IIIAMMA1IO

Al
IIIAII
INFLAMMATION AND REPAIR
DEFINITION:
1. Reaction oI vascularized tissues to local iniury
2. Series oI changes which take place in living tissue II.
iniury
3. Local reaction oI the body to iniury
4. Reaction oI irritated and damaged tissues which still retain
viability
CARDINAL SIGNS OF INFLAMMATION
1. Calor ( heat)
2. Rubor (redness)
3. Tumor (swelling)
4. Dolor (pain)
5. Functio laesa (loss oI Iunction)
INFLAMMATION AND REPAIR
CAUSES OF INFLAMMATION
1. Physical Agents: Heat, Trauma, irradiation
2. Chemical Agents: Organic and Inorganic
3. Microbial InIections: most important
4. Hypersensitivity Reactions:
5. Necrosis oI Tissues
MAJOR COMPONENTS OF ACUTE INFLAMMATOrY
RESPONSE
1. Alterations in vascular caliber
2. Structural changes in microvasculature
3. Emigration oI leucocytes/ Accumulation in Iocus oI iniury
INFLAMMATION AND REPAIR
CAUSES OF INFLAMMATION
1. Physical Agents: Heat, Trauma,
irradiation
2. Chemical Agents: Organic and
Inorganic
3. Microbial InIections: most important
4. Hypersensitivity Reactions:
5. Necrosis oI Tissues
Stages of Inflammation
Stages oI InIlammatory
Responses
V-E-R
Stages of Inflammation
STAGE I: Vascular & Cellular Response
initial vasoconstriction (blood vessels) at the
site oI iniury (lasting Ior only a Iew moment)
Followed by rapid dilatation oI small vessels
(result Irom histamine release) marked by
increased in blood supply (Hyperemia)
responsible Ior the characteristic sign oI
redness & heat
Stages of Inflammation
STAGE I: Vascular & Cellular Response
increased in vascular permeability with:
dilatation oI the vessels in response to tissue
necrosis
release oI chemical mediators (bradykinin,
serotonin, prostaglandin)
release oI histamine
outpouring oI Iluid, proteins, leukocytes into the
interstitial spaces (clinically maniIested by signs oI
swelling & pain)
Stages of Inflammation
STAGE I: Vascular & Cellular Response
pain: caused by:
pressure oI accumulating Iluid on local nerve endings
chemical mediators which irritates nerve endings
Blood Ilows shows in the dilated vessels
Altered rate oI Ilow Iacilitates the mobilization oI increased
number oI leukocytes (WBC) to the iniured tissues
Stages of Inflammation
STAGE I: Vascular & Cellular Response
Processes
Migration leukocytes aggregate or line-up along inner
surIace oI the blood vessels
Emigration leukocytes move through the blood vessel
wall into the aIIected tissue spaces
Diapedesis actual passage oI blood corpuscles through
blood vessel wall
Chemotaxis process through which leukocytes are
attracted to iniured cells. A locomotion oriented along a
chemical gradient
CELLULAR AAD JASCULAR CHAACES
Stages of Inflammation
STAGE II: Exudate
Iluid that escape Irom blood vessels, dead
phagocytic cells & dead tissues &
products they release produce
inIlammatory exudates
Stages of Inflammation
STAGE II: Exudate
Fibrinogen plasma protein
converted to Iibrin when released into the
tissue
Thromboplastin products released
by iniured tissue cells
Platelets
Stages of Inflammation
STAGE II: Exudate
Nature and amount oI exudates
depends
tissue involved
intensity & duration oI
inIlammation
Stages of Inflammation
STAGE II: Exudate Formation
Maior Types oI Exudates: Serous,
Purulent and Sanguineous
Stages of Inflammation
STAGE II: Exudate
Serous exudates contains chieIly oI serum
(clear portion oI blood) derived Irom: blood
& serous membranes oI the body
(peritoneum, pleura, pericardium &
meninges)
watery in appearance & has Iew cells
e.g. blister Irom a burn
Stages of Inflammation
STAGE II: Exudate
Purulent exudates thicker than serous
contain pus (consists oI leukocytes,
liqueIied dead tissue debris, dead & living
bacteria)
suppuration process oI pus Iormation
pyogenic bacteria produces pus
color oI purulent exudates: depends on the
causative organism
Stages of Inflammation
STAGE II: Exudate
Sanguineous (hemorrhagic) exudates
consists oI large amount oI RBC indicating damage
to capillaries that is severe enough to allow the escape
oI blood cells Irom the plasma
bright sanguineous exudates Iresh bleeding
dark sanguineous exudates older bleeding
serosanguinous exudates consists oI clear & blood-
tinge drainage commonly seen in surgical incisions
Stages of Inflammation
STAGE III: Reparative
involves repair oI iniured tissues by:
Regeneration
Scar Iormation
Stages of Inflammation
STAGE III: Reparative
involves repair oI iniured tissues by:
Regeneration and Scar Iormation
replacement oI destroyed tissue cells by
cells that are identical or similar in structure
& Iunction
involves not only replacement oI damaged
cells one by one BUT also organization oI
these cells to restore its architectural
structure & Iunction
Proliferative Potential of Cells.
