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Infection Control

Chapter 29

Infection- invasion and multiplication of microorganisms, results in injury


Colonization- invasion and multiplication of micro organisms without tissue injury
Normal Defense mechanism-
Immune system, skin, normal flora, mouth, respiratory tract, coughing, sneezing, urinary tract, GI tract,
vagina, urination, inflammation, sebum
Localized infection- area specific; redness, inflammation
Systemic infection- entire body, multiple organs, vomiting, sickness
4 stages of infection:
Incubation period- contagious, infection is multiplying
Prodromal stage- contagious, multiplying
Illness stage- sickness, symptoms
Convalescent stage- returning to previous state of health
Nosocomial infection- hospital acquired, multiple drug resistant organisms, compromised host easily get
infection
Pathogen- microorganism that produces disease
Virulence- the degree of pathogenicity of an finfectious microorganism
Anthropogenic- reflecting changes in the relationship between humans and environment
Etiologic agent- infectious agent, autoclaving killing infection, red bag material, removed and destroyed.
Chain of infection:
Agent- biological (bacteria, virus, fungi), chemical (pesticides, food additives, medications, industrial
chemicals), physical- (heat, light, noise, radiation, machinery)
Host- Susceptible host- lack resistance, vulnerable to disease, does not have pre-existing illness
Compromised host- immunodeficiency, pre existing illness
Reservoir-environment that allows the pathogen to multiply- ex bread, water, food on counter
Portal of entry- how it gets into person, ex skin, nose, mouth,
Portal of exit- needed to spread the disease- skin urinary, gi, reproductive, blood
Mode of transmission- how it moves from one person to another
Modes of transmission: bridges gap among chain of infection.
Contact- direct contact, close contact with secretions
Air-borne- droplets and dust, through the air
Vehicle-contaminated inanimate object infects host, ex food, h2o, milk, drugs, blood
Vector-borne- animals carrying disease ex. Mosquito, fleas, ticks
NANDA Statements
Risk for infection
Inadequate primary defense -ex skin
Inadequate secondary defense -ex acquired immunity, immunosuppression
environmental exposure
Chronic diseases and malnutrition
Invasive procedures and pharmaceutical agents
Insufficient knowledge
Implement
Surgical asepsis- eliminate microorganisms and spores
Surgical attire, technique
Sterile gloves, hand antisepsis
Isolation precautions- contact, droplet, airborne
Client education
Evaluation
Client free from infection
Planning outcome identification
Manipulate external environment to reduce risk of infection
Client and caregiver education

CHAPTER 37
Skin Integrity and Wound Healing

---Maintaining skin integrity is a primary responsibility of the nursing personnel---


