGF attracts fibroblasts chemotacticallyLeading to collagen deposition in later
stages of wound healing
Fibrinogen → FibrinThus providing the structural support for
the cellular components of inflammation
Inflammatory Phase
Capillary dilatation occurs due to:HistamineBradykininProstaglandinsNOThis dilatation allows inflammatory cells to
reach the wound site
Inflammatory Phase
These PMNs or leukocytes have several functions:
• Scavenge for debris
• Debride the wound
• Help to kill bacteria by:
-oxidative burst mechanisms
-opsonization
Inflammatory Phase
Opsonin“factor which enhances the efficiency of
phagocytosis because it is recognized by receptors on leucocytes
2 major opsonins are:Fc fragment of IgGA product of complement, C3b
Inflammatory Phase
Monocytes now enter the wound and become macrophages
They have numerous functions
Macrophage functions in healing
Secretion of numerous enzymes and cytokines
Collagenases and elastasesTo break down injured tissuesPDGF, TGFβ, IL, TNFTo stimulate proliferation of fibroblasts,
endothelial and smooth muscle cells
Proliferative Phase
AngiogenesisThe formation of new blood vesselsFormed by endothelial cells becoming new
capillaries within the wound bedAngiogenesis stimulated by TNFα
Proliferative Phase
Collagen depositionType III collagen is laid down by
fibroblastsFibroblasts are attracted by TGFβ and
PDGFTotal collagen content increases until day
21
Proliferative Phase
Granulation TissueIs the combination of collagen deposition
and angiogenesis
Granulation Tissue
Definition:Newly formed connective tissue, often
found at the edge or base of ulcers and wounds made up of : capillaries, fibroblasts, myofibroblasts, and inflammatory cells embedded in a mucin rich ground substance during healing
Granulation Tissue
Granulation Tissue
Granulation Tissue
Occasionally overgranulation can occur (as above following a flexor tendon repair)
Treatment is steroid topical cream (1% hydrocortisone cream)
Proliferative Phase
Re-epithelialization occurs next:By upward migration of epithelial cells if
BM is intactOr from wound edges
Remodelling Phase
Fibroblasts become myofibroblastsAnd wound begins to contractCan contract 0.75mm per dayCan over contract howeverContraction allows wound to become
smallerA large wound can contract by up to 40-
80%
Remodelling Phase
Type III collagen is degraded And replaced with Type IWater is removed from the scar, allowing
collagen to cross-linkWound vascularity decreasesCollagen cross linkage allows: Increased scar strength Scar contracture Decreased scar thickness
Microbiology: Dr. Lynda Fenelon
Wound Strength
During phase 1 and 2 (inflammatory and proliferative phases)
Wounds have very little strengthDuring remodelling: Wounds rapidly gain strengtho @ 6 weeks: wound is 50% of final strengtho @12 months: wound is maximal strength: but
this is only 75% of pre-injury tissue strength
Abnormal Scars
Hypertrophic ScarsKeloid Scars
Hypertrophic Scars
Raised, red and thickenedLimited to boundaries of scarOccurs shortly after injuryCommon on anterior chest and deltoidsRegresses over timeRelated to wound tension and prolonged
inflammatory phase of healing
Hypertrophic Scars
Hypertrophic Scars
Hypertrophic Scars
Treatment:Surgical excisionIntralesional Triamcenelone acetate
injection
Hypertrophic Scars
No racial or familial preponderanceElectron microscopy: flattened collagen
bundles parallel in orientation
Keloid Scars
Raised, red and thickened scarExtends beyond original scar boundaryOccurs months after injuryDoes not regressCommoner in darker skinned peopleFamilial tendency? Autoimmune phenomenonWorsened by surgery and in pregnancyRegresses post menopause
Keloid scar
Keloid scar
Keloid scar
Treatment:Surgical excision : caveat- recurrence =
65%Compression treatmentCO2 lasersCryotherapy
Factors influencing scarring
These can be broken down into:
i. Patient factors
ii.Surgical factors
Patient Factors
AgeElderly scar well
-? 2° wrinklesSkin typeCeltics : hypertrophic scar tendencyDark skinned: keloid scars
Patient Factors
Anatomic regionMidlineDeltoid regionSternotomy post CABG
Patient Factors
Patient morbidityNutritional stateDiabetesWound infections
Patient Factors
Local tissueOedemaPrevious radiotherapyVascular insufficiency
Surgical factors
Atraumatic skin handlingEversion of wound edgesInversion places keratinised epidermis
between the healing surfaces = delayed healing
