COPD

Definition: Disorder of lung that is characterized by expiratory airflow obstruction that is not fully reversible. The airway obstruction is usually progressive and associated with an abnormal inflammatory response.

  • Chronic bronchitis: is defined clinically as cough productive of sputum, approx 2 tbsp on most days of 3 consecutive months in 2 consecutive years, in the absence of other lung diseases, that could account for the symptoms.

  • Emphysema: is defined pathologically as enlargement of the distal airways with destruction of the acinus, and abscence of associated fibrosis.

Epidemiology:

  • 10 - 24 million American are affected.

  • 4th leading cause of death in U.S

  • Death rates in males and females are equal.

Risk factors:

  • Smoking, occupation and environmental dusts and gases, chemicals, wood-burning stove.

  • Alpha-1-antitrypsin deficiency should be considered in a patient with emphysema who is young <45 years of age, family histroy of lung diseases, has minimal smoking history, and has lower lobe predominant emphysema.

  • Underdiagnosed condition, therefore, it is recommended that all sx pts with COPD, as well those who are asymptomatic but with risk factors of COPD, and persistent airflow obstruction of PFT, be screened for alpha-antitrypsin deficiency.

History:

  • Progressive dyspnea, cough, sputum production, and wheezing.

  • Nocturnal sx are unusual in COPD, except in patients with other comorbidities such as cardiac disease, CHF, sleep apnea, Gerd,

  • Smoking history, exposure to environmental and occupational risk factors: dust, fumes, smoke, etc.

  • Wt. loss seen in end-stage emphysema, but consider associated malignancy and depression.

  • Acute exacerbations of COPD in a year.

  • Family history of lung disease

PE:

  • Significant impairment of lung function FEV1 <50% need to make physical signs of COPD clinically sensitive and specific.

  • Prolonged breath sounds (> 6 sec) on maximal forced exhalation, decreased breath sounds, use of accessory muscles or resp, chest hyperresonance to percussion, and enlarged thoracic volume.

  • Expiratory wheezing may or may not be present.

  • Clubbing not a feature of COPD, if seen check for other etiologies, such as lung cancer.

  • Signs of pulmonary hypertension (PH) and right heart failure may be present.

  • Respiratory distress, paradoxical abdominal motion, and fatigue need mechanical ventilation.

DDx:

  • Asthma, bronchiectasis, cystic fibrosis, constrictive bronchiolitis, diffuse panbronchiolitis, mycobacterial infection (TB and nontuberculous), eosinophilic granuloma, lymphangioleiomyomatosis, airway tumors, tracheal stenosis, tracheobronchomalacia.

Labs/Dxtic:

  • CXR: chest hyperinflation, flattening of the diaphragm, increasing retrosternal/retrocardiac air spaces, and lung hyperlucency with diminished vascular markings. Bullae may be seen, usually in the upper zones, so emphysema is present in the upper zones, unlike in alpha-1-antitrypsin def. which is seen in basilar zones. CXR during acute exac. needed to check of complications like PTx, and pneumonia.

  • CT chest is not routinely indicated for diagnosing COPD, but used to rule out other diagnoses. Used routinely to assess patients with COPD for lung volume reduction surgery (LVRS) and lung transplantation.

  • PFT: spirometry is the only reliable means of dx COPD. Limited ability in acute illness.

    • Dx of COPD requires the presence of expiratory airflow obstruction, defined as FEV1/FVC ratio of < 0.70

    • FEV1 defines the severity of expiratory airflow obstruction and is a predictor of mortality.

    • TLC, FRC, RV increase to supranormal values in patients with COPD, indicating thoracic hyperinflation and air trapping.

    • Emphysema produces a reduction of DLCO (diffusing capacity of the lungs for CO).

    • GOLD Classification of COPD Severity:

      • Stage I: mild.

        • Symptoms: with or without chronic cough or sputum production

        • Spirometry: FEV1:FVC < 0.7 and FEV1 ≥ 80% predicted

      • Stage II: moderate.

        • Symptoms: with or without chronic cough or sputum production

        • Spirometry: FEV1:FVC < 0.7 and FEV1 50 – 79% predicted

      • Stage III: severe.

