PATOLOGI ANATOMI

PADA INFEKSI OPERASI

KELOMPOK 4
 dipicu oleh sistem kekebalan
Jika sistem kekebalan
tubuh, yang merupakan
mendeteksi cedera atau
sistem seluler dalam tubuh.
Inflamasi  respons normal adanya patogen, ia
Sistem kekebalan tubuh
dan protektif tubuh terhadap memasang respons yang
memantau cedera pada
cedera atau infeksi. disebut respons inflamasi dan
tubuh dan mendeteksi
memberi sinyal sel ke lokasi
patogen seperti bakteri dan
cedera atau infeksi.
virus.
 INFLAMAS GEJALA
INFEKSI
I KLINIS
 The steps of
the inflammatory
response

Could be acute and chronic

INFLAMMATION
ACUTE INFLAMMATION
Infections and microbial toxins

Trauma

Physical and chemical agents

Stimuli for Acute Inflammation
Tissue necrosis

Foreign bodies

Immune reactions (hypersensitivity reactions)

Vascular changes Cellular events

• Changes in Leukocyte
Vascular Caliber Recruitment and
and Flow Activation
• Increased Vascular
Permeability
 Induced by mediators (e.g. Histamines)

Transient arteriolar vasoconstriction followed by vasodilation

Opens new capillary beds in the area and increase Blood flow
Vascular Changes
Heat and redness at the inflammatory site

Changes in Vascular
Caliber and Flow Vasodilation is quickly followed by increased permeability of the microvasculature,
with an exudate into the extravascular tissues
(Vasodilatation)
The loss of fluid and increased vessel diameter lead to slower blood flow and
increased viscosity of the blood. These changes externally as localized redness
(erythema) of the involved tissue.

As stasis develops, blood leukocytes, principally neutrophils, accumulate along the

vascular endothelium. Leukocytes then adhere to the endothelium, and soon
afterward they migrate through the vascular wall into the interstitial tissue.
Increased Vascular
Permeability
(Vascular Leakage)
 Histamines, bradykinins, leukotrienes cause an early, brief (15 – 30 min.),
immediate transient response

Cytokine mediators (TNF, IL-1) induce endothelial cell junction retraction

through cytoskeleton reorganization (4 – 6 hrs post injury, lasting 24 hrs or
more)

Mechanism Endothelial injury results in vascular leakage by causing endothelial cell

Causing necrosis and detachment.
Vascular Leakage

Accumulation of activated leukocytes along the vessel wall may pile-up and
damage the endothelium through activation and release of toxic oxygen
radicals and proteolytic enzymes

Certain mediators (VEGF) may cause increased transcytosis of proteins via

intracellular vesicles which lead to venular permeability.
 A : 32 mmHg
V : 12 mmHg

25 mmHg

fluid with low protein content

(most of which is albumin)
and a specific gravity of less
than 1.012

inflammatory extravascular fluid that

has a high protein concentration, cellular
debris, and a specific gravity above
1.020
Cellular Events
Leukocyte recruitment and activation

Recruitment - Margination and rolling Phagocytosis and degranulation

- Adhesion and transmigration Leukocyte-induced tissue injury

Activation Chemotaxis
• Leukocytes follow chemical gradient (chemotactic substances)
to site of injury
 Bacterial products
 Complement components (C5a)
 Cytokines (chemokine family e.g., IL-8)
 LTB4 (AA metabolite)
Leukocyte Activation
• Stimuli for activation include microbes, products of necrotic
cells, and several mediators
 Histamine, NO
increasing blood
viscosity and
slowing the circulation Vascular dilation and
increased blood flow
(causing erythema and
stasis warmth)

leukocytes (principally
neutrophils) begin to
accumulate along
the vascular
endothelial surface
extravasation and
leukocyte deposition of plasma
emigration and fluid and proteins
accumulation in the (edema)
site of injury
 Summary of Mediators of Acute Inflammation
    Action
Mediator Source Vascular Leakage Chemotaxis Other
Histamine and serotonin Mast cells, platelets + -  
Bradykinin Plasma substrate + - Pain
C3a Plasma protein via liver + - Opsonic fragment (C3b)
Leukocyte adhesion,
C5a Macrophages + +
activation
Mast cells, from
Potentiate other
Prostaglandins membrane - Vasodilation, pain, fever
mediators
phospholipids
Leukotriene B4 Leukocyte adhesion,
Leukocytes - +
activation

Leukotriene C4, D4, E4 Bronchoconstriction,

Leukocytes, mast cells + -
vasoconstriction
Endothelial damage,
Oxygen metabolites Leukocytes + -
tissue damage
Bronchoconstriction,
PAF Leukocytes, mast cells + +
leukocyte priming
Acute-phase reactions,
IL-1 and TNF Macrophages, other - +
endothelial activation
Chemokines Leukocytes, others - + Leukocyte activation
Macrophages,
Nitric oxide + + Vasodilation, cytotoxicity
endothelium
 Differences of Acute and Chronic
ACUTE
Rapid response to an injurious agent
Predominantly neutrophilic (PMN)
infiltration
Activation to eliminate the offending
agent
CHRONIC
Inflammation of prolonged duration
(weeks or months)
Infiltration with mononuclear cells,
which include macrophages,
lymphocytes, and plasma cells
Attempts at healing by connective tissue
replacement of damaged tissue,
accomplished by proliferation of small
blood vessels (angiogenesis) and, in
particular, fibrosis
 SSI ? PATHOGENESIS
RISK FACTOR: Microbial
HOST FACTORS invasion
SURGERY SURGICAL WOUND

ENVIRONTMENTAL Cell & organ

Treatment WOUND
FACTOR injury
FACTOR
factor
RISK FACTORS
RISK FACTORS
RISK FACTORS
 Pathophysiology

Primmed Inflammation,
Inflammation & infection and
Immune innate immune
suppression response
Immuno-inflammatory response model
PAMPs and DAMPS in cellular injury
Primmed inflammation & Immune Response
Inflammation , infection & innate immune
receptors
Early and late mortality due to Surgical Site
Infection
Principles of treatment
TERIMA KASIH