COPD with acute
exacerbation
What is COPD?
COPD is a chronic slowly progressive
disorder characterized by airflow
obstruction (FEV1 < 80% predicted and
FEV1/FVC ratio < 70%) which does not
change markedly over several months.
It encompasses three clinical entities :
EMPHYSEMA
CHRONIC BRONCHITIS
SMALL AIRWAYS DISEAES
DEFINITIONS
CHRONIC BRONCHITIS : It is defined as
cough with sputum on most days for at least
three consecutive months for more than two
successive years.
EMPHYSEMA : It is defined as permanent
destructive enlargement of the air spaces
distal to the terminal bronchioles.
SMALL AIRWAYS DISEASE : A condition in
which small bronchioles are narrowed.
RISK FACTORS
SMOKING: studies have shown accelerated
decline in FEV1 in a dose response relationship to
the intensity of cigarette smoking which is
expressed as pack years.
AIR WAY RESPONSIVENESS: Increased air way
responsiveness is a significant predictor of
subsequent decline in pulmonary function.
RESPIRATORY INFECTIONS: Though respiratory
infections are an important cause of exacerbation
of COPD , their association to the development
and progression of COPD remains to be proven.
RISK FACTORS contd..
OCCUPATIONAL EXPOSURE: Including coal
mine , gold mining and cotton textile dust have
been suggested as risk factors.
AMBIENT AIR POLLUTION: with high rates of
COPD in non smoking women in developing
countries indoor air pollution associated with
cooking has been suggested as potential
contributor.
ALPHA 1 ANTI TRYPSIN DEFICIENCY: Cigarette
smokers with alpha 1 anti-trypsin deficiency are
more likely to develop COPD at early ages.
CLINICAL PRESENTATION
HISTORY: three most common symptoms of
COPD are cough, sputum production and
exertional dyspnea.
As disease progresses dyspnea occurs with mild
activity and in severe cases at rest.
Hallmark of COPD is frequent exacerbation of
illness.
Pneumonia , pulmonary HTN , cor pulmonale
and chronic respiratory failure characterize the
late stages of the disease.
SIGNS OF COPD
Nicotine staining of finger nails.
Pursed lip breathing.
Characteristic tripod position.
Use of accessory muscles.
Barrel shaped chest.
Excavation of suprasternal and
supraclavicular fossae during respiration.
Cyanosis.
Weight loss , bitemporal wasting.
Hoover’s sign : paradoxical inward
movement of rib cage during inspiration.
SIGNS OF COPD contd..
Tracheal tug
Loss of cardiac dullness
Prolonged expiratory phase with wheezing
Signs of hypercapnia i.e bounding pulse, warm
extremities and flapping tremors
Signs of cor pulmonale namely elevated JVP ,
right ventricular heave , loud P2 , S3 , hepatic
congestion , ascities . Peripheral edema
Clubbing is not a sign of COPD ; CA lung is the
most likely explanation for clubbing in COPD.
INVESTIGATIONS
PFTs: Reduction in FEV1 and FEV1/FVC ratio.
1.
2.
3.
ABGs: Indicated if
Hypoxemia or hypercapnia is suspected.
FEV1 is less than 40% of predicted.
Clinical signs of heart failure.
SPUTUM EXAMINATION for micro organisms in acute
exacerbation
ECG may show sinus tachycardia , signs of RVH and
Supraventricular arrythmias.
HAEMATOLOGY may show polycythemia.
INVESTIGATIONS contd..
CXR may show hyperinflation with flattening of
diaphragm or peripheral arterial deficiency ,
parenchymal bullae and enlargement of central
pulmonary arteries.
CT SCAN is the current definitive test for the
establishing the presence or absence of
emphysema.
ALPHA 1 ANTI TRYPSIN LEVEL in patients
presenting with age < 50 yrs, strong family history
, predominant basilar disease or with minimal
smoking history.
