Concept: Inflammation
Review
•
•
•
Normal immune responses
o Nonspecific: inflammation
§ Cells: mast and phagocytic
§ Plasma protein systems: complement, kinin, & clotting
o Specific: lymphocytes (B-cell and T-cell mediated)
§ B-cell antibodies
§ Cytotoxic T-cells
Autoimmune disease
Hypersensitivity reactions
2
3
Arthritis
•
•
Arthritis: inflammation of joint(s)
o Most forms affect women more than men
Osteoarthritis (OA): slowly progressive noninflammatory disorder of the diarthrodial (synovial) joints
o Most common chronic joint condition
o Gradual loss of articular cartilage w/ formation of bony outgrowths (spurs or osteophytes) at
joint margins
o Factors: age, genetics, trauma to joint, biological differences (estrogen changes), obesity,
physical activity & occupational activity
o Development
Cartilage changes: becomes dull, yellow, granular
• Over time, becomes softer & less elastic
o Cartilage repair falls behind
§ Collagen structure changes further
• Articular surfaces become worn & cracked
• Joint edges thicken & osteophytes form
• Surfaces become uneven, affecting dist of stress across joint, causing reduced
motion
§ Bone cysts, outgrowth of bone, loss of cartilage
§ Inflammation is usually not typical
• Secondary synovitis may occur when phagocytes try to rid joint of small pieces of
cartilage torn from joint surface
Above changes cause early pain & stiffness of OA. Pain in later disease occurs when articular
cartilage is lost & bony joint surfaces rub against each other.
§
•
o Associated outcomes
§ S/S may be mild to significant
§ Pain: main symptom. Worsens w/ joint use,
relieved by rest
§ Stiffness: occurs after periods of rest or
unchanged position
• Early morning stiffness is common,
usually resolves w/i 30 min
o Distinguishes OA from
inflammatory joint disorders, such
as Ra
o Overactivity can cause mild joint
swelling, temporarily increasing
stiffness
• Crepitation: grating sensation caused by
loose cartilage particles in joint cavity
o Can also cause stiffness
o Common in pts w/ knee OA
§ Deformities
• Heberden’s nodes: occur on DIP joints
due to osteophyte formation & loss
of space
• Bouchard’s nodes: on PIP joints
indicate similar disease involvement
• Either are often red, swollen, &
tender
o Do not usually cause
significant loss of function
o Visible deformity may
bother pt
o Diagnosis
§ Bone scan, CT, MRI, x-ray
• Joint changes & bone thickening
§ Fatigue, fever, & organ involvement are NOT present. Important distinction between
OA & inflammatory joint disorders like RA
§ No labs or biomarkers for diagnosis
• Erythrocyte sedimentation rate (ESR) is normal, aside from slight increases
during acute inflammation
o Treatments
§ Pain management: acetaminophen, NSAIDs
§ Rest & joint protection
§ Heat & cold applications (heat = stiffness)
§ Nutritional therapy & exercise
§ Surgical interventions
Rheumatoid arthritis (RA): chronic, systemic, autoimmune disease chr by inflammation of connective
tissue in diarthrodial (synovial) joints
o Autoantibodies: rheumatoid factor (RF)
4
o Typically marked by periods of remission & exacerbation
o Often has extra-articular manifestations
o One of most disabling forms of arthritis
§ w/o adequate treatment, pt may need mobility aids or joint reconstruction. May have
loss of independence & self-care ability
o Disease process
5
Inflammation
• Rheumatoid synovitis: early pathologic change
o Synovium becomes inflamed
o Lymphocytes & plasma cells increase greatly
§ Pannus forms: articular cartilage destruction occurs over time, vascular granulation
tissue grows across cartilage surface (pannus) from edges of joint
• Joint surface shows loss of cartilage beneath extending pannus, most marked at
joint margins
§ Bone Destruction: inflammatory pannus causes focal destruction of bone
• Osteolytic destruction of bone occurs at joint edges, causing erosions seen on xrays
• Phase associated w/ joint deformity
o Clinical manifestations
§ Joints
• Subtle onset, nonspecific manifestations (fatigue, anorexia, weight loss,
generalized stiffness) can precede onset of joint symptoms
o Stiffness becomes more localized in following weeks to months
• Specific joint involvement marked by pain, stiffness, limited motion, & signs of
inflammation (heat, swelling, tenderness)
• Joint symptoms occur symmetrically & often affect small joints of hands (PIP &
MCP) & feet (MTP)
§
o Larger peripheral joints may be involved
§ EX: wrists, elbows, shoulders, knees, hips, ankles, & jaw
§
§
§
§
§
Stiffness
• Typical after periods of inactivity
• Morning stiffness may last 60 min to several hours or more, dep on disease
activity
MCP & PIP typically swollen
Early disease: fingers may become spindle shaped from synovial hypertrophy &
thickening of joint capsule. Joints are tender, painful, & warm.
