Asthma

Definition and epidemiology

• Chronic inflamm. disorder w/ airway hyperrespons. + var. airflow obstruction

• Affects 5% population; 85% of cases by age 40; ? link to ADAM-33 (N£jw 2002.-947:936) Clinical manifestations (nejm 2001:344:350)

• Classic triad wheezing, cough, and dyspnea; others include chest tightness, sputum;

symptoms typically chronic with episodic exacerbation

respiratory irritants (smoke, perfume, etc.) & allergens (pets, dust mites, pollen, etc.) infections (URI, bronchitis, sinusitis)

drugs (eg. ASA via leukotrienes,/3B via bronchospasm. morphine via histamine release) emotional stress, cold air. exercise

• Exacerbations: important to note frequency, severity, duration, and required treatment including need for steroids, ED visits, hospitalizations, and intubations

Physical examination

• Wheezing and prolonged expiratory phase

• Presence of nasal polyps, rhinitis, rash -* allergic component

• Exacerbation -> î RR. use of accessory muscles of respiration, pulsus paradoxus Diagnostic studies

• PFTs: i peak expiratory flow rate (PEFR)

spirometry: i FEV,. 1 FEV,/FVC. coved flow-volume loop: lung volumes: • î RV + TLC ® bronchodilator response (T FEVi -12%) strongly suggestive of asthma methacholine challenge (i FEV, --20%) if PFTs nl:Se -90% <ajrccm 2000.161 309)

• Allergy suspected -» consider ✓ serum IgE. eosinophils, skin testing/RAST

• Sputum: eos >3% — 86% Se. 88% Sp; can also see Curschmann's spirals (mucus casts of distal airways) and Charcot-Leyden crystals (eosinophil lysophospholipase); normalization of sputum eos count may help guide outPt Rx (tancée 2002;360:1715)

• Fractional excretion of NO (FeNO) proportional to airway inflammation and sputum eosinophils: >20 ppb Se 88%. Sp 79% {ajrccm 2004:169:473) Ddx ("all that wheezes is not asthma...")

• Mechanical airway obstruction or structural airway abnormalities (eg, tumor)

• Laryngeal or vocal cord dysfunction (eg. due to GERD or postnasal drip)

• COPD. CHF. vasculitis: consider in older Pts with new dx of "asthma"

• Other pulmonary causes: bronchiectasis. PE. aspiration, sarcoidosis. ILD

• "Asthma + " syndromes (Lancet 2002;360:1313)

Atopy asthma * allergic rhinitis + atopic dermatitis

ASA-sensitive asthma (Samter s syndrome) = asthma + ASA sensitivity 1 nasal polyps ABPA asthma - pulmonary infiltrates • allergic rxn to Aspergillus Churg-Strauss asthma + eosinophil • granulomatous vasculitis Classification of severity

• Intermittent: sx <1/wk. noctural sx - 2/mo. brief exacerb.. PEF or FEV, -80%

• Mild persistent: sx -1/wk but <1/d. noctural sx -2/mo; exacerb. may affect activity &

• Mod. persistent: sx qd. noctural sx >1/wk; exacerb. may affect activity & sleep.

daily use of short-acting fo-agonist. PEF or FEV, 60-80%

• Sev. persistent: sx qd. freq. nocL sx & exacerb.. limited physical activity. PEF or FEV, r=60% "Quick-relief" medications

• Short-acting inhaled Pî-agonists (eg, albuterol): treatment of choice levoalbuterol (R-isomer) 2x potency with similar side effect profile, no outcome benefit

• Inhaled anticholinergics (ipratropium) improve (Jj-agonist delivery

• Systemic corticosteroids

"Long-term-control" medications

• Inhaled or systemic corticosteroids: treatment of choice (SOCS.jama 200i;28S:2S83)

FeNO can predict responsiveness (ajrccm 2005:172:453) and guide Rx (nejm 2005:352.2163)

• Longocting inhaled f^-agonists (salmeterol): use w/ caution given concern for î mortality

(SMART. Chest 2006:129:15; Annoh 2006:144:904) possibly due to descnsitization of |i-receptOrs Pts w/ p2 receptor genetic polymorphism Arg/Arg (1/6* of asthmatics) do not appear to derive long-term benefit and may be harmed by LAB A (Lancet 2004:364:1505)

• Nedocromil/cromolyn: useful in young Pts. exercise-induced bronchospasm;

ineffective unless used before trigger or exercise exposure

• Theophylline: useful in hard to control Pts. PO convenience, but high side effect profile

• Leukotriene modifiers: some patients very responsive, especially aspirin-sensitive asthma (ajrccm 20011653); may consider trial in all patients

Other

• Behavior modification: identify and avoid triggers

• Immunotherapy (eg. desensitization): may be useful if significant allergic component

