NCM50 It is debilitating can produce long-

lasting effects
Care of Clients w/Problems in Inflammatory and
Immunologic Response and Perception and
Coordination
Manifestation of Inflammation:
INFLAMMATORY and Immunologic Response
 Protective mechanisms of the body from
injury and invading microorganisms
 Once barrier is penetrated protective
responses are activated
 These are the inflammatory and immunologic
response
INFLAMMATION
 Is a localized rxn intended to neutralize,
control, or eliminate the offending agent to
prepare the site for repair
 It is a nonspecific response that is meant to
serve a protective function
Does not serve a beneficial and serve
protective and beneficial function
Can result to permanent tse damage
 Redness (rubor) – hyperemia from
vasodilation
 Heat (calor) – increase metabolism
@inflammatory site
 Pain (dolor) – nerve stimulation by chemicals
fluid exudate
 Swelling (tumor) – fluid shift to interstitial
spaces; fluid exudate
 Loss of function (function laesa) – swelling
and pain
INFLAMMATORY RESPONSE
Disruption of tse integrity

Immunologic response
 Takes longer to develop and highly specific injury Ischematic Immune rxn
 It destroys particular infectious damage
microorganisms and foreign molecules @ the
site of nfxn throughout the body

Inflammation and immunologic response: Inflammatory response

 Almost any injury or nfxn will lead to an
inflammatory response
 Example: a skin cut by a dirty piece of glass
- or an infected pimple
Vascular changes:
 Short term inflammation develops in the CT, Vasodilation: Cellular changes:
and produces sx.  Capillary Phagocytosis:
permeability  Leukocytes
1. Heat (calor)
 Bld flow (granulocytes and
2. Redness (rubor)  Local tse monocytes)
3. Swelling/edema (tumor) congestion  Release of chemical
4. Pain (dolor) mediators (mast
cells and
5. Loss of function (function laesa)
macrophages)