Wounds may occur b/c
Trauma, Surgery, Prolonged pressure- immobility, Laceration, Irritation of skin
Skin- largest organ & primary defense
Wound- disruption in body tissue
Types of healing
Primary—minimal tissue loss, edges are well approximated ex. Surgical, paper cut
Secondary—extensive tissue loss, edges can not be approximated, wound left open, scaring greater
Tertiary—known as delayed or secondary closure, wound closed after all edema and debris removed
Defensive Phase:
Hemostasis- cessation of bleeding occurs by vasoconstriction and activation of platelets and clotting
cascade provide wound closure
Stages of the inflammatory process: p678
Stage 1—initial injury: release chemicals histamine, activates inflammation process
Stage 2—increase blood flow to injured area- erythema, redness and warmth
Stage 3—leakage of plasma, fibrogen clots formed, initiate inflammation process
Stage 4—produce purulent exudate
Stage 5—destroyed cells replaced, scar tissue forms
Remember in these steps-- Phagocytes leukocytes, vasodilatation=inflammation bringing P&L
Reconstructive phase
Collagen- replenish dead cells, elasticity of skin
Angiogenesis- formation of new blood vessels increases blood flow
Epithealization-growth of epithelial tissue begins
Maturation phase
Final stage of healing begins about the 21st day and continue for 2+yr
Scar tissue reconstructed by collagen
scar tissue weaker than tissue it replaces
white scar tissue due to lack of blood supply
Chemical mediators released during the inflammatory response
Functions of fluid released in tissues: dilution of toxins produced by bacteria, transport leukocytes and
plasma, transport debris away from site
Kinds of Wound Drainage:
Serous— serum- clear portion of blood, watery ex blisters after burn
Purulent— Pus- severe inflammation, may include infection, thicker due to leukocytes
Hemorrhagic— large RBC count
Debridement- cleaning out and scraping wound so it will begin to bleed and bring new blood to site for healing
medicate before performing procedure; in healthy individuals wounds natural defense keeps wound debride
Exception: do not debride dry, stable eschar on heel or toes w/o signs of edema or drainage b/c natural
barrier to infection
Hemorrhage: persistent bleeding
Hematoma: Bruise-localized collection of blood underneath the tissues aka. Ecchimosis
Dehiscence: partial or complete separation of the wound edges and layers below the skin caused by vomiting,
coughing, obesity, poor nutrition, suturing
Evisceration: clients viscera protrude through the disrupted wound
Table 37-1 p. 1212
Factors affecting wound healing
Age- older slower wound healing, old and young risk for infection
Nutrition- obesity decrease ability for blood vessels to deliver nutrients to site
Oxygenation- decrease o2 wounds heal slowly
Smoking- hemoglobin lvl decrease cause decrease o2
Drug therapy- steroids, anti-inflammatory, antibiotics superinfection risk
Diabetes mellitus- small vessels disease

Intentional Wounds- occurs during treatment ex surgical incisions and venipuncture


Unintentional wounds- unanticipated result of trauma or accident
Cleanliness of wound:
Clean wounds—intentional, no inflammation was created
Clean contaminated wounds—intentional created by entry into alimentary, respiratory, genitourinary,
oropharyngeal tract
Contaminated wounds—open traumatic wounds or intentional in which there was a break in aseptic
technique
Dirty and infected wounds—retained dead tissue or intentional wound created where drainage was
present
Table 37-2 nutrients that enhance wound healing
Amino acids- neovascularization, lymphocyte formation, fibroblast proliferation
Albumin- osmotic equlibrium, edema prevention
Carbs- cellular energy
Fats- cellular energy, cell membrane
Copper- collagen cross-linking
Iron- collagen synthesis
Zinc- cell proliferation
A- collagen synthesis and epithealization
Thiamine-antibody and WBC formation, cofactors of enzyme systems
C-resist infection, collagen synthesis, capillary formation
K- coagulation

Skin Loss:
Stage I- Superficial- epidermis, 1st degree, red skin
Stage II- Partial thickness- epidermis to dermis, 2ed degree ex. blister
Stage III- Full thickness- extends through epidermis, dermis, subq; 3ed degree
Stage IV-involves epidermis, dermis, subq, muscle and bone
The RYB wound classification: Assists nurse in assessing the wound color surface
Red wounds: color of normal wound, recent without infection need to be protected and kept moist and
clean
Yellow wounds- have fibrinous slough or purulent exudate from bacteria; needs to be cleaned to remove
pus and slough; irrigate and cover with wet to dry
Black wounds- gray or brown contain necrotic tissue (eschar- scab or dry crust results from skin death);
wounds need debridement
*Always treat the worst color first
Assessment
Health history
Allergies and Family History
Aggravating factors- touch move cough make it hurt
Alleviating factors- medication, holing stomach
Personal social history- chronic issues to require narcotics
Functional ability- to provide self care
Physical exam- any concurrent conditions assessed
Wound assessment- location, size, general appearance/ drainage, pain
Laboratory data- elevate WBC indicate infection; decreased leukocytes increased risk infection, albumin
decreased increased wound healing and culture of wound drainage presence of infection
Sinus tract and undermining- wound healing from outside in, common w/ puncture wounds
Planning outcomes: wound healing primary intention
Implementation:
Emergency measures- surgical repair and vitals, pressure stop bleeding
Cleanse wound- clean to dirty
Dress the wound- keep wound moist, keep it clean, protect from physical trauma or bacteria
Monitor drainage- penrose drains- function by gravity & closed suction drains reservoir creates negative
pressure
Suture care- check numbers to be removed
Bandages, binders, slings- secure, immobilize or support body part
Heat cold therapy- vasodialation and vasoconstriction- precautions: neurosensory impaired, impaired
mental status, impaired circulation; moist open wounds vs. dry for sprains and closed wounds
NANDA Statements
Impaired skin integrity
Risk for infection
Acute pain
Chronic pain
Disturbed body image
Deficient knowledge
Pressure ulcers- bed sores- decubitus ulcers
Caused by ischemia, common on boney prominences- sacrum, heels
Blanching- white color of skin, when pressure relieved skin remains red
Shearing- friction
Risk factors: immobility, inactivity, incontinence, malnutrition, decreased mental status,
diminished sensation, age related changes
Braden’s scale for pressure ulcer risk
Sensory perception, moisture, degree of physical activity, mobility, nutrition, friction
Vascular ulcers
Arterial ulcers- weak or absent pulses, thin skin, lack of hair
Neuropathic ulcers- diabetic ulcers

