The Surgical Wound

Cormac Joyce

Final Med 2009

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

Surgery

But wound infections can occur despite these measures causing:

• Death

• Morbidity

• Longer hospital stays

• Cosmetically displeasing wounds

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

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

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

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

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

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

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

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

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

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

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

Gridiron: appendix

Surgical Incisions

Lanz: appendix

Surgical Incisions

Nephrectomy/ loin

Surgical Incisions

Kochers

Surgical Incisions

Inguinal : hernia, orchidectomy (for Ca) not for torsion

Surgical Incisions

Midline sternotomy

Surgical Incisions

Mercedes Benz/Chevron

Surgical Incisions

Midline laparotomy

Surgical Incisions

Rutherford Morrison : renal transplant

Surgical Incisions

Lap Chole

Surgical Incisions

Lap appendix