NCM 50

Inflammatory Response Body response

Inflammation :
 a localized rxn intended to neutralize, control,
or eliminate the offending agent to prepare
the site for repair
 it is a nonspecific response that is meant to Local effects: Systemic effects:
serve a protective function  Redness  Fever
types of Inflammation:  Warmth  Leukocytosis
a. ACUTE INFLAMMATION – characterized by  Swelling  Malaise
the local vascular and exudative changes and  Pain  Anorexia
 Loss of function  Sepsis
serves a protective function
b. CHRONIC INFLAMMATION – develops if the
injuries agent and acute response is
perpetuated
Exudate formation Major Components:
 Exudate consists of fluid and leukocytes that a. REGENERATION – is the replacement of lost
move from the circulation to the site of injury cells and tss w/cells of the same type
 The nature and quantity of exudate depend
on the type and severity of the injury and the Regenerative ability of different types of tss.
tss involved Tse type Regenerative ability
1. Epithelial
Types of Inflammatory Response Skin, linings of bld Cells readily divided and
a. Serous – result from outpouring of fluid that vessels, mucous regenerate
has low cell and CHON content; seen in early membrane
stage of inflammation or when injury is mild. 2. Connective
(ex. Skin blister; pleural effusion) tse
b. Catarrhal – found in tss where cells produce Bone -active tse heals rapidly
mucus. Mucus production is accelerated by Cartilage -regeneration possible but
inflammatory response. (ex. Runny nose Tendons and slow
associated w/URTI) ligaments
c. Fibrinous – occurs w/increasing vascular Blood -cells actively regenerate
permeability and fibrinogen leakage into 3. Muscles
interstitial spaces. Excessive amts. Of fibrin Smooth - Regeneration usually
coating tse surface may cause them to adhere possible (particularly GI tract)
(ex. adhesion) Cardiac - damaged muscle replaced
d. Purulent – consist of WBC microorganism by connective tse
(dead and alive), liquified dead cells and other Skeletal - connective tse replaces
debris (ex. Abscess, furuncle [boil]) severely damaged muscle;
e. Hemorrhagic – results from rupture or soe regeneration in
necrosis of bld vessel walls, consists of RBC moderately damaged muscle
that escape into tss occurs
4. Nerve
INFLAMAMTORY RESPONSE: Neuron - generally nonmitotic, do not
 A sequential rxn to cell injury replicate and replace
 Neutralizes and dilutes the inflammatory themselves if irreversibly
agent, removes necrotic materials and damaged
establishes an environment suitable for Cilia - cells regenerate , scar tse
healing and repair often forms when neurons
are damaged
MEDIATORS of INFLAMMATIO
Mediator Source MOA CELL TYPE
Histamine Stored in Vasodilation a) LABILE CELLS – divide constantly (injury to
granules of these organs is followed by rapid
basophils, mast regeneration)
cells, platelet Skin, lymphoid organs, bone marrow,
Serotonin Stored in Vasodilation, mucus membrane of the GIT, urinary,
platelet, mast stimulates reproductive tracts
cells, smooth b) STABLE CELLS – retain their ability regenerate
enterochromaffin muscle but do so only if the organ is injured (have
cells of GIT contraction latent ability to regenerate)
Bradykinin Produced from Contraction of Liver, pancreas, kidney, bone cells
precursor factor smooth c) PERMANENT CELLS – have left the cell cycle
kininogen muscle and and do not divide. Destruction of neurons is
dilation of bld permanent, however axons may regenerate
vessel Neurons of the CNS; skeletal and
cardiac muscle cells
HEALING OF SKELETAL AND CARDIAC
WOUND HEALING MUSCLE IS WITH SCAR TISSUE
 Healing is the final phase of the inflammatory
response
 b. REPLACEMENT – heal by connective tse repair  Occurs when a contaminated wound is left
open and sutured closed after the nfxn is
REPAIR HEALING controlled
1. Primary Intention – takes place when wound  Results in a larger and deeper scar than
margins are neatly approximated, such as primary and secondary intentions
surgical wound
WOUND CLASSIFICATION
Phase in Primary Intention Healing a. Surgical or nonsurgical
PHASE ACTIVITY b. Acute or chronic
INITIAL (3-5days)  Approximation of c. Depth of tse affected; superficial, partial-
incision edges; thickness, full thickness
migration of epithelial
cells; clot serving as
meshwork for starting RED – YELLOW – BLACK
capillary growth
 Acute inflammatory rxn RED WOUND
occurs  Characteristics:
GRANULATION  Migration of Traumatic or surgical wound,,
(5days – 4wks) fibroblastic; secretion possible presence of serosanguineous
of collagen, abundance drainage, pink to bright or dark red
of capillary buds; healing or chronic wound
fragility of wound, @ w/granulating tse
risk for dehiscence and  Purpose of tx.
resistant to nfxn Protection and gentle atraumatic
 Wound is pink and cleansing
vascular, wound closely  Dressing and therapy
resembles the adjacent Transparent film dressing ex.
skin Tegaderm
 Fibroblastic, Hydrogels ex. Tegagel
proliferative, Gauze dressing w/antimicrobial
reconstructive phase ointment or sol’n
SCAR  Remodeling of YELLOW WOUND
CONTRACTURE collagen; strengthening  Characteristics
(7days – several of scar Presence of slough or soft tse, liquid
mos.)  Maturation phase semiliquid slough w/exudate ranging
from creamy ivory to yellow-green
2. SECONDARY INTENTION HEALING  Purpose of tx.
 Wound edges are not approximated and the Wound cleansing to remove
wound fills w/granulation tse nonviable tse and absorb excess
 Wounds that occur from trauma, ulceration drainage
and nfxn have large amt of exudates and  Dressing and Therapy
wide, irregular wound margins w/extensive Wound irrigation
tse loss Hydrotherapy
 This result in more debris, cells and exudate Moist gauze w/or w/o antibiotic or
(infection reopened wounds heal by antimicrobial agent
secondary intention) BLACK WOUND
 Greater defect, healing and granulation tse –  Characteristics
resulting in a larger scar Black, gray, or brown adherent tse
 Debridement is done possible presence of purulent
drainage
3. TERTIARY INTENTION  Purpose of tx.
 Occurs w/delayed suturing of a wound in w/c Debridement of eschar and nonviable
two layers of granulation tse are sutured tse
together  Dressing and therapy
Topical enzyme debridement
Surgical debridement
 Hydrotherapy
Chemical debridement
Moist gauze dressing
Absorptive dressing covered
w/dressing

FACTORS DELAYING WOUND HELAING

Factor Effect on wound healing
Nutritional
deficiency
Vit. C delays formation of collagen
fibers and capillary development
CHON decreases supply of amino acid
for tse repair
Zn Impairs epithelialization
Inadequate bld Decreases of nutrients to injured
supply areas, inhibits inflammatory
response
Corticosteroids Impair phagocytosis by WBC,
drugs inhibit fibroblast proliferation
and function
Infection Increases inflammatory
response and tse destruction
Smoking Nicotine is a potent
vasoconstrictor and impedes
bld flow to healing areas
Advanced age slows collagen synthesis by
fibroblasts, impairs circulation,
requires longer time for
epithelialization of skin
Obesity decreases bld supply in fatty tse
DM Decreases collagen synthesis,
retards are capillary growth,
impairs phagocytosis, reduces
supply of O2 and nutrient s/t
vascular dse
Anemia Supplies less O2 @ tse level
Poor general causes generalized absence of
health factors necessary to promote
wound healing
Mechanical Destroys granulation tse,
friction on prevents approximation of
wound wound edges
Mechanisms of Wound Healing