Dressing Guidelines chart page 1221


Transparent adhesive films- cover IV sites, easily viewed, body fluid can not enter
DuoDerm- ulcers, comfortable
Hydrogels- conform to wound bed sooothing and cooling ex. burns
Absorbers- wounds with moderate to large amounts of exudate 20x their weight absorbed
Foams- for minimal exudate
Lubricating sprays- moisturize wound and stimulate local circulation
Nonadherent dressings- skin donor sites, abrasions, tears, lacerations, full thickness
Gauze dressing- wounds with dead space tunneling or sinus tracts necrotic or exudate
Antibiotics
LILLY p 569-593

Gram positive- have cell wall with thicker constituent known as peptidoglycan- purple gram stain
Gram negative organisms harder to treat due to complex cell wall- red gram stain
Morphology- coccus, bacillus, coccobacillus, fusiform bacillus, spirillum, vibrio, spirochete
Signs and symptoms of infection: fever, chills, sweats, redness, pain, swelling, fatigue, weight loss, increase
WBC, formation of pus
Empiric therapy- when life threatening complications is high and micro-organism can not be identified yet after
cultures antibiotic is given immediately
Prophylactic antibiotic therapy- used to prevent infection when a procedure increases likelihood of dangerous
microbial contamination
Superinfection-caused when antibiotics reduce or completely eliminate the normal bacterial flora; bacteria or
fungi needed to maintain normal function of organs are eliminated. Ex yeast infection from antibiotics
Signs- fever, perineal itching, oral leasions, vaginal irritation, cough, lethargy
Green or yellow sputum is indicative of bacterial infection during a viral respiratory illness
Inappropriate antibiotic prescribing, patients not complete antibiotic regiment, cause antibiotic resistant
medication
Drug –drug interactions and drug- food interactions
Host factors- patient age, allergy history, kidney liver function, pregnancy, genetic characteristicts, defenses
Infants children- can not take tetracyclines b/c affect bone teeth growth
Penicillin and sulfonamides common allergies
Teratogens- drugs that cause development abnormalities and birth defects in the fetus b/c several
antibiotics can pass through the placenta
Genetic host factor- adverse effects b/c- Glucose-6-phosphate dehydrogenase deficiency and slow
acetylation , sulfonamides and nirtofunantoin to person w/ G6PD def may result in hemolysis
Bacteriostatic- inhibit growth of bacteria but not kill them
Bactericidal- directly kill bacteria
B-lactamases is one way bacteria can fend off the effects of antibiotics
Antibiotics interfere with
Bacteria cell wall synthesis, interference with protein synthesis, inference with replication of nucleic
acids DNA and RNA, antimetabolite action that disrupts critical metabolic reactions of cell