Joint pain increases w/ motion
Extraarticular manifestations
• Sjogren’s syndrome: affects moistureproducing glands of eyes, sometimes
mouth. May have more widespread
effects
• Keratoconjunctivitis: inflammation of
sclera &/or cornea
• Episcleritis: inflammation of sclera
• Amyloidosis: build-up of amyloid protein
kidney
• Raynaud’s phenomenon: reduced blood
flow to extremities
o Blueish in appearance
• Felty syndrome: enlargement of spleen
• Rheumatoid nodules: fibrin ass nodules
that can develop t/o body, esp ass w/
body tissue
6
7
o Diagnostic studies
§ Positive RF in 80% of adults
§ Titers rise during active disease
§ ESR & CRP increased as general indicators of active inflammation
§ Synovial fluid analysis in early disease often shows slightly cloudy, straw-colored fluid w/
many fibrin flecks
• WBC count of synovial fluid increased
• Tissue biopsy can confirm inflammatory changes in synovial membrane
§ X-rays alone are not diagnostic of RA
• Early disease: may show only soft tissue swelling & possible bone
demineralization
• Later disease: narrowed joint space, articular cartilage destruction, erosion,
subluxation, & deformity
• Advanced disease: poor alignment & fusion
• Baseline x-rays may be used to monitor disease progression & treatment
effectiveness
• Bone scans more useful in detecting early joint changes & confirming diagnosis
so that treatment can be started
8
•
o Medical management (Lewis 64.9)
§ Nonsteroidal Anti-Inflammatory Drugs
• Ibuprofen: first-generation NSAID
• Celecoxib: COX-2 inhibitor
§ Corticosteroids: during disease flare
§ Disease-Modifying Antirheumatic Drugs (DMARDs)
• Methotrexate: immunosuppressant. 1st line therapy in early stages
• Etanercept: tumor necrosis factor antagonist
o Other management strategies
§ Heat & cold application – can be used several times a day
• Can help relieve stiffness, pain, & muscle spasm
• Ice useful during periods of increased disease activity
o Should not exceed 10-15 min at a time
• Heat can relieve stiffness to allow pt to take part in therapeutic exercise
o EX: heating pads, moist hot packs, paraffin baths, & earm baths or
showers
§ Sitting/standing in warm shower, sitting in tub w/ warm towels
around shoulders, or soaking hands in basin of warm water can
relieve joint stiffness to complete ADLs more comfortably
§ Weight management
§ Exercise
§ Rest & joint protection
§ Complementary & alternative therapies – herbal products, nutritional supplements,
acupuncture
§ Surgical: joint replacement
Impaired physical mobility
o Assistive devices – walkers, canes
o Exercise – safe practices to protect joints
o Heat & cold applications
o Analgesics
o Assistive devices for ADLs – long-hailed reacher, long-handled shoe horn
9
10
Inflammatory Bowel Disease Overview
•
•
•
•
•
•
•
Types: Crohn’s disease, ulcerative colitis
Genetics
o We have found over 200 genes ass w/ IBD
§ Auto-immune mediated disease process – many of these are related to body immune
function
o Certain genetic mutations ass w/ Crohn’s, others w/ UC, and many w/ both
Immune dysfunction -> inflammation
About 1.3 million Americans have IBD
Often begins during teenage years & early adulthood. Second peak 6th decade
Risks
o Greatest risk factor: family member with IBD
o Environmental factors (diet, smoking, stress) increase susceptibility by changing env of GI
microbial flora