1. LABILE CELLS (Continuously dividing)
surIace epithelia, vagina, gastrointestinal cells, urinary tract,
bone marrow
2. QUIESCENT ( STABLE CELLS)
low level oI replication, but can undergo rapid division in
reponse to stimulus
glandular organs, liver, pancreas,kidneys, Iibroblasts, smooth
muscle cells
3. PERMANENT CELLS (NONDIVIDING)
can not undergo mitotic division in postnatal liIe
nerve cells, skeletal muscles, cardiac muscle cells
Stages of Inflammation
STAGE III: Reparative Phase
Good Reparative capacity:
Epithelial tissue oI the skin,
Digestive & respiratory tract (provided
Underlying support structures are intact)
Osseous, lymphoid &bone marrow tissues
Little regenerative capacity:
Nervous, muscular & elastic tissue
Stages of Inflammation
STAGE III: Reparative
Fibrous tissue formation
occur if regeneration not possible
fibrous (scar) tissue - has the capacity to proliferate
under the unusual conditions of ischemia & altered
pH
inflammatory exudates with its interlacing network of
fibrin - provides the framework for this tissue to
develop
damaged tissues are replaced with the CT elements of
collagen. blood capillaries. lymphatics. & other
tissue-bound substances
Stages of Inflammation
STAGE III: Reparative
disadvantages oI scar tissue:
can reduce Iunctional capacity oI the tissue or
organ
mechanical obstruction
AC1ORS AEC1IAC
IALAMMA1ORY-REPARA1IJE
RESPOASE
Systemic:
Adequacy oI blood supply
Nutritional status oI the host
Presence or absence oI Diabetes Mellitus
Glucortico-steroid therapy
Denervation oI an area
Inadequate levels oI circulating white cells
AC1ORS AEC1IAC
IALAMMA1ORY-REPARA1IJE
RESPOASE
Local
Presence or absence oI inIection
Foreign material (including large areas oI dead
tissues)
Radiation exposure
Type, size , location oI wound
Mechanical Iactors
Inflammation
Interventions
Reduce inIlammatory process
Minimize swelling
Relieve pain
Provide adequate nutrition: high calorie, high
protein, high vitamin C
Promote rest
Administer prescribed medications
$:22arv of Infla22ation
Stage Description
V Initial injury releases chemicals
(histamine. Prostaglandin and
Bradykinin)
This activates the
inflammatory process
Vasodilatation and increased blood Flow Cause the REDNESS
and HEAT
Increased capillary permeability causes
leakage of fluids from the plasma into
the damaged tissues
There is compression of the surrounding
tissues
Causes the
SWELLING and the
PAIN
The damaged tissue is infiltrated by
leukocytes which engulf the
microorganisms
MigrationEmigration
diapedesis
$:22arv of Infla22ation
Stage Description
E The inflammatory fluid and the WBC.