Category of antibiotics:
Sulfonamides- bacteriostatic- also antimetabolites, only organisms that syntise their own folic acid are
inhibited by sulfonamides.
B-Lactam- some bacterias enzymes can break the chem bond between carbon and nitrogen in b lactam
ring causing an ineffective antibiotic- b lactamase inhibitors increase effectiveness of antibiotics
4 classes of b lactam antibiotics, if patient is allergic to penicillin have 4fold risk of alergy to other b-
lactam antibiotics- cross sensitivity
Penicillins- bactericidal, inhibit cell wall synthesis
b-lactamases destroy penicillins- clavulanic acid, tazobactam, sulbactam
natural penicillin V&G- treat syphilis
penicillinase-resistant pen.- nafcillin- resist breakdown by penicillinase
broad spectrum- aminopenicillins- effective against gram negative
amoxicillin
ampicillin
extended spectrum penicillins- antipseudomonal- able to treat pseudomonas,
Cephalosporins- bacteriacidal, most widely used antibiotic,cross sensitivity with penicillin and
bind to penicillin binding proteins, not active against fungi or viruses, produced by a fungus,
gram -/+ variable on generation 1-4
Carbapenems- broadest antibacterial of any antibiotic to date
MonoBactams-aztreonam only 1, g- bact, e coli, klebsiella,psudomonas
Macrolides— erythromycin - bacteriostatic w/ high concentration bacteriocidal, affects
Gi motility, can benefit in pt. with decrease GI mobility, treat AIDS
To be used if pt. is allergic to penicillin
Ketolides--
Tetracyclines- bacteriostatic, binds to ca2+ mg2+ and al3+, can not be used 8yrs b/c tooth discoloration,
not to be used preg women and nursing mothers, differ from one another by: oral absorption, body tissue
penetration, half-life
Broad spectrum; inhibit protein synthesis
Treat syndrome of ineffective antidiruretic hormone, cause formation of necessary scar tissue in lungs

Nursing process relating to antibiotics:


Assessment
History of hypersensitivity, liver function, pt. age weight willingness to learn,
Sulfonamides- renal, skin, blood count assessment
Penicillins- hypersensitivity, neurologic, abdominal, bowel, electrolyte tests should be completed
Carbapenems- allergy to penicillin, neurologic funct, hearing values, Gi
Cephalosporins-
Tetracyclines-
Macrolides-

