INFLAMMATION

INFLAMMATION
Reaction of the microcirculation
Movement of fluid and WBC, RBC, P. from
the blood to extravascular tissues
Host attempt to localize and eliminate:
– altered cells,
– foreign particles,
– Microorganisms.
 INFLAMMATION
Reaction of the body to injury
Under normal circumstances inflammation
is a protective response
The goal is to eliminate both the cause of
injury and the consequences of it (dead
cells and tissues)
If triggered can itself become harmful
leading to cell, tissue and organ
destruction
 INFLAMMATION

This process accomplishes:

- regeneration of the normal tissue and
return to normal function

- formation of a scar tissue to replace what

was destroyed
 INFLAMMATION

Further extension of injury may lead to:

– Loss of function

– Loss of tissue
 INFLAMMATION
AULUS CELSIUS- 4 cardinal signs:
– Rubor = redness
– Calor = heat
– Tumor = swelling
– Dolor = pain
In the affected area
 INFLAMMATION
JOHN HUNTER- vasodilatation,
RUDOLF VIRCHOW-reaction to prior
tissue injury
JULIUS COHNHEIM- migration of WBC
ELI METCHNIKOFF-phagocytosis
THOMAS LEWIS- chemical mediators
 INFLAMMATION
INFLAMMATORY RESPONSE OCCURS
WITHIN THE MICROCIRCULATION
WITHIN THIS NETWORK ARE
COMPONENTS OF INFLAM.RESPONSE
– PLASMA
– PLATELETS
– RBC
– WBC
 INFLAMMATION

Changes in the vascular wall:

– Vasoconstriction then vasodilation
– Loss of endothelial wall integrity
– Leakage of fluid and plasma components
– Migration of WBC, RBC out of vessels
 INFLAMMATION

A quick-response system effective against

a wide range of pathogens and foreign
substances

It always gives the same response

 INFLAMMATION

ACUTE INFLAMMATION
– PMN LEUKOCYTES

CHRONIC INFLAMMATION
– LYMPHOCYTES, PLASMA CELLS,
MACROPHAGES
VASCULAR PERMIABILITY
Starling’s law
Pressure gradient across the vascular wall
depends on both hydrostatic and oncotic
pressure differential between IV/EV
compartments
Increase of IV hydrostatic pressure /
decrease of IV oncotic pressure =
extravasation of fluid across the vessel
wall
 INFLAMMATORY EDEMA

Three events following the injury:

– Transient vasoconstriction
– Vasodilatation
– Increase in the permeability of the endothelial
cell barrier
NON INFLAMMATORY EDEMA

PULMONARY EDEMA

SOFT TISSUE EDEMA:

– DVT
– NEPHROTIC SDR.

OBSTRUCTION OF LYMPHATIC FLOW

 Pulmonary edema, CHF –heart is
unable to pump the necessary amount
of blood throughout the body, blood
backs up in the veins, fluid pools in ALV
PE-high pulmonary venous pressure
due to high LV diastolic pressure
shortness of breath, orthopnea
DEEP VENOUS THROMBOSIS
DEEP VENOUS THROMBOSIS
Contributing factors:
– Venous stasis
– Trauma
– Hypercoagulation
– Age
– Heart failure
– Previous DVT
The clot can break loose and cause a
pulmonary embolism
First degree (superficial) burns
Redness, swelling, pain
 Second degree (partial thickness)
burns: blisters, swelling, severe pain
Frostbite
FROSTBITE
CELLULITIS
NEPHROTIC SYNDROME
NEPHROTIC SYNDROME
LYMPHEDEMA
LYMPHEDEMA AFTER BREAST
CANCER SURGERY
EDEMA
EFFUSION
TRANSUDATE
EXUDATE
SUPPURATIVE INFLAMMATION
CAUSES OF INFLAMMATION

MECHANICAL TRAUMA
INFECTIONS
CHEMICAL AND PHYSICAL INJURY
ISCHEMIA
ALLERGY
OUTCOMES OF INFLAMMATION
RESOLUTION
ABSCESS FORMATION
CELLULITIS
FISTULA FORMATION
LYMPHANGITIS
BACTERAEMIA, SEPTICEMIA
CHRONIC INFLAMMATION
FIBROSIS WITH SCARRING
 FISTULAS
INTERNAL FISTULAS
– GASTRO-COLIC FISTULA
– BILIARY-DUODENAL FISTULA
– ENTERO-COLIC FISTULA
– COLO-VAGINAL FISTULA

EXTERNAL FISTULAS
– ENTERO-CUTANEOUS FISTULA
– EXTERNAL BILIARY
– EXTERNAL DIGESTIVE
– PERIANAL
 CAUSES OF FISTULAS

CONGENITAL
TRAUMA
INFLAMMATION
MALIGNANCY
RADIATION
COMPLICATIONS OF FISTULAS

MALNUTRITION
FLUID AND ELECTROLYTE IMBALANCE
SEPSIS
SKIN EXCORIATION
HEMORRHAGE
TREATMENT OF FISTULAS
HYDRATION AND DEFFICITS
CORRECTION
ANTIBIOTICS
BOWEL REST AND PARENTERAL
NUTRITION
INHIBITION OF DIGESTIVE
SECRETIONS
OPERATIVE REPAIR
 CAUSES OF DEATH

SEPSIS

RENAL FAILURE