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8/2/2019 Acute Exacerbation of Copd by Dr Irappa Madabhavi
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ACUTE EXACERBATION OF COPD
DR.IRAPPA MADABHAVI
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DEFINITION OF AE-COPD
An event in the natural course of the disease
characterized by a change in the patients
baseline dyspnea, cough, and/or sputum that
is beyond normal day-to-day variations, is
acute in onset, and may warrant a change in
regular medication in a patient with
underlying disease
GOLD, 2006 (Rabe et al. 2007)
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FREQUENCY OF EXACERBATION
Exacerbation rates according to baseline lung function. Vestbo J,Epidemiology of AECOPD, AECOPD Lung Biology in Health and Disease,
vol183, 2004
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The Study to Understand Prognosis and Preferencesfor Outcomes and Rates of Treatment (SUPPORT)
In-hospital mortality
rate of 11% in patients
with acute hypercapnic
respiratory failure. The
180-day mortality rate
was 33% and the
2-yr mortality rate was49%
Am J Respir Crit Care Med 1996; 154: 959
967.
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Triggers of COPD exacerbation
Wedzicha JA et al
Lancet 2007
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AETIOLOGY OF EXACERBATION
Infectious agents, including bacteria, viruses
and atypical pathogens are currently
implicated in up to 80% of acute exacerbation.
Bacteria likely playing a role in 50% ofexacerbations
Sethi S. Infectious etiology of acute exacerbations of chronic bronchitis. Chest2000; 117:380S385Stions
Sethi S. New developments in the pathogenesis of acute exacerbations of
chronic obstructive pulmonary disease. Curr Opin Infect Dis 2004; 17(2):113
119.
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BACTERIAL ETIOLOGY
The three predominant bacterial species isolated are
60% cases
Nontypeable Haemophilus influenzae,
Moraxella catarrhalis
Streptococcus pneumoniae.
. 10% - Atypical Chlamydia
Other less frequently isolated potential pathogens include
Pseudomonas aeruginosagram-negative enterobacteria
Staphylococcus aureus
Haemophilus parainfluenzae
Haemophilus hemolyticusNseir S et al, Respiration 2008
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Eller J et al Chest, 1998
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ROLE OF VIRAL INFECTION
Respirology (2010) 15, 536542
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VIRAL INFECTION AND AE-COPD
More severe as reflected by
Longer length of hospitalization
Decrease in FEV1, FEV1%, FEV1/FVC% anddiffusion capacity
Trend towards greater hypoxaemia.
Longer median symptom recovery time thandid non-viral exacerbations (13 and 6 days
respectively).
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AIR POLUTION and AECOPD
Hospital admissions for AECOPD were increasedwith increased environmental pollution.
London: Thorax (50) 1995 p.1188
6 European cities: ERJ (10) 1997 p. 1064
Taiwan: J. Tox. Env. Health (70), 207
Brazil: Cod Saudi P (22) 2006 p. 2669
Hong Kong: Thorax, 2007
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Secondary Causes of AECOPD and/or
comorbidities
Pneumonia
Left or Right heart failure
Arrhythmias
Pulmonary embolism
Spontaneous pneumothoraxInappropriate oxygen therapy
Drugs (hypnotics, diuretics, etc)
Metabolic diseases
Poor nutritional stageOther acute disease (GI Bleeding)
End-Stage disease (fatigue resp. muscles)
[1st ERS Guidelines 1995]
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Prevalence of Pulmonary Embolism in acuter
exacerbations of COPD: a systematic review andmetaanalysis.
Rizkallah J et al. Chest 2009;135(3):786-93.
Conclusions: One of four COPD patients who requirehospitalization of an acute exacerbation may havePE. A diagnosis of PE should be considered inpatients with exacerbation severe enough to warranthospitalization, especially in those with anintermediateto-high pretest probability of PE.