o Dietary factors unique to industrialized countries may contribute to dev
§ High intake of refined sugar, total fats, polyunsaturated fatty acid (PUFA), & omega-6
fatty acids ass w/ increased risk for IBD
Cardinal signs
o Chron’s: abd pain, diarrhea (w/ or w/o gross bleeding), fatigue, weight loss
§ Small intestine may be involved = greater risk of nutrient malabsorption
o UC: bloody stools & dehydration
o Both: relapsing & remitting, may have triggers
§ Risks increase w/ severity of disease
11
12
•
Pattern of inflammation differs
o Chron’s
§ Can occur anywhere in GI from
mouth to rectum, but most often
involves distal ileum & proximal
colon
§ Skip lesions: segments of normal
bowel that can occur between
diseased portion
§ Inflammation involves all layers of
bowel wall, so microscopic leaks
can allow bowel conents to enter
peritoneal cavity & form
abscesses or produce peritonitis
§ Cobblestone appearance:
ulcerations usually deep,
longitudinal, & penetrate between
islands of inflamed edematous
mucosa
§ Strictures at areas of inflammation can cause bowel obstruction
§ Fistulas common during active disease
o UC: disease of colon & rectum
§ Usually starts in rectum, moves in continual fashion toward cecum
• Mild inflammation may occur in terminal ileum
§ Inflammation occurs in mucosal layer (innermost layer of bowel wall)
• Fistulas & abscesses are rare b/c it doesn’t extend thru all the layers
§ Water & electrolytes not absorbed thru inflamed mucosa
• Diarrhea w/ large F/E loss common
§ Protein loss thru stool from breakdown of cells
•
•
•
•
13
Pseudopolyps: tongue-like projections into bowel lumen formed by areas of inflamed
mucosa
Extra-intestinal manifestations & risks
o Systemic vs. GI complications
§ Hemorrhage
§ Strictures
§ Perforation w/ possible peritonitis
§ Abscesses
§ Fistulas
§ Toxic megacolon (colonic dilation)
o Systemic (inflammatory-related) diseases
often occur during exacerbations
o Other IBD-related diseases tied to
malabsorption issues
o Cancer screening at regular intervals
§ Increased colorectal cancer risk
§ Chron’s: increased risk for small
intestinal cancer
UC clinical manifestations
o Primary: bloody diarrhea & abd pain
§ Pain may vary from mild lower abd
cramping ass w/ diarrhea to severe,
constant pain ass w/ perforations
o Mild disease: diarrhea may consist of 4 or
less semi-formed stools daily w/ small
amounts of blood
§ Pt may have no other manifestations
o Moderate: increased stool output (up to
10/day), increased bleeding
§ Systemic symptoms: fever, malaise, mild anemia, anorexia
o Severe: diarrhea is bloody, contains mucus, 10-20/day
§ Fever, rapid weight loss (greater than 10% of total body weight), anemia, tachycardia,
dehydration
Chron’s clinical manifestations
o Diarrhea & cramping abd pain
o Small intestine involved? Weight loss.
§ Inflammation causing malabsorption
o Rectal bleeding sometimes, not as often as w/ UC
Diagnosis
o Symptoms: abdominal pain, cramping, fatigue, frequent liquid stools, may be bloody, mucusy
o Labs
§ Serum
• Non-specific inflammation: Elevated c-reactive protein, elevated ESR
• Anemia
o B12 & folate deficiencies due to malabsorption
o Iron deficiency due to bleeding
§ CBC
§
•
•
High WBC count may be sign of toxic megacolon or perforation
Hypoalbuminemia present w/ severe disease because of poor nutrition or
protein loss.
