Transcript COPD - QStation

COPD
Eric J Milie, D.O.
Goals and Objectives
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Compare and contrast chronic bronchitis and
emphysema with regards to physical exam,
pathogenesis, and clinical history
Discuss treatment options for outpatient
management of COPD
Construct a plan for in hospital management
of a COPD exacerbation
Introduction
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Estimated to effect 32 million people in the
U.S.
Fourth leading cause of death in U.S.
Classic symptoms of chronic bronchitis
and/or emphysema
Triad now recognized as including asthma
Background
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Early 19th century Western Europe: Badham
and Laennec made the classic descriptions of
chronic bronchitis and emphysems
British medical textbook in 1860 described
chronic bronchitis as an advanced lung
disease with recurrent infections that ended
in right heart failure
Background continued
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Caused greater than 5% of all death in the
middle ages
More common among poor, attributed to “bad
living”
1958: Ciba symposium- proposed definitions
for both chronic bronchitis and emphysema,
encorporating spirometry and air flow
obstruction
Definition
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Disease state characterized by the presence
of airflow obstruction
Airflow obstruction progressive
Accompanied by airway hyper-reactivity,
May be partially reversible
Pathophysiology
Combination of 3 disease entities:
1. Chronic Bronchitis
2. Emphysema
3. To a lesser extent, asthma
Pathophysiology continued
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Increased number of polymorphonuclear
leukocytes and macrophages, which leads to
lung destruction
Oxygen free radicals from cigarette smoke
further damage lung tissue
Human leukocyte esterase primary offender
among inflammatory cytokines
Chronic Bronchitis
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Defined clinically as the presence of a
productive cough for three consecutive
months for two consecutive years
Characterized by excessive mucus
production with airway obstruction and
notable hyperplasia of mucus producing
glands
Chronic Bronchitis
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Damage to epithelium impairs response to bacteria
Inflammation and mucus provide obstruction
Body responds by decreasing ventilation and
increasing cardiac output
Hypercapnea and respiratory acidosis develop with
time
Lead to cor pulmonale and “blue bloater”
appearance
Chronic Bronchitis: Schematic
Chronic Bronchitis:
Bronchoscopy
Cor Pulmonale: EKG
Blue
Bloater
Emphysema: Three Subtypes
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Centriacinar: focal destruction limited to
respiratory bronchioles. Associated with
cigarette smoking
Panacinar: Involves entire alveolus, worst in
lower lung zones. Associated with alpha 1antitrypsin deficiency
Distal Acinar: Limited to fibrous septa, forms
bullae
Emphysema
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Gradual destruction of alveola and pulmonary
capillary bed
Results in decreased ability to keep blood
oxygenated
Body compensated with decreased cardiac output
and hyperventilation
Body tissue suffers from low cardiac output, develop
pulmonary cachexia
“Pink puffers”
Emphysema: Schematic
Pink
Puffer
Emphysematous Lung
Centriacinar Emphysema
Emphysema: Apical Bullae
COPD: Frequency
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In the U.S., between 14.2 million diagnosed
with COPD (estimated 32 million with
disease)
12.5 million diagnosed with Chronic
Bronchitis
1.7 with Emphysema
Since 1982, number of U.S. citizens
diagnosed with COPD increased by 41.5%
Frequency continued
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Researchers estimate prevalence of 8-17%
of men and 10-19% of women
Global initiative for Obstructive Lung Disease
(GOLD) estimates international prevalence
between 9-10% of adults over the age of 40
COPD: Morbidity and Mortality
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Absolute mortality rates for U.S.patients
between the ages of 55 and 80 were 200 per
100,000 males and 80 per 100,000 females
Mortality rate in women expected to increase
due to increased number of women smokers
Between 1979 and 1998, death rates
increased by 9% in men, 159% in women
COPD: Cost
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In 2004, cost to the nation in health care
dollars for COPD was approximately 37.2
billion dollars
20.9 billion in direct health care cost
7.4 billion in indirect morbidity cost
8.9 billion in indirect mortality cost
Risk Factors: Smoking
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Smoking is primary risk factor: 80-90% of all
COPD deaths are related to smoking
