Acute exacerbation of COPD

Diagnosis, treatment, and follow-up of acute exacerbation of COPD in a 67-year-old man.


Morning Report is an occasional feature in ACP Hospitalist that will analyze the clinical and administrative aspects of a fictional but realistic hospital case from admission to discharge. Authors of this feature will discuss the patient's clinical course and will also provide a brief overview of background, diagnosis, and management, emphasizing whether the case was optimally managed and whether the patient was appropriately discharged with efforts to prevent readmission. Tips on effective documentation will also be reviewed.

The patient

Photo by Thinkstock
Photo by Thinkstock

Chief symptoms: Progressive shortness of breath, cough, and wheezing for 4 days

History: A 67-year-old man with a history of chronic obstructive pulmonary disease (COPD), hypertension, and dyslipidemia was brought into the ED by his daughter with 4-day history of worsening shortness of breath, wheezing, and increased productive cough with change in color of sputum from clear tan to greenish. He was experiencing dyspnea on exertion. He did not report fever, night sweats, chest pain, or palpitations. He had had multiple hospitalizations for COPD exacerbations due to nonadherence to medications. The most recent admission was a month previously.

He reported no other pertinent medical or surgical history. He had a family history of hypertension and diabetes in his mother and hypertension and myocardial infarction in his father. He had a 40-pack-year smoking history but did not report using alcohol or illicit drugs. He retired 2 years ago and lived alone. He had no known drug allergies. His medications were lisinopril, 20 mg/d; atorvastatin, 20 mg/d; fluticasone propionate/salmeterol, 250/50 inhaler, 1 puff twice daily; tiotropium inhaler, 18 µg, 1 cap daily; ipratropium bromide/albuterol, inhaled 0.5 mg/2.5 mg/3 mL nebulizer every 6 hours as needed; and levalbuterol, inhaled 0.63 mg/3 mL nebulizer every 8 hours as needed.

His most recent spirometry results, from a month ago, showed an FEV1 of 1.56 L, 30% of predicted (predicted FEV1, 3.07 L), FVC of 2.28 L, and FEV1/FVC ratio of 0.68 (68%).

Physical examination: Vital signs were as follows: blood pressure, 110/60 mm Hg; heart rate, 110/min; temperature, 98.7 °F; respiratory rate, 34/min; oxygen saturation, 81% on room air.

The patient was a thin man who appeared awake and alert but in moderate respiratory distress, using accessory muscles. On cardiac examination, he was tachycardic with regular rhythm and normal S1, S2 heart sounds with audible S3 gallop. Auscultation of the lungs revealed coarse rhonchi and diffuse wheezing. He had no cyanosis or lower-extremity pitting edema. The rest of the examination was unremarkable.

Labs: Arterial blood gases showed a pH of 7.20, a Paco2 of 67 mmHg, a Pao2 of 61 mmHg, and an HCO3 of 30 mmol/L on nasal cannula at 2 L/min. White blood cell count was 14,000 cells/µL, hemoglobin level was 15.1 g/dL, and hematocrit was 48%. Comprehensive metabolic panel was within normal limits.

Imaging: Electrocardiogram revealed sinus tachycardia (heart rate, 115/min) with a normal interval and no ST, T-wave changes. Chest X-ray revealed lung hyperinflation and flattened diaphragm. No acute infiltrates were seen.

Clinical course

The patient was admitted to the inpatient unit with the diagnosis of COPD exacerbation. He was treated with oxygen therapy by nasal cannula, 6 L/min. He was also given inhaled albuterol, 2.5 mg, by nebulizer every 2 to 4 hours, together with oral prednisone, 60 mg/d. On day 2 of admission, the patient's clinical state deteriorated with severe hypoxemia and increasing respiratory fatigue. He required endotracheal intubation and was transferred to the ICU. Levofloxacin, 500 mg, and a systemic corticosteroid were started intravenously along with frequent albuterol/ipratropium nebulization. After daily weaning trials, he was successfully liberated from invasive mechanical ventilation on day 8. His antibiotic course was completed, and he was subsequently discharged on day 10 with a taper course of oral corticosteroids. He was advised to go to the nearest ED if the symptoms developed again.

Case review

Q: Was our patient diagnosed correctly?

A: Yes. The diagnosis of COPD exacerbation is based on the clinical presentation (acute change in symptoms from baseline dyspnea, cough and/or sputum production, that is beyond normal day-to-day variation) (1). Our patient had an extensive smoking history along with multiple admissions for COPD exacerbation. The worsening of his respiratory symptoms (dyspnea, cough, and/or sputum production) along with his medical history pointed toward COPD exacerbation. However, the severity of his COPD exacerbation was not identified at the time of admission. Our patient had respiratory failure based on his difficulty breathing and abnormal arterial blood gas values, so hypoxic hypercapnic respiratory failure should have been documented. This improper documentation would have resulted in inappropriate coding of the diagnosis-related group (DRG), leading to lower than expected geometric mean length of stay and lower reimbursement to the hospital.