14
Increased erythrocyte sedimentation rate, C-reactive protein, & WBCs reflect inflammation.
•
Decreased serum sodium, potassium, chloride, bicarbonate, magnesium levels
o F/E losses from diarrhea & vomiting
§ Stool examined for blood, pus, & mucus. Cultures can determine if infection is present
§ Decreased serum sodium, potassium, chloride, bicarbonate, magnesium levels
• F/E losses from diarrhea & vomiting
o MRI of bowel with contrast
§ NPO Q8H
§ Administer glucagon IV to slow gut motility
§ Ingest contrast medium
o Endoscopy, biopsy if needed
§ Or small bowel imaging for suspected Chron’s
• Much of small bowel not accessible by direct endoscopic visualization, also
demonstrates disease distribution and extent.
Pathognomonic finding of UC is presence of continuous
colonic inflammation chr by erythema, loss of normal
vascular pattern, granularity, erosions, friability,
bleeding, and ulcerations, w/ clear distinct demarcation
between inflamed and non-inflamed bowel.
Dominant endoscopic feature in Crohn’s is presence of
ulcerations.
•
Fistula: erosion
o Risk mainly w/ Chron’s disease due to
transmural involvement
o May require surgical repair
o Management of enterocutaneous fistula
drainage
o Enterocutaneous fistula: bowel has
adhered to abd wall, erosion
communicating w/ outside
o Enteroenteric fistula: communication
between 2 sections of bowel b/c they
become adhered together thru tissue
changes & erosion in wall
§ Can result in dilated or perforated
bowel
Treatment of IBD
•
•
•
No cure. Treatment relies on drugs to treat
inflammation & maintain remission
o Drugs preferred treatment for Chron’s bc
recurrence rate is high after surgical
treatment
o Hospitalization needed if pt doesn’t
respond to drug therapy, disease is
severe, or complications are suspected
Goals
o Decreased number of diarrhea stools
o Maintain body weight
o Maintain nutrition & hydration
o Pain relief
Approaches
o Rest bowel
o Control inflammation
o Combat infection
15
16
•
•
•
o Correct malnutrition
o Provide symptomatic relief
o Improve quality of life
Long-term management concerns
o Exacerbation/remission cycles
o Diet and nutrition
§ Malabsorption, vitamin deficiencies
§ Eating ® worse pain ® anorexia, weight loss, malnutrition, dehydration
§ Ongoing diarrhea ® dehydration, blood loss
o Surgery: bowel diversion ostomy
§ Total colectomy eliminates bowel symptoms of UC
Nutritional approaches
o Goals
§ Provide adequate nutrition w/o worsening symptoms
§ Correct & prevent malnutrition
§ Replace F/E losses
§ Prevent weight loss.
o Dietary guidelines
§ Small, frequent meals
§ Low fiber
§ Lean protein
§ Refined grains
o During acute exacerbation, pts may not be able to tolerate regular diet
o Liquid enteral feedings preferred over PN b/c atrophy of gut & bacterial overgrowth occur
when GI tract not used
o EN is high in calories & nutrients, lactose-free, easily absorbed. Help achieve remissions &
improve nutritional status
o Supplement selected usually based on clinician preference, pt tolerance, availability, & cost
Drug therapy
o Choice dep on location & severity of inflammation
o Pts treated w/ either step-up or step-down approach
§ Step-up: pt w/ mild symptoms begins w/ amin salicylate or antimicrobial & adds a more
toxic medication (e.g., biologic therapies) when initial therapies do not work
• 5-aminosalicylic acid (5-ASA): mainstay to achieve & maintain remission,
prevent flare-ups
§
•
Step-down: uses immunosuppressant & biologic therapy first
17
Surgical therapy
o Indications for surgery for UC: see table below
§ Procedures used include
• Total proctocolectomy w/ ileal pouch/anal anastomosis (IPAA)
o Most common procedure for UC
o Initially: may have 4-6+ stools/day
§ Adaptation over next 3-6 mos will result in fewer BMs
o Pt can control defecation at anal sphincter
• Total proctocolectomy w/ permanent ileostomy.