Female smokers 13 times more likely to die
of COPD than non-smokers
Male smokers 12 times more likely to die
than nonsmokers
Risk Factors: Other
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Air pollution
Second hand smoke
History of childhood respiratory infections
Heredity
Atopic patients
Alpha-1-antitrypsin deficiency
Occupational exposures (involved in 19% of COPD
cases, 31% of nonsmokers)
History
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Most present with combination of signs of
chronic bronchitis, emphysema, asthma
Worsening dyspnea
Progressive exercise intolerance
Altered mental status
History: Chronic Bronchitis
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Productive cough, with progression to
intermittent dyspnea
Frequent, recurrent pulmonary infections
Progressive cardiac/respiratory failure over
time
Edema
Weight gain
History: Emphysema
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Long history of progressive dyspnea
Late onset of nonproductive cough
Occasional mucopurulent relapses
Cachexia
Overt respiratory failure
Physical Exam: Chronic
Bronchitis
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Obese patient
Productive cough
Coarse breath sounds
Accessory muscle usage
Signs of right heart failure
Physical Exam: Emphysema
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Thin with barrel chest
Little cough
Pursed lip breathing
Hyperresonant chest, distant heart sounds
Wheezing
Clubbing of Digits
Pursed Lip Breathing
Nicotine Staining
Cyanotic Nails
Barrel Chest
Lab Studies: ABG
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ABG provides clues as to acuity and severity
Renal compensation almost always present,
usually with near-normal pH
pH below 7.3 sign of acute respiratory
compromise
Lab Studies: Serum
Chemistries
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Tend to be sodium retainers
Tend to have low potassium: diuretics,
theophylline, and beta-agonists all lower
serum K
Beta-agonists also enhance renal excretion
of magnesium and calcium
CBC may show polycythemia secondary to
cigarette smoking
Imaging Studies
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Chronic bronchitis: increased vascular
markings, cardiomegaly
Emphysema: hyperinflation, flat diaphragm,
small heart, possible bullous changes
Chronic Bronchitis: CXR
Emphysema: CXR
Emphysema: CXR and CT
Other Tests: Pulse Oximetry
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Not as accurate as ABG
No info on CO2
May precipitate iatrogenic CO2 narcosis if
used inappropriately
Other Tests: EKG
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Underlying cardiac disease likely
Need to determine if hypoxia causing
ischemia
Rule out cardiac as cause of shortness of
breath
PFT’s
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Decreased FEV1 with concomitant reduction
in FEV1/FVC ratio
Poor or absent reversibility with
bronchodilators
FVC normal or reduced
TLC normal or increased
Increased RV
Normal or reduced defusing capacity
Normal
Obstructive
GOLD Criteria
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FEV1/FVC <70%
FEV1 <80% post-bronchodilator
Severity Based on Spirometry
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Moderate: FEV1 <80% predicted
Severe: FEV1 <50% predicted
Very Severe: FEV1 <30% of predicted
Treatment: Improving Survival
Time
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Smoking cessation
Oxygen therapy
Lung Volume Reduction Surgery
Noninvasive mechanical ventilation in acute
exacerbation
Treatment: Symptom Improvement
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Pharmacotherapy
Pulmonary Rehab
Surgery
Smoking Cessation
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Most important component of COPD therapy
in smokers
Smoking cessation programs should involve
multiple interventions
Smoking cessation materials available at
http://www.surgeongeneral.gov/tobacco/defa
ult.htm
Pharmacotherapy:
Bronchodilators
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Alleviate symptoms of COPD
Improve exercise tolerance
Decrease number and severity of
exacerbations
Decrease lung hyperinflation in response to
increased respiratory demand
Elderly patients: difficulty with MDI
Proper Usage of MDI
Step 1: Shake inhaler and remove the cap as
instructed
Step 2: Hold the inhaler upright with the
mouthpiece at the bottom
Step 3: Tilt head back slightly, breathe out slowly
and completely
Step 4: Place the inhaler
2.5 cm (1 in.) to 5 cm (2
in.) in front of your open
mouth, without closing
your lips over it
Place the inhaler in your
mouth.
This method is easier for
most people and reduces
the risk that any of the
medication will get into
your eyes.
Step 5: Start breathing in slowly, evenly, and deeply,
and press down on the inhaler one time (inhale and
press).
