Inflammation, Healing, Immunity

purpose of inflammatory response (chronological reaction to cell injury)

1. neutralizes and dilutes the inflammatory agents
2. removes necrotic materials
3. establish an environment suitable for healing and repair

inflammation is always present with \________________

infection

inflammatory response is caused by:

-heat
-radiation
-trauma/injury
-chemicals
-allergens
-autoimmune reaction
-non-fungi
-non-bacterial
-sunburn

Infection is \___ present with inflammation

NOT always
ex: neutropenic patient

infection

involves invasion of tissues or cells by microorganisms like bacteria, fungi, and viruses

vascular inflammatory response

1st response

1. cellular injury
2. brief transient vasoconstriction
3. release of chemical mediators (histamine causes vasoD and increases capillary permeability BF)
4. VasoD and capillary permeability are responsible for redness, heat, and swelling
5. inflammatory exudates made of serous fluid containing plasma proteins and albumin (this attracts water moving fluid into the interstitial space)

What best describes the nature of the fluid associated with swelling of tissue in acute inflammation?

protein-rich exudate

clinical manifestations of inflammation vascular response

cell death or injury, momentary vasoconstriction, and
release of chemical mediators (histamine, kinins, prostaglandins) leads to:

-local vasodilation
-hyperemia (redness)
-increased cap permeability (BF)
-local edema

which all lead to fluid/cell inflammatory exudate

Cellular inflammatory response

2nd response
-WBCs move from circulation to the site of injury using chemotaxis

margination

cells line up against the endothelium

rolling

close contact w and roll along the endothelium
-mediated by IL1 and TNF

adhesion

connecting to the endothelial wall (blood vessel wall)

diapedesis

cells move through the vessel wall

what has to happen for diapedesis to occur?

vascular response bc it increases capillary permeability allowing for cells to move across vessel wall

chemotaxis

the directional migration of WBCs to the site of injury

WBC count

5,000-10,000/mm3

types of WBC

1. neutrophils
2. monocytes
3. lymphocytes (B & T)

Neutrophils

1st responders w short lifespan (6-12 hrs) that phagocytize(engulf) the bacteria, foreign materials, and damaged cells that become pus
-mature neutrophils
-immature neutrophils

mature neutrophils are \_________________ neutrophils

segmented 55-70%

immature neutrophils are \_________________ neutrophils

band (shift to the left) 0-8%

Monocytes

2-8% WBC w long lifespan (3-7 days) that eventually transform into macrophages once they enter tissue, they phagocytize (engulf) inflammatory debris in cleaning the area and orchestrating the healing process
-macrophages can accumulate to form a multinucleated giant cell called granuloma to wall off bacteria

monocytes transform into \_________ once they are in the tissue

macrophages

Granuloma

macrophages that accumulated to form a multinucleated giant cell to isolate the bacteria (defensive immune response)
ex: tuberculosis of the lung

Lymphocytes

B and T 20-40% WBC that arrive later at the site of injury and function mainly for immune response
-play a primary role in humoral and cell-mediated immunity

inflammatory exudate is made up of:

fluid/cell exudate & WBCs that move from the circulation to the site of injury

Catarrhal exudate

found in tissues where cells produce mucus
-inflammatory response accelerates mucus production

ex: runny nose associated w URI

fibrinous exudate

excessive amounts of fibrin that coats tissue surfaces

ex: adhesions, gelatinous ribbons seen in surgical drain tubing, frequently covers fluid-exuding wounds, such as venous injuries

hemorrhagic exudate

results from rupture or necrosis of blood vessel walls

ex: hematoma, bleeding after surgery or tissue trauma

purulent (pus) exudate

consists of WBCS, microorganisms (dead & alive), liquified dead cells, and other debris

ex: furuncle (boil), abscess, cellulitis (diffuse inflammation in connective tissue)

Serosanguineous exudate

semiclear pink and may have red streaks that's composed of RBCs and serous fluid
-found during midpoint in healing after surgery or tissue injury

ex: surgical drain fluid

serous exudate

clear to pale yellow watery fliud that results from outpouring of fluid seen in the early stages of inflammation or when injury is mild

ex: skin blisters, pleural effusion

local clinical manifestations of inflammation

-heat
-redness
-pain
-swelling
-loss of function

systemic clinical manifestations of inflammation

-increased WBC count
-shift to the left (immature/band neutrophils)
-malaise
-nausea
-anorexia
-increased pulse and respiratory rate
-fever

acute inflammation

Healing occurs in 2 to 3 weeks, usually leaving no residual damage

what is the predominant cell type at the site of acute inflammation?