together with the dead tissues and
microorganisms will accumulate in the
injured site
This will produce the
EXUDATE
R The destroyed tissues are replaced by
the same cells
The destroyed tissues can be replaced
by fibrous tissue or cicatrix
Regeneration
Scar formation
OUTCOME OF ACUTE
INFLAMMATION
1. Complete resolution
2. healing by connective tissue
replacement
3. abscess Iormation
4. progression to chronic inIlammation
ENEFICIAL EFFECT$ OF
INFLAMMATION
A. INFLAMMATORY EXUDATES
dilution oI toxins
protective antibodies
Iibrin Iormation
promotion oI immunity
cell nutrition
B. PHAGOCYTOSIS
digestion /elimination oI inIectious agents
digestion/removal oI debris
ARMFUL EFFECT$ OF
INFLAMMATION
Anaphylactic shock
Crippling Rheumatoid Arthritis
Acute Glomerulopathy
Disfigurement (scars and keloids)
Post-operative obstructive adhesions
Cirrhosis
Valvulitis in Rheumatic Heart Disease
CRONIC INFLAMMATION
DEFINITION:
Inflammation of prolonged duration in which
active inflammation. tissue destruction and
attempts of healing are proceeding
simultaneously
CHARACTERISTICS:
1. infiltration by mononuclears
2. tissue destruction
3. repair by connective tissue replacement
CRONIC INFLAMMATION
SETTINGS OF CHRONIC INFLAMMATION
1. Persistent inflammation
2. prolonged exposure to potentially
toxic agents
3. autoimmune disease
CRONIC INFLAMMATION
Components oI Fibrosis:
Formation oI new blood vesssels
Migration and proliIeration oI Iibroblasts
Deposition oI extracellular matrix
Maturation and Organization oI Iibrous tissue
Morphologic Jariants of Patterns in
Inflammation
1. Serous InIlammation
2. Fibrinous InIlammation
3. Suppurative or Purulent InIlammation
4. Granulomatous InIlammation
5. Ulcer
CRONIC INFLAMMATION
Serous InIlammation
outpouring oI thin Iluid, either Irom serum or as
secretions oI mesothelial cells called effusion
Fibrinous InIlammation
greater vascular damage causing larger molecules
such as Iibrin to pass the vascular barrier
Iibrin stimulates Iormation oI blood vessels and
Iibroblasts (Scarring) called organization
fibrinous pericarditis
CRONIC INFLAMMATION
Suppurative inIlammation
production oI purulent exudates consisting oI
neutrophils, necrotic cells, and edema Iluid
pyogenic organisms (Staphvlococci)
Abscess is localized collection oI purulent
inIlammatory caused by suppuration buried in a ,
tissue, an organ or a conIined space
eventually walled oII by connective tissue
CRONIC INFLAMMATION
Granulomatous InIlammation
distinctive pattern oI Chronic InIlammation
predominant cell type is an activated macrophage
with epithelial-like (epithelioid) appearance
Granuloma - consists oI microscopic aggregates oI
epithelioid macrophages surrounded by lymphocytes
and occasionally lymphocytes
. Foreign body granuloma
Tuberculous (Langhan`s type giant cells)
leprosy
CRONIC INFLAMMATION
Ulcer
local deIect or excavation on the surIace oI an organ
or tissue that is produced by sloughing oI
inIlammatory necrotic tissue
COMPONENT$ OF FIRO$I$
1. FORMATION OF NEW BLOOD VESSELS`
2. MIGRATION AND PROLIFERATION OF
FIBROBLASTS`
3. DEPOSITION OF EXTRACELLULAR MATRIX
4. MATURATION AND ORGANIZATION OF
FIBROUS TISSUE
`GRANULATION TISSUE
INFLAMMATORY REACTION$
A$ED ON LOCATION
ABSCESS
CELLULITIS
ULCER
MEMBRANOUS
INFLAMMATION
CATARRHAL
INFLAMMATION
ABSCESS
GRANULOMA
EPITHELOID CELL
LANGHAN`S TYPE GIANT CELL
