COPD exacerbation

Dr. Ibrahim Abuasbeh

 Definition and Classification

• an acute change in a patient's baseline

– dyspnea
– cough
– sputum
• that is beyond normal variability, and that is
sufficient to warrant a change in therapy.
• Classification of COPD exacerbations :
– Mild
– Moderate
– Severe
• based on the intensity of the medical
intervention required to control the patient's
symptoms
• In addition to the hallmark symptoms of a
COPD exacerbation
– (cough, dyspnea, and increased sputum),
• systemic inflammation also causes
extrapulmonary symptoms
 Etiology

• Infection of the tracheobronchial tree and air

pollution
– (e.g., tobacco smoke, occupational exposures,
ozone)
• are the most common identifiable causes of
COPD exacerbations.

• One third of exacerbations have no

identifiable cause.
• Other medical problems, such as :
– congestive heart failure
– nonpulmonary infections
– pulmonary embolism
– Pneumothorax
• can also prompt a COPD exacerbation
 4 steps for evaluation
• The first step is an appropriate medical history
which identifies :
– one or more of the three cardinal symptoms:
• increased shortness of breath,
• increased sputum volume
• increased sputum purulence.
– These symptoms have to be interpreted in the context
of other clinical conditions such as
• disease severity,
• frequency of previous acute episodes,
• the presence of co‐morbidities (cardiovascular, diabetes,
skeletal muscle),
• and the socioeconomic environment.
• The second step is a physical examination to
identify :
– the principal respiratory signs (rapid and shallow
breathing, use of accessory respiratory muscles,
paradoxical chest wall motion, wheezing,
attenuated or absent breath sounds,
hyperresonance on percussion, purse lip
breathing),
– cardiovascular signs (increased and/or abnormal
pulse heart rate, right heart failure, peripheral
oedema, haemodynamic instability),
– and general signs (altered mental status, central
cyanosis).
• The third step involves the recognition of
clinical conditions that are often associated
with COPD for example:
– pulmonary conditions (pneumonia,
pneumothorax, pleural effusion, lung cancer,
upper airway obstruction, rib fracture)
– cardiovascular conditions (pulmonary embolism,
right/left heart failure), and drug related causes
(sedatives, narcotics).
• All the latter are considered complications
that easily mimic exacerbations.
• The fourth step includes several standard
diagnostic procedures such as:
– arterial blood gas analysis,
– chest radiography,
– routine blood tests,
– ECG,
– Gram stain and culture when sputum is purulent.
• The use of pulse oximetry alone to measure
arterial oxygen saturation (SaO2) is only
recommended for mild exacerbations.
• Forced spirometry is of limited usefulness for the
management of exacerbations but is mandatory
during the recovery or follow up period to
confirm the diagnosis of COPD or to monitor
further slow improvement.
 Indications for Hospitalization

• About 50 percent of COPD exacerbations are

not reported to physicians, suggesting that
many exacerbations are mild.
• The risk of death from an exacerbation
increases with the development of
– respiratory acidosis,
– the presence of significant comorbidities,
– and the need for ventilatory support.
• Patients with symptoms of :
– respiratory distress
– and those at risk of distress
• should be admitted to the hospital to provide access to
critical care personnel and mechanical ventilation.

• Inpatient mortality for COPD exacerbations is 3 to 4

percent.
• Patients admitted to the intensive care unit have a 43
to 46 percent risk of death within one year after
hospitalization.
 TREATMENT
• Identifying and ameliorating the cause of the
acute exacerbation, if possible
• Optimizing lung function by administering
bronchodilators and other pharmacologic agents
• Assuring adequate oxygenation and secretion
clearance
• Averting the need for intubation, if possible
• Preventing complications of immobility, such as
thromboemboli and deconditioning
• Addressing nutritional needs
 OXYGEN THERAPY
• Supplemental oxygen is a critical component
of acute therapy.
• It should target
– an arterial oxygen tension (PaO 2 ) of 60 to 70
mmHg,
– with an oxyhemoglobin saturation of 90 to 94
percent
 PHARMACOLOGIC TREATMENT
• The major components of managing an acute
exacerbation of COPD include:

– inhaled short-acting bronchodilators :

• beta adrenergic agonists

• anticholinergic agents

– Glucocorticoids
– and antibiotics
• Inhaled short-acting beta adrenergic agonists
(eg, albuterol ) are the mainstay of therapy for an
acute exacerbation of COPD because of:
– their rapid onset of action
– and efficacy in producing bronchodilation
• Typical doses of albuterol for this indication are
2.5 mg (diluted to a total of 3 mL) by nebulizer
every one to four hours as needed,
• Increasing the dose of nebulized albuterol to 5
mg does not have a significant impact on
spirometry or clinical outcomes
• Similarly, continuously nebulized beta agonists
have not been shown to confer an advantage.
• Inhaled short-acting anticholinergic agents
(eg, ipratropium bromide) are used with
inhaled short-acting beta adrenergic agonists
to treat exacerbations of COPD
• This is based on several studies that found
that combination therapy produces
bronchodilation in excess of that achieved by
either agent alone in patients with a COPD
exacerbation.
• Typical doses of ipratropium for this indication
are 500 mcg by nebulizer every four hours as
needed.
 Glucocorticoids

