Therapy of COPD Exacerbations

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An exacerbation is a sustained worsening of the patient's symptoms from his or her usual stable state that is beyond normal day-to-day variations. It is acute in onset and sufficient to warrant a change in management. Commonly reported symptoms are worsening of dyspnea, increased sputum production, and change in sputum color. The most common causes of an exacerbation are respiratory infection and air pollution, but

the cause cannot be identified in about one-third of severe exacerbations.

Treatment depends on the symptoms and severity of the exacerbation. Mild exacerbations can often be treated at home with an increase in bronchodilator therapy with or without oral corticosteroids (Fig. 15-3). Antibiotics are indicated when there are specific signs of airway infection (e.g., change in color of sputum and/or increased sputum production or dyspnea) or when mechanical ventilation is needed. Moderate to severe exacerbations require management in the emergency department or hospital. Management should consist of controlled oxygen therapy, bronchodilators, oral or IV corticosteroids, antibiotics if indicated, and consideration of mechanical ventilation (noninvasive or invasive).

Bronchodilators

Albuterol is the preferred bronchodilator for treatment of acute exacerbations because of its rapid onset of action. Ipratropium can be added to allow for lower doses of albuterol, thus reducing dose-dependent adverse effects such as tachycardia and tremor. Delivery can be accomplished through MDI and spacer or nebulizer. The nebulizer route is preferred in patients with severe dyspnea and/or cough that would limit delivery of medication through an MDI with spacer. If response is inadequate, theophylline can be considered; however, clinical evidence supporting its use is lacking.

Oral Corticosteroids

Systemic corticosteroids shorten the recovery time, help to restore lung function more quickly, and may reduce the risk of early relapse.34 The GOLD guidelines recommend that corticosteroids be considered in addition to bronchodilators in all hospitalized patients and in outpatients with baseline FEVi less than 50% predicted.2 Other authorities recommend corticosteroids for all patients experiencing a COPD exacerbation.1 Oral prednisone 30 to 40 mg/day for 10 to 14 days is recommended. Prolonged treatment does not result in greater efficacy and increases the risk of adverse effects. If inhaled corticosteroids are part of the patient's usual treatment regimen, they should be continued during systemic therapy.

Gold Copd Treatment Algorithm

FIGURE 15-3. Algorithm for the management of an exacerbation of COPD at home. (From Ref. 2.) Antibiotics

The role of antibiotic treatment in treating COPD exacerbation is evolving, and recent

FIGURE 15-3. Algorithm for the management of an exacerbation of COPD at home. (From Ref. 2.) Antibiotics

The role of antibiotic treatment in treating COPD exacerbation is evolving, and recent evidence suggests that subsets of patients may benefit from antibiotic treatment. Antibiotics should be used in patients with COPD exacerbations who: (a) have all three cardinal symptoms (increased dyspnea, increased sputum volume, and increased purulence); (b) have increased sputum purulence along with one other cardinal symptom; or (c) experience a severe exacerbation requiring mechanical ventilation.

The predominant bacterial organisms in patients with mild exacerbations are Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. In patients with more severe underlying COPD, other bacteria such as enteric Gramnegative bacilli (Escherichia coli, Klebsiella pneumoniae, and Enterobacter cloacae) and Pseudomonas aeruginosa may be more common. Selection of empiric antibiotic therapy should be based on the most likely organism(s) thought to be responsible for the infection and on local resistance patterns. A risk stratification approach has

been advocated to help guide antibiotic selection. ' ' This approach is based on risk factors found to be predictive of treatment failure or early relapse. Patients at risk for poor outcome are candidates for more aggressive initial antibiotic treatment. Table

15-5 provides recommended antibiotic treatment based on this risk stratification ap-

2 35

proach. Antibiotic treatment for most patients should be maintained for 3 to 7 days, until the patient has been afebrile for 3 consecutive days. Exacerbations due to certain infecting organisms (P. aeruginosa, E. cloacae, and methicillin-resistant Staphylococcus aureus), while not common, require more lengthy courses of therapy (21-42 days).

If there is worsening clinical status or inadequate clinical response in 48 to 72 hours, reevaluate the patient, consider sputum Gram stain and culture if not already obtained, and adjust antimicrobial therapy. If Gram stain and culture results are available, narrow the antibiotic therapy according to cultured organism(s) and sensitivities. If no cultures have been obtained, or cultures remain negative, consider additional antibiotics and/or change to antibiotics with a broader spectrum of activity.

Oxygen

The goal of oxygen therapy is to maintain PaO2 above 60 mm Hg (7.98 kPa) or SaO2 above 90% to prevent tissue hypoxia and preserve cellular oxygenation.1 Increasing the PaO2 much further confers little added benefit and may increase the risk of CO2 retention, which may lead to respiratory acidosis. ABGs should be obtained after 1 to 2 hours to assess for hypercapnia.