Q: Was our patient managed and discharged appropriately?

A: No. Our patient had COPD exacerbation with respiratory failure from the time of admission. Signs of severity for diagnosis of a COPD exacerbation consist of accessory respiratory muscles usage, worsening or new-onset central cyanosis, development of peripheral edema, hemodynamic instability, and deteriorated mental status (1). The need for noninvasive positive-pressure ventilation and antibiotics should have been addressed from the time of admission given his degree of gas exchange impairment. Based on guidelines (2, 3), antibiotics should be given to patients with COPD exacerbation who have worsening dyspnea, increased sputum volume, and purulent sputum. In the GOLD (Global Initiative for Chronic Obstructive Lung Disease) classification, our patient fits the criteria for stage D COPD. Therefore, he should have been on a short- and long-acting bronchodilator, inhaled corticosteroid, and oxygen therapy (1). Our patient was not on oxygen therapy at home, and the requirement for oxygen therapy was not assessed upon discharge. His home medications should have also been reviewed and reconciled upon discharge. Influenza and pneumococcal vaccinations should have been given. He should also have been educated on inhaler technique and medication adherence, as well as being offered smoking cessation counseling.

Q: Was the transition of care properly handled at the time of discharge?

A: No. Poor coordination of the transition and communication with the patient increased his risk of recurrent COPD exacerbation. Home oxygen therapy requirements should have been assessed and arranged prior to discharge. Follow-up within 4 to 6 weeks should have been scheduled. Case management should ensure adequate social support and follow-up adherence. A referral for pulmonary rehabilitation should have been provided to promote long-term adherence to health-enhancing behaviors, since research has shown that pulmonary rehabilitation referral within 28 days of discharge from an acute exacerbation of COPD decreased the chance of readmissions (4).

Overview

Acute exacerbation of COPD is defined by worsening of the patient's respiratory symptoms (baseline dyspnea, cough, and/or sputum production) that is beyond normal day-to-day variations and leads to a change in medication (1, 5, 6). There are several precipitating factors for COPD exacerbation—70% of exacerbations are due to either viral or bacterial respiratory infections (7), whereas the rest are due to pollution, pulmonary embolism, or unknown cause (8).

Diagnosis

COPD exacerbation can be diagnosed on the basis of a patient's medical history, clinical signs of severity, and laboratory tests. Relevant medical history includes severity of COPD based on degree of airflow limitation, duration of worsening or new symptoms, and number of previous episodes (including whether hospital or ICU admission resulted). The best predictor of future exacerbations is past exacerbations. Signs of severity for diagnosis of COPD exacerbation include use of accessory respiratory muscles, paradoxical chest wall movements, worsening or new-onset central cyanosis, development of peripheral edema, hemodynamic instability, and deteriorated mental status (1).

Treatment

The goals of treatment in COPD exacerbation are to minimize the impact of the current exacerbation and prevent subsequent exacerbations (9). Depending on the severity of an exacerbation and/or severity of underlying disease, COPD exacerbation can be managed in an outpatient or inpatient setting. More than 80% of exacerbations can be treated on an outpatient basis.

The decision to hospitalize is based on a marked increase in intensity of symptoms, such as sudden development of resting dyspnea, severe underlying COPD, onset of new physical signs such as cyanosis or peripheral edema, failure of exacerbation to respond to medical management, presence of serious comorbidities (e.g., heart failure or newly occurring arrhythmias), frequent exacerbations, older age, and insufficient home support.

In the ED, physicians should assess the patient's ability to protect his airway, his hemodynamic stability, and the need for respiratory support. If needed, the patient should be admitted to the ICU immediately based on the following criteria: severe dyspnea that responds inadequately to initial emergency therapy; changes in mental status (confusion, lethargy, coma); persistent or worsening hypoxemia (Pao2 <40 mm Hg); and/or severe respiratory acidosis (pH <7.25) despite supplemental oxygen and noninvasive ventilation, need for invasive mechanical ventilation, and hemodynamic instability (including need for vasopressors) (1).

Inpatient management of a COPD exacerbation includes pharmacologic therapy (bronchodilators, corticosteroids, antibiotics, other adjunct therapies) and respiratory support (oxygen therapy, mechanical ventilation).

A bronchodilator, such as an inhaled short-acting beta-agonist (albuterol, 2.5 mg diluted to 3 mL via nebulizer or 4 to 8 inhalations from a metered-dose inhaler [MDI]), is typically given every hour. Increasing the nebulized albuterol dose to 5 mg does not have a significant impact on spirometry or clinical outcomes (10), and a meta-analysis showed no significant difference in FEV1 between the routes of delivery (nebulizers versus MDI with or without a spacer device) (11). Because of significant side effects, IV methylxanthines (theophylline or aminophylline) should be considered as second-line therapy only in selected cases, including insufficient response to short-acting bronchodilators (12).