CLINICO-PATOLOGIC DIFFERENCE$
ETWEEN ACUTE AND CRONIC
INFLAMMATION
ACUTE CHRONIC
1. 1. Fotho|og|c Feotures Fotho|og|c Feotures
A. Gross orgon |orger thon normo| ...smo||er A. Gross orgon |orger thon normo| ...smo||er
8 . H|sto|og||c exudot|ve, po|vs pro|||erot|ve, monos 8 . H|sto|og||c exudot|ve, po|vs pro|||erot|ve, monos
2. 2. C||n|co| Feotures C||n|co| Feotures
A. Onset rop|d |ns|duous A. Onset rop|d |ns|duous
8. Durot|on short |ong 8. Durot|on short |ong
SCHEMA OF INFLAMMATORY RESPONSE
INJbkY INJbkY
VA$CbLAk kE$FON$E VA$CbLAk kE$FON$E
INFLAMMAIOkY kE$FON$E INFLAMMAIOkY kE$FON$E
INVADEk$ FkOMFILY DE$IkOYED INVADEk$ NOI FkOMFILY INVADEk$ FkOMFILY DE$IkOYED INVADEk$ NOI FkOMFILY DESTROYED DESTROYED
NO NECkO$I$ OF CELL$ NECkO$I$ OF CELL$ NO NECkO$I$ OF CELL$ NECkO$I$ OF CELL$
EXbDAIE kE$OLVED EXbDAIE$ OkGANIIED $IA8LE / LA8ILE FEkMANENI EXbDAIE kE$OLVED EXbDAIE$ OkGANIIED $IA8LE / LA8ILE FEkMANENI
kE$IIIbIION OF NOkMAL $CAkkING FkAMEWOkK $CAkkING kE$IIIbIION OF NOkMAL $CAkkING FkAMEWOkK $CAkkING
$IkbCIbkE$ INIACI DE$IkOYED $IkbCIbkE$ INIACI DE$IkOYED
kEGENEkAIION kEGENEkAIION
kE$IIIbIION kE$IIIbIION
MiId Heart Injury Fibrinous Pericarditis Lobar Pneumonia Amebic Abscess M . I. MiId Heart Injury Fibrinous Pericarditis Lobar Pneumonia Amebic Abscess M . I.
Infection
InIection is the invasion oI the body tissue by
microorganisms & their proliIeration there.
An inIection occurs as a result oI a cyclic
process, consisting oI six components:
InIectious agent, reservoir, Portal oI exit,
means oI transmission, portal oI entry and
susceptible host.
Infection
In order Ior a client to acquire inIection, a
series oI elements needs to be PRESENT.
Each element or 'LINK is necessary to result
in an inIection
The process is known as INFECTIOUS
PROCESS
IMPOR1AACE O S1UDYIAC
IALAMMA1ORY RESPOASES
Preventing transIer oI microorganisms is a
very important concern.
Preventing inIection is one step in promoting a
healthy liIestyle
We are involved in identiIying, preventing,
controlling and teaching the patient about
inIection.
Definition of terms
InIection invasion oI body tissues by
microorganisms and their proliIeration. It is a
disease state that results Irom the presence oI
pathogens
Virulence the degree oI pathogenicity or
seriousness oI the disease
Pathogenicity ability to produce disease or
pathologic changes in the body
Definition of terms
Asepsis Ireedom Irom disease causing
microorganisms
Medical Asepsis includes all practices intended to
conIine a speciIic microorganism to a speciIic area,
limiting the number, growth and transmission
Surgical Asepsis includes all practices that keep an
area Iree oI all microorganisms
Sepsis a state oI generalized inIection, 'poisoning
oI tissues
Definition of terms
Microorganisms bacteria, viruses, Iungi and
parasites
Colonization - a process by which strains oI
microorganisms become resident Ilora, but
their presence does not cause disease
Local inIection limited to a speciIic area
where the microorganisms remain
Systemic inIection generalized inIection
which spread to diIIerent body parts
Definition of terms
Acute inIection sudden, short-lived, intense
inIection
Chronic inIection slow and prolonged
inIection
Nosocomial inIection arising Irom a health
Iacility
Iatrogenic inIection due to direct result oI
diagnostic or therapeutic procedures.