 Wound bed: necrosis and granulation tse

Healthy granulation tse is pink
Dark red, easily bleeds on contact,
may indicate wound infection
Excess granulation may be associated
w/infection or non-healing wound
Necrotic tss (black areas)
 Surrounding skin: color, moisture, suppleness
Periwound – the tse surrounding the
wound
Cellulitis – nfxn of the skin and
underlying soft tse
Maceration – softening and breaking
of skin from prolonged exposure to
moisture
 Wound edge – not diagnostic but may help
identify its etiology from hx.

WOUND ASSESSMENT LAB. TEST

 TcPO2 – transcutaneous oximetry
Albumin – CHON, produced by liver
diminished in severe burn wounds,
malnutrition, liver dse
 Prealbumin – CHON, produced by the liver, a
better indicator for changes in nutritional
status. Diminished in widespread tse damage,
malnutrition, CHON wasting
 Hgb AIc – composed of hgb A w/a glucose
molecule, an indicator of long-term glucose
control
 CBC  Odor and exudates
 Size, depth and location of the wound  Infection
Measure @ 1st presentation, and  Quality of life
regularly thereafter
Mgnt. Of clients w/wounds: Medical and Surgical
mgnt.
 Management depends on the type of wound
 Wound from surgical procedure:
1. Ongoing assessment of the surgical site:
Approximation of wound edges
Integrity of sutures or staples
Redness, discoloration, warmth,
swelling, unusual tenderness
Rxn to tape of trauma to tight
bandage
2. Caring for surgical drains
Penrose, Jackson-Pratt

