COPD exacerbation

80 year old female with past history of moderate COPD( 3L oxygen all the time), HTN, hyperlipidemia, osteoporosis, glaucoma and CAD present with shortness of breath since yesterday morning. Patient is getting SOB every day in the morning since last month. She has been taking Proair(albuterol) and Duoneb (albuterol/ipratropium), SOB normally can improve and go back to baseline within 1 hour. yesterday morning, her SOB couldn't improve with same medications, therefore, she came to ER. She had COPD exacerbation in Dec 2012, Mar 2013. She has always cough with clear phlegm. there is no fever, chills, no chest pain, orthopnea, paroxysmal nocturnal dyspnea. She smoke all her life for 60-70 years, but quit smoking 2 weeks ago. at ER, she received solu medrol 125 mg IV once, and Duoneb once. vital, RR 22, SaO2 95% on 3L, cxr no acute infiltrate, EKG is normal sinus rhythm. assessment and plan: 1, COPD exacerbation, solu medrol 60mg IV q8h, for 1-2 days, then transtion to po steroid, plus azithromycin 500mg once for 3 days. 2, HTN, continue lisinopril and metoprolol 3, CAD, continue ACEi, beta blocker, aspirin and statin 4, start omeprazol as she will be on steroid. Management of acute exacerbations of chronic obstructive pulmonary disease defines an exacerbation of chronic obstructive pulmonary disease (COPD) as an acute increase in symptoms beyond normal day-to-day variation. This generally includes an acute increase in one or more of the following cardinal symptoms: ■Cough increases in frequency and severity ■Sputum production increases in volume and/or changes character ■Dyspnea increases Constitutional symptoms, an unchanged chest radiograph, a variable decrease in pulmonary function, and tachypnea are typical in acute exacerbations Rapid overview: Emergency management of severe acute COPD exacerbations General points Chronic obstructive pulmonary disease (COPD) exacerbations are most often precipitated by infection (viral or bacterial) Differential diagnosis includes: Acute decompensated heart failure, pulmonary embolism (PE), pneumonia, pneumothorax Clinical manifestations Cardinal symptoms: Increase or change in character of dyspnea, cough, sputum production Diagnostic testing Assess oxygen saturation with pulse oximetry Obtain arterial blood gas in severe exacerbations Obtain chest radiograph to assess for signs of pneumonia, acute heart failure, pneumothorax Obtain complete blood count and measures of basic electrolytes and renal function Obtain electrocardiogram Pharmacotherapy Oxygen to target saturation of 90 to 94 percent and PaO2 of 60-70 mmHg; Venturi mask can be useful for titrating FiO2; high FiO2 usually not needed and can contribute to hypercapnia (high FiO2 requirement should prompt consideration of alternative diagnosis (eg, PE)) Inhaled beta agonist (eg, albuterol 2.5 mg diluted to 3 mL via nebulizer) Inhaled anticholinergic agent (eg, ipratropium 500 micrograms via nebulizer) Systemic corticosteroid (eg, methylprednisolone 60 mg IV) Antibiotic therapy: Levofloxacin (750 mg IV) or alternative based on likely pathogens (including risk of pseudomonas infection) and local patterns of antibiotic resistance Noninvasive Positive Pressure Ventilation (NPPV) Indicated for moderate to severe exacerbations Use only if tracheal intubation not immediately necessary and no other contraindications Contraindications to NPPV include: Severely impaired consciousness, inability to clear secretions or protect airway, high aspiration risk Initial settings for bilevel NPPV: 8 cm H2O inspiratory pressure (may increase up to 15 cm H2O if needed to aid ventilation); 3 cm H2O expiratory pressure Monitoring and initial interventions Perform continual monitoring of oxygen saturation, cardiac rhythm, and vital signs Place two peripheral IV catheters Tracheal intubation For patients with severe respiratory distress in whom NPPV is contraindicated or who fail to improve with NPPV and aggressive pharmacotherapy Disposition Criteria for hospitalization include: Patients with high-risk comorbidities (pneumonia, cardiac arrhythmia, heart failure, diabetes mellitus, renal failure, liver failure) Inadequate improvement of symptoms with initial therapies Marked increase in dyspnea Inability to eat or sleep due to symptoms Worsening hypoxemia or hypercapnea PRECIPITANTS — It is estimated that 70 to 80 percent of COPD exacerbations are due to respiratory infections, including: Haemophilus influenzae 13 to 50 Moraxella catarrhalis 9 to 21 Streptococcus pneumoniae 7 to 26 Pseudomonas aeruginosa 1 to 13 The remaining 20 to 30 percent are due to environmental pollution or have an unknown etiology. The single best predictor of exacerbations was a history of exacerbations, regardless of COPD severity. The GOLD guidelines suggest using a combination of an individual’s FEV1 and history of exacerbations to assess the exacerbation risk [1]. The number of exacerbations in the previous 12 months is stratified: a history of zero or one exacerbation suggests a low future risk of exacerbations, while two or more suggest a high future risk. Severity of airflow limitation in COPD (based on postbronchodilator FEV1) In patients with FEV1/FVC <0.7: GOLD 1 Mild FEV1 ≥80 percent predicted GOLD 2 Moderate 50 percent ≤FEV1 <80 percent predicted GOLD 3 Severe 30 percent ≤FEV1 <50 percent predicted GOLD 4 Very severe FEV1 <30 percent predicted ■Low risk: Typically GOLD 1 or 2 (mild to moderate airflow limitation) and/or 0 to 1 exacerbation per year ■High risk: Typically GOLD 3 or 4 (severe or very severe airflow limitation) and/or ≥2 exacerbations per year DIFFERENTIAL DIAGNOSIS — Patients with COPD who present to the hospital with