Acute Exacerbation of Copd by Dr Irappa Madabhavi

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

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Acute Exacerbation of Copd by Dr Irappa Madabhavi

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