ECHO for suspected pulmonary HTN,
GOLD CRITERIA FOR COPD SEVERITY
Gold
stage
severity
symptoms
spirometry
0
At risk
Ch cough,sputum production
normal
I
mild
With or without ch cough or
sputum production
FEV1/FVC<0.7
AND FEV1>80
%
II
moderate
As above
FEV1/FVC<0.7
AND
50%<FEV1<80%
III
severe
As above
FEV1/FVC<0.7
AND
30%<FEV1<50%
IV
Very severe
As above
FEV1/FVC<0.7
AND FEV1<30%
TREATMENT
STABLE PHASE COPD:
1.
Smoking cessation is one of the two interventions that
influence the natural history of patients with COPD. Nicotine
transdermal patch, nicotine gum and bupropion increase
cessation rates in motivated smokers.
2.
Oxygen therapy also influence natural history of disease in
patients with resting hypoxemia. Survival in hypoxemic
patients with COPD is directly proportionate to the no. of hrs
/ day oxygen is administered.
ABG analysis is prefered over oximetry to guide initial oxygen
therapy. Oxygen by nasal prongs must be given for at least
15 hrs a day.Transtracheal oxygen is alternative method of
delivery in pts. who require high flows of oxygen than can be
deliverd by nasal prongs.
BRONCHODILATORS
Anticholinergic agents like ipratropium bromide is first line
agent because of its longer duration of action and absence
of sympathomimetic side effects. Dose 2 puffs every 6 hrs.
1.
2.
Beta agonists
Short acting: like salbutamol are less expensive, have
rapid duration of action and have bronchodilator effect
equal to ipratropium bromide but may cause tachycardia,
tremor and hypokalemia.
Long acting: like salmeterol appear to achieve
bronchodilation that is equivalent or superior to
ipratropium but their role in stable COPD is under
research.
THEOPHYLLINE
Theophylline is third line agents in COPD patients
who fail to achieve adequate symptoms with
anticholinergics and beta 2 agonists.
SR theophylline improve arterial oxygen Hb
saturation during sleep in COPD pts and is a first
line agent for those with sleep related breathing
disorders.
Its benefits may result from anti inflammatory
properties and extra pulmonary effects on
diaphragm strength , myocardial activity and renal
function.
CORTICOSTEROIDS
Apart from acute exacerbation , COPD is
not generally steroid responsive disease.
A trial of inhaled glucocorticoids should be
considered in pts with frequent
exacerbations defined as 2 or more per
year, and in pts who demonstrate a
significant amount of acute reversibility in
response to inhaled bronchodilators.
Chronic use of oral glucocorticoids for
treatment of COPD is not recommended.
OTHER AGENTS
N ACETYL CYSTEINE: has been used in
pts of COPD for its mucolytic and anti
oxidant properties.
ALPHA 1 ANTI TRYPSIN THERAPY for
severe anti trypsin deficiency.
Pts over 18 years of age with air flow
obstruction on spirometry and level less
than 11 umol/l are candidates for
replacement therapy.
NON PHARMACOLOGICAL
THERAPIES
General medical care : influenza vaccine annually.
Pneumococcal vaccine is also recommended.
Pulmonary rehabilitation: graded aerobic physical
exercise programs
walking 20 mins at least thrice weekly,
bicycling are helpful for preventing deterioration of physical
condition and to improve patient’s ability to carry out daily
activities.
Pursed lip respiration to slow the rate of breathing and
abdominal breathing exercises to relieve fatigue of accessory
muscles of respiration may reduce dyspnea in some pts.
Adequate systemic hydration and cough training methods for
mobilization of secretions in pts with ch bronchitis.
SURGICAL TREATMENT
1.
LUNG TRANSPLANTATION: for pts with FEV1
less than 25% and severe limitation in quality of
life esp with hypercapnia and hypoxemia.It is
not an option for elderly pts.
2.
BULLECTOMY: Is considered in pts with COPD
and dyspnea in whom a bulla or bullae occupy
50% of hemithorax.
3.
LUNG VOLUME REDUCTION SURGERY: In
highly selected pts with severe COPD due to
emphysema.
