Inflammatory
m e d s u r g
I N F L A M M A T I O N
Vascular and cellular response to trauma. It’s
purpose is to initiate the healing of the injured
tissue.
The body’s attempt to dispose of micro-organisms,
foreign material, and dying tissues so that tissue
repair can occur.
An inflammatory response may result from external
or internal factors (infection)
Protects the body by localizing and removing the
injury agent.
SIGNS OF INFLAMMATION
REDNESS - RUBOR
SWELLING - TUMOR
PAIN- BOLAR
WARMTH- CALOR
LOSS OF RANGE OF MOTION (ROM)
1. REDNESS OR RUBOR
Caused by blood vessel dilation (the arterioles)
Chemical mediators promote vessel dilation
(contained in the capillary walls or endothelium
resulting in immediate response)
CHEMOKINES - Histamines, serotonin, Bradykinins
and Prostaglandins
NOTE: A 1X INCREASE IN ARTERIOLE DIAMETER
YIELDS A 4X INCREASE IN BLOOD FLOW
2. SWELLING OF TUMOR
Edema fluid varies with the stage of inflammation
Initially, vessel permeability is only slightly altered
and no cells or protein escapes and the fluid is
mainly water and dissolved electrolytes
(transudate); like synovial fluid.
As capillary permeability increases and plasma
proteins escape the extravascular fluid becomes
cloudy and more viscous. This is called exudate
(containes a large amount of leukocytes called PUS
CAUSES OF EDEMA/ SWELLING
Bleeding from torn vessels
Cell death due to anoxia allows fluid leakage
(permeability increases)
Increased proteins raise extracellular osmotic
pressure, drawing fluid from the capillaries.
Chemicals alter cell permeability to proteins and
fluid
Gravity may increase swelling (Capillary filtration
pressures)
Mishca Daizel G. Lotino
GGCSN2025
To cease hemorrhage/ swelling/ edema
Pressure gradient
Vessel repair
3. PAIN OR BOLAR
Results from irritation of nerve ending by physical or
chemical factors
Physical trauma may irritate pain receptors
Chemical mediators release when cell damage
occurs sensitize pain receptors.
Trauma may result in cell anoxia because of
interference with blood flow due to capillary
damage.
4. WARMTH OR CALOR
The result of chemical activity and increased blood
flow in the injured area.
5. LOSS OF ROM
This may occur due to pain causing reflex guarding
or muscle spasm
Spasm decreases metabolic activity and constricts
blood flow which causes more pain due to ischemia:
thus the pain/ spasm cycle.
PHASE 1: EARLY PHASE INFLAMMATION-
VASODILATION
Chemical mediators are released:
Histamines, bradykinins and prostaglandins increase
vascular permeability released from mast cells and
blood platelets into traumatized tissue.
As fluid filtrates through gasps in the extravascular
spaces this is called EXUDATION
The accumulation of excess fluid is called edema
(swelling)
Vascular permeability due to action of the histamine
is short-lived, lasting less than 1 hour.
PHASE 1: EARLY PHASE INFLAMMATION-
LYMPHATIC CHANNELS ARE BLOCKED
Local lymphatic channels are blocked by fibrin
plugs formed during coagulation. Obstruction of
the local lymphatic channels prevents drainage of
fluid from the injured site, thus localizing the
inflammatory reaction.
PHASE 1: LATE PHASE: PHAGOCYTOSIS
Body’s cellular defense to remove toxic material via
lymphatic system.
PHAGOCYTOSIS: a process when leukocytes
capture and digest foreign matter and dead tissues.
1
Inflammatory
m e d s u r g
Mishca Daizel G. Lotino
GGCSN2025

1st line of defense: neutrophiles (in most

abundance from 1-3 days)- phagocytic activity
reaches maximum effectiveness within 7-12 days.
2nd line of defense: monocytes (which convert into
large cells called macrophages) and lymphocytes
consume large amounts of bacteria and cellular
debris. Monocytes are critical in the initiation of
tissue repair because they attract fibroblast.

PHASE 2: REGENERATION

The replacement of destroyed cells by reproducing

Pus is the end result- it contains leukocytes, dead
healthy cells adjacent to the wound (humans
tissue and phagogenic material.
capacity to regenerate tissue is limited and further
Prolonged puss accumulation can prevent fibroplasia
affected by age and nutritional state)
which begins wound healing.
Fibroblasts are connective tissue responsible for PHASE 2: COLLAGEN SYNTHESIS
collagen synthesis (ligaments, joint, capsule,
tendon) Tissue healing times
Osteoblasts: responsible for bone syntheis MUSCLES- APPROX 3 WEEKS
PHASE 1: EARLY PHASE INFLAMMATION
TENDONS- 4-6 WEEKS
MARGINATION Extend of the tissue damage and vascularity will aid
in determining healing time
When trauma occurs the endothelial wall is
Age may also be a factor in healing
disrupted exposing collagen fibers creating a
“stickiness” CHRONIC INFLAMMATION
WBC’s concentrate in the injury site to rid the body Inflammation which continues past 1 month
of foreign substances and dead (necrotic) tissue. Marked by a loss of function
As circulation slows, leukocytes migrate and adhere Fibroblast activity continues forming granuloma.
to the walls of post- capillary veinuels (approx. 1
hour) COMPLICATIONS
The leukocytes pass through the walls of the vessels Granuloma- large mass of weaker scar tissue
(diapedesis) and travel to the site of injury. (usually due to large inflammation and activity
(Chemotaxis) without regard to healing time.
Retardation of muscle fiber: with excessive
PHASE 1: LATE PHASE BLOOD CLOTTING granuloma fibroblasts cannot reach damaged tissue
Adhesions/ contractures in tissue
Ruptured vessels release enzyme factor X Keloid/ hypotrophic scars
Factor X reacts with prothrombin (free floating
Abnormal scarring- hypertrophic scar or keloid
in blood)
scar, their difference is not well understood but
Thrombin then stimulates fibrogen into its
clinically hypetrophic scar is contained withing the
individual from fibrin.
boundaries of the original wound while keloid
Fibrin grouped together to from “lattice” around
extends beyond borders of the original wound
injured area.
Fibrin lattice contracts to remove plasma and
compress platelets forming a “patch”
Prothrombin- (protein) A glycoprotein, produced
in the liver, that is converted into thrombin during
bleeding and subsequent clotting.
Thrombin (enzyme) An enzyme in blood that
facilitates blood clotting by converting fibrinogen to
fibrin (by means of ionized calcium). 2