Step 6: Hold your breath for 10 seconds. This will let
the medication settle in your lungs
Beta Agonists
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Increase cyclic adenosine monophosphate
levels
Promote smooth muscle relaxation in the
bronchioles
Available in short and long acting
preparations
Side effects include tachyarrhythmias and
hypokalemia
Short Acting Beta Agonists
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Work quickly to relieve shortness of breath
(15-20 minutes)
“Rescue agents”
Albuterol (Proventil® and Ventolin®) and
Metsproterenol (Alupent®) commonly used
Levalbuterol (Xopenex®) newer preparation,
less side effects of tachycardia
Long Acting Beta Agonists
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No immediate effect, last longer (12 hours)
Not to be used as rescue agent
Use on twice daily basis
Salmeterol (Serevent®) and Formeterol
(Foradil®) commonly used
Anticholnergics
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Effect muscarinic receptors
Slower onset of action but longer acting than
Albuterol
Ipratroprium (Atrovent®) used up to four
times daily
Tiotroprium (Spiriva®) revolutionizing COPD
treatment; once daily administration with
increased functional capacity and less
exacerbations
Spiriva®
Theophylline
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Increases cyclic adenosine monophosphate
levels
Induces smooth muscle relaxation
Improves respiratory drive, diaphragmatic
motion, and increases exercise tolerance
Limited by side effects: tachyarrhythmias,
seizures, nausea, vomiting
Corticosteroids
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Consider in patients who don’t improve on
bronchodilators
Several clinical trials failed to show benefit in
mild to moderate COPD
Large metanalysis showed decreased
symptoms, improved functional capacity in
patients with severe COPD
May be inhaled or systemic
Other Anti-Inflammatory
Agents
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Cromolyn (Intal®) and Nedocromil (Tilade®),
despite role in asthma, not indicated in COPD
Leukotriene inhibitors (Singulair®) data not
promising with regards to COPD
Antibiotics
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2/3 of COPD exacerbations infectious, 80%
bacterial
Accepted utility of antibiotics in the face of
COPD exacerbation
Outpatient treatment with Bactrim or
Doxyxyxline
Inpatient treatment more involved
Most Common Infectious Causes of COPD
Exacerbations
Mild to moderate exacerbations
Streptococcus pneumoniae
Haemophilus influenzae
Moraxella catarrhalis
Chlamydia pneumoniae
Mycoplasma pneumoniae
Viruses
Severe exacerbations
Pseudomonas species
Other gram-negative enteric
bacilli
Antibiotics Commonly Used in Patients with COPD Exacerbations
Mild to moderate exacerbations* Moderate to severe exacerbationsÝ
First-line antibiotics
Doxycycline (Vibramycin), 100 mg
twice daily
Trimethoprim-sulfamethoxazole
(Bactrim DS, Septra DS), one
tablet twice daily
Amoxicillin-clavulanate
potassium(Augmentin), one 500
mg/125 mg tablet three times daily
or one 875 mg/125 mg tablet twice
daily
Macrolides
Clarithromycin (Biaxin), 500 mg
twice daily
Azithromycin (Zithromax), 500 mg
initially, then 250 mg daily
Fluoroquinolones
Levofloxacin (Levaquin), 500 mg
daily
Gatifloxacin (Tequin), 400 mg daily
Moxifloxacin (Avelox), 400 mg daily
Cephalosporins
Ceftriaxone (Rocephin), 1 to 2 g IV
daily
Cefotaxime (Claforan), 1 g IV every 8
to 12 hours
Ceftazidime (Fortaz), 1 to 2 g IV every
8 to 12 hours
Antipseudomonal penicillins
Piperacillin-tazobactam(Zosyn), 3.375
g IV every
6 hours
Ticarcillin-clavulanate potassium
(Timentin), 3.1 g IV every 4 to 6 hours
Fluoroquinolones
Levofloxacin, 500 mg IV daily
Gatifloxacin, 400 mg IV daily
Aminoglycoside
Tobramycin (Tobrex), 1 mg per kg IV
every 8 to 12 hours, or 5 mg per kg IV
daily
Stepwise Approach to
Management
STEP 1 For mild, variable symptoms
Selective beta2-agonist MDI aerosol, 1-2 puffs q2-6h prn (not
to exceed 8-12 puffs/24 hr)
STEP 2 For mild to moderate, continuing symptoms
Long-acting beta2-agonist MDI aerosol, 1 puff bid OR
Long-acting anticholinergic, 1 capsule qd OR
Ipratropium bromide (Atrovent) MDI aerosol, 2-6 puffs q6-8h
(not to be used more frequently) PLUS
Selective beta2-agonist MDI aerosol, 1-4 puffs prn qid (for
rapid relief, when needed or as regular supplement)
Alternative: Combine a long-acting beta2-agonist MDI
aerosol, 1 puff bid, and a long-acting anticholinergic, 1
capsule qd
Continued
STEP 3 If response to step 2 is unsatisfactory or for a mild to
moderate increase in symptoms
Add a timed-release formulation of theophylline, 200-400 mg bid OR
400-800 mg hs for nocturnal bronchospasm
STEP 4 If control of symptoms is suboptimal or patient has frequent
exacerbations
Consider adding inhaled corticosteroids
STEP 5 For severe exacerbations
Increase beta2-agonist dose (eg, MDI with spacer, 4-6 puffs q1/2-2h;
inhalant solution, unit dose q1/2-2h)
Increase ipratropium dose (eg, MDI with spacer, 6-8 puffs q3-4h, or
