Bronquiectasias tratamiento.docx

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INTRODUCTIONBronchiectasis is a syndrome of chronic cough and daily viscid sputumproduction associated with airway dilatation and bronchial wall thickening. Multiple conditionsare associated with the development of bronchiectasis, but all require an infectious insult andusually also impairment of drainage, airway obstruction, and/or a defect in host defense.

Of the broad spectrum of causes of noncystic fibrosis bronchiectasis, only a few respond todirect treatment (eg, certain immunodeficiencies, nontuberculous mycobacterial infection,allergic bronchopulmonary aspergillosis). Instead, treatment of bronchiectasis is aimed atcontrolling infection and improving bronchial hygiene [1,2]. Surgical extirpation of affected areasmay be useful in selected patients.

The treatment of bronchiectasis will be reviewed here. The diagnosis and treatment of cysticfibrosis and the clinical manifestations and diagnosis of bronchiectasis are discussedseparately. (See"Cystic fibrosis: Clinical manifestations and diagnosis"and"Cystic fibrosis:Overview of the treatment of lung disease"and"Cystic fibrosis: Antibiotic therapy for lungdisease"and"Clinical manifestations and diagnosis of bronchiectasis in adults".)

TREATING THE UNDERLYING DISEASEFor most causes of bronchiectasis, treatment ofthe underlying disease is not possible, as the bronchiectasis is a manifestation of scarring thatresulted from a prior injury or infection (eg, severe pneumonia, pertussis in childhood) or aresult of an ongoing problem with secretion clearance that does not have a specific treatment(eg, primary ciliary dysfunction). However, some disease processes can be controlled toprevent further scarring. The evaluation and diagnosis of the underlying causes ofbronchiectasis are discussed separately (table 1andtable 2andtable 3). (See"Clinicalmanifestations and diagnosis of bronchiectasis in adults".)

Examples of disease processes in which specific therapies may prevent progression ofbronchiectasis include the following:

While nontuberculous mycobacterial infection can be an opportunisticinfection in a patient with bronchiectasis, it can also be a primary causeof bronchiectasis. It is usually treated directly to prevent further lunginjury. (See"Overview of nontuberculous mycobacterial infections in HIV-negative patients"and"Treatment of nontuberculous mycobacterialinfections of the lung in HIV-negative patients".)

Certain primary immunodeficiencies can be treated with immunoglobulinpurified from pooled human plasma given intravenously (IVIG) orsubcutaneously (SCIG). The use of these preparations is discussedseparately. (See"Immune globulin therapy in primaryimmunodeficiency".)

Treatment of recurrent aspiration due to swallowing difficulties or severegastroesophageal reflux with aspiration may help prevent progression ofbronchiectasis. (See"Diagnosis and treatment of oropharyngealdysphagia"and"Approach to refractory gastroesophageal reflux diseasein adults".)

Allergic bronchopulmonary aspergillosis, in which central bronchiectasisis caused by an inflammatory response to aspergillus colonization of theairway, is treated with glucocorticoids and antifungal agents.(See"Allergic bronchopulmonary aspergillosis", section on 'Treatment'.)

While unproven, it is hoped that treating the underlying disease willprevent progression of bronchiectasis due to rheumatic or otherinflammatory diseases, such as rheumatoid arthritis, inflammatory boweldisease, and sarcoidosis. (See"Overview of lung disease associated
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with rheumatoid arthritis", section on 'Bronchiectasis'and"Pulmonarycomplications of inflammatory bowel disease", section on 'Airwayinvolvement'and"Treatment of pulmonary sarcoidosis withglucocorticoids".)

Patients with symptomatic bronchiectasis due to tracheobronchomegaly

may benefit from placement of a stent or tracheobronchoplasty tomaintain airway patency and improve secretion clearance. (See'Airwaystabilization for tracheobronchomegaly'below and"Tracheomalacia andtracheobronchomalacia in adults", section on 'Treatment'.)

TREATMENT OF ACUTE EXACERBATIONSDeciding when a patient has an acuteexacerbation depends upon symptomatic changes rather than any specific laboratory feature.Acute bacterial infections are usually heralded by increased production of sputum that is moreviscous with darker color, often accompanied by lassitude, shortness of breath, and pleuriticchest pain. Systemic complaints such as fever and chills are generally absent. Sputum isobtained for gram stain and culture prior to antibiotic administration. A chest radiograph is

performed in patients with respiratory distress or systemic complaints to exclude the possibilityof pneumothorax or pneumonia.