Definition of terms
InIectious agent microorganism that cause the
inIection
Asymptomatic or subclinical no clinical evidence
oI the disease
Disease detectable alteration in normal tissue
Iunction
Opportunistic Pathogen causes disease only in a
susceptible pathogen
Definition of terms
Etiology study oI cause; identiIication oI the
invading microorganism
Resident Ilora microorganisms that are always
present in speciIic areas oI the body usually in
numbers compatible with the individual`s health
Transient Ilora microorganisms that are present
episodically in speciIic areas oI the body
Definition of terms
Non-speciIic deIenses protect the person
against all microorganisms regardless oI
prior exposure
SpeciIic (immune) deIenses- directed
against identiIiable bacteria, viruses, Iungi,
or other inIectious agents
1he chain of infection
1. Etiologic agent
2. Reservoir
3. Portal oI exit Irom reservoir
4. Method oI transmission
5. Portal oI entry to the susceptible host
6. Susceptible host
Links of Infection
Chain oI InIection: (6) Links in the Chain
1. Etiologic Agent (microorganism)
This can be bacterium, parasite, virus
or Iungus
Links of Infection
Chain of Infection: (6) Links in the Chain
1. Etiologic Agent (microorganism)
Extent to which any microorganism or parasite is
capable of producing an infectious process depends on:
Numbers of organism present
Virulence and potency of the organism
(pathogenicity)
Ability of the organism to enter the body
Susceptibility of the host
Ability of the organism to live in the host`s body
Colonization: the presence of organism in the body
secretions or excretions that does not cause illness
Links of Infection
2. Reservoir
Source of infection
Needed for the agent to survive
This is required for the survival of
the agent while waiting for the host
Links of Infection
2. Reservoir
The reservoir for growth of microorganisms is the
natural habitat of the organism.
Common sources: other humans. client`s own
microorganisms. plant. animals or general
environment
Reservoirs must have certain characteristics for
organism to live & grow: food. water. (+) or (-)
oxygen. optimal temperature & pH & minimal
light
Carrier state maybe: short and long duration
Links of Infection
3. The portal oI exit
the point of escape for the organisms from
the reservoir. The pathway of escape.
The organisms cannot extend its influence
unless it moves away from the carrier.
Within human: the microorganism have a
number of exits. depending on the site of the
reservoir- gastrointestinal. respiratory.
genitourinary. body fluids and break in the
skin.
Links of Infection
4. Method oI Transmission
3 Mechanisms:
Direct
Indirect
Air borne
Links of Infection
Method of Transmission
1. Direct Transmission
Involves immediate & direct transfer of
microorganisms from person to person
through touching. biting. kissing. or
sexual intercourse
Links of Infection
Method oI Transmission
DIRECT transmission
Droplet spread a Iorm oI direct contact
Occur only iI the source & the host are
within 3 feet apart
Links of Infection
Method of Transmission
2. Indirect Transmission
1. Vehicle-borne transmission
Fomites. inanimate objects
Other vehicles: water. foods. mild. blood.
serum. plasma
2. Vector-borne transmission- mosquitoes.
ticks. and lice can transmit organisms
form one human to another.
Links of Infection
Method of Transmission
3. Airborne Transmission
Droplet nuclei (residue of evaporated
droplets that may remain in the air for long
periods of time)
Dust particles containing an infectious agent
Links of Infection
. Portal of Entry
Microorganism can enter the body
through the same routes they use to
leave the body
The urinary. respiratory and the
gastrointestinal tracts are the most
common entry points.
Links of Infection
6. Susceptible Host
Microorganisms can continue to exist only in
a source that is acceptable
Susceptibility is the degree of resistance the
potential host has to the pathogen
Susceptible host: person who is at risk
for infection
Compromised host: person "at increased
risk
Stages of Infectious Disease
The course oI inIection that results in
disease state is a dynamic series oI events
that express competition between the host
and the invading organism.
The pattern oI most disease Iollows a
predictable course.
Stages of Infectious Disease
Communicable disease when the
causative agent oI the disease is
transmissible between one individual to
another.
II it passes with ease Irom one host to
another, it is called contagious disease.
Stages of Infectious Disease
The inIection progresses through the
Iollowing phases:
Incubation
Prodromal
Full stage oI illness
Convalescence.