        • Symptoms: with or without chronic cough or sputum production

        • Spirometry: FEV1:FVC < 0.7 and FEV1 30 – 49% predicted

      • Stage IV: very severe

        • Symptoms: with or without chronic cough or sputum production

        • Spirometry: FEV1:FVC < 0.7 and FEV1 < 30% predicted or FEV1 < 50% predicted with respiratory failure (PaO2 <60 mm Hg +/- PaCO2 >50 mm Hg while breathing room air at sea level), or signs of right heart failure.

  • Classification based on pathologic type:

    • Centriacinar emphysema

      • Type most frequently associated with cigarette smoking

      • Most prominent in upper lobes and superior segment of the lower lobes of the lungs

    • Panacinar emphysema

      • Usually observed in patients with α1AT deficiency

      • Most prominent in lower lobes

  • ABG to detect acute and chronic hypoxemia and hypercapnia, and the development of acute respiratory acidosis may signal need for assisted ventilation.

  • Elevated HCO3 may signify a metabolic response to chronic hypercapnia

  • Polycythemia may reflect a physiologic response to chronic hypoxemia and inadequate supplemental oxygen use.

Tx:

  • Long term: improve quality of life, decrease frequency and severity of acute exacerbations, slow the progression of disease, and prolong survival.

  • Smoking cessation and supplemental oxygen to correct hypoxemia have been shown to improve survival.

  • LVRS improves survival in select patients.

  • Stepwise Approach to COPD therapy

    • Gold Stage

      • Mild: smoking cessation, vx (flu and pneu), SABA prn

      • Moderate: above + LABA, pulm. rehab

      • Severe: above + ICS if repeat exac, O2

      • Very severe: all the above + consider surgical treatments.

  • Tiotropium (Spiriva), 1 puff (18 mcg) qd, use resulted in significant improvement in lung function, quality of life, and COPD exacerbations, although the rate of decline of FEV1 was unaffected.

  • ICS reduces frequency of COPD exacerbations, may increase FEV1, but do not slow the rate of decline of lung function over time.

  • Theophylline is a xanthine derivative is a PDE inhibitor with bronchodilator properties. Used when standard therapy does not work. Sustained release theophylline is dosed once or twice a day. Serum levels should be maintained between 8 - 12 mcg/mL to avoid toxicity.

    • Side effects: anxiety, tremor, HA, insomnia, nausea, vomiting, dyspepsia, tachycardia, tachyarrhythmia, and seizure. In the event of toxic sx, theophylline must be stopped and serum level is checked.

  • IV alpha-antitrypsin (A1AT) augmentation therapy may benefit select patients with A1AT deficiency and COPD. Weekly infusion of 60 mg/kg is the standard treatment.

  • Supplemental O2 decreases mortality. O2 indicated for patients with PaO2 <55 mm Hg and less or SaO2 < 88% or less. If a patient has PaO2 < 60 mm Hg or SaO2 < 90% and evidence of PH, polycythemia (Hct > 55%), or heart failure, O2 therapy is indicated.

    • O2 requirement is more during exertion, and sleep. Least when awake at rest. It is reasonable to set the O2 flow rate 1 L/min greater than that required during rest while awake.

  • Pulmonary rehab

  • Vaccinations: influenza and pneumococcal.

  • Surgical Management: BODE score of 7 - 10 or at least one of the following:

    • History of hospitalization for a COPD exacerbation associated with acute hypercapnia (PaCO2 >50)

    • PH, RHF or both, despite supplemental O2 therapy

    • FEV1 <20% and either a DLCO <20% or homogeneous distribution of emphysema.

    • LVRS may provide quality of life and survival benefits in patients with upper lobe predominant emphysema and significantly reduced exercise capacity.

Acute Exacerbation of COPD

    • Increased dyspnea, cough, sputum production, sputum purulence, wheezing, chest tightness, and worsening respiratory status, in the absence of an alternative explanation, define Acute exacerbation of COPD.

    • Preceding viral or bacterial inf - rhinosinusitis; air pollution are typical triggers

    • DDx: PTx, pneumonia, pleural effusion, CHF, cardiac ischemia, and PE.

We will admit Pt. to Medical floor.

Condition: critical-guarded

Patient is a full code.