IMMUNITY CH 46 LILLY p.702

Immunity- specific resistance of the body to infection; protection from disease


Humoral immunity- specific
Antibody mediated defense; B- Lymphocytes
Antibodies produced by B-cells in body fluids
Form- Antibodies- Immunoglobulins
Released from plasma
Cell Mediated immunity- non specific response
T- Cell system- stimulate protective immune response ex. Release cytokines- nasal secretions
Exposure to antigen release large # activated T-cells into lymph to general circulation
Antigen: can stimulate antibody production, foreign to a host ex. Viruses and allergens
Antibody: protein molecule, combine with specific antigen resulting in agglutination, precipitation,
neutralization, increases susceptibility to phagocytosis, synthisized in humoral immune system
Primary immune response- first interaction between antigen and antibody
Types of immunity people develop:
Natural- inherited, genetics, born with it
Acquired- specific acquired after exposure to a disease agent
Active immunity- development long-lasting immunity; you produce your own antibodies in response to antigen
Active natural- chicken pox; antibodies formed in presence of infection
Active artificial- antigens in vaccines are given to stimulate antibody production
Passive immunity- produced by another source animal or human
Passive natural- mother gives antibodies through placenta; mothers milk to child antibodies lasts 4-8 mo
Passive artificial- antibodies produced in body of others given antibodies produced in body of other;
used when you need fast reaction ex snake bite, rabies, hepatitis, bypass own immune system
Nonspecific Immunity- T cells, stimulate cell mediated immunity,
Specific Immunity- B cells, humoral immunity antigen specific
Immunoglobulin- glycoproteins, used to kill all substances foreign to the body-non specific antibody
Always passive immunizing drugs
Immune response:
# of lymphocytes that react to antigen increase
Increase triggers production of antibodies that act to destroy antigen
Lymphoid tissue macrophages make antigen susceptible to attack
Memory lymphocytes
Allergic response
Allergic reaction- antibody antigen reaction due to release of histamine
Number of exposures vary not always sensitized
Fatigue, stress, infection contribute to allergic reactions
Allergens: substances cause allergic reaction
Inhalants- dust, feathers, pollen, hair
Contactants- dyes-hair, clothes, wool, nylon, cosmetics
Ingestants- eggs, seafood, nuts, chocolate
Drugs- ex. Penicillin
Treatment of allergies
Avoidance, modify behaviors, read labels, desensitizing treatment
Anaphylactic reaction: severe allergic reaction
Bronchospasm, labored breathing, edema of the larynx and pharynx, gi distress
Immunization
Active immunization- long lasting
Exposure to relatively harmless form of antigen, imprint memory, develop antibodies, toxoids
Passive immunization
Bypass immune system obtained from humans or animals, immunoglobulin, antitoxins, snake and spider
antivenins
Toxoids- artificial active immunity, detoxified with chemicals or heat, stimulate own immune system
Vaccines- suspension of live attenuated or killed microorganisms that stimulates antibody production
Herd immunity- entire community population (95%) or large portion of members immune to disease
Adverse effects- unexpeced, serious or unusual is reported to Vaccine adverse reporting system
Mild(fever, rash) to severe (anaphalactic and fever higher than 103F)
Side effects- expected
Serum Skickness— Symptoms usually do not develop until 7 - 21 days after the first dose of antiserum or
exposure to the medication. However, some people may develop symptoms in 1 - 3 days if they have previously
been exposed to the substance. after antiserum administration the immune system misidentifies a protein in
antiserum as a potentially harmful substance (antigen).
Antitoxin- antiserum against toxin, usually obtained from animals to give humans artificial passive immunity
ex tetanus immunoglobulin
Antivenin- antiserum against a venom (posion produced by an animal ex. Snake bite, spider bite
Nursing implications for immunizations:
Hx, med hx, allergies, pregnancy, previous reactions, contraindications
Don not give asprin to children, discomfort at injection site
Bioterrorism agents- certain areas at higher risk
Anthrax, smallpox, botulism
Immunizations interactions examples
Hep B interacts with other live vaccines
Meningococcal, pertussis and typhoid should not be given together b/c large endotoxin content
Active immunizing drugs:
Hep B virus vaccine- recombinant Dna technology, contraindicated for yeast sensitivity
Influenza virus vaccine- high risk groups should receive vaccine- elderly adolescents on asprin therapy,
health care workers,
Measles mumps and rubella- do not administer if egg or neomycin allergy or pregnant
Pneumococcal vaccine--
Polio vaccine
Rabies virus vaccine
Varicella virus vaccine (chicken pox)-
Diphtheria and tetanus toxoids-
Passive immunizing drugs:
Hep B immunoglobulin
Rh0D immunoglobulin- supress antibodies of negative blood person exposed to Rh+ blood
Rabies immunoglobulin
Tetanus immunoglobulin
Varicella-zoster immunoglobulin
Immunizations Nursing Process
Assessment
Diagnoses-
Risk for injury related to possible adverse effects of or allergic reactions to immunizing drug
Acute pain related to local and or systemic effects of the injection
Deficient knowledge related to use of immunizing drugs
Anxiety related to suspected risk of bioterrorism
Planning
Patient states adverse effects
Patient experiences minimal discomfort
Patient remains compliant with therapeutic regimen
Patient returns for follow up injections
Implementation
Check manufactures guidelines
Evaluation

OTHER NOTES:
Antifungal agents
Systemic mycotic infections
Superficial mycotic infections
Cutaneous infections
Retrovirus- replicate using reverse transcriptase RNA

Cytopathic Effect- refers to cellular degeneration due to viral entry and replication and usually results in cell
lysis
Viral Transformation- involves mutation of host genetic material that results in cancerous cells (oncogenic
viruses)

RESOURCES:
Fundamentals of Nursing 3rd edition, DeLaune
Pharmacology and the Nursing Process, 5th edition, Lilley, Harrington, Snyder