• Anti-lgE (omalizumab): allergic asthma uncontrolled on inhaled steroids (nejm 2006:354 2689)

• TNF antagonists may be helpful in Pts w/ refractory asthma (Níjm 2006:354:697)

• Bronchial thermoplasty (exp'tal): radiofrequency destruction of airway smooth muscle no A in FEV,. but 1 in sx and # of exacerbations (nejm 2007:356:1327)

Principles of treatment

• Education and avoidance of environmental triggers for all Pts

• Use quick-relief rescue medication as needed for all Pts

• Rather than fixed Rx based on severity, new goal is to achieve complete control daily sx 2/wk. 0 nocturnal sx or limitation of activity, reliever med - 27wk, nl PEFR or FEV,

• Step up treatment as needed to gain control, step down as tolerated

Asthma Stepwise Therapy

Step 1

Step 2

Step 3

Step 4

StepS

Rapid-acting ßj-agonists prn

S

Select one

Select one

Do one or more

Add one or both

i

Low-dose

Low-dose ICS ♦

A low-dose ICS to

Oral steroids

ICS

LABA

med/high dose (w/LABA)

(lowest dose)

P

LTA

Med/high-dose ICS

Add LTA

Anti-lgE Rx

s g

Low-dose ICS + LTA

Add Theo

Ô

Low-dose ICS • Theo

ICS inhaled corticosteroid; LABA - long-acting {Ji-agonist: LTA = leukotriene antaguTheo = sutuirx>d-re) theophylline Boldfaced treatments are preferred options.

(Adapted from Global Initiative for Asthma (GINA)-Global Strategy for Asthma Management and Prevention 2006)

ICS inhaled corticosteroid; LABA - long-acting {Ji-agonist: LTA = leukotriene antaguTheo = sutuirx>d-re) theophylline Boldfaced treatments are preferred options.

(Adapted from Global Initiative for Asthma (GINA)-Global Strategy for Asthma Management and Prevention 2006)

Exacerbation

Direct evaluation

Previous asthma: baseline PEFR. steroid requirement. ED visits, hospital admissions;

previous need for intubation a good predictor of risk of death (Thorax 1986:41.833) Current exacerbation: duration, severity, potential précipitants, medications used

• Physical exam

Signs of severity: tachypnea, tachycardia, diaphoresis, cyanosis, fragmented speech, absent breath sounds, accessory muscle use. pulsus paradoxus, abdominal paradox Assess for barotrauma: asymmetric breath sounds, tracheal deviation, subcutaneous air — pneumothorax, precordial (Hamman s) crunch pneumomediastinum

• Diagnostic studies

ABG. not always considered essential because exam and SjO? provide equivalent info;

low P.COj initially, nl or high P»COî may signify tiring; may respond to bronchodilacor PEFR: used to follow clinical course; CXR: not essential unless suspicion for PNA or PTX

Acute Pharmacologic Treatment

Agent

Dose

Comments

Oxygen

Titrate to achieve S,Oj >90%

Albuterol

MDI 4-8 puffs q20min or nebulizer 2.5-5 mg q20min continuous nebulizer if severe

First-line therapy (Chest 2002:121:1036)

Corticosteroids

prednisone 60 mg PO or methylprednisolone 80 mg IV

IV not superior to PO {jama 1988:260527)

Ipratropium

MDI 4-8 puffs q30min, or nebulizer 0.5 mg q30min *3

1 bronchodilation when combined w/ albuterol

(Chest 2002:121:1977)

Magnesium

2g IV over 20 rnin (lancet 2003:361:2114)

T PEFR & FEV,

Other treatments

• Epinephrine (0.3-0.5 mL SC of 1:1000 dilution): no advantage over inhaled fr-agonists

• Antibiotics: not needed unless evidence of bacterial infection, although evidence of improved symptoms/ FEV, may be related to anti-inflammatory effect (NEJM 2006:3S41S89)

• IV montelukast/zafirlukast: improves FEVj acutely {Ajrccm 2003:167488);. relapse after d/c from emergency department (0*« 2004:1261480)

I Classification of asthma exacerbation severity

• Mild: PEFR -80%. dyspnea on exertion, end-expiratory wheezes

• Moderate: PEFR 50-80%. dyspnea w/ talking, expiratory wheezes, accessory muscle use

• Severe: PEFR 50%. S,Oj 91%.PlCOj 42. dyspnea at rest, inspiratory and expiratory wheezes, accessory muscle use. pulsus paradoxus 25 mmHg

Figure 2-2 Iratlal aueumcnt oI auhma exacerbation

Initial Assessment

Oxygen to maintain Sa02 >90% Inhaled |i agonists q 20 mins x 3 Corticosteroids PO or IV x 1 consider Magnesium IV