The colonizing bacterial flora in patients with bronchiectasis is slightly different from that seenwith chronic bronchitis. Frequently isolated pathogens in bronchiectasis include Haemophilusinfluenzae, Moraxella catarrhalis, Staphylococcus aureus, Pseudomonas aeruginosa(especiallymucoid types), and, less frequently, Streptococcus pneumoniae[3,4]. The likelihood of resistantorganisms tends to increase with the number of prior courses of antibiotics. The presence of P.aeruginosa, particularly if the patient has had prior courses of anti-pseudomonal agents, oftennecessitates hospital admission for intravenous antibiotics.

Outpatient treatmentMost afebrile, clinically stable patients with an exacerbation of

bronchiectasis can be treated as outpatients. The initial selection of an oral antibiotic for anexacerbation of bronchiectasis is generally based on previous sputum bacteriology results, thehistory of success or failure of prior regimens, and the presence of allergy to antimicrobialagents.

Sputum showing sensitive organisms For patients whose sputumcultures do not show beta-lactamase-positiveH.influenzaeor Pseudomonas, reasonable initial antibiotic choicesincludeamoxicillin,500 mg three times daily, or a macrolide, based onthe typical colonization patterns noted above. Alternatively, otherantibiotics with a similar spectrum of coverage may be used. High-dose

regimens (amoxicillin 1 gram three times daily, or 2 grams twice daily)may be needed in patients with severe bronchiectasis who arechronically colonized with H. influenzae, but may be difficult to toleratedue to gastrointestinal adverse effects such as diarrhea[2]. The initialantibiotic selection can be modified in a couple of days based on theresponse to therapy and results of the sputum culture and sensitivity.

Sputum culture growing beta-lactamase-positive organism In thepresence of beta-lactamase producing H. influenzae, antibiotic choicesincludeamoxicillin-clavulanate,a second or third generationcephalosporin,azithromycinorclarithromycin,doxycycline,or afluoroquinolone [2]. (See"Microbiology, epidemiology and treatment ofHaemophilus influenzae", section on 'Treatment'.)
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Sputum culture data not available For those without cultureinformation, a fluoroquinolone (eg,levofloxacin,moxifloxacin)is areasonable, broad spectrum, therapeutic option [5].

Sputum growing sensitive Pseudomonas For patients with knowncolonization with Pseudomonas, the initial antibiotic selection depends

on the sensitivity patterns of the organisms isolated. In the absence ofknown resistance to quinolones, the usual choice isciprofloxacin,500 to750 mg twice daily [2].

Because of the propensity of P. aeruginosato develop resistance andthe limited of availability of oral agents, the efficacy of addinginhaledtobramycinsolution (TS) to oral ciprofloxacin was studied. In amulticenter trial, 53 patients with known P. aeruginosainfection whowere having exacerbations of bronchiectasis were randomly assigned toreceive ciprofloxacin plus inhaled TS or ciprofloxacin plus placebo for twoweeks [6]. The addition of inhaled TS to ciprofloxacin did not improve

clinical outcomes compared to ciprofloxacin alone, although there was amarked reduction of Pseudomonasdensity in the sputum of patients whoreceived inhaled TS plus ciprofloxacin. Wheezing was more common inthe inhaled TS plus ciprofloxacin group.

Based on current data, inhaled aerosols of antibiotics, such as TS,cannot be recommended alone or in combination with ciprofloxacin foracute exacerbations in bronchiectasis. Certain aerosolized antibioticsmay be helpful for prophylaxis. (See'Inhaled antibiotics'below.)

Sputum growing resistant Pseudomonas The nonquinoloneantibiotics typically used for resistant Pseudomonasare not availableorally and require intravenous administration for a systemic effect.Intravenous antibiotics for exacerbations due to resistant Pseudomonasare discussed below and separately. (See'Inpatient treatment'belowand"Treatment of Pseudomonas aeruginosa infections", section on'Antibiotic choices'.)

As noted above, inhaled aerosols of antipseudomonal antibiotics are notadequate treatment for exacerbations of bronchiectasis.