Since UC affects only the colon, a total proctocolectomy is curative.
o Indications for surgery for Crohn’s - complications such as strictures, obstructions, bleeding, &
fistula
§ Most pts with Crohn’s eventually need surgery
§ Most common surgery involves resecting diseased segments w/ reanastomosis of the
remaining intestine
• Disease often recurs at anastomosis site
o Repeated removal of sections of the small intestine can lead to short bowel syndrome
§ Short bowel syndrome (SBS): either surgery or disease leaves too little small intestine
surface area to maintain normal nutrition and hydration
• Lifetime fluid boluses and parenteral nutrition (PN) may be needed
o Strictureplasty: opens narrowed areas obstructing bowel
§ Intestine stays intact.
§ Risk for short-bowel syndrome & associated complications reduced
§ Recurrences at site are uncommon
18
•
Ileostomy & colostomy
o Output initially liquid, becomes thicker/pasty/semi-formed over time, dep on location of stoma
o Management
§ Assess regularly, record bleeding, excess drainage, unusual odor. Color every 4 hr
§ Complications: delayed wound healing, hemorrhage, fistulas, infections
§ Color should be rosy pink to red, mildly swollen
• Dusky blue – ischemia
• Brown-black – necrosis
§ Excess gas common for first 2 weeks
§ First 24-48, drainage from ileostomy may be negligible
• Peristalsis returns – may be as high as 1500 – 1800 mL/hr
• May be greater if small bowel shortened by surgery
o Lost absorptive functions provided by colon & delay provided by ileocecal
valves
§ Should thicken to paste-like consistency, volume decrease to ~500 mL/day
§ Pt’s w/ chron’s are risk for dev bowel obstruction during first 30 post-op days
§ Colostomy starts functioning when peristalsis returns
§ Ileostomy
• Regularity not possible, should wear drainable pouch. Lasts 4-7 days
• Increase fluid intake to 2-3+ L/day when losing excess fluid from heat/sweat.
May need to ingest extra sodium.
•
•
•
•
Susceptible to obstruction b/c lumen less than 1 inch in diameter, may narrow
further where bowel passes thru fascia/muscle layer of abd
Chew food well before swallowing! (nuts, popcorn, mushrooms, olives, dried
fruits, stringy veggies, coconut, food with skins, meats w/ casings, etc.)
19
o Risks
§ Peristomal skin breakdown
o Preventing skin
breakdown
§ Skin barrier:
powder, adhesive
§ Cut adhesive
barrier to fit
stoma, cover all skin
• Body image disturbance
• Self-care deficit: resistance to learning self-care
• Altered relationships
• Social isolation – embarrassment
§ Well-maintained ostomy should not smell bad. If it smells, there’s a leak.
Toxic megacolon: colonic dilation r/t IBD, involves inhibited smooth muscle tone
o Suspect in pts w/ abd distention & diarrhea
o Risk factors: hypokalemia, antimotility agents, opiates, anticholinergics, antidepressants, abrupt
cessation of glucocorticoids, barium enemas, & colonoscopy/bowel preparation
o Diagnosis based on clinical signs of systemic toxicity combined w/ radiographic evidence of
colonic dilatation (diameter >6 cm)
§ Criteria
• Radiographic evidence of colonic dilation (diameter >6 cm)
• PLUS at least three of the following:
o Fever >38ºC
o Heart rate >120 beats/min
o Neutrophilic leukocytosis >10,500/microL
o Anemia
• PLUS at least one of the following:
o Dehydration
o Altered sensorium
o Electrolyte disturbances
o Hypotension
o Treat: bedrest, gut rest (parenteral feeding), systemic management of relate pathos
(antibiotics, anti-inflammatory drugs)
o Absolute indications for surgery at any time
§ Frank intraperitoneal perforation
§ Life-threatening hemorrhage or increasing transfusion requirements
§ Worsening systemic toxicity
§ Worsening colonic dilatation
§
Nursing implications
o Acute phase
§ Hemodynamic stability
20
§ Pain control
§ F/E balance
§ Nutritional support
o Assessment findings
§ Objective Data
• General: Intermittent fever, emaciated appearance, fatigue
• Integumentary: pale skin w/ poor turgor, dry mucous membranes. Skin lesions,
anorectal irritation, skin tags, cutaneous fistulas
• Gastrointestinal: abd distention, hyperactive bowel sounds, abd cramps
• Cardiovascular: tachycardia, hypotension
• Possible diagnostic findings: Anemia, leukocytosis. Electrolyte imbalance,
hypoalbuminemia, vitamin, & trace metal deficiencies. Guaiac-positive stool.
