COPD Guidline in MMH
1. Admission criteria
Indications for Hospital Assessmentor Admission for Exacerbations of
COPD*
• Worsening symptoms & sign then general condition,
such as sudden development of resting dyspnea
• Underlying condition  Stage 3
• New physical findings, eg. Cyanosis, lower legs edema.
• Poor response to initial management.
• Other severe comorbidities.
• New arrythmia.
• Diagnostic uncertainty..
• Older age.
• Insufficient home support.
2. ICU admission criteria
Indications for ICU Admission of Patients with Exacerbations of COPD*
• Respiration distress:
Severe dyspnea that responds inadequately to initial emergency
therapy.
• CNS depression: (most important sign of severe excerbation)
Confusion, lethargy, coma.
• ABG abnormality:
- Persistent or worsening hypoxemia (PaO 2 < 50 mm Hg#), and/or
- Severe/worsening hypercapnia (PaCO 2 > 70 mm Hg#), and/or
- Severe/worsening respiratory acidosis (pH < 7.30#)
despite supplemental oxygen and NIPPV.
#
Post local modification by Taiwain chest association
On Duty Dr. for MANAGE EXACERBATIONS
A. History:
Key Indicators for Considering a Diagnosis of COPD
Chronic cough: Present intermittently or every day.
Often present throughout the day;
Seldom only nocturnal.
Chronic sputum production: Any pattern of chronic sputum production
may indicate COPD.
Dyspnea that is: Progressive (worsens over time).
Persistent (present every day).
Described by the patient as an
“increased effort to breathe,”
“heavi-ness,” “air hunger,” or “gasping.”
Worse on exercise.
Worse during respiratory infections.
History of exposure to risk factors, especially:
Tobacco smoke.
Occupational dusts and chemicals.
Smoke from home cooking and heating fuels.
Spirometry is needed to establish a diagnosis of COPD
A detailed medical history of a new patient known or thought to have
COPD should assess:
• Patient’s exposure to risk factors
a. Smoking
b. Occupational
c. Environmental exposures
d. Family history
Host Factors
Exposures
Risk Factors for COPD
• The major environmental factors are tobacco
• Genes (e.g., alpha-1 antitrypsin deficiency)
• Airway Hyperresponsiveness
• Lung Growth
•Tobacco Smoke
• Occupational Dusts & Chemicals
• Indoor and Outdoor Air Pollution
• Infections
• Socioeconomic Status
• Past medical history
including asthma, allergy, sinusitis or nasal polyps, respiratory
infections in childhood, other respiratory diseases
.
• Family history of COPD or other chronic respiratory disease
• Pattern of symptom development & exacerbation
(COPD typically develops in adult life &
Most patients are conscious of increased breathlessness &
More frequent “winter colds,” & some social restriction
for a number of years before seeking medical help.)
• Collect the message and make a differential diagnosis
• History of exacerbations or previous hospitalizations for respiratory
disorder
a. What’s the symptoms?
b. What’s the diagnosis?
c. How to relieve it?
d. Does it need oxygen, intubation or mechanical ventilation?, (Patients
may be aware of periodic worsening of symptoms even if these
episodes have
not been identified as exacerbations of COPD.)
• Presence of comorbidities
such as heart disease and rheumatic disease, which may also contribute
to restriction of activity.
• Appropriateness of current medical treatments
eg. beta-blockers commonly prescribed for heart disease are
usually contraindicated in COPD.
• Impact of disease on patient’s life:
including limitation of activity &
Missed work and economic impact &
Effect on family routines
Feelings of depression or anxiety.
• Social and family support available to the patient
• Possibilities for reducing risk factors
esp. smoking cessation.