Research has shown that systemic corticosteroids can shorten recovery time; improve FEV1 and arterial hypoxemia (PaO2); and reduce the risk of early relapse, treatment failure, and length of hospital stay (13-15). A daily dose of prednisone, 40 mg, for 5 days is recommended (16). Oral therapy appears to be as efficacious as IV glucocorticoids for treating most exacerbations of COPD. A randomized trial found no difference between oral versus IV prednisolone, 60 mg daily for 5 days, in the rate of treatment failure, length of hospital stay, improvement in spirometry, or quality of life (17).

Antibiotics should be given to patients who have 3 cardinal symptoms (increase in dyspnea, sputum volume, and sputum purulence); those who have 2 of the cardinal symptoms, 1 being increased sputum purulence; and those who require invasive or noninvasive mechanical ventilation (2, 3). Five to 10 days of antibiotic therapy is usually recommended (1). Other adjunct therapies such as smoking cessation treatment should also be strongly promoted.

Supplemental oxygen should be titrated to improve hypoxemia with a target saturation of 88% to 92% (18). Arterial blood gases should be checked 30 to 60 minutes after oxygen is started. Although Venturi masks are less likely to be tolerated by the patient, they offer more accurate and controlled oxygen delivery than nasal prongs (19).

Noninvasive mechanical ventilation (NIV) is indicated if the patient has respiratory acidosis (arterial pH ≤7.35 and/or PaCO2 ≥45 mm Hg) or severe dyspnea with clinical signs suggestive of respiratory muscle fatigue or increased work of breathing, such as use of respiratory accessory muscles, paradoxical motion of the abdomen, or retraction of the intercostal spaces (20, 21).

Invasive mechanical ventilation is indicated for patients who are unable to tolerate NIV or who have NIV failure; in patients with respiratory or cardiac arrest; or in those who have respiratory pauses with loss of consciousness or gasping for air, diminished consciousness, psychomotor agitation inadequately controlled by sedation, massive aspiration, persistent inability to remove respiratory secretions, heart rate below 50/min with loss of alertness, severe hemodynamic instability without response to fluids and vasoactive drugs, or severe ventricular arrhythmias and life-threatening hypoxemia (22).

Discharge

According to the 2014 GOLD guidelines, discharge criteria for COPD exacerbation include being able to use long-acting bronchodilators, either beta-2 agonists and/or anticholinergics with or without inhaled corticosteroids; requiring inhaled short-acting beta-2 agonist therapy no more than every 4 hours; being able to walk across the room (if previously ambulatory); being able to eat and sleep without frequent awakening by dyspnea; being clinically stable for 12 to 24 hours; and having stable arterial blood gas values for 12 to 24 hours. The patient (or home caregiver) should also fully understand correct use of medications and follow-up and home care arrangements should have been completed (e.g., visiting nurse, oxygen delivery, meal provisions), with the patient, family, and physicians feeling confident that the patient can manage successfully at home (1). The GOLD guidelines also provide a checklist to assess patients at the time of discharge (Table 1) (1).

Repeated COPD exacerbations and hospitalizations can be minimized by smoking cessation; influenza and pneumococcal vaccines; patient knowledge of current therapy, including inhaler technique; and treatment with long-acting inhaled bronchodilators (with or without inhaled corticosteroids) and possibly phosphodiesterase-4 inhibitors (23-25). Early outpatient pulmonary rehabilitation after hospitalization for an exacerbation results in clinically significant improvements in exercise capacity and health status at 3 months (4).

Some predictors of readmission include patient factors such as male sex; history of heart failure; lung cancer; osteoporosis; depression; and care factors such as no prior prescription of statin within 12 months of the index hospitalization and no prescription of short-acting bronchodilator, oral steroid, and antibiotic on discharge. Other factors such as length of stay less than 2 or more than 5 days and lack of follow-up visit after discharge have also been associated with early readmission (26).

Documentation

It is crucial to specify the primary diagnosis in COPD exacerbation. For example, one should document an acute exacerbation of COPD or exacerbated COPD or acute on chronic COPD, all of which are equivalent for coding purposes. Clinicians should not document respiratory insufficiency as a diagnosis by itself. Complications and comorbidities should also be documented to allow coding to reflect accurate severity of illness and ensure appropriate DRG classification (Table 2) (27, 28).

Improper coding will result in lower reimbursements to hospitals. In the case of our patient, inappropriate coding of the DRG leading to lower reimbursement to the hospital would result from the incomplete documentation of severity (respiratory failure) of the disease.

In conclusion, this case demonstrates potential opportunities for better management of a COPD exacerbation, including adhering to guideline-directed medical therapy, improving transitions of care, and optimizing documentation, which can result in better patient outcomes, lower readmissions, and higher reimbursement.