ACUTE EXACERBATION
Exacerbations are commonly considered to
be episodes of increased dyspnea and
cough and change in amount and
character of sputum.
It may or may not be accompanied by
fever, myalgias and sore throat.
Approach to the pt includes assesment of
severity , identification of the precipitating
factor and institution of therapy.
PRECIPITATING CAUSES
Bacterial infections play a role in
many episodes.
(H.influenzae,S.pneomoniae,M.catarr
halis and Mycoplasma)
Viral infections are involved in 1/3 rd
of cases. (Influenza and Adenovirus)
In 20 – 35% no specific precipitant
can be identified.
PATIENT ASSESMENT
History include degree of dyspnea , by asking
about breathlessness during activities , ask about
fever , change in character of sputum and
associated symptoms as nausea , vomiting ,
diarrhea , myalgias and chills.
Inquire about frequency and severity of previous
exacerbations.
Physical examination : process degree of distress.
CXR and ABGs
INSTITUTION OF THERAPY
OXYGEN to achieve and maintain PaO2 > 55-60 mm Hg
and to keep arterial saturation > 90%. Hypoxic respiratory
drive plays a small role in pts of COPD.
INHALED BRONCHODILATORS
1.
Short acting beta agonists are first line agents as albuterol
has reduced duration of action in acute exacerbation
allowing a treatment frequency of every 30 – 60 mins as
tolerated. Subsequent treatment can be reduced to 2- 4
puffs every 4 hrs.
2.
Anticholinergic agents are equally effective to short acting
beta 2 agonists. Dose : 2 puffs QID can be increased to 46 puffs every 4-6 hrs.
3.
Combination therapy has synergistic bronchodilation ,
rapid onset of action and fewer S/E.
Contd..
GLUCOCORTICOIDS: GOLD guidelines
recommend 30 – 40 mg of oral prednisolone over
10 – 14 days. They reduce hospital stay , hasten
recovery and reduce the chance of subsequent
exacerbation or relapse for a period upto 6 mths.
ANTIBIOTICS: First line antibiotic regimes are
Septran (160/800 mg every 12 hrs) , Amoxycillin (
500mg tds) Doxycycline (100mg bd) for 7-10 days.
For severe exacerbation recommended antibiotics
include Azithromycin , Clarithromycin ,
Levofloxacin and Gatifloxacin.
Contd..
PSYCHOACTIVE DRUGS :low dose
anxiolytics may reduce anxiety .
Buspirone 5-10 mg tds is usually
tolerated well.
INDICATIONS FOR ICU
ADMISSION
SEVER DYSPNEA
MENTAL STATUS CHANGES
PERSISTENT WORSENING
HYPOXEMIA
HYPERCAPNIA
RESPIRATORY ACIDOSIS ALL
DESPITE MEDICAL THERAPY.
MECHANICAL VENTILATORY
SUPPORT
Non Invasive positive pressure pressure
ventilation (NIPPV) in pts with respiratory
failure , defined as Pco2 > 45 mm Hg
results in significant reduction in mortality,
need for intubation , complication of
therapy and duration of hospital stay.
IPPV with ETT is indicated for pts with
severe respiratory distress despite initial
therapy , life threatening hypoxemia ,
severe hypercapnia and/or acidosis ,
impaired mental status , respiratory arrest
and hemodynamic instability.
DISCHARGE CRITERIA
Use of inhaled bronchodilators less
frequently than every 4 hrs.
Clinical and ABG stability for at least
12 – 24 hrs and
Acceptable ability to eat , sleep and
ambulate.
THANK YOU !
SCENARIO
50 years oil male presented in
emergency department with history of
severe shortness of breath associated
with productive cough with yellow
color sputum and fever.
He has past history of cigarette
smoking 2 pack year for last 35 years.
What physical signs you can suspect
in this case ?
SCENARIO
BP 100/60mmHg
Pulse 110 beats/min
R/R 34/min
Temp 101 F
Pt is cyanosed a
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