Duration of therapy The optimal duration of therapy is not well-defined. Clinical experience favors a duration of 10 days for patients with

a first time or few exacerbations [5,7,8]. For patients with resistantorganisms such as P. aeruginosa, a 14 day course is preferred [2].Sputum culture and sensitivity to help define antibiotic selection areindicated in patients who fail to respond to the initial antibiotic, or whohave repeated symptomatic attacks over a short period of time.

Inpatient treatmentInitial inpatient treatment of an exacerbation is appropriate for patientswith characteristics such as increased respiratory rate 25/minute,hypotension, temperature38C, hypoxemia (pulse oxygen saturation


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If the reason for hospital admission is to initiate intravenous antibiotics because the patient hasknown colonization withPseudomonasresistant to oral quinolones (rather than due to severity ofillness), the initial antibiotic choice is based on the sensitivity profile from culture data andhistory of allergy to antibiotics.

If sputum culture data are not available, local antibiotic resistance patterns and responses to

recent antibiotics guide empiric antibiotic selection. For example, if the patient has failed an oralquinolone, coverage for resistant Pseudomonasand methicillin resistant Staphylococcusaureusshould be included, pending updated culture results.

It is controversial whether single or dual (eg, beta-lactam plus aminoglycoside) antibiotictherapy is preferable for flares of bronchiectasis due to Pseudomonas[2]. A meta-analysis ofstudies examining this question in patients with cystic fibrosis was unable to determine whichcourse of therapy is better [9]. We typically use a single agent (eg, antipseudomonal penicillinwith or without a beta-lactamase inhibitor,ceftazidime,aztreonam)unless the patient appearsacutely ill such that an incipient Pseudomonaspneumonia seems possible. In the latter case,we typically add a second agent (eg, fluoroquinolone, aminoglycoside). Aminoglycosides should

not be used as monotherapy. The question of single versus dual therapy and antibiotic selectionand dosing for Pseudomonaspneumonia are discussed in greater detail separately.(See"Pseudomonas aeruginosa pneumonia", section on 'Treatment'and"Treatment ofPseudomonas aeruginosa infections".)

Use of aminoglycoside antibiotics requires careful dosing and monitoring to avoid renal orototoxicity. (See"Aminoglycosides".)

Once the patient has stabilized and results of initial cultures are available, the antibiotic regimencan be narrowed to the most effective/least toxic regimen.

Atypical pathogensTwo colonizing organisms that are particularly problematic and difficult

to eradicate are Mycobacterium avium complex (MAC) and Aspergillus species.Mycobacterium avium complexMycobacterium avium complex (MAC) refers to infectionscaused by one of two nontuberculous mycobacterial species, either M. aviumor M.intracellulare. MAC and other nontuberculous mycobacteria are often harbored in damaged lungtissue and bronchiectatic airways. A detailed discussion about the treatment of MAC and othernontuberculous mycobacteria in the lung is presented elsewhere. (See"Treatment ofnontuberculous mycobacterial infections of the lung in HIV-negative patients"and"Microbiologyof nontuberculous mycobacteria".)

Aspergillus speciesAllergic bronchopulmonary aspergillosis is a cause of centralbronchiectasis in patients with asthma and can also develop in patients with bronchiectasis due

to another cause. For patients with allergic bronchopulmonary aspergillosis and a total serumIgE level >1000 IU/mL (>2400 ng/mL), the usual initial therapy is oralprednisone0.5 to1 mg/kg per day for two weeks followed by alternate day therapy tapered over three to sixmonths. A 16 week course of an antifungal agent, such asitraconazoleorvoriconazole,may beadded in patients who require substantial doses of glucocorticoids. (See"Allergicbronchopulmonary aspergillosis", section on 'Treatment'.)

PREVENTION OF EXACERBATIONSInfection plays a major role in causing andperpetuating bronchiectasis, so reducing the microbial load and attendant mediators is acornerstone of therapy [10]. A variety of suppressive or preventive antibiotic regimens havebeen studied as methods to reduce the frequency of exacerbations and prevent further loss oflung function.
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One difficult issue is colonization with Pseudomonas aeruginosa, which has a propensity topersist in damaged (eg, bronchiectatic) airways, possibly due to its ability to produce virulencefactors and to circumvent immune defenses with quorum signaling and biofilmproduction. Pseudomonascan also interact adversely and directly with the airway epithelialsurface and the cystic fibrosis conductance regulator (CFTR) protein [11]. (See"Cystic fibrosis:

Genetics and pathogenesis", section on 'Chronic lung infection'and"Epidemiology andpathogenesis of Pseudomonas aeruginosa infection", section on 'Chronic infection in cysticfibrosis'.)

