COPD Exacerbation:

An exacerbation of COPD (Chronic obstructive pulmonary disease) is defined as “an event in the natural course of the disease characterized by a change in the patient's baseline dyspnea, cough, and/or sputum and beyond normal day-to-day variations, that is acute in onset and may warrant a change in regular medication in a patient with underlying COPD”

Differential diagnosis of Acute Dyspnea

Respiratory

Airway COPD exacerbation, asthma exacerbation, acute bronchitis, infectious exacerbation of bronchiectasis, foreign body obstruction

Parenchyma pneumonia, cryptogenic organizing pneumonia, ARDS, acute exacerbation of interstitial lung disease

Vascular pulmonary embolism, pulmonary hypertension

Pleural pneumothorax, pleural effusion

Cardiac

Myocardial HF exacerbation, myocardial infarction

Valvular aortic stenosis, acute aortic regurgitation, mitral stenosis, endocarditis

Pericardial pericardial effusion, Tamponade

Systemic sepsis, metabolic acidosis, anemia

Others neuromuscular, psychogenic, anxiety

Pathophysiology

Precipitants of COPD Exacerbation infections, lifestyle/environmental (10%, cigarette smoke, dust, pollutants, cold air), non adherence, pulmonary embolism, pulmonary edema, pneumothorax, progression of COPD

Clinical Features

Rational clinical examination series:

Does the clinical examination predict airflow limitation?

	Sens	Spc	LR+	LR
History
Smoking >70 pack year	40%	95%	8	0.63
Smoking ever	92%	49%	1.8	0.16
Sputum ¼ cup	20%	95%	4	0.84
Chronic bronchitis Sx	30%	90%	3	0.78
Wheezing	51%	84%	3.8	0.66
Any exertional dyspnea	27%	88%	2.2	0.83
Coughing	51%	71%	1.8	0.69
Any dyspnea	82%	33%	1.2	0.55
Physical
Wheezing	15%	100%	36	0.85
Barrel chest	10%	99%	10	0.90
Decreased cardiac dullness	13%	99%	10	0.88
Match test	61%	91%	7.1	0.43
Rhonchi	8%	99%	5.9	0.95
Hyperresonance	32%	94%	4.8	0.73
FEV1 >9 s			4.8
FEV1 6 9 s			2.7
FEVI < 6 s			0.45
Subxyphoid cardiac apical impulse	8%	98%	4.6	0.94
Pulsus paradoxus (>15 mmHg)	45%	88%	3.7	0.62
Decreased breath sounds	37%	90%	3.7	0.70
Accessory muscle use	24%	100%		0.70
APPROACH ‘‘no single item or combination of items from the clinical examination rules out air flow limitation. The best findings associated with increased likelihood of airflow limitation are objective wheezing, FEV1 >9 s, positive match test, barrel chest, hyperresonance and subxyphoid cardiac impulse. Three findings predict the likelihood of airflow limitation in men: years of cigarette smoking, subjective wheezing and either objective wheezing or peak expiratory flow rate’’

Stereotypes (not useful clinically)

Blue bloater (more chronic bronchitis) cough and sputum, hypoxemia, CO2 retention, pulmonary hypertension, right sided heart failure

Pink Puffer (more emphysema) cachexia, relatively preserved blood gases, dyspnea even at rest

Prediction rule for Obstructive Airway Disease

Self reported history or chronic obstructive airway disease LR+ 7.3

Maximum laryngeal height < 4 CM [< 1.6 IN.] Distance between the top of thyroid cartilage and suprasternal notch at end of expiration. LR+ 2.8

Investigations

Basic

Labs CBCD, electrolytes, urea, Cr, troponin/CK, Ca, Mg, PO4

Microbiology sputum Gram stain/AFB/C&S/ fungal

Imaging CXR

ECG left atrial enlargement, atrial fibrillation, sinus tachycardia

Spirometry/PFT FEV1/FVC < 0.7 partially reversible. Severity based on FEV1

ABG if acute respiratory distress

Special

BNP if suspect HF

D dimer if suspect PE

Echocardiogram

Prognostic Issues

Prognosis of patients with acute exacerbation of COPD in hospital mortality 5 10% Gold classification 2007 all have FEV1/FVC <0.7

Stage I (Mild) FEV1 80% predicted >80% predicted

Stage II (Moderate) FEV1 50 79% predicted

Stage III (Severe) FEV1 30 49% predicted

Stage IV (very severe) FEV1 < 30% predicted, or < 50% predicted + cor pulmonale

Body Index

BMI 0= >21, 1= 21

Obstruction (post bronchodilator FEV1) 0 <65% predicted, 1=50 64%, 2=36 49%, 3= <35%

Distance walked in 6 min 0= >350 m, 1=250 349 m, 2=150 249 m, 3= <149 m

Exercise MMRC Dyspnea 0=0 1, 1=2, 2=3, 3=4

Scoring hazard ratio for death from any cause per one point increase in BODE score is 1.34

ABC O2 to keep sat >90%, or 88 92% if CO2 retai ner, IV

Bronchodilators salbutamol 2.5 5 mg NEB q4h ATC + q1h PRN and ipratropium 0.25 0.5 mg NEB q4h. Puffers preferable for acute management if proper technique used

Steriods prednisone 40 60 mg PO daily 14 days (tapering dose not necessary in all cases) or methylprednisolone 60 125 mg IV daily (inpatient)

Antibiotics give if any two of the following criteria are met: raised sputum purulence, raised dyspnea or raised sputum volume. Other considerations include the need for non invasive mechanical ventilation and ‘‘at risk’’ for poor outcome (substantial comorbidities, severe COPD, frequent exacerbations >3/year, recent antibiotics within 3 months); choices depend on clinical circumstance (levofloxawcin 500 mg PO daily x 7 days, doxycycline 100 mg PO BID x 7 to 10 10 days, amoxicillin 500 mg PO BID x days, cefuroxime 250 500 mg PO BID x 10 days, or azithromycin 500 mg PO x 1 day then 250 mg PO daily x 4 days)

Mechanical ventilation BIPAP, intubation OTHERS DVT prophylaxis (heparin 5000 U SC BID), physiotherapy.