3. Changing the dressing

By surgical team member, then by a
nurse
Reasons for applying dressing to
wound:
a. To provide proper environment
for proper wound healing
b. To absorb drainage
c. To immobilize the wound
d. To protect wound and new
epithelial tse from injury
e. To protect wound from bacterial
contamination
f. To promote hemostasis like in
pressure dressing
g. To provide mental and physical
comfort
Observe sterile or clean technique
when doing dressing change
 Wound cleansing: usually w/normal
saline
Povidone-Iodine (betadine) and
hydrogen peroxide should not go
deep into the tse w/o thru rinsing,
only used for initial cleansing
Hypoallergenic tape if necessary,
porous prevents maceration
Disinfect sol’n per MD
During dressing change, the nurse has
the opportunity to educate the px.
4. Px education =: wound care instructions. Until
sutures are removed:
a. Keep wound dry and clean
b. Immediately report any signs of nfxn
c. For soreness and pain, apply dry cool
pack, or take prescribed medication
d. Elevate affected part as swelling is
common postop
: After sutures are removed
a. Cont. monitoring, still tender and
continues to heal
WOUND DEBRIDMENT
GOALS OF DEBRIDEMENT:
1. Removal of devitalized tse or burn eschar in
preparation for grafting and wound healing
2. Removal of tse contaminated by bacteria and
foreign bodies
TYPES OF DEBRIDEMENT:
1. Natural debridement
2. Mechanical debridement
3. Chemical debridement
4. Surgical debridement
WOUND GRAFTING
 A surgical procedure of removing skin from
one area of the body and transplanting it to a
different area of the body
 May be done when there is lost of protective
covering of skin from deep burns, skin nfxn,
large open wounds, or bedsores or other ulcer
that have not healed well
 Can reduce risk of nfxn, prevent further loss
of CHON and electrolytes
 Aesthetics
 Autografting – the preferred autologous
method for definitive burn wound closure
after excision
 Autografts are px. Own skin therefore are not
rejected by our immune sys.
 CEA (Cultured Epidermal Autograft)
A tse grown from one’s own skin cells
for use in placing on the person’s own
body
Maintenance or growth of cells in the
incubator after removal from the
body
Care of the Graft Site:
1. Protection is the key goal
Occlusive dressing initially to
immobilize the graft
OT may construct splint to immobilize
grafted area
Homograft, xenograft or synthetic
dressings are used to protect grafts
2. 1st dressing change usually performed 2-5
days
3. Monitor sign of bleeding and nfxn
4. Px is turned and positioned carefully to avoid
disturbing the graft or putting pressure to
graft
5. Exercise of the grafted area may begin 5-7
days
6. If extremity has been grafted elevate to
minimize edema
Disorders of Wound Healing
1. Delayed wound healing
2. Wound nfxn
3. Wound disruption
4. Others
 Delayed wound healing or non-healing
chronic wound
There is interruptions, aberrancies or
prolongation of the healing process
From tse trauma from surgery,
previous radiation therapy,
inadequate nutrition, or infection
 Mgnt: delayed wound healing
Determine cause
Minimize pressure on he wound site
to promote circulation to the tss
Aseptic, non traumatic dressing
promotes healing
Monitoring of lab results to initiate
interventions that promotes
homeostasis and wound healing
Repositioning px frequently to
prevent further skin breakdown
Medical and surgical mgnt
Special therapeutic bed
 Wound nfxn
For surgical incision, the doctor will
remove suture and put a drain
 Deep wound may require incision and  Common form is WET-TO-
drainage antimicrobial therapy DRY dressings – an open
mesh gauze is moistened
 Wound disruption w/NSS packed on or into the
Dehiscence and evisceration wound surface and allowed to
Serious complications esp. for dry
abdominal incision  Topical antimicrobials ex.
Place px in a Low Fowler’s and Betadine; Dakin’s sol’n (Na+
instruct to lie quietly hypochlorine); hydrogen
Cover w/a sterile dressing moistened peroxide; chlorhexidine
w/normal saline  Wound irrigation
Notify surgeon immediately  Whirlpool
Note: mechanical debridement should not be used in
Complication of wound Healing a clean granulating wound
a) Hypertrophic scars – an inappropriately large, 3. Autolytic debridement
red, raised and hard  Semiocclusive or occlusive
b) Keloid formation – greater protrusion of scar dressings used to promote
tse that extends beyond the wound edges and softening of eschar by
may form tumor like a mass; permanent autolysis
c) Contracture – shortening of muscle or scar tse 4. Enzymatic debridement
result from excessive fibrous tse formation,  Use of drugs that are topically
esp. near the joint applied to the necrotic tse in
d) Evisceration – separation of wound edges, the wound and then covered
intestine protrudes thru the wound w/saline – moistened gauze
e) Adhesion – bands of scar tse b/n or around ex. Collagenase
organs Hyperbaric O2 Therapy – delivery of O2 @increased
atmospheric pressure
Mgnt:
a) Drug therapy
Antipyretic drugs
Anti-inflammatory
 Salicylates
 Corticosteroids – interfere
w/tse granulation, induce
immunosuppressive effects
 NSAIDS
Vitamins
 Vit. A – accelerates
epithelialization
 Vit. B complex – act as
coenzymes
 Vit. C – synthesis of collagen
and new capillaries
 Vit. D – facilitates Ca
absorption
b) Nutritional therapy
c) RICE – rest, ice, compression, elevation
d) Immobilization – decrease metabolic needs
e) Debridement
1. Surgical debridement
2. Mechanical debridement
 Use when minimal debris is
present
NCM 50 PRELIM 12 – 06 – 19
IMMUNE RESPONSE
Inflammation vs immunologic response
Inflammation
- is a localized rxn intended to neutralize, control,
or eliminate the offending agent to prepare the
site for repair
- it is a nonspecific response that is meant to
serve a protective function
Immunologic response
- takes longer to develop and highly specific
- it destroys particular infectious microorganisms
and foreign molecules @ the site of nfxn
throughout the body
Function of the Immune System
- to remove foreign antigens such as viruses and
bacteria to maintain homeostasis
TYPES OF IMMUNITY:
a) Natural Immunity
- nonspecific, provides a broad spectrum of
defense against resistance to infection
- first line of host defense following antigen
exposure
- coordinates the initial response to
pathogens through the production to
cytokines and other effector molecules,
which either activate cells for control of
the pathogens or promote the
development of acquired immune
response
- natural immunity is present at birth
b) Acquired Immunity
- develop as a result of prior exposure to
antigen through immunization; or by
contracting a disease – both of which
generate a protective immune response
TYPE OF ACQUIRED IMMUNITY:
a) Active Acquired Immunity – immunologic
defenses developed by the person’s own
body, it lasts lifetime.
b) Passive Acquired Immunity- temporary
immunity transmitted from a source
outside the body that has developed
immunity through previous disease or
immunization
RESPONSE IN INVASION
1. Phagocytic Immune Response
- the first line of defense, primarily involves
the WBC (granulocytes and macrophages),
which have the ability to ingest foreign
particles and destroy the invading agents.
Apoptosis – programmed cell death, is the
body’s way of destroying worn out cells such
as blood or skin cells that need to be renewed.
2. Humoral Immune Response (antibody
response)
- begins with the B lymphocytes which can
transform themselves into plasma that
manufacture antibodies. These antibodies
are highly specific proteins that are
transported in the blood stream and
attempt to disable invaders.
3. Cellular Immune Response
- involves the T lymphocytes which can turn
into special cytotoxic T cells that can attack
pathogens.