Tension free closureClean and healthy wound edges
Everted Edges
Inverted Edges
Surgical factors
Scar orientationParallel to lines of relaxed skin tensionLangers linesSuture tension“Thou shall not commit tension”Over-tight: pressure necrosisUnder-tight: wound gaping and widened
scar
Langers Lines
Langers Lines
Acute Inflammation
Definition
o The cellular and vascular response to injury
o Short in duration
o Has cellular and chemical components
Acute Inflammation: Causes
Injury by:o Pathogens Bacteria, viruses, parasiteso Chemical agents Acids, alkaliso Physical agents Heat, trauma (surgery), radiationo Tissue death Infarction
Stages of Acute Inflammation
Dilatation of local capillaries endothelial permeabilityLeakage of protein-rich fluid into interstitial
space – including fibrinogenFibrinogen → fibrinMargination of leukocytes to peripheries of
capillariesMostly neutrophils
Stages of Acute Inflammation
Acute Inflammation is mediated by:Chemicals: interleukins and histamineProteins: complement cascade
Complement Cascade
Component of innate immune system Cascade of proteins Resulting in formation of Membrane-
Attack-Complex (MAC) which can
I. Destroy invading bacteria
II. Recruit other cells ie neutrophils Can also act as opsonins: enhancing
phagocytosis
Complement Cascade
2 main activating arms of CC:
I. Classic pathway: consists of antigen-antibody complexes
II. Alternative pathway: activated directly by contact with micro-organisms
Acute Inflammation: Neutrophils
The role of the NeutrophilFirst cellular component to appearAttracted by inflammatory mediators
o By chemotaxisThey can move: margination in blood
vessels – by adhering to vascular endothelium: roll between endothelial cells: emigrate to interstitium
Acute Inflammation: Neutrophils
Function:Phagocytosis of micro-organisms
• With lysosomal free radical degradation of pathogens
Chemical messengers in AI
These allow cells to communicate with each other and mediate the immune response
Chemical messengers in AI
ChemokinesCause direct migration of target cells to
site of release
CytokinesSoluble, biologically active molecules
secreted by cells which have a variety of effects on the target cells
Cytokines: Examples
IL-1: neutrophil adhesion and vascular adhesion molecules
IL-2: proliferation of B cells and NK cellsTNF: causes fever and promotes
inflammationIFN: activates macrophagesHistamine: vasodilation and permeability
Effects of AI: beneficial
• Dilution of bacterial toxin
• Defence mechanisms are brought to the pathogen
neutrophils;: phagocytosisComplement: cell lysisAntibodiesDrug delivery
Effects of AI: beneficial
• Drainage to LNs: immune response stimulated
• Fibrin traps the pathogen in place so it can be attacked
Effects of AI: non beneficial
Destruction of normal tissue: RALethal swelling in certain parts of the body
ie epiglottitisHypersensitivity reactionsAsthmaAnaphylaxis
Outcomes of Acute Inflammation
ResolutionTissues restored to normalPus/abscessOrganizationTissues replaced by granulation tissuesChronic InflammationIf causative agent not removed
Ruptured Abscess
Chronic Inflammation
Definition
o Tissue response to persistent injury
o Long in duration
o Cellular components differ from acute inflammation
Chronic Inflammation
CausesForeign bodies: ie suturesBacteria: ie TBChronic abscess: ie osteomyelitisTransplant: ie chronic rejectionIBDProgression from AI
Chronic Inflammation
Key pointsHistological pattern not as predictable as
acute inflammationThere may be areas of acute inflammation
occurring simultaneouslyGranulation tissue and fibrosis may both
be present: indicating the tissues attempts at repair
Chronic Inflammation
Lymphocytes predominateMacrophages present too
• In granulomatous inflammation they fuse forming multinucleate Langhans giant cells
Plasma cells are also present
Chronic Inflammation
MacrophagesDerived from monocytesPhagocytosis and killing of pathogens by
lysosomesAntigen presentationLanghans giant cell formation
Chronic Inflammation: Effects
Secondary infection ie chronic epithelial injury
ScarringResolution: restoration of normalityLocal lymphadenopathy
Surgical Incisions
Surgical Incisions
Surgical Incisions
Surgical Incisions
Surgical Incisions
Surgical Incisions
Surgical Incisions
Surgical Incisions
Surgical Incisions
Surgical Incisions
Thank You
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