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IMPACT OF EXACERBATION
Lancet 2007; 370: 786
96
Increase economic burden
Increase systemic
inflammation and co-
morbidity
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Corticosteroids in the Management of
Acute Exacerbations
Faster improvement in the FEV1 by
about 100 mL over the first 3 days of
treatment Reduce treatment failure, relapse and
length of hospital stay
Induce side effects (such ashyperglycaemia)
N Engl J Med 1999; 340:1941
1947
(SCCOPE TRIAL)
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ANTIBIOTIC THERAPY
Three levels of severity of exacerbation weredefined:
The most severe (type 1) comprisedworsening dyspnea with increased sputumvolume and purulence,
Type 2 was only two of these symptoms
Type 3 was any one of the symptoms withevidence of fever and/or an upper respiratorytract infection
Anthonisen criteria of severity of exacerbation
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ERS-ATS COPD Guidelines
Indications for hospitalisation of patients
with a COPD exacerbation Presence of high-risk co-morbid conditions, including
pneumonia, cardiac arrhythmia, congestive heartfailure, diabetes mellitus, renal or liver failure
Inadequate response of symptoms to outpatientmanagement
Marked increase in dyspnoea Inability to eat or sleep due to symptoms
Worsening hypoxaemia
Worsening hypercapnia
Changes in mental status Inability of the patient to care for her/himself
Uncertain diagnosis
Inadequate home care
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INDICATION FOR ICU ADMISSION
Severe dyspnea that responds inadequately to initial
therapy
Changes in mental status
Persistent or worsening hypoxaemia
PaO260 mmHg,
pH< 7.25 despite supplemental oxygen and NIV
Need for invasive mechanical ventilation and
vasopressor therapy
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Etiology of primary AECOPD
Sethi et al. Chest 2000; 117: 380s-5s
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Indication for Empiric Antibiotic
Therapy in AECOPD
Severity of AECOPD
judged by 3 Anthonisen criteria:
Worsening of dyspnea
Increased sputum volume
Increased sputum purulence
3/3 Type 1 or severe AE
2/3 Type 2 or moderate AE
1/3 Type 3 or mild AE
AB indicated/useful in
Type 1 or severe AE,
and Type 2 or
moderate AE if sputum
is purulent
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STRATIFICATION OF AE-COPD PATIENTSGROUP DEFINITIONS MICROORGANISMS
GROUP-A MILD EXACERBATIONS, NORISK FACTORS FOR POOR
OUTCOME
Streptococcus pneumoniaeH. influenzae
Moraxella catarrhalis
C.PNEUMONIAE
VIRUSES
GROUP-B MODERATE
EXACERBATIONS, WITH RISKFACTORS FOR POOR
OUTCOME
GROUP-A PLUS RESISTANT
ORGANISM, BETA-LACTAMASE PRODUCING
PENICILLIN RESISTANT
STREPTOCOCCI
PNEUMONIAE,ENTEROBACT
ERIACEAE
GROUP-C SEVERE EXACERBATIONS,
WITH RISK FACTORS FOR
PSEUDOMONAS
AERUGINOSA
GROUP-B PLUS
PSEUDOMONAS
AERUGINOSA
Presence of comorbid diseases, frequent exacerbations >3/year, severe COPD,
Antimicrobial use within past 3 months
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Antibiotic therapy in AE-COPD
GROUP-A Patients withonly one cardinalsymptoms should notreceive antibiotics
If indicated, thenBeta-lactam, TetracyclineTMP-SMX
Alternative: beta-lactam/beta lactamase
inhibitor, advancedmacrolides, 2 or 3rdgenerationcephalosporine
GROUP-B
beta-lactam/betalactamase inhibitor,
Alternative oral therapy
fluoroquinolones-gemi,levo and gatifloxacin
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GROUP-C patients at risk for PS.aeruginosa
Ciprofloxacin or levofloxacin at high doses
Antibiotics therapy in patients of COPD couldbe given for 5-7 days
Antibiotic therapy in AE-COPD
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INDICATIONS FOR NIV IN AE-COPD
Moderate-to-severe respiratorydistress with use of accessory muscleand abdominal paradox
Moderate to severe acidosis (pH7.35) and/ or hypercapnia (Paco2 > 45mm Hg)
Tachypnea (respiratory rate > 25/min)
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Do not use this therapy if the patient
Has Respiratory arrest
Is medically unstable (hypotensive shock, uncontrolledcardiac ischemia or arrhythmias)
Cannot protect the airway (impaired cough or
swallowing mechanism) Has excessive secretions
Is agitated or uncooperative
Has facial trauma, burns, or surgery, or anatomic
abnormalities interfering with mask fit Has an Acute Physiology and Chronic Health Evaluation
(APACHE) score > 29RESPIR CARE 1997; 42:364369
EUR RESPIR J 2005; 25:348355;
THORAX 2002; 57:192
211.
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INDICATION FOR INVASIVE
MECHANICAL VENTILATION
NPPV failure (worsening of arterial blood gasesand/or pH in 12 hr or lack of improvement inarterial blood gases and/or pH after 4 hr)
Severe acidosis (pH < 7.25) and hypercapnia[PaCO2 >60 mm Hg]
Life-threatening hypoxemia [PaO2/FiO2 < 200mm Hg]
Tachypnea >35 breathsmin
Other complications include metabolicabnormalities, sepsis, pneumonia, pulmonaryembolism, barotraumas, and massive pleuraleffusion.