acute worsening of dyspnea should be evaluated for potential alternative diagnoses, such as heart failure, pulmonary thromboembolism, and pneumonia. TREATMENT: OXYGEN THERAPY — Supplemental oxygen is a critical component of acute therapy. It should target an arterial oxygen tension (PaO2) 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 and anticholinergic agents), glucocorticoids, and antibiotics. Beta adrenergic agonists — Inhaled short-acting beta adrenergic agonists (eg, albuterol) are the mainstay of therapy for an acute exacerbation of COPD.These medications may be administered via a nebulizer or a metered dose inhaler (MDI) with a spacer device. Despite evidence that MDI devices may have equal efficacy during acute exacerbations of COPD, many clinicians prefer nebulized therapy on the presumption of more reliable delivery of drug to the airway [1]. We favor nebulized therapy because many patients with COPD have difficulty using proper MDI technique in the setting of an acute exacerbation. Patients with severe COPD are at risk for hypercapnia with administration of supplemental oxygen, so concern has been raised about the risk of hypercapnia during bronchodilator treatments using oxygen-driven nebulizers.We concur with the British Thoracic Society guidelines that suggest using air-, rather than oxygen-driven bronchodilator nebulization, or limiting oxygen-driven treatments to 6 minutes. Anticholinergic agents — Inhaled short-acting anticholinergic agents (eg, ipratropium bromide) are used with inhaled short-acting beta adrenergic agonists to treat exacerbations of COPD. Glucocorticoids 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. As an example, a randomized trial assigned 210 patients hospitalized with a COPD exacerbation to receive oral or intravenous prednisolone (60 mg daily) for five days and found no difference between the two groups in the rate of treatment failure, length of hospital stay, improvement in spirometry, or improvement in quality of life. 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). Antibiotics — Antibiotics are indicated for many patients having a COPD exacerbation. 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 — Noninvasive positive pressure ventilation (NPPV) refers to mechanical ventilation delivered through a noninvasive interface, such as a face mask, nasal mask, or nasal prongs. It improves numerous clinical outcomes and is the preferred method of ventilatory support in many patients with an acute exacerbation of COPD. Invasive ventilation — Invasive mechanical ventilation should be administered when patients fail NPPV, do not tolerate NPPV, or have contraindications to NPPV. PROGNOSIS — Acute exacerbations of COPD are associated with increased mortality after hospital discharge. ■It is estimated that 14 percent of patients admitted for an exacerbation of COPD will die within three months of admission [47,48]. ■Among 1016 patients with an acute exacerbation of COPD and a PaCO2 of 50 mmHg or more, the 6 and 12 month mortality rates were 33 and 43 percent, respectively [49]. ■In a study of 260 patients admitted with a COPD exacerbation, the one year mortality was 28 percent [50]. Independent risk factors for mortality were age, male gender, prior hospitalization for COPD, PaCO2 ≥45 mmHg (6 kPa), and urea >8 mmol/L. ■Patients hospitalized for a COPD exacerbation who have a Pseudomonas aeruginosa in their sputum have an increased risk of mortality at three years than those without (59 versus 35 percent, HR 2.33, 95% CI 1.29-3.86), independent of age, comorbidity, or COPD severity SUMMARY AND RECOMMENDATIONS ■A table to assist with emergency management of severe acute exacerbations of COPD is provided (table 1). ■An acute exacerbation of COPD is characterized by an acute increase in symptoms beyond normal day-to-day variation. (See 'Introduction' above.). ■We recommend that all patients having a COPD exacerbation receive both an inhaled short-acting beta adrenergic agonist and an inhaled short-acting anticholinergic agent, rather than either medication alone (Grade 1B). (See 'Beta adrenergic agonists' above and 'Anticholinergic agents' above.) ■We recommend that all patients having a COPD exacerbation receive systemic glucocorticoids (Grade 1A). A reasonable dose for patients not requiring intensive care unit admission is prednisone 30 to 60 mg orally once daily, or the equivalent, for 10 to 14 days, although preliminary data suggest that a 5 day course may be an acceptable alternative. (See 'Glucocorticoids' above.) ■Antibiotics are indicated for many patients having a COPD exacerbation. (See "Management of infection in acute exacerbations of chronic obstructive pulmonary disease", section on 'Summary and recommendations'.) ■Mucoactive agents, mechanical techniques to augment sputum clearance, and methylxanthines have not been shown to confer benefit for patients with a COPD exacerbation. (See 'Mucoactive agents' above and 'Chest physiotherapy' above and 'Methylxanthines' above.) ■We suggest that all patients who are hypoxemic be given supplemental oxygen targeting a PaO2 of 60 to 70 mmHg, with an oxyhemoglobin saturation of 90 to 94 percent (Grade 2C). (See 'Oxygen therapy' above.) ■Noninvasive positive pressure ventilation (NPPV) improves numerous clinical outcomes and is the preferred method of ventilatory support in many patients with an acute exacerbation of COPD. Invasive mechanical ventilation is required in patients with respiratory failure who fail NPPV, do not tolerate NPPV, or have contraindications to NPPV. Both NPPV and invasive mechanical ventilation for patients with an acute exacerbation of COPD are discussed separately.