Stages of Infectious Disease
Incubation Period
Time between the entry of
microorganisms into the body and the
onset of non-specific symptoms
Length of the incubation period varies
depending on the microorganisms
Viral infection usually average 2 weeks
Stages of Infectious Disease
Prodrome Period
The time from the onset of non-specific
symptoms to the appearance of the
SPECIFIC symptoms of the infection
This is where most people are MOST
infectious and most likely to spread the
disease
Early manifestations are present but are
vague and non-specific.
Short in duration. usually hours to few days.
Stages of Infectious Disease
Illness Period
The presence of SPECIFIC signs and symptoms
indicates the full stage of the infection.
The type of infection determines the length of the
illness and the severity of the manifestations.
Usually appearance of exanthem and enanthem
If manifestations appear in one area of the body it is
called localized infection. If it involves the whole
body. it is called generalized / systemic infection.
Stages of Infectious Disease
Convalescence
Extends from the time the symptoms start
to abate until the time the person returns
to the normal state of health
Recovery period from the illness
Signs and symptoms disappear and the
client becomes healthy again.
Type Antigen or antibody source duration
Active Immunity Antibodies are produced by the body in
response to an antigen
long
Aatural active Antibodies are formed in the presence of
active infection
lifelong
Artificial active Antigens (vaccines/toxoids) are injected
to stimulate antibody production
Many years
Passive Immunity Antibodies are produced by another
source
Short
Aatural passive Antibodies are transferred naturally
from an immune mother to her baby
through the PLACENTA or BREAST
FEEDING
About 6 months
to 1 year
Artificial passive Immune serum (antibodies) comes from
another source (humans/animals)
injected to another human
2 to 3 weeks
Immunitv
Immunity Examples
ACTIVE natural Infectious disease
ACTIVE artificial Immunization with vaccines
and toxoids
PASSIVE natural Placenta and Breastfeeding
PASIVE artificial Injection of Immune serum,
anti-toxins
Breaking the Chain of Infection
Interruption oI the inIectious process: Surgical
and Medical Asepsis
Antiseptics agents that inhibits the
growth oI some microorganisms
DisinIectants agents that destroy
pathogens other than spores: inanimate
Sterilization
Hand-washing
The single most important measure
to prevent inIection
Rubbing together oI all surIaces
and crevices oI the hands using
soap or chemical and water
Hand-washing
For routine care, it is required that
vigorous hand washing with soap
under a stream oI water Ior
At least 10 seconds-15 seconds (CDC,
Kozier)
At least 15-30 seconds (Udan)
Asepsis
DisinIectant chemical preparation (phenol or
iodine compounds) use to treat inanimate
obiects; Irequently caustic & toxic to tissues
Antiseptic chemical preparation used on skin
& tissue
Bactericidal: destroys bacteria
Bacteriostatic: prevents growth & reproduction
oI some bacteria
AGENT USES
Antiseptics
Povodine Iodine
BETADINE
Kills bacteria; applied to skin. in
wounds & for irrigations
Chlorhexidine
Kills g (+) bacteria; skin cleansing &
irrigations
Hydrogen peroxide (3)
Decomposes necrotic tissues; wound
irrigations
Disinfectants
Isopropyl Alcohol
Kill bacteria but not spores. virus or
fungi
Chlorine
Kills most microorganisms; used to
clean countertops
Surgical Asepsis
Sterilization a process that
destroys all microorganisms;
including spores and viruses
Sterilizing
ME1HODS
Moist heat (steam)
Steam under pressure
Attains temperature higher
than boiling point
Autoclave: pressure 15-17
pounds
Sterilizing
ME1HODS
Temperature - 121-123 C (2-24 F)
Free steam
Temperature: 1 c (212 F)
Used to sterilize objects that would be
destroyed at the higher temperature and
pressure of the autoclave
Necessary to steam the article for 3mins
on 3 consecutive days
Sterilizing
ME1HODS
Gas (Ethylene Oxide Gas)
Destroys microorganisms by
interIering with metabolic process
EIIective against spores
Advantages: good penetration;
eIIective Ior heat sensitive items
toxic to humans
Sterilizing
ME1HODS
Boiling Water
Most practical & inexpensive (home)
Disadvantage: do not kill spores &
some viruses
Temperature not higher than boiling
point 100 c (212 F)
Duration: minimum oI 15 minutes
Sterilizing
ME1HODS
Radiation
Ionizing radiation - used to sterilize foods.