Abnormal sigmoidoscopy, colonoscopy, & /or barium enema findings
Concept: Gas Exchange
Gas Exchange: Peds Considerations
•
•
•
•
•
Difference from adults
o Smaller airways
o Less developed muscles
o Lung capacity less
o Decreased alveoli surface
o Large obstructive tongue
o Life experience
Upper airway
o Tongue much bigger
o Large occiput
o Size matters
o Obligate nose breathers
Protecting airway for gas
exchange
o Suction
o Positioning
o Coughing
o Reduce swelling?
Weaker muscles
o Compensation
mechanism
o Tired
o Chest shape
o Barrel chest
o Pectus excavartum
Lung sounds
o Resonating sounds
o Inspiratory
o Expiratory
o Wheezing
o Stridor
21
•
o Nothing
Assessing child
o Methods: slowly, cross room,
w/ parents
o VS, compensation, cap refill, RR
Asthma
•
•
•
•
•
•
Asthma: chronic inflammatory disorder chr by wheezing, breathlessness, chest tightness, & cough
o Most common chronic disease in children, primary cause of school absence
o Any age
§ 80% aged 4-5 yrs
§ Multiracial
§ Black
§ Male
§ Genetics
o Eczema & GERD
Triggers
o Allergens
o Exercise
o Nose & sinus issues
o Resp infections
o Cigarette smoke
o Food additives
Allergic response: histamine response, increased mucous,
inflammation
Diagnosis
o Frequency
o Treatments
o Triggers
o Severity
Assessment
o Position of comfort
o Keep parent near
o Look then listen
Initial plan of care
o Bronchodilators?
o Steroids?
o Beta Agonists?
o Chest Xray?
22
o Oxygen?
o IV fluids?
•
•
Drugs
o Albuterol
o Atrovent
o Prednisone / Prednisolone
o Aminophylline / Theophylline
How to dose
o Nebulizer
o Inhaler MDI
o Disk DPI
o IV Fluids?
23
•
•
•
•
Side effects & pt care
o Weakness
o HR
o Lung sounds
o Shaking
o Re-evaluate
Nursing diagnosis
o Impaired breathing
o Activity intolerance
o Anxiety
o Lack of knowledge
Bedside teaching
o MDI Use
o MDI doses #
available
o Action plan
o Position of comfort
Health promotion
o Action plan
o Trigger identification
o Obesity
o Activity
o Fluid intake
o Planning
o PCP & follow-up
24
25
Bronchiolitis
•
•
•
•
•
•
•
•
•
Causes
o Viral
§ RSV
§ Influenza?
o Super imposed infections
§ Ear infections
§ Pneumonia
Symptoms
o Runny/stuffy nose
o Cough
o Slight fever – not always
present
o Shortness of breath
Clinical manifestations
o Increased WOB
o SOB
o Wheezing
o Lots of snot
o Lung sounds
§ Wheezing
§ Wet/moist
§ Upper airway
Assessment
o Across room: RR
o Listen to lung sounds
o Cap refill
o HR
Treatment
o Fever: Tylenol or motrin
o Respiratory distress
§ Albuterol?
§ Atrovent?
§ Oxygen?