Patients colonized with P. aeruginosahave reduced quality of life indices, more extensivebronchiectasis on CT, accelerated decline in pulmonary function, and increased number ofhospitalizations, compared to patients colonized with Haemophilus influenzae[12,13]. For thisreason, attempts are often made to eradicate P. aeruginosainfection with variable success.

MacrolidesFor patients with bronchiectasis who have recurrent exacerbations, we suggestpreventive therapy with a macrolide antibiotic. Our threshold for the initiation of preventiveantibiotics is two or more exacerbations within one year. Chronic low-dose administration of

macrolide antibiotics appears to have an effect that is not solely antimicrobial [14]. A variety ofalternative mechanisms have been proposed to explain the observed benefit, includingreduction of biofilm around virulent gram negative organisms such as P. aeruginosa, retardationof neutrophilic influx, stabilization of nuclear and cellular membranes, and promotion of gastricemptying that may reduce potential for acid reflux. Daily or three times weekly use of amacrolide has been found to be efficacious in the management of cystic fibrosis even in patientscolonized withPseudomonas. (See"Cystic fibrosis: Overview of the treatment of lung disease",section on 'Macrolide antibiotics'.)

Three multicenter, randomized trials have shown reduced rates of exacerbations with use of amacrolide as compared to placebo in patients with noncystic fibrosis bronchiectasis. The trialsare small but have a consistent finding of a reduction in exacerbations.

In the Effectiveness of Macrolides in patients with BronchiectasisusingAzithromycinto Control Exacerbations (EMBRACE) trial, 141patients with at least one exacerbation of bronchiectasis in the prior yearwere randomly assigned to take azithromycin 500 mg or placebo, orallythree times a week for six months [15]. Azithromycin was associated witha decrease in exacerbations compared with placebo (RR 0.38, 95% CI0.260.54). However, no significant difference was noted in lung functionor quality of life.

In the Bronchiectasis and Long-termAzithromycintreatment (BAT) trial,

83 patients with three or more exacerbations of noncystic fibrosisbronchiectasis in the prior year were randomly assigned to takeazithromycin 250 mg or placebo daily for 12 months [16]. The mediannumber of exacerbations was zero in the azithromycin group and two inthe placebo group. Thirty-two placebo-treated versus 20 azithromycin-treated individuals had at least 1 exacerbation (hazard ratio, 0.29 [95%CI, 0.16-0.51]). However, the rate of colonization with azithromycinresistant organisms was 88 percent in the azithromycin group and 26percent in the placebo group. Abdominal pain and diarrhea were morecommon in the azithromycin group.

The Bronchiectasis and Low-doseErythromycinStudy (BLESS)

randomly assigned 117 patients two or more exacerbations of noncysticfibrosis bronchiectasis in the prior year to take erythromycin 250 mg or
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placebo twice daily for one year [17]. Protocol defined pulmonaryexacerbations were modestly reduced in the erythromycin group (mean1.29 versus 1.97 per patient per year, incidence rate ratio [IRR], 0.57[95% CI 0.42-0.77]). The volume of sputum produced and rate of declinein forced expiratory volume in one second (FEV1) were also decreased,

although the clinical importance of these changes appears small.Erythromycin increased the proportion of macrolide-resistantoropharyngeal streptococci.

The impact of adverse effects, such as gastrointestinal symptoms, hepatotoxicity, decreasedhearing, and increased bacterial resistance, will need ongoing review and attention. In addition,macrolide antibiotics are associated with the potential for prolongation of the QT interval.Clinicians should assess the risk of torsades de pointes when considering a macrolide for long-term treatment in patients at risk for cardiovascular events. Patients at particular risk includethose with existing QT interval prolongation, hypokalemia, hypomagnesemia, significantbradycardia, bradyarrhythmias, uncompensated heart failure, and those receiving certain

antiarrhythmic drugs. (See"Azithromycin, clarithromycin, and telithromycin", section on 'QTinterval prolongation'.)