Medical history of a patient known have COPD should assess beside
above:
• General condition of symptoms
• Usual medication, usage, dosage, frequency
• Previous data of Arterial blood gas & pulmonary function test
• Recent symptoms change, any new symptoms
• Previous hospitalization, intubation, mechanical ventilation
Classification of Severity of COPD
Stage
Characteristics
0: At Risk
• normal spirometry
• chronic symptoms (cough, sputum production)
I: Mild COPD
• FEV 1 /FVC < 70%
• FEV 1  80% predicted
• With or without chronic symptoms(cough,
sputum production)
II: Moderate COPD
• FEV 1 /FVC < 70%
• 50% ≤ FEV 1 < 80% predicted
• with or without chronic symptoms (cough,
sputum production)
III: Severe COPD
• FEV 1 /FVC < 70%
• 30% ≤ FEV 1 < 50% predicted
• With or without chronic symptoms(cough,
sputum production)
IV: Very Severe COPD
• FEV 1 /FVC < 70%
• FEV 1 ≤ 30% predicted or
FEV 1 < 50% predicted plus chronic
respiratory failure
More detail in Medical history
Symptoms
1. Cough
- D.D.
Causes of Chronic Cough with a Normal Chest X-ray
Intrathoracic
• Chronic obstructive pulmonary disease
• Bronchial asthma
• Central bronchial carcinoma
• Endobronchial tuberculosis
• Bronchiectasis
• Left heart failure
• Interstitial lung disease
• Cystic fibrosis
Extrathoracic
• Postnasal drip
• Gastroesophageal reflux
• Drug therapy (e.g., ACE inhibitors)
2. Sputum production
( Sputum production is often difficult to evaluate because patients
may swallow sputum
rather than expectorate it. )
3. Dyspnea
a. Hallmark symptom of COPD,
b. reason most patients seek medical attention
c. major cause of disability and anxiety associated with the disease.
d. As a sense of increased effort to breathe, heaviness, air hunger, or
gasping4.
4. Assessment of symptoms worsening
Differential Diagnosis
Differential Diagnosis of COPD
Diagnosis
Suggestive Features*
COPD
Onset in mid-life.
Symptoms slowly progressive.
Long smoking history.
Dyspnea during exercise.
Largely irreversible airflow limitation.
Asthma
Onset early in life (often childhood).
Symptoms vary from day to day.
Symptoms at night/early morning.
Allergy, rhinitis, and/or eczema also present.
Family history of asthma.
Largely reversible airflow limitation.
Congestive
Fine basilar crackles on auscultation.
Heart Failure Chest X-ray shows dilated heart, pulmonary edema.
PFT: indicate volume restriction, not airflow limitation.
Bronchiectasis Large volumes of purulent sputum.
Commonly associated with bacterial infection.
Coarse crackles/clubbing on auscultation.
X-ray/CT: Bronchial dilation, bronchial wall thickening.
Tuberculosis Onset all ages.
Chest X-ray shows lung infiltrate.
Microbiological confirmation.
High local prevalence of tuberculosis.
Bronchiolitis May have Hx of rheumatoid arthritis or fume exposure.
CT on expiration shows hypodense areas.
Panbronchiolitis Smokers.
Almost all have chronic sinusitis.
X-ray & HRCT: Diffuse small centrilobular nodular
Opacities & hyperinflation.
( *These features tend to be characteristic of the respective diseases, but do not occur in every case. For example, - a person who
has never smoked may develop COPD (especially in the developing world, where other risk factors may be more important
than cigarette smoking); - asthma may develop in adult and even elderly patients.)
Etiology of exacerbation
Primary
Secondary
Common Causes of Exacerbations of COPD
• Tracheobronchial infection.
• Air pollution.
• Pneumonia.
• Pulmonary embolism.
• Pneumothorax.
• Rib fractures/chest trauma.
• Inappropriate use of sedatives,narcotics,
-blocking.
• Right and/or left heart failure or arrhythmias.
1. 1st causes of an exacerbation are infection of the tracheobronchial tree
&
air pollution,
2. But the cause of about 1/3 of severe exacerbations cannot be identified
(Evidence B).
3. Bacterial infections, once believed to be the main cause of COPD
exacerbations, is controversial.
B. Physical Examination
General appearance
• Consciousness level & content
• Vital sign: BP, RR, HR, BT
Inspection.
• Central cyanosis,
or bluish discoloration of the mucosal membranes, may be(+)
but is difficult to detect in artificial light and in many racial groups.
• Pursed-lip breathing,
which may serve to slow expiratory flow & permit more efficient lung
emptying.
• Common chest wall abnormalities,
which reflect the pulmonary hyperinflation seen in COPD, include
- horizontal ribs,
- “barrel- shaped” chest, &
- protrudingabdomen.