Bone Bone Bone
marrow marrow
marrow
IMMUNOLOGIC RESPONSE
Lymphocytes
- the most effective of our defense cells
- repeatedly move between the circulatory
vessels and the connective tissue –
RECIRCULATION
- must pass through several stages before
they are ready to attack antigens, from
infancy to childhood, as well as adulthood
- like other blood cells, they originate from
the hematopoietic stem cells in the bone
marrow
B and T Lymphocytes
- some immature lymphocytes enter the
bloodstream and travel the thymus and
stay there for 2-3 days and divide rapidly
- as they divide, the T lymphocytes begin to
recognize its specific antigen, this is called
IMMUNOCOMPETENCE
- B lymphocytes achieve
immunocompetence in the bursa of the
bone marrow (in birds bursae of Fabricius)
- B and T lymphocytes become fully
activated only when they travel to the
infected loose CT and encounter their
antigen there, called ANTIGEN CHALLENGE
- T lymphocytes – attack host cells infected
w/viruses, fungi, transplanted human cells and
cancerous cells/ must have actual physical contact
w/victim cell in order to destroy it – CELL –
MEDIATED IMMUNITY
- B lymphocytes combat bacterial and some viral
nfxns by secreting antibodies into the bld and
lymph – HUMORAL IMMUNITY
INFECTION
- the successful invasion of the host’s body
tissues by dse causing agents (pathogens)
such as bacteria, viruses or parasites, their
multiplication and the reaction of host
tissues to these organisms, and the toxins
they produce.
- a condition in which a host interacts
physiologically and immunologically with a
microorganisms.
INFECTIOUS DISEASE
- any dse caused by the growth of
pathogenic microbes in the body
- it may or may not be communicable
- modern science has controlled, eradicated
or decreased the incidence of many
infectious dses.
INFECTIOUS PROCESS
Chain of infection – the process by which
infections spread
Infectious Agent/Causative Agent
 bacteria, viruses, protozoa, fungi, helminthes,
rickettsiae
Reservoir
 the source of infection: any person, plant,
animal, substance, or location where
pathogens survive and multiply
Mode of Exit
 mode of exit from reservoir to another
organisms or environment for transmission to
occur
 EXIT: respiratory tract, GIT, GUT, blood, breast
milk, vomitus, semen, saliva
Route of Transmission
 necessary to connect the infectious source
with its new host
 may be transmitted through direct or indirect
contact
- Direct contact – kissing, sexual
intercourse, touching
- Indirect contact – contact with fomite, a
contaminated object that transfers the
pathogen
 CARRIER – a person who carries or transmits
an organism but does not have the apparent
signs and symptoms of infxn
 Note: Specific organisms require specific
routes of transmission
Portal of Entry
 access to the host
 Normal body openings – conjunctiva of the
eye, nares, mouth, urethra, vagina, anus
 Potential portal of entry – abnormal openings
– cuts bites, scrapes, insertion sites for tubes
and needles
Susceptible Host SECONDARY INFXN – infxns following primary
infxn, especially in immunocompromised pts.
 a person with inadequate defenses against the
invading pathogen EXOGENOUS INFXN – the pathogen is acquired
- immunocompromised from healthcare environment
- elderly ENDOGENOUS INFXN – pathogens arises from the
patient’s normal flora

FACTORS THAT DETERMINE WHETHER THE

PERSON DEVELOPS INFECTION
1. Virulence of the microorganism (the
power to cause dse)
2. The number of microorganisms
transmitted – the greater the number, the
more likely they are to cause dse
3. Ability of the host’s defenses to prevent
infxn

FACTORS AFFECTING SUSCEPTIBILITY TO INFXN

 Immunosuppression
 Malignancy
 Neutropenia
 Cellular Immune Dysfunction
 Humoral Immune Dysfunction
 Bone marrow Immune Dysfunction
 Splenectomy
 Chemotherapeutic agents
 Health status and health habits of the host
 Exposure to pathogens
 Virulence of the microorganisms

INFECTION CAN BE CLASSIFIED BY LOCATION

AND DURATION
LOCAL – infxn in limited region of the body
SYSTEMIC – when infxns invade the blood stream
or lymph and spread throughout the body
BACTEREMIA – the clinical presence of bacteria in
the blood
SEPTICEMIA – symptomatic systemic infxns
spread via the blood
PRIMARY INFXN – first infxn that occurs in the pt.