Table 15-5 Recommended Antibiotic Therapy in Acute Exacerbations of COPD

Pïticnl Ch»r*ctrnsHci

Likgljf Pathogeny

Rrcommendcd Antibiotic*1

Mild Ejia<tjbatl$n Wilhoul Rllk Fjî (firî for Poor Outcome

Mot requirirq iiospilalizatlon liH thjri thnr esKiitutions per yraf

Ho cianoil>d lllnesi fEV, joar« than 501& p<odic ted

Si HEPfOCDCCUi pneumoniae Htï£liTK3phi*J> yiÎIÎA'iliKIT

¿(TJjf/kiiii CNawydia pneumoniae VUuitt

Onaf FiriKine Therapy: £ LiK (jrn (high (*nt JmOsicillirii

Lac tdmr^laciamaie Inh: :>iIih bmorit ilhnclaYuljiiah!) Tetracaine

Meinotw Ûror Tfvnapy:

MjtnAJCi Ça/i(hfloWtn.in. (liiiliiiCaflKiifl ietond- îk ihlrd-ffiYififliiofictffltviImpoiIrti fcifuroxlme, ccfpodaHme, ctidinh, ccipraell} M ihtfapr. tfor rpcommerytefl

M nifrraiT E »iwrbïtion With Hïtk F«Cti>ri for Poor Owtcornr fEtf, Ira îfjn H** ptcdhMfri Comafbtd disi1«« TTlf»(y |TiOfOC*Jtfi|>MiCfi! i^.ji Antibiotic therapy In 11« pie--out 3 mOnlhi

ALove organisms plut; Reiisrarii pocuiftatoiti «H«™™«* podudnç, pot »¿¡llit-rcsnlant), £Sitmichio foii Awftrt îp(j.

imeumwMie

Qralf irjriine Thetapy:

fHjclamjJMKBmKtlinliiHtcr (j«rieHjtiliin-cFivulj<viije) A) WrUJiiVie Ofll thtfopy f luoroquinolonc with enhanced piveumococcal activity

IJfcnC'VïJtddi* tfCrnirkwatjn. nwïirkwjtirD NThçifjpy;

placlanvfl- lac Lamjsi ■ inhibant (impie J «-sulbiitaiiU ietond tu thircJ tfcncratkjfi otpiultspctin fatfuOiinw, «iUiixO«}

I luOroquiriOtonC with enhanced pWurntXùttJl activity (levelkHcliiiHidkndlil

Severe Exicorbailon With Risk Factors for fàeudomonas aeitiginow

COPCLchiont obmuctlw? pulmonary drfe™; FEtf,, for«ii volume in I wîotkJ.

'AntlbkHJcs ate iridlcSled for patlenli wilhfOfOrMioittHiofts (a) have all ihuv cardinal *fmplnnw (Increase! dyspnc.i, Inc leased sputum volume, and inc. ilmvnJ puiutrKc'i, lL>: have Increased sputum uuiulencc along with ate Ullwt cardinal symptom;« (0 espcrienco J sc^e fïjoertMtioo requiring «>«h)nicai ventilation

All! t:Hifl[ thOfCOi ■■">i>ij!:I Ijhï ink? 11 ¡fiMdri.il kjn hX'il ItthUIIW |hiEliti

■] HiJh-tJiiiC ^KiCftiiillln Is riiomiï^rxlid OilC (0 |ly [iiCvilCXie Of penicillin reliant S .pniunNyiAje.

In advanced COPD, caution should be used because overly aggressive administration of oxygen to patients with chronic hypercapnia may result in respiratory depression and respiratory failure. In these patients, mild hypoxemia, rather than CO2 accumulation, triggers their drive to breathe.

Assisted Ventilation

R«Cfl( UKCiialliJtlOrt

IUHIVI' iyi|.ïn nnjpfcV"

OrnjfFirsrii'W Tfi&Qpy;

Amlpseudomorul f luofoqulnotaw If Ipcrf lonacln. h (jh-dixo

Icvoftiïjclri} I\fJîjiiflw:

Aniipîp udomonal ^-Lk tima^î-Ksiiiarït (Vfiii'iiin rpipftacilliiv tazobaclam)

1 hn : ! ■ H fi ¡Liilth . |i-iiif.ilKiri wish . ii ;rl[ A4in\H liI

acllvity (jctitaAdinie.celepirini?] Anllpuudomonal riuwtx]ulnalore'{dpof kxcacin, h<jh dou kwtoedfi)

Four 01 moie couim of antlbiaici In the fîjvru^'nou lait yit'a'

VHy «wftCCHtXGf?! P «*0e IV] fuevlous Isolation of f. oeiuqifiow

Mechanical ventilation can be administered as follows: (a) invasive (conventional) mechanical ventilation through an endotracheal tube; and (b) noninvasive mechanical ventilation using either negative (e.g., iron lung—not recommended) or positive pressure devices. Noninvasive positive pressure ventilation (NPPV) is preferred whenever possible. It improves signs and symptoms, decreases the length of hospital stay, and most importantly, reduces mortality. 6 Appropriate patients to consider for NPPV include those with the following characteristics: (a) moderate-to-severe dyspnea with use of accessory muscles and paradoxical abdominal motion; (b) moderate-to-severe acidosis (pH between 7.25 and 7.35) and hypercapnia (PaCO2 between 45 and 60 mm Hg [6-8 kPa]); and (c) respiratory rate between 25 and 35 breaths/min. Invasive mechanical ventilation should be used in patients with more severe symptoms and in those failing NPPV.

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