neutrophils bc they are the 1st responders

subacute inflammation

Has same features as acute inflammation but persists longer (weeks to months)

chronic inflammation

lasts for weeks, months, or even years. Possible physical deterioration

Outcomes of acute inflammation

1. complete resolution
2. formation of an abscess
3. chronic inflammation
4. fibrosis and scar formation

Outcomes of acute inflammation: complete resolution

completely repaired and destroyed the inflammatory agent

Outcomes of acute inflammation: formation of an abscess

localized collection of pus surrounded by granulation tissue

Outcomes of acute inflammation: chronic inflammation

from a persisting insult

Outcomes of acute inflammation: fibrosis and scar formation

occurs in cases of significant inflammation

what's the best management of inflammation?

PREVENTION of infection, trauma, surgery, and contact with potentially harmful agents

why is adequate nutrition essential for inflammation?

bc for every degree your temp increases above your normal your metabolic rate increases by 7% which will increases your need for more calories
-high fluid intake will replace fluid loss from perspiration

RICE

rest, ice, compression, elevate
-used primarily for acute inflammation

How does a fever help the body fight infection?

-increased killing of microorganisms
-increased phagocytosis of neutrophils
-increased proliferation of T cells

what can happen if a patients fever is too high?

damage body cells and delirium/seizures can occur

drug therapy for fever

Antipyretics
-acetominophen
-NSAIDs
-salicylates

when should an antipyretic be considered?

if the patient is:
-really old/really young
-extremely uncomfortable
-has significant medical problems

when should an immunocompromised patient with a fever be treated with antibiotics?

immediately

When to give antipyretics?

give on a regular basis, not PRN

what is the last phase of the inflammatory response?

healing process

2 major components of the healing process

regeneration and repair

regeneration

replacing lost cells w the same cell type

the ability for cells to regenerate depends on the \____________

cell type

cell types with rapid regeneration

-skin
-lymphoid organs
-bone marrow

these cells divide constantly therefore \= rapid regeneration

cell types with slow regeneration

-liver
-pancreas
-kidney
-bone cells

only regenerate if the organ is damaged therefore \= slow regeneration

cell types with NO regeneration

-neurons of the CNS
-cardiac/skeletal muscles

they do not divide leading to permanent loss

Repair

replacing lost cells with connective tissue
-usually results in scar formation
-more common/complex than regeneration
-most injuries heal by connective tissue repair

Repair 3 intentions

-primary intention
-secondary intention
-tertiary intention

repair: Primary intention healing

wounds have been neatly approximated (minimal scaring)

3 phases of primary, secondary, and tertiary intention healing

1. initial
2. granulation \***
3. maturation

initial phase

inflammatory, 3-5 days, approximation of edges
-area fills with erythrocytes, fibrin, neutrophils, and platelets (clot serves as a meshwork for starting capillary growth)

granulation phase

5 days-4 weeks, granulation tissue of fibroblasts, WBC, exudate, capillary sprouts (angioblasts),

*risk for dehiscence*

maturation phase

7 days to several months/years
-remodeling of collagen fibers and strengthening of scar

Fibroblasts

immature connective tissue cells that migrate into the healing site and secrete collagen
-the collagen is then organized and restructured to strengthen the healing site (fibrous/scar tissue)

Secondary intention healing

heals from the bottom up and occurs from trauma, ulceration, or infection
-edges of the wound cannot be approximated
-inflammatory reaction may be greater than primary intention
-debridement may be appropriate before healing can take place
-the healing process is the same as primary except that healing in the granulation takes place from the edges inward and from the bottom of the wound upward leaving a larger scar

tertiary intention healing

occurs when delayed suturing of a wound is sutured together or when primary wound becomes infected
-contaminated wound is left open and sutured closed after the infection is controlled
-larger and deeper scar than primary or secondary intention

wound

a break or opening of the skin
-can range from minor to deep wounds like bones, blood vessels, and nerves

causes of wounds

surgical, non-surgical, acute, chronic

depth of wounds can be:

-superficial
-partial thickness
-full thickness
-skin tear

superficial wound

involves only the epidermis

partial thickness wound

wound extends into the dermis

full-thickness wound

involves the subcutaneous tissue and sometimes extends into the fascia and underlying structures of muscle, tendon, and bone (deepest layer)

skin tear wound

can be partial thickness or full thickness resulting in separation of skin layers, commonly seen in older adults/critically ill adults
-can be a shear tear or frictional tear

shear skin tear wound

opposite force has been applied to rip off layer

friction skin tear wound

rubbing of the skin

wound management

1. protecting a clean wound from trauma so that it can heal normally
2. cleaning a wound to remove any dirt and debris from the wound bed
3. treating infection to
prepare the wound for healing

factors delaying would healing

anything that can put you at risk

-advanced age
-anemia
-corticosteroid drugs
-diabetes mellitus
-inadequate blood supply
-infection
-mechanical friction on wound
-nutritional deficiency (vitamin C, Protein, Zinc)
-obesity
-poor general health
-smoking

complications of healing

-adhesions
-contractures
-dehiscence
-evisceration
-fistulas
-infection
-hemorrhage
-hypertrophic scars
-keloids

adhesion complication

bands of scar tissue that form between or around organs
-may occur in the abdominal cavity or between the lungs and the pleura
-those in the abdomen may cause an intestinal obstruction
-risk for separation

contractions complication

wound contraction is a normal part of healing but complications occur when excessive contraction results in deformity
-shortening of scar tissue, especially over joints, results from excessive fibrous tissue formation

deshiscence

separation of wound edges that usually occurs when a primary healing site bursts open and may be caused by:
-infection causing an inflammatory process
-granulation tissue not strong enough to withstand forces involved on wound
-obesity (bc adipose tissue has less blood supply and may slow healing)
-pocket of fluid (seroma, hematoma) developing between tissue layers and preventing the edges of the wound from coming together

fistula complication

an abnormal passage between organs or a hollow organ and skin (abdominal/perianal fistula)

infection complication

increased risk of infection when:
-wound contains necrotic tissue
-inadequate blood supply
-immunocompromised pt's (could be from immunosuppressive drugs)
-inadequate nutrition
-multiple stressors
-hyperglycemia in diabetes

hemorrhage complication

abnormal internal or external blood loss may be caused by:
-suture failure
-clotting abnormalities
-dislodged clot
-infection
-the erosion of a blood vessel by a foreign object (tubing/drains)

hypertophic scarring

hard, large, red, and raised scar that occurs when too much collagen is made during healing
-usually goes away

keloid scarring

a great protrusion of scar tissue that extends beyond wound edges and mat form tumor like masses of scar tissue( excessive collagen formation that goes beyond boundaries)
-dark-skinned people more prone
-patients often have tenderness, pain, and hyperparesthias in early stages
-permanent without any tendency to subside

evisceration of abdomen

laceration of abdominal wall, occurs when wound edges separate to the extent that intestines protrude through wound
-immediate surgical treatment

why do pressure injuries occur?

because of intense and/or prolonged pressure in combination w shear

ex: pulling the patient up in bed

risk factors for pressure injuries

-old age
-critically ill
-immobility
-peripheral vascular disease
-incontinence
-major trauma

common place for pressure injury to occur

-sacrum(most common)
-heals (2nd most common)
-elbows
-shoulder blades

pressure injury: stage 1

blancchable/non-blanchable erythema of intact skin
-intact skin with a localized area of non-blanchable erythema which may appear differently in dark skin

pressure injury: stage 2

partial-thickness skin loss w exposed dermis

pressure injury: stage 3

full-thickness skin loss w exposed adipose tissue
-adipose is visible in the injury
-granulation tissue and epibole (rolled wound edges) are often present
-slough and/or eschar (types of dead tissue) may be visible
-undermining and tunneling may occur

pressure injury: stage 4

full-thickness skin and tissue loss
-exposed or directly palpable fascia, muscle, tendon, ligament, cartilage, or bone in the injury
-slough and/or eschar may be visible
-epibole, undermining, and/or tunneling often occur

pressure injury: stage 5 (unstageable)

Obscured full-thickness skin and tissue loss
-extent of tissue damage within the injury cannot be confirmed bc it's obscured by slough or eschar
-stage 3 or 4 PI is present after removing slough or eschar
-stable eschar (dry, adherent, intact w/o erythema or fluctuance) on the heel or ischemic limb should not be softened or removed!!
-has necrotic tissue

deep tissue pressure injury

Persistent non-blanchable deep red, maroon, or purple discoloration
-stage 1 but purple

primary nursing responsibilities for PI

1. identifying patients at risk for developing a PI
2. implementing pressure injury prevention strategies for those who are at risk

\__________________ is the best treatment for pressure injuries

prevention