inhalant solution of ipratropium, 0.5 mg q4-8h) AND
Provide methylprednisolone sodium succinate (A-Methapred, SoluMedrol) dose IV, giving 50-100 mg stat, then 40 mg q6-8h; taper as soon
as possible (treat for <2 wk) AND
Occasionally, consider giving theophylline dose IV with calculated
amount to bring serum level to 8-12 micrograms/mL
Add an antibiotic, if indicated
Oxygen Therapy
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Aside from smoking cessation, only intervention
shown to prolong life
1970: Barach and Petty recognized value of long
term oxygen in patients with severe COPD
Nocturnal Oxygen Therapy Trial and Medical
Research Council studies demonstrate long term
oxygen therapy extends life in hypoxemic COPD
patients and that survival benefit related to number
of hours on oxygen daily
Oxygen Therapy Continued
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Medical necessity must be completed
Indications are PaO2<55mmHg or
SPO2<88%
No survival benefit with PaO2<55mmHG
Delivery via nasal canula or CPAP (if
hypercapnic)
Oxygen-Hemoglobin
Dissociation Curve
CPAP: Whole Face Mask
CPAP: Nasal Pillows
CPAP: Chin Strap
Pulmonary Rehab
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American Thoracic Society: “a
multidisciplinary program of care for patients
with chronic respiratory impairment that is
individually tailored and designed to optimize
physical and social performance and
autonomy”
Controlled studies have shown significant
improvement in areas of exercise tolerance,
quality of life, decreased dyspnea, and fewer
hospitalizations
Surgery
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Surgical options last resort
Lung volume reduction and lung transplant
Clinical trials showed increase in FEV1 of
45% and decrease in residual volume by
25% at one year
One year mortality >10%
Pictured: the usual sites of the
small incisions used to
accomplish the thoracoscopic
approach to lung volume
reduction surgery. Diseased
lung tissue is removed to
restore lung elasticity and
improve the function of the
diaphragm muscle.
Acute Exacerbations
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Pharmacologic therapy initiated with same
agents used for day to day management
Rule out other sources of SOB (MI, CHF,
Pneumonia, PE)
Anticholinergics and beta agonists
administered with greater frequency via
nebulized route
AECOPD contnued
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Systemic corticosteroids should be added via
intravenous or intramuscular route
Appropriate antibiotic selection
Noninvasive mechanical ventilation (BiPAP or
CPAP) in patients who are hypercapnic, not
septic, and can participate in their own care
reduces ICU stays, hospital length, and
intubation rates
Intubation if indicated
Question 1
A fifty five year old white female presents to
your office with a chief complaint of shortness
of breath, getting progressively worse over
the past few months. On further questioning,
she admits to a productive cough for the last
few months, and notes a similar history over
the past three or four years. She smokes 2
packs of cigarettes daily. An ABG shows a
PAO2 of 60%, with a pulse oximetry reading
of 90% on room air.
Question 1 continued
Which of the following interventions will prolong
this patient’s life?
A. Beginning the patient on short acting betaagonist albuterol
B. Low flow oxygen via nasal canula
C. Smoking cessation
D. Introduction of theophylline
E. Tapered dose of prednisone
Question 2
The same patient comes back t the office for a
follow up visit four months later. She
continues to smoke. She’s complaining of a
cough today, productive for green sputum, as
well as fevers and chills. Her x-ray is
shown…
Question 2 continued
Which of the following antibiotic choices would
be appropriate in this patient?
A. Metronidazole 250mg PO TID for 14 days
B. Keflex 500mg PO QID for 10 days
C. Pen VK 250mg PO QID for 10 days
D. Trimethoprim/Sulfamethoxazole one tablet
POtwice daily for 10 days
E. Ciprofloxacin 250mg PO Bid for 10 days
Question 3
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Your patient responds well to the antibiotic
and improves clinically. Six months later, she
arrives in the emergency department short of
breath. She’s been off of her medicatins. She
continues to smoke. On exam, she’s
tachycardic with a blood pressure of 100/56.
Wheezes are noted bilaterally. The following
tests are procured in the emergency
department…
Question 3 continued
What is the appropriate next step in thie patient’s management?
A.
Inhaled beta agonists, intravenous corticosteroids,
supplemental oxygen, and intravenous theophylline for a
COPD exacerbation
B.
Intravenous levofloxacin 500mg daily for a right upperlobe
pneumonia
C.
Chest tube placement for spontaneous pneumothorax
secondary to a ruptured bleb
D.
Acute coronary syndrome protocol for acute inferior wall MI
E.
Intravenous loop diuretic for decompensated right sided heart
failure
F.
Intravenous heparin for a saddle-embolus