Repeat assessment at 3 h (more freq il severe exacerbation) symptoms, exam. PEFR, Sa02)

no dyspnea improve <25% se v. dyspnea wheezing no or mild wheezing mild-mod dyspnea.'wheezing P»CÖ2 >42 mmHg response sustained 60' after Rx i i

Good response Incomplete response Poor response

Discharge home Admission to hospital ward Admission to ICU Inhaled fe-agonists Systemic corticosteroid taper Close follow-up

Hospital ward-level care

• ✓ PEFR q8h. SaOj q8h (continuous if 90%). provide supplemental O2

• Bronchodilators and steroids usually sufficient continue inhaled (^-agonist as needed for sx. watch for tachycardia and hypokalemia start steroids at prednisone 60 mg qd or equivalent, begin taper when PEFR 50% ICU-level care

• High-dose steroids: methylprednisolone 125 mg IV q6h (Arehnes 1983:143:1324)

• Noninvasive ventilation: may I need for intubation </nt Con Med 2001:27 486)

• Heliox: ? helpful in first hour, especially in more severe Pts <Che*t 2003:123882)

• Invasive ventilation large ET tube, keep Pp*,, 30 (predicts barotrauma better than PIP), watch for auto-PEEP

paralysis, inhalational anesthetics, bronchoalveolar lavage w/ mucolytic, and ECMO have been used with success

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Definition and epidemiology (NE/m 2004:35036)

• Progressive airflow limitation caused by airway and parenchymal inflammation

Emphysema vs. Chronic Bronchitis

Emphysema

Chronic Bronchitis

Definition Dilation/destruction of airspaces (pathologic definition)

Productive cough -3 mo/yr x s2 yrs (clinical definition)

Pathophysiology Parenchyma affected Matched V/Q defects Mild hypoxemia

Small airways affected V/Q mismatch

Severe hypoxemia, hypercapnia PHT. cor pulmonale

Clinical Severe, constant dyspnea manifestations Mild cough

Intermittent dyspnea Copious sputum production

Physical exam "Pink puffer"

Tachypneic. noncyanotic. thin Diminished breath sounds

"Blue bloater" Cyanotic, obese, edematous Rhonchi & wheezes

Pathogenesis (lancct 2003:362:1053)

• Caused by: cigarette smoke (centrilobular emphysema, affects 15-20% of smokers).

a i-antitrypsin deficiency (panacinar emphysema), recurrent airway infections

Clinical manifestations

• Chronic cough, sputum production, dyspnea; later stages — freq exac.. a.m. HA. wt loss

• Exacerbation triggers: infxn. other cardiopulmonary disease, ind. PE (Annoa 2006:144 390)

Infxn: overt tracheobronchitis/pneumonia from viruses. S. pneumoniae. H. influenzae. M. catarrhalis. or triggered by changes in strain of colonizers (NE}M 2002:347 465)

• Physical exam: t AP diameter of chest ("barrel-chest"), hyperresonance. i diaphragmatic excursion, i breath sounds. T expiratory phase, rhonchi. wheezes during exacerbation: tachypnea, accessory muscle use. pulsus paradoxus, cyanosis Diagnostic studies

• CXR: hyperinflation, flattened diaphragms. • interstitial markings and bullae

Obstruction: .. FEVi. I FVC.i FEVi/FVC. expiratory scooping of flow-volume loop Hyperinflation: " RV. T TLC. T RV/TLC Abnormal gas exchange: 1 DiCO (in emphysema)

• ABG: i PjOj, - ? P.COj (in chronic bronchitis, usually only if FEV, -1.5 L) and . pH

• ECG: PRWP. S1S2S3. R-sided strain. RVH. T P waves in lead II ("P pulmonale")

Chronic treatment ("COPDer") tfama 2003:290:2301.2313; nijm 2004:350:2689)

• Corticosteroids: (inhaled)

-20% i in exacerbations if FEVi 2.0 L (Lone« 1998:351:773; BM) 2000:320:1297) may slow FEVi loss (NiJM 2000:343:1902 & 2007;3S6:775) t in pneumonia; no A in mortality with inh steroids alone (ne¡m 2007:356 775)

• Oxygen: if P,Oj - 55 mmHg or S,Oj - 89% (during rest, exercise, or sleep) to prevent cor pulmonale and . morality (a/inah 1980:93:391 A tone« 198U681)

• Prevention: Flu/Pneumovax; smoking cessation — 50% i in lung function decline (AjRCCM

2001166:675) and 1 long-term mortality (Annoh 2005:142323)