• Blow by
• Nasal Cannula
• Non-rebreather
• High flow
• Intubation
Drugs
o Viral: no antibiotics, antivirals!
o Comfort care: Tylenol or motrin
Pt care: comfort, fluids, oxygen
Oxygen titration: RR, SaO2
High flow O2
o Empty space
•
•
o That first breath
§ Percentage
§ Flow
Nursing diagnosis
o Ineffective airway clearance
o Sleep Deprivation
o Fluid volume deficit
Health promotion
o Immunizations
o Handwashing
o Social Distancing!!!
o Expectations of disease process
26
Atelectasis
•
•
•
•
•
•
•
•
•
Atelectasis: alveola collapse
Causes:
o Mucous
o Infection
o Surface tension-surfactant-surgery
o Surface tension –trauma-air in
o Foreign body
o Tumor
Few alveola filled with fluid? PNEUMONIA
Large areas of alveola collapse? PNEUMOTHORAX
Nursing interventions to prevent
o Coughing
o IS
o Deep breathing
o Ambulation
Manifestations
o Shortness of breath
o Chest pain
o Cough
o Rapid breathing
Interventions
o Deep breathes
o Ambulation
o Incentive spirometry
o Monitor for infection
Diagnosis
o Chest Xray
o Pulse Ox
o Bronchoscopy
Treatment
o Coughing etc
§ Percussion
o Antibiotics-infection
o Chest tube
o CPAP: increased pressure forces alveolar open
27
Pneumonia
•
•
•
•
•
•
•
•
•
Pneumonia: infection in the lung
Presents as a cough or sepsis and everything in between
Causes
o Viral
§ Flu, COVID
o Bacterial
§ Streptococcus, mycoplasma
o Fungal
§ Chronic
o Aspiration
Risk factors
o Age- Old and young
o Smoking
o Chronic disease
o Immune system issues
Complications
o Empyema
o Pleural effusion
o Bacteremia
Manifestations
o Cough
o Shortness of breath
o Chest pains
o Nausea
o Fatigue
o Confusion-Why
o Temperature High or Low
Diagnosis
o Chest Xray
o Blood culture
o Pulse oximetry
o Sputum culture
o Pleural fluid culture
Treatment
o Antibiotics
o Cough suppressants
o Expectorants
o Oxygen
o Intubation
o Support
Prevention
o Incentive spirometry
o Cough/deep breath
o Fever/pain meds
o Immunizations!
28
Chronic Obstructive Pulmonary Disease
•
•
•
•
•
29
Prevention
COPD: persistent airflow limitation
o Chronic bronchitis: cough & sputum production for at least 3 months in each of 2 consecutive
years.
o Emphysema: destruction of alveoli w/o fibrosis
Risks
o Cigarette smoking
o Occupational chemicals and
dusts
o Infection
o Asthma
o Air pollution
o Aging
o Genetics
o Alpha-1 Antitrypsin
Deficiency
S/S
o Slow and progressive
o Chronic cough or sputum production
o Dyspnea, usually w/ exertion
o Chest heaviness
o Air hunger
o Shortness of breath at rest (late)
o Flatten diaphragm
o Chest breather - relying on the intercostal and accessory muscles
o Wheezing
o Chest tightness
o Fatigue
o Weight loss
o Anorexia
o Decreased breath sounds and/or wheezes lung fields
o “Barrel chest” - from the chronic air trapping
o Tripod position
o Naturally purse lips on expiration & use accessory muscles
o Hypoxemia: PaO2 < 60 mm Hg or O2 saturation < 88% on room air
o Hypercapnia: PaCO2 > 45 mm Hg
o Bluish-red color of the skin results from polycythemia and cyanosis.
o Abnormal hemoglobin
Treatment/management
o Avoid smoke-filled rooms & air pollutants
o Influenza immunization yearly
o Pneumococcal vaccine for all smokers ages 19+ & all patients w/ COPD
o Smoking cessation
o Drug therapy (inhaled route)
o Surgery
o Oxygen therapy
o Breathing retraining
o Airway clearance techniques
o Nutritional therapy
30