drugs. and other items sensitive to heat
Non-ionizing radiation (ultraviolet rays) -
do not penetrate deeply
Advantage: effective for items difficult to
sterilize
Disadvantage: equipment is very
expensive
Standard precaution
Intended to prevent transmission of blood-borne
and moist body substance pathogens
1. Wearing of clean gloves
2. Performing hand washing immediately
3. Wear mask. eye shield during procedures that
generate splashes
4. Wear gown if splashes. sprays. secretions cause
soiling
. Prevent injuries from needle & sharp objects
Precaution
Standard
Precaution
Used in care of ALL hospitalized persons-
applies to blood. all body fluids. secretions.
excretions
1RAASMISSIOA-based
precaution
Airborne, Droplet and Contact
AIRBORNE
Airborne droplet nuclei less
than microns
Measles, Varicella and TB
Private room, negative air pressure and N95
respirator when entering room
DROPLET
Particles greater than
microns
Diphtheria, pneumonia, pertussis,
mumps, German measles
Contact
GIT, Respi, Skin and wound inIection easily
transmitted by direct client contact or contact
with client items
AOSOCOMIAL IAEC1IOA
Associated with the delivery oI health
care services in a health care Iacility
Develop during client`s stay in the
Iacility or maniIest aIter discharge
May also be acquired by: health
personnel working in the Iacility
AOSOCOMIAL IAEC1IOA
Usually occurs 3 days aIter
hospitalization
3-15 oI in-patients may develop
nosocomial inIection
The most common inIection is UTI
The most common agent is E. coli
AOSOCOMIAL IAEC1IOA
Sources:
Endogenous Source: originate
Irom clients themselves
Exogenous Source: Irom
hospital environment or
hospital personnel
AOSOCOMIAL IAEC1IOA
Contributing Factors:
Direct result oI diagnostic & therapeutic
procedures
Iatrogenic inIections
Presence oI compromised host
InsuIIicient hand washing
AC1ORS IACREASIAC
SUSCEP1IBILI1Y 1O IAEC1IOA
AGE
Newborns and older adults have reduced defenses against infection
HEREDITY
Genetic susceptibility
STRESS
Stressors elevate blood cortisone. epinephrine
NUTRITIONAL STATUS
Adequate nutritional status will increase resistance to infection
MEDICAL THERAPIES
Chemotherapy and Radiotherapy decrease resistance
CO-MORBID CONDITIONS
Diabetes. COPD. Chronic Diseases will all weaken the defense
barriers
Normal WBC count -1.
Increased WBC
(Leukocytosis)
More than 1.
Increased Neutrophils ACUTE bacterial infection
Increased Lymphocytes CHRONIC bacterial infection
VIRAL infection
Increased Eosinophils PARASITIC infection
In Summarv
Agents that cause inIection are everywhere in
the environment, on body surIace, in Iood
and in products used in normal activities oI
daily living.
Humans have deIenses against the invading
microorganisms- physical barriers, non-
speciIic immune responses and speciIic
immune responses
Intact skin and mucus membrane are the Iirst
line deIense oI the body
In Summarv
The inIlammatory response oI the body
limits physical, chemical and microbial
iniury and it promotes tissue repair
InIlammation has the Iive characteristics
signs- rubor, calor, dolor, tumor, Iunctio
laesa
InIlammation has 3 stages- Vascular and
cellular response; Exudate production; and
Repair
In Summarv
An inIection can develop iI the links in the
chain remain uninterrupted
The chain contains the Iollowing links-
etiologic agent, source/reservoir, portal oI
exit, method oI transmission, portal oI
entry and the susceptible host.
In Summarv
Nosocomial inIections are associated
with the delivery oI healthcare
services in the health Iacility.
The most common is UTI
In Summarv
we can break the chain oI inIection Irom
one person to another by Iollowing steps
in inIection control practices.
In Summarv
we can break the chain oI inIection
Irom one person to another by
Iollowing steps in inIection control
practices.
In Summarv
Proper Hand washing is the single
most important inIection control
technique!
EIIective control oI inIection
necessitates medical and surgical
asepsis