Consult:

Pulmonary – Dr. re:

Cardiology – Dr. re:

Consult RT for DC education

Consult Pharmacy for medication education

Smoking Status:

Has Pt smoked in last 12 months  Yes  No

Consult smoking cessation counseling/program

Vitals: q4hr x 12hrs, then qshift

Activities

Bed rest (HOB elevated to 45°)

Up in chair tid

OOB with assistance

BRPs as tolerated

OOB ad lib

Allergies:

Nursing:

O2 at 2 l/min via NC

Check SpO2 now & q4h x 12 hrs, then qshift

(maintain SpO2>92%). Notify HO, if SpO2 ≤92% on 2L O2 via NC.

PEFR measurements, now & q4h x 12, then qshift

(PEFR >50% predicted = mild moderate severity)

(PEFR <50% predicted or 250 L/min = severe)

ABGs: A normal or increased PaCO2 is a sign of impending respiratory failure. Hypercapnia occurs when PEFR <25% of normal.

Intermittent SCDs

Diet:

Labs/Dxtics: CCP, CBC with diff, BC x 2, ECG, CXR, blood sugar check AC/HS or q4 hrs

ABGs, BNP, D-dimer, aPTT, PT/INR.

Saline lock – IV

0.9% NaCl @ ____ ml/hr

Other: ______ @ _____ ml/hr

Steroids:

Methylprednisolone 125 mg IV x 1. 1st dose now. Also can be given IM.

Methylprednisolone 40 - 60 mg IVP q 6h

Taper after clinical improvement (36 – 48 h)

Prednisone, 60 mg PO q6-8 h (preferred in Pts able to tolerate/absorb oral meds. Start taper only after clinical improvement, usually 36 – 48 h).

Taper x 7 – 14 days. Start Advair at the beginning of tapering schedule.

Respiratory Treatments: (unit clerk to notify respiratory)

Nebulizer Tx:

Albuterol, 2.5 mg in 3 ml saline q20 min until improvement obtained or toxicity noted, then q2-4 h.

Ipratropium 0.5 mg q 3 – 4 h

(anticholinergic may cause dry mouth, BOO, exac. of acute angle glaucoma. Caution in Pts on MAO-I, and in whose asthma is induced by beta-blockers)

Albuterol 10 – 15 mg cont. x 1 h in severe obst.

Xopenex (levalbuterol), 0.63 – 1.25 mg q6-8h

Fluticasone/salmeterol diskus (Advair Diskus):

(do not use concomitantly with fluticasone inhaler, not used in acute exacerbation. Used for chronic Tx).

250/50 mcg 2 puffs IH q12h

500/50 mcg 2 puffs IH q12h

Start at the beginning of tapering schedule

ABX (for ABECB- COPD only): Consider only in presence of purulent sputum and increased sputum volume.

TMP/SMX 160/800 mg (DS) PO bid OR

Amoxicillin, 500 mg PO q8h, OR

Doxycycline, 100 mg PO q12h, OR

Azithromycin, 500 mg PO on day 1, and 250 mg PO on days 2 – 5), OR

Clarithromycin 500 mg PO bid or ER 1 gm PO qd, OR

Levofloxacin, 500 mg PO qd OR

Gatifloxacin 400 mg PO qd, Or

Moxifloxacin, 400 mg PO qd

Initiate DMC Influenza / Pneumococcal immunization protocol (refer to immunization order form)

Discharge Criteria for Pts with Acute exacerbation of COPD:

Use of SABA frequency < q4h

Clinically stable for at least 12 - 24 hrs

ABG stable for at least 12 - 24 hrs

Ability to walk and talk, eat, sleep, poop, and peep.

Pt. understanding of HHC and other home therapies.

Prior to discharge from hospital, chronic therapy issues, supplemental O2, vaccinations, smoking cessation, assessment of inhaler technique, and pulmonary rehabilitation should be readdressed.

Complications:

    • Severe COPD and chronic hypoxemia may lead to PH and RHF.

    • COPD predisposes to lung CA, PTx, arrhythmias (MAT, AF, SVT, etc), psychiatric disturbances such as anxiety and depression.

    • Zolpidem is safe for COPD insomniacs.

Links resources:

www.goldcopd.com

www.aarc.org/resources/confronting_copd/exesum.pdf