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COPD exacerbation

Etiology: 1) infections (most common) a) bacterial 1] Streptococcus pneumonia 2] Haemophilus influenza, Haemophilus parainfluenza 3] Moraxella catarrhalis [49] 4] Mycoplasma pneumonia b) viral 1] influenza virus 2] adenovirus 2) heart failure, cor pulmonale 3) myocardial infarction 4) cardiac arrhythmias 5) pneumothorax 6) pulmonary embolism (as high as 25%) [6]; up to 6% [44] 7) bronchogenic carcinoma 8) environmental exposure to bronchospastic agents - each 1 degree C increment in outdoor temperature associated with a 2% increased risk of COPD exacerbation [46] 9) oversedation 10) non-compliance with medications 11) excessive oxygen use (suppression of respiratory drive) 12) tachyphylaxis to beta-2 adrenergic agonists 13) mucus plugging 14) emotional factors 15) vitamin D status is not a risk factor [9] 16) risk factors for early hospital readmission - multiple comorbidities (most significant) [6] - heart failure, lung cancer, depression. anxiety, osteoporosis, alcoholism - rate of early hospital readmission increases as the number of comorbidities increases [6,28] - inadequate hospital discharge medications - length of hospital stay < 2 days or > 5 days - male gender 17) gabapentinoid use increases risk for severe COPD exacerbation Pathology: - persistent or recurrent COPD exacerbations are driven mostly by residual airway inflammation, not by infection [43] - auto-PEEP contributes to increased work of breathing during exacerbations of obstructive lung disease Clinical manifestations: 1) increase in severity of cough 2) dyspnea, respiratory failure may occur 3) sputum may be increased or changed in character with exacerbations 4) fatigue 4) purulent sputum predicts need for antibiotics in patients with mild-to-moderate COPD* [17] * mild-to-moderate COPD defined as FEV1 > 50% of predicted * severity of exacerbationis determined by dyspnea intensity, respiratory rate, heart rate, & oxygen saturation [53] Laboratory: 1) SaO2 2) arterial blood gas (ABG) a) hypercarbia over baseline - a decrease in pCO2 of over baseline suggests pulmonary embolism [5] b) pH < 7.30 c) carboxyhemoglobin level to identify continued smoking 3) D-dimer in plasma: rule out pulmonary embolism 4) complete blood count - eosinophilia: blood eosinophils > 2% predicts favorable response to glucocorticoids [10] - patients with eosinophil count < 300/mL may not need oral glucocorticoids [39] 5) basic metabolic panel 6) serum C-reactive protein patients with mild-to-moderate COPD* [17,38] a) < 20 ng/mL unlikely to benefit from antibiotics b) 20-40 ng/mL possible benefit of antibiotics c) > 40 mg/dL predicts need for antibiotics 7) low serum procalcitonin may identify patients hospitalized with COPD exacerbation for which antibiotic therapy > 24 hours does not reduce readmission rates [33] 8) sputum culture not indicated (rarely affects management) [6] 9) for mild COPD exacerbations, clinical assessment is sufficient - if physical examination is unremarkable, laboratory testing &/or imaging is unlikely to beneficially alter management * mild-to-moderate COPD defined as FEV1 > 50% of predicted Special laboratory: - electrocardiogram (see Complications: below) - pulmonary angiography if pulmonary embolism suspected Radiology: - chest X-ray - rule out pulmonary embolism - CT angiography or ventilation perfusion scan - computed tomography (CT): - pulmonary artery enlargement predicts COPD exacerbation [11] Complications: - pulmonary embolism in 17% [56] - patients with purulent sputum at lower risk (RR=0.43) [56] Differential diagnosis: - need for large amounts of supplemental oxygen suggests diagnosis other than obstructive lung disease (asthma, COPD) - pulmonary embolism [13] - unstable angina - deep symmetric T-waves with flat ST segment in leads V2 & V3 suggest stenosis of the proximal left anterior descending coronary artery - heart failure, cor pulmonale Management: 1) observation units may reduce need for hospitalization (63% vs 78%) [31] 2) combination therapy a) glucocorticoids plus antibiotics - for hospitalized patients [12] - beneficial regardless of severity [42] - antibiotics for patients with purulent sputum (GOLD) b) short-acting inhaled beta-2 adrenergic receptor agonist - albuterol MDI &/or nebulizer c) anticholinergic agent: ipratropium (Atrovent) MDI &/or nebulizer d) continue maintenance theophylline 3) glucocorticoids may preferentially benefit patients with eosinophilia [10,58] a) prednisone 40 mg/day [6] for 5 days sufficient (ACP) [6,16] - equivalent to higher &/or longer doses &/or IV administration [6] b) personalized prednisone dosing better than standard dosing 40 mg/day - based on 5 factors including symptom scales, previous steroid dosing, inflammatory markers, & blood gas results - optimal dose 40-60 mg prednisone/day for 5 days [47] c) avoid glucocorticoid therapy for > 2 weeks [1,28] d) NNT = 10, NNH = 7 (adverse effects) e) reserve intravenous glucocorticoids for patients that cannot tolerate oral therapy [6] f) methylprednisolone 2 mg/kg/day in divided doses - 80-160 mg/day may be sufficient in ICU patients [19] g) manage glucocorticoid-induced hyperglycemia in patients who are eating with basal, prandial & correctional insulin [6] 4) antimicrobial therapy: a) for severe exaberbations [1,4] 1] all hospitalized patients with COPD exacerbation [15] 2] limited to patients with purulent sputum or mechanical ventilation (GOLD) 3] see pneumonia for empiric antibiotic therapy b) for mild-moderate exacerbations with: 1] increased dyspnea 2] increased sputum volume 3] increased sputum purulence [17] 4] increased cough & sputum purulence [21] c) 5 day course of oral antibiotics [45] (previously 7-10 days) d) complicated exacerbation - older age > 65 years, FEV1 < 50%, heart disease, >= 2 COPD exacerbations/year - amoxicillin/clavulanate or - respiratory fluoroquinolone [21]: - 2 days of levofloxacin non inferior to 7 days [52] e) amoxicillin 250 mg PO TID f) Bactrim DS 1 PO BID (works as well as Cipro [7]) g) doxycycline 100 mg PO BID h) azithromycin (Zithropac) 250 mg, 2 tabs day 1, then 1 tab PO QD - 500 mg QD for 3 days, then 250 mg QOD [40] i) increased cardiovascular mortality noted 1 year after treatment of COPD exacerbation with clarithromycin [14] 5) chest physiotherapy a) may improve clearance of secretions b) increased hypoxia may occur during chest percussion or postural drainage 6) supplemental oxygen a) maintain an oxygen saturation (of hemoglobin) of 88-90%, even in the face of increasing hypercapnia - higher oxygen flow rates associated with increased mortality [8] b) a Venturi mask provides good control over oxygen delivery 7) criteria for ICU admission - PaO2 < 40 mm Hg - respiratory acidosis, pH < 7.25 requiring enndotracheal intubation - mental status changes - hemodynamic instability 8) ventilatory support a) non-invasive positive pressure ventilation (NPPV) is needed in 10-20% of patients [2,18] - reduces mortality (relative risk 0.41) - is associated with lower in-hospital mortality (NNT=12) [30], length of stay (3.4 days shorter), & cost compared with mechanical ventilation [22,30] - reduces need for endotracheal intubation (RR 0.42) - BiPAP is NPPV of choice - acute on chronic hypercapneic respiratory failure - high inspiratory flow rates (80-100 L/min) - high-pressure NPPV may result in the need for fewer intubations than standard low-pressure NPPV [60] - CPAP can open the upper airway to treat obstructive sleep apnea, but will not help patients ventilate & clear carbon dioxide - superior to high-flow nasal cannula in patients with moderate hypercapnic respiratory failure during COPD exacerbation [59] b) mechanical ventilation - obtundation, delirium, or other mental status changes preclude cooperation necessary for NPPV - inability to protect airway - loss of gag reflex - vomiting, excessive secretions, upper GI bleed - failure of CPAP/BiPAP trial [6] - hypoxemic respiratory failure, acute respiratory distress syndrome (ARDS) - complications: auto-PEEP, use low tidal-volume ventilation (see ARDS) [41] 9) pulmonary rehabilitation after hospital discharge - may be helpful [3,6] - reduces rate of rehospitalizations after COPD exacerbation [47] - reduces 1 year mortality when pulmonary rehabilitation started within 90 days of hospitalization for COPD [50] - progressive exercise rehabilitation should not be started during the early stages of recovery [20] 10) see chronic obstructive pulmonary disease for outpatient supplemental oxygen - no mortality benefit if oxygen desaturation with exercise between 80-89% [51] 11) prevention of COPD exacerbation - smoking cessation, ensure pneumococcal vaccination & influenza vaccination, ensure proper inhaler technique [6] - see COPD 12) home care for COPD exacerbation is increasingly common [6] - reasonable for mild-moderate exacerbation in patients without significant comorbidities [6] - home non-invasive positive pressure ventilation (NPPV) reduces hospital readmissions 4.3 months vs 1.4 months for oxygen alone in patients with persistent hypercapnia (PaCO2 >53 mm Hg) 13) risk factors for early hospital readmission (see etiology above) 14) surgery: - delay elective surgery until resolution of exacerbation [6]

General

chronic obstructive pulmonary disease (COPD) exacerbation

References

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