Long Term management

Education smoking cessation Disease specific self management program. Puffer technique education and review

Vaccinations influenza vaccine annually and pneumococcal vaccine booster at 5 years

Rehabilation exercise training (increases quality of life and exercise tolerance)

First line short acting b2 agonist or short act ing anticholinergic on an as needed basis

Second line long acting β 2 agonist or long acting anticholinergic (tiotropium 1 puff [18 µmg/ puff] INH daily) plus short acting β 2 agonist PRN. Consider early initiation of long acting agents if requiring regular PRN short acting agents as long acting agents are superior

Third line long acting β 2 agonist plus long acting anticholinergic, with short acting β 2 agonist PRN

Fourth line long acting anticholinergic plus long acting β2 agonist/inhaled corticosteroid combination (e.g. Advair, Symbicort). No role for inhaled corticosteroid alone in COPD

Fifth line fourth line plus theophylline 400 mg PO daily 3 days, then 400 600 mg PO daily, therapeutic level 10 20 mg/mL

Sixth line fifth line plus home O2

Seventh line lung volume reduction surgery (may be beneficial if upper lobe involvement and poor functional capacity) or lung transplant

Treatment Issues

Factors for Impending Intubation cardiac or respiratory failure, hemodynamic instability, markedly elevated respiratory rate (>35/min), fatigue and labored respiration, use of accessory muscles, worsening hypercapnia, acidosis (especially lactic), stridor (impending upper airway obstruction), agonal breathing (impending respiratory arrest)

Life prolonging measures for COPD smoking cessation, supplemental O2

Indications for supplemental home O2 ABG done in room air. PaO2 <55 mmHg alone or PaO2 ><60 mmHg in the presence of bilateral ankle edema, cor pulmonale, or hematocrit >56% <55 mmHg alone or PaO2 <60 mmHg in the presence of bilateral ankle edema, cor pulmonale, or hematocrit >56%

Specific Entitis

α1 Anttrupsin deficiency

Pathophysiology production of an abnormal protease inhibitor (homozygous ZZ) with impaired transport out of the liver. Serum level is only 10 15% of normal increased protease activity leads to emphysema and cirrhosis (10%)

Diagnosis a1 antitrypsin levels

Treatments similar to COPD, a1 antitrypsin replacement

Bronchiolitis obliterans

Pathophysiology severe inflammation of bronchioles airflow obstruction. Very different from bronchiolitis obliterans organizing pneumonia (BOOP)/cryptogenic organizing pneumonia (COP), a parenchymal lung disorder

Causes infection (viral, mycoplasma), inflammatory (ulcerative colitis, rheumatoid arthritis), transplant (bone marrow, lung), toxic fumes, idiopathic

Treatments bronchiolitis obliterans (with an organizing intraluminal exudates and proliferative granulation tissue polyp) is usually steroid responsive. Constrictive bronchiolitis (late, fibrotic, concentric) is not responsive to glucocorticoids

Bronchiectasis

Pathophysiology airway obstruction, destruction, altered immunity increased  cellular and mediator inflammatory response raised elastase, sputum production  recurrent infections vicious cycle permanent dilatation of bronchi. Major types of bronchiectasis include

Cylindrical or Tubular Bronchiectasis dilated airways alone, sometimes represents residual effect of pneumonia and may resolve

Varicose Bronchiectasis focal constrictive areas along the dilated airways

Saccular or Cystic Bronchiectasis most severe form. Progressive dilatation of the air ways, resulting in large cysts or saccules

Causes

Focal broncholith, post infectious, tumor, extrinsic lymph node compression, post lobar resection, recurrent aspiration

Diffuse

Post-Infections bacterial (Pseudomonas, Haemophilus), mycobacterium, fungal, viral (adenovirus, measles, influenza, HIV)

Immunodeficiency cancer, chemotherapy, hypogammaglobulinemia, immunosup pression, sequelae of toxic inhalation or aspiration of foreign body

Interstitial Lung Disease traction bronchiectasis

Inflammatory RA, SLE, Sjogren’s syndrome, relapsing polychondritis, IBD

Inherited a1 antitrypsin deficiency, cystic fibrosis, primary ciliarydyskinesia (Kartagener’s syndrome, Young’s syndrome), tracheobronchomegaly (Mounier Kuhn syndrome), cartilage deficiency (Williams Campbell syndrome), Marfan’s syndrome

Diagnosis high resolution CT chest (signet ring sign), PFT (obstruction reversibility).
Treatments exercises, chest physiotherapy, and bronchodilators similar to COPD; however, if reversible, inhaled corticosteroids should be given early. Ensure adequate systemic hydration. Effective treatment of exacerbations