• Flattening of the hemidiaphragms may be associated with
- Paradoxical indrawing of the lower rib cage on inspiration,
- Reduced cardiac dullness &
- Widening xiphisternal angle.
• Resting respiratory rate is often increased to
- > 20 breaths per minute &
- Breathing can be relatively shallow12
.
• Resting muscle activation while lying supine.
Use of the scalene and sternocleidomastoid muscles is a further
indicator of respiratory distress.
• Ankle or lower leg edema & Jugular vein engorgement
can be a sign of right heart failure.
Palpation and percussion.
• Detection heart apex beat,
may be difficult due to pulmonary hyperinflation.
• Increase in the ability to palpate the liver,
Hyperinflation also leads to downward displacement of this organ
without it being enlarged.
Auscultation.
• Often have reduced breath sounds,
but this finding is not sufficiently characteristic to make the diagnosis13
• The presence of wheezing during quiet breathing,
is a useful pointer to airflow limitation.
However, wheezing heard only after forced expiration is of no
diagnostic value.
• Inspiratory crackles
occur in some COPD patients but are of little help diagnostically.
• Heart sounds are best heard over the xiphoid area.
C. Laboratory data
1. Arterial blood gases. is essential to assess the severity of an
exacerbation.
a. Respiratory failure
- PaO 2 < 60 mm Hg and/or SaO 2 < 90% with or without
- PaCO 2 > 50 mm Hg
- when breathing room air.
b. Life-threatening episode that needs critical management
- PaO 2 < 50 mm Hg
- PaCO 2 > 70 mm Hg,
- pH < 7.3025.
2. Chest X-ray. Chest radiographs (posterior/anterior plus lateral)
- Useful in identifying alternative diagnoses that can mimic the
symptoms
of an exacerbation.
- Evaluation the heart size, esp. Right side
3. ECG aids in the diagnosis
- Right heart hypertrophy,
- Arrhythmias
- Ischemic episodes
- Pulmonary embolism
4. Other laboratory tests
- CBC/DC
a. Polycythemia (hematocrit > 55%) or bleeding.
b. White blood cell counts
- Purulent sputum (sufficient indication for starting empirical antibiotic
treatment.)
- Sputum culture and an antibiogram
(If an infectious exacerbation does not respond to the initial
antibiotic treatment)
- Biochemical tests can reveal
a. Electrolyte disturbance(s)(hyponatremia, hypokalemia, etc.),
b. Diabetic crisis, or
c. poor nutrition (low proteins)
D. General rules of treatment for exacerbations of COPD
1. Find exacerbation factors for excerbation
2. Oxygenation (base).
3. Inhaled Bronchodilator (Evidence A).
4. Theophylline
5. Systemic steroid, preferably orally (Evidence A)
6. NIPPV(Evidence A).
- Improves blood gases & pH
- Reduces in-hospital mortality,
- Decreases the need for invasive mechanical ventilation & intubation
- Decreases the length of hospital
7. Antibiotics when infection suspected(Evidence B)
- Signs of airway infection, e.g
a. Increased volume and change of color of sputum, and/or
b. fever
- most common bacterial pathogens
a. Streptococcus pneumoniae,
b. Hemophilis influenzae, and
c. Moraxella catarrhalis
8. Smoking cessation
Management of Severe but Not Life-Threatening Exacerbations of COPD
in the Emergency Department or the Hospital*
• Assess severity of symptoms, blood gases, chest X-ray.
• Administer controlled oxygen therapy
- repeat arterial blood gas measurement after 30 minutes.
• Bronchodilators:
– Increase doses or frequency.
– Combine ß 2 -agonists and anticholinergics.
– Use spacers or air-driven nebulizers.
– Consider adding intravenous aminophylline, if needed.
• Add oral or intravenous glucocorticosteroids.
• Consider antibiotics:
– When signs of bacterial infection, oral or occasionally intravenous.
• Consider noninvasive mechanical ventilation.
• At all times:
– Monitor fluid balance and nutrition.
– Consider subcutaneous heparin.
– Identify and treat associated conditions
(e.g., heart failure, arrhythmias).
– Closely monitor condition of the patient.
Controlled oxygen therapy.