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OXYGEN THERAPY IN AE-COPD
The goal is to maintain SaO2 at >90%.
Main delivery devices include nasal cannula andventuri mask. Alternative delivery devices include
nonrebreather mask, reservoir cannula, nasalcannula or transtracheal catheter.
ABG should be monitored for PaO2, PaCO2 and pH.
Prevention of tissue hypoxia supercedes CO2retention concerns. If CO2 retention occurs, monitorfor acidaemia.
If acidaemia occurs, consider mechanical ventilation.
Risk factors for poor outcome and/or
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Risk factors for poor outcome and/or
for antibiotic-resistant pathogens in
AECB >3 exacerbations in the past 12 months
Comorbidities (especially cardiac disease)
Severe or very severe airflow obstruction atbaseline (FEV1 50% predicted)
Recent (within past 3 months) systemic
antibiotic use
Table 16.1
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Hypoxia at exacerbation of COPD is primarilythe consequence of ventilation-perfusion(V/Q) imbalance and may be life threatening,
for example through cardiac arrhythmia. Oxygen should therefore be used to correct
hypoxia in respiratory failure.
This should be administered in a controlledmanner, to prevent the hypercapnia which willoccur in a minority of patients
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GOLD recommendations, antibiotics should be given topatients with exacerbations with the three majorsymptoms, to those with two symptoms provided increasedsputum purulence is present, and to those who arecritically ill and needing mechanical support.
The oral route is preferred and is cheaper. Theiradministration should be based on the patterns of localbacterial resistance and their use should be maintained fora period of 310 days
If an exacerbation responds poorly to empirical antibiotictreatment, the patient should be re-evaluated forcomplications with microbiological reassessment ifnecessary.
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NON-PHARMACOLOGICAL TREATMENT
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OXYGEN THERAPY
Administer controlled low inspired oxygenconcentrations (either 24% or 28%) through high flow(Venturi) masks at flow rates of 24 l/min.
This strategy increases PaO2 sufficiently to maintain
optimal values above 60 mm Hg and to ensureadequate SaO2 levels (>90%) without riskingdetrimental carbon dioxide retention and acidosis.
Low flow devices such as nasal prongs or cannulae are
less accurate as they deliver a variable and higherinspired oxygen concentration which can result insuppression of respiratory drive, carbon dioxidenarcosis, and eventually respiratory arrest, if the
patient is not appropriately monitored
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BRONCHODILATORS
Short acting inhaled b2 agonists and
anticholinergic agents remain the main treatment
modality for exacerbations as they reduce
symptoms and improve airflow obstruction
No significant differences in FEV1 between the
use of hand held MDIs with a good inhalertechnique (with or without a spacer device) and
nebulizers
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The first step is an appropriate medical history whichidentifies one or more of the three cardinal symptoms:increased shortness of breath, increased sputumvolume, and increased sputum purulence
The second step is a physical examination to identifythe principal respiratory signs (rapid and shallowbreathing, use of accessory respiratory muscles,paradoxical chest wall motion, wheezing, attenuated orabsent breath sounds, hyperresonance on percussion,
purse lip breathing), cardiovascular signs (increasedand/or abnormal pulse heart rate, right heart failure,peripheral oedema, haemodynamic instability), andgeneral signs (altered mental status, central cyanosis)
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The third step involves the recognition of
clinical conditions that are often associated
with COPDfor example, pulmonary
conditions (pneumonia, pneumothorax,pleural effusion, lung cancer, upper airway
obstruction, rib fracture), cardiovascular
conditions (pulmonary embolism, right/leftheartfailure), and drug related causes
(sedatives, narcotics)
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The fourth step includes several standard diagnosticprocedures such as arterial blood gas analysis, chestradiography, routine blood tests, ECG, and Gram stain andculture when sputum is purulent. The use of pulse oximetryalone to measure arterial oxygen saturation (SaO2) is only
recommended for mild exacerbations. Forced spirometry isof limited usefulness for the management of exacerbationsbut is mandatory during the recovery or follow up period toconfirm the diagnosis of COPD or to monitor further slowimprovement. Peak expiratory flow rate (PEFR), used as an
alternative measurement of airflow limitation, correlateswell with forced expiratory volume in 1 second(FEV1),although the clinical implications of this
correlation remain unclear
Recommended