• Dilators: anticholinergics. 3i-agonists. theophylline anticholinergic > (^-agonist; combination may be more effective (Chea 1999:115:635) LA anticholinergic (tiotropium): 1 exac.. T QoL 1 FEVi decline in mod/severe disease vs. ipratropium (Cochrane 2005;CD002876), superior to LA fr-agonist as monotherapy (O»« 2004:125:249). and Combination ! FEVi (Chat 2006:129:509) LABA: -15% i in exacerbations, i FEVi decline, trend towards i mort. (ne)m 2007356:775) LABA + inhaled steroid may 1 mort- (TORCH nqm 2007:356:775)

• Experimental

Lung volume reduction surgery (LVRS): i exer. capacity, i mort. rf FEVi -20%. upper-

lobe emphysema, i baseline exer. capacity (NQM 2000:343:239; nett. 2003:348 2059) Bronchoscope LVRS safe and effective (Oku 2006:129518). await outcome data Roflumilast (PDE III inhibitor): T FEVi (Lancet 200S:366:563)

• Rehabilitation: i dyspnea and fatigue. T exercise tolerance. T QoL (Cochrane 2001CD003793)

COPD Staging and Recommended Therapies by GOLD Criteria

Stage

PFTs (of predicted)

Therapies

0: t risk

Normal but • sx

n/a

1: Mild

FEV, -80%

Dilator prn

v

FEV, 50-80%

c o a c

Standing Dilator (tiotropium >fi ag) Corticosteroid if response Rehabilitation

IIB: Mod

U g

FEV, 30-50%

>

Above ♦

a.

Corticosteroid if t exacerbations

III: Severe

¿ u_

FEV, <30% or respiratory failure or right heart failure

Oxygen if respiratory failure Experimental as indicated

(Adapted from Global Iniuauve lor Chronic Obstructive Pulmonary Disease.WHO/NHLßl 1998)

Exacerbation

COPD Exacerbation Treatment

Agent

Dose

Comments

Ipratropium

MDI 4-8 puffs q1-2h or Nebulizer 0.5 mg q1-2h

First-line therapy

Albuterol

MDI 4-8 puffs q1-2h or Nebulizer 2.5-5 mg q1-2h

Benefit if component of reversible bronchoconstriction

Corticosteroids

Methylprednisolone 125 mg IV q6h * 72 h then

Prednisolone 60 mg PO qd x 4 d then taper by 20 mg q3-4d or

Prednisone 30 mg qd x 2 wks if pH -7.26 (Lancet 1999:354:456)

30% 1 in death, intubation, readmit for COPD or need for t Rx (NEJM 1999:340:1941: Archim 2002:162:2527)

OutPt Rx after ED visit i relapse (N£/M 2003.348:2618)

Antibiotics

Amoxicillin. TMP-SMX. doxycydine. clarithromycin, anti-pneumococcal FQ. etc.. all reasonable (no single abx proven superior)

H. influenzae, M. catarrhal, S. pneumonia freq. precip. T PEFR & chance of clinical resolution (/AMA 1995:273:957)

Oxygenation

T F.Oj to achieve P,Oj ?55-60 or S,02 90-93%

Watch for CO2 retention

(due to T V/Q mismatch, loss of hypoxic resp. drive. Haldane effect) but must maintain oxygenation!

Noninvasive positive-pressure ventilation

Endotracheal intubation

Initiate early if mod/severe dyspnea, i pH / T P.COj, RR >25 Results in 58% 1 intubation. 1 LOS by 3.2 d. 59% i mortality Contraindications: A MS. inability to cooperate or clear secretions, hemodynamic instability. UGIB

(Cochrane 2004.CD004104:Annoli 2003:138:861. N£/M 1995333:817; £«/ 2005:25:34«)

Consider if P.Oj - 55-60. T'ing P,C02. i'ing pH. T RR. respiratory fatigue. A MS. or hemodynamic instability

Other measures

Chest physiotherapy, mucolytics not supported by data Monitor for cardiac arrhythmias

Prognosis

• FEVi: 60% predicted - 5-y mort 10%; ■ 40% -. 50%; - 20% - - 90%

• BODE 10-point scale: HR 1.62 for resp. mort for each 1-point '

Obstruction (FEV,): 50-64% (.1). 36-49 (-2).-3S (-3)

Pyspnea (MMRC scale): walking level (-1), after 100 yds (+2). with ADL (+3)

ixs capacity (6 min walk):250-349 m (■ 1). 150-249 (• 2).: 149 (-3)

superior to FEVi (N£JM 20CW;3SCH00S); can predict survival from LVRS (Ctai 2006:129.873)

• Continued smoking, frequent exacerbations also associated w/ poorer prognosis

• Lung transplant 0 A survival (tone« 1998.35124). but may improve QoL and symptoms

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