• Efficacy :
– Systemic glucocorticoids, when added to the
bronchodilator therapies described above

• improve symptoms and lung function,

• and decrease the length of hospital stay
• Route :
• Oral glucocorticoids are rapidly absorbed
(peak serum levels achieved at one hour after
ingestion)
• with virtually complete bioavailability and
appear equally efficacious as intravenous
glucocorticoids for treating most
exacerbations of COPD.
• However, intravenous glucocorticoids are
typically administered to patients who present
with a severe exacerbation:
– who respond poorly to oral glucocorticoids,
– who are unable to take oral medication,
– or who may have impaired absorption due to
decreased splanchnic perfusion (eg, patients in
shock).
• The efficacy of inhaled glucocorticoids on the
course of a COPD exacerbation has not been
studied in randomized trials. Thus, they should
not be used as a substitute for systemic
glucocorticoid therapy.
• Dose :
• The optimal dose of systemic glucocorticoids for
treating a COPD exacerbation is unknown .
• Frequently used regimens range from :
– prednisone 30 to 60 mg, once daily,
– to methylprednisolone 60 to 125 mg, two to four
times daily.
– A growing body of evidence favors using a moderate,
rather than high dose of glucocorticoids, for the
majority of patients with an exacerbation of COPD.
• The Global Initiative for Chronic Obstructive Lung
Disease (GOLD) guidelines advise using:
• the equivalent of prednisone 30 to 40 mg once daily
for the majority of COPD exacerbations .
• For patients with impending or actual acute respiratory
failure due to a COPD exacerbation, most clinicians
would use an intravenous formulation at a higher dose,
such as the equivalent of methylprednisolone 60 mg
intravenously, one to four times daily, although
outcomes data to guide this practice are not available
• Duration :
• The optimal duration of systemic
glucocorticoid therapy is not clearly
established and often depends on the severity
of the exacerbation and the observed
response to therapy .
• The Systemic Corticosteroids in COPD
Exacerbations (SCCOPE) trial compared two
and eight week regimens and did not find any
additional benefit to the longer course .
Patients in the eight week group experienced
more glucocorticoid-related side effects.
• As a rough guide :
• most exacerbations are treated with full dose
therapy (eg, prednisone 30 to 40 mg daily) for 10
to 14 days .
• After this time, glucocorticoid therapy may be
discontinued.
• Alternatively, the dose is tapered over another
seven days, as a trial to determine whether
continued glucocorticoid therapy is required.
• Tapering solely because of concerns about
adrenal suppression is not necessary if the
duration of therapy is less than three weeks (a
duration too brief to cause adrenal atrophy).
• Mucoactive agents :
• There is little evidence supporting the use of
mucoactive agents (eg, N-acetylcysteine) in
acute exacerbations of COPD .
• Some mucoactive agents may worsen
bronchospasm.
• Methylxanthines ( Aminophylline and
theophylline ):
• are NOT recommended for the treatment of
acute exacerbations of COPD
• CHEST PHYSIOTHERAPY :
• Mechanical techniques to augment sputum
clearance, such as directed coughing, chest
physiotherapy with percussion and vibration,
intermittent positive pressure breathing, and
postural drainage, have not been shown to be
beneficial in COPD and may provoke
bronchoconstriction.
• Their use in acute exacerbations of COPD is
not supported by clinical trials
 MECHANICAL VENTILATION
• Noninvasive ventilation
• Invasive ventilation
 Noninvasive ventilation
• In patients with mild to moderate ARF,
characterized by
– pH levels between 7.25 and 7.35
• NIV was administered for few hours per day
(<12h/day) with low failure rates ranging from
15% to 20%
• In these patients, NIV is indicated to prevent
endotracheal intubation
• In more severely ill patients (pH < 7.25),
• the rate of NIV failure was inversely related to the
severity of respiratory acidosis, rising up to 52%–
62%
• The use of NIV in alternative to the invasive
ventilation
– does not affect the mortality rate and the duration of
ventilatory support,
– but the patients treated with NIV are subjected to a
lower rate of complications (VAP, difficult weaning).
• In these patients, although exposed to high risk
of failure, a NIV trial may be justified, if
intubation is not strictly required because the
need of protecting the airways, loss of
consciousness or gasping.
• In patients with “mild” exacerbations, not
complicated by respiratory acidosis,
– the use of NIV was investigated by few studies,
including patients in large majority with pH > 7.35,
who failed in demonstrate a better effectiveness of
NIV than standard medical therapy in preventing the
occurrence of the ARF.
– No significant improvement in mortality and
hospitalization duration was found, and the tolerance
of the patients to the NIV was less than 50%
• Absolute contraindications for NIV:
• Cardiac or respiratory arrest
• Severe encephalopathy
• Severe gastrointestinal bleeding
• Severe haemodynamic instability with or without
unstable cardiac angina
• Facial surgery or trauma
• Upper airway obstruction
• Inability to protect the airway and/or high risk of
aspiration
• Inability to clear secretion
Invasive ventilation
Thank you