1. Adequate levels of oxygenation (PaO 2 > 60 mm Hg, or SaO 2 > 90%)
2. CO 2 retention can occur insidiously with little change in symptoms.
3. Once oxygen is started, arterial blood gases should be checked 30
minutes later to ensure
- Satisfactory oxygenation
- Without CO 2retention or acidosis.
4. Venturi masks are more accurate sources of controlled oxygen
than are nasal prongs
- but are more likely to be removed by the patient.
5. Note Haldane effect.
Bronchodilator therapy.
1. Short-acting inhaled ß 2 -agonists are usually the preferred bronchodilators
(Evidence A).
2. If a prompt response to these drugs does not occur, the addition of an
anticholinergic is recommended.
3. More severe exacerbations
- Addition of an oral or intravenous methylxanthine can be considered
- Close monitoring of serum theophylline is recommended
to avoid the side effects of these drugs
Short-acting inhaled ß 2 -agonists
- Salbutamol( ventolin) nebuliser solution 1Amp st & qid
- Turbutaline( Bricanyl) turbuhaler 1 puff qid~ q4hr
Anticholinergic agent
- Ipratropium bromide(Atrovent) nebuliser solution 1Amp st & qid
Fixed combination bronchodilator preparation
- Ipratropium+Sambutamol( Combivent) MDI 1,2 puff tid, qid
Aminophylline
- Loading: 6mg/kg IVD for 20-30mis
- Maintenance dose: 0.5mg/kg/hr
- Decrease Doses to 1/2 should in
a. Already taking theophylline in general
b. Factors decrease clearance
Drugs and Physiological Variables that Affect Theophylline Metabolism
in COPD
Increased
Decreased
• Tobacco smoking
• Old age
• Anticonvulsant drugs
•Arterial hypoxemia (PaO 2< 45
• Rifampicin
mm Hg)
• Alcohol
• Respiratory acidosis
• Congestive cardiac failure
• Liver cirrhosis
• Erythromycin
• Quinolone antibiotics
• Cimetidine (not ranitidine)
• Viral infections
• Herbal remedies (St. John’s Wort)
Glucocorticosteroids
1. Oral or intravenous glucocorti-costeroids are recommended
2. The exact dose that should be recommended is not known, but
-30 ~ 40 mg of oral prednisolone daily for 10 to 14 days is a reasonable
compromise between efficacy and safety
- Solumedrol(40)(Methylprednisolone) 1 Amp IV q6h~q8h iv
Antibiotics.
1. Only effective in increased sputum volume and purulence4.
2. The choice of agents should reflect local patterns of antibiotic sensitivity
among
a. S. pneumoniae,
b. H. influenzae,
c. M. catarrhalis.
Indications and Relative Contraindications for NIPPV47,56
Selection criteria
• Moderate to severe dyspnea with use of accessory muscles and
paradoxical abdominal motion.
• Moderate to severe acidosis (pH ≤ 7.35) and
hypercapnia (PaCO 2 > 45 mm Hg)
.• Respiratory frequency > 25 breaths per minute.
Exclusion criteria (any may be present)
• Respiratory arrest.
• Cardiovascular instability (hypotension, arrhythmias, myocardial
infarction).
• Somnolence, impaired mental status, uncooperative patient.
• High aspiration risk; viscous or copious secretions.
• Recent facial or gastroesophageal surgery.
• Craniofacial trauma, fixed nasopharyngeal abnormalities.
• Burns.
• Extreme obesity.
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2. Harrison’s on line, Internal medicine
3. Chronic obstructive pulmonary disease.New Yo rk: Marcel Dekker; 1989.
1-22.
4. Vermeire PA, Pride NB. A "splitting" look at chronic non-specific lung
disease (CNSLD): common features but diverse pathogenesis.
Eur Respir J 1991; 490-6.
5. Fletcher C, Peto R. The natural history of chronic airflow obstruction. BMJ
1977; 1:1645-8.
4. Leitch AG. Pulmonary tuberculosis: clinical features. In Crofton J, Douglas A,
eds. Respiratory diseases. Oxford: Blackwell Science; 2000. 507-27.
5. Birath G, Caro J, Malmberg R, Simonsson BG. Airway obstruction in
pulmonary tuberculosis. Scand J Resp Dis 1966; 47:27-36.