Referat Bedah Plastik

Inflammatory Mediators
Role of Granulation
Progress In Infection
Advisor :
dr. Amru Sungkar, Sp. B, Sp. BP-RE

Infection
The invasion and multiplication of
microorganisms such as bacteria, viruses, and
parasites that are not normally present within
the body

Immune Response
Physical barrier
Chemical barrier,
secretes oil and
sweat (lower Ph
skin), tears
(contain enzyme
called lysozyme)
and saliva
Sheds constantly
(1 million cells per
hour)

Immune Response

Inflammation

Inflammation Mechanism
Hiperemis

Stagnation

Resolution

Inflammation Mediators

ACTION
Mediator

Source

Vascular Leakage

Inflammation

Chemotaxis

Other

Histamineand
serotonin

Mastcells,platelets

Bradykinin

Plasmasubstrate

Pain

Opsonicfragment(C3b)

Plasmaproteinvialiver
C3a
Mediator
C5a

Macrophages

Leukocyteadhesion,
activation

Prostaglandins

Mastcells,from
membrane
phospholipids

Potentiateother
mediators

Vasodilatation,pain,fever

LeukotrieneB4

Leukocytes

Leukocyteadhesion,
activation

Leukotrienes
C4D4E4

Leukocytes,mastcells

Bronchoconstriction,
vasoconstriction

Platelet
ActivatingFactor
(PAF)

Leukocytes,mastcells

Bronchoconstriction,
leukocytepriming

IL-1andTNF

Macrophages,other

Acute-phasereactions,
endothelialactivation

Chemokines

Leukocytes,others

Leukocyteactivation

Macrophages,
endothelium

Vasodilatation,cytotoxicity

Granulation Process

Bleeding stops and

fibrin begins to form
to prevent blood loss.
Last from a few
hoursto a few days in
severe cases.

Body is working to
repair the damaged
skin area. Cells divide
to fix injured tissues
and blood vessels
aswound begins to
close.
Lasts from a few days
to a few weeks.

Newly formed collagen

restorethe functions
of cells. Collagen is
remodeled, becomes
stronger & more
dense.
Lasts from a few
weeks to a few
months.

Primaryintention
healing
Wound healing by primary
intention is typical for
noncomplicated surgical
wounds.
Wound edges are approximated
and kept together with sutures
or staples and healing occurs
by wound epithelialisation and
connective tissue deposition.
These wounds usually heal
quickly provided there is no
infection.

Secondaryintention healing
Typical for chronic wounds such as
venous leg ulcers. The wound is
left open and healing occurs by
granulation tissue formation,
contraction of the wound edges
and subsequently epithelialisation.
These wounds show delayed
healing due to the volume of
connective tissue required to fill
the defect. Since there is no
epidermal barrier, the risk of an
infection is significantly higher in
these wounds.

Growth Factors
Growth factor

Abbreviati
on

Main origins

Effects

Epidermal
Growth Factor

EGF

Activated
macrophages
Salivary glands
Keratinocytes
Platelets

Keratinocyte and
fibroblast mitogen
Keratinocyte
migration
Granulation tissue
formation

Transforming
growth factor-

TGF-

Activated
macrophages
T-lymphocytes
Keratinocytes
Platelets

Hepatocyte and
epithelial cell
proliferation
Expression of
antimicrobial
peptides
Expression of
chemotactic
cytokines

Growth Factors
Growth factor

Abbreviati
on

Main origins

Effects

Hepatocyte
Growth Factor

HGF

Mesenchymal
Cells

Epithelial and
endothelial cell
proliferation
Hepatocyte
motility

Vascular
endothelial
growth factor

VEGF

Mesenchymal
cells
Endothelial cells

Vascular
permeability
Endothelial cell
proliferation
Promote
angiogenesis
during tissue
hypoxia

Growth Factors
Growth
factor

Abbreviati
on

Platelet
PDGF
derived
growth factor

Main
origins

Effects

Platelets
Granulocyte,
Macrophage macrophage, fibroblast
s
and smooth muscle cell
Endothelial
chemotaxis
cells
Granulocyte,
Smooth
macrophage and
muscle cells
fibroblast activation
Keratinocyt Fibroblast, endothelial
es
cell and smooth muscle
cell proliferation
Matrix
metalloproteinase,
fibronectin and
hyaluronan production
Angiogenesis
Wound remodeling
Integrin expression
regulation

Growth Factors
Growth
factor

Abbreviati
on

Transforming TGF-
growth factor

Main origins

Effects

Platelets
Tlymphocyte
s
Macrophage
s
Endothelial
cells
Keratinocyt
es
Smooth
muscle cells
Fibroblasts

Granulocyte,
macrophage,
lymphocyte,
fibroblast and
smooth muscle cell
chemotaxis
TIMP synthesis
Angiogenesis
Fibroplasia
Matrix
metalloproteinase
production inhibition
Keratinocyte
proliferation

Wound Infection

Infection (in wound)

About 2-3% surgical wounds are complicated

by infection; the risk of infection is greatest

during the first 48 to 72 hours.
Infection is defined as the presence of

replicating microorganisms in a wound,

leading to subsequent host injury. It should
be distinguished from wound
contamination where microorganisms are
not replicating.

Surgical or acute wound infection is most

frequently due toStaphylococcus aureusand
sometimesStreptococcus pyogenesand aerobic
gram-negative bacilli.

Infection is considered a major

factor in delayed wound healing
due to:

reduced tissue tensile

strength gain
formation of exuberant
granulation tissue
dehiscence following
wound closure

Pathogenic bacteria may have or do

the following
Adhere/bind to extracellular matrix
proteins of exposed tissue which may
have a direct effect on wound healing
Produce cytotoxic causing more tissue damage
and creating a microenvironment conducive to
their survival
Those with thick capsules are more resistant
to phagocytosis by leukocytes.
Liberate endotoxins can cause; thrombosis of
the microvasculature, systemic organ or
immune dysfunction, and activate
macrophages to release more
inflammatory mediators.

Pathogenic bacteria may have or do the following

1) Adhere/bind to extracellular matrix proteins of exposed

tissue which may have a direct effect on wound healing.
Binding makes the protein unavailable for promoting tissue
adherence
2) Produce cytotoxic exotoxins (e.g. Clostridium spp, S
pyogenes, S aureus) causing more tissue damage and
creating a microenvironment conducive to their survival. 3)
Those with thick capsules (e.g. S pyogenes, S aureus and
Klebsiella pneumoniae) are more resistant to phagocytosis
by leukocytes. 4) Liberate endotoxins can cause; thrombosis
of the microvasculature, systemic organ or immune
dysfunction, and activate macrophages to release more
inflammatory mediators. Circulatory alterations decrease
the efficiency of glucose and oxygen delivery, the
polymorphonuclear leukocyte, is deprived of the materials
necessary for optimum bacterial killing.

Characteristic of delayed wound

healing
Necrotic bioburden
Cellular dysfunction and biochemical imbalance
number of growth factors is reduced due to
- inadequate production by the cells of the wound bed (e.g.
macrophages or fibroblasts)
- rapid breakdown of growth factors by high levels of proteases
imbalance between inflammatory and proliferative cytokines
cellular senescence (aged cells)
- decreased or non-existent replicative ability of fibroblasts
- deficiency of growth factor receptor sites on host target cells
(fibroblasts)
Increased exudation

THANK
YOU