In order to avoid development of nontuberculous mycobacteria that are macrolide resistant,some experts (and we agree) obtain sputum stains and cultures for nontuberculousmycobacterial (NTM) infection prior to initiating long-termazithromycintherapy. Preventivemonotherapy with a macrolide antibiotic is NOT initiated if NTM are identified on culture.(See"Cystic fibrosis: Overview of the treatment of lung disease", section on 'Macrolideantibiotics'and'Mycobacterium avium complex'above.)

Daily suppressive nonmacrolide antibioticsDaily oral nonmacrolide antibiotic treatmenthas been studied in small case series, but not randomized trials. As an example, among 10patients treated withciprofloxacin(500 to 1500 mg/day in two to three divided doses) for at least90 days, symptomatic improvement occurred in seven [18]. A major concern with long-termquinolone suppressive therapy is the development of resistant strains of P. aeruginosa [2].Based on clinical experience, we usually reserve daily suppressive nonmacrolide antibioticregimens (eg,amoxicillin500 mg twice daily,doxycycline100 mg twice daily) for patients withthree or more exacerbations a year who are not candidates for long-term macrolideadministration and are not colonized with P. aeruginosa [2]. Patients who are colonized with P.aeruginosamay be candidates for inhaled antibiotic therapy, as described below.

Inhaled antibioticsThe role of inhaled antibiotics in noncystic fibrosis bronchiectasis isunclear. Inhaled antibiotics (eg,tobramycin,gentamicin)have been investigated primarily in

patients with cystic fibrosis when P. aeruginosais present in the respiratory secretions. Benefitsin these patients include reduced sputum Pseudomonasdensity, improved FEV1, anddecreased hospitalizations. Inhaled antibiotics may also play a role in the management of somepatients with noncystic fibrosis bronchiectasis and Pseudomonascolonization, but no agent isapproved for this purpose by the US Food and Drug Administration (FDA). (See"Cystic fibrosis:Antibiotic therapy for lung disease", section on 'Inhaled antibiotics'.)

Studies of inhaled antibiotics in noncystic fibrosis bronchiectasis include the following:

Aerosolizedtobramycin The use of aerosolized tobramycin has beenstudied in patients with noncystic fibrosis bronchiectasis [19-22]. One trial

randomly assigned 74 patients with non-CF bronchiectasis andbacteriologic evidence of P. aeruginosainfection to receive aerosolized
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tobramycin (300 mg, twice daily) or aerosolized placebo for 28 days [19].Patients in the treatment group demonstrated a 10,000-fold reductionin Pseudomonasdensity, but no change in FEV1as compared tocontrols.

In a six month crossover study of aerosolized tobramycin versus placeboin 30 patients, there was no difference in the exacerbation rate, but thenumber of hospitalizations and duration of hospital stay were modestlyreduced during the tobramycin phase [23]. Of concern, four patients inthe tobramycin group and one in the placebo group died during thestudy.

In a small, uncontrolled study, aerosolized tobramycin (300 mg, twicedaily) was administered to 41 patients with non-CF bronchiectasis and ahistory of P. aeruginosainfection. The protocol alternated two weeks oftreatment with two weeks without therapy for a total of 12 weeks [20].

Treatment was associated with a decrease in symptoms andimprovements in health-related quality of life (QOL). However, 10 of 41patients (24 percent) were unable to complete the protocol because ofside effects (cough, wheezing, worsened dyspnea), and two of thepatients who completed the trial acquired tobramycin-resistant P.aeruginosa.

Aerosolizedgentamicin Aerosolized gentamicin, prepared by dilutingthe intravenous preparation with saline, was assessed in 58 patients withnon-CF bronchiectasis, who were randomly assigned to use nebulizedgentamicin 80 mg twice daily or normal saline placebo for a year [22].Patients were aware of their medication assignment. The primaryendpoint of reduction in sputum bacterial density was achieved in thegentamicin cohort as compared to no reduction in the saline group.Thirty-one percent of the gentamicin cohort had complete eradicationof Pseudomonasat the end of 12 months. Favorable secondaryendpoints in subjects taking gentamicin included reduction inexacerbations and improved patient outcomes by analysis of twoquestionnaires. However, no differences were seen in the 24 hoursputum volume or in spirometric parameters. In addition, the sputumbacterial density was no longer different from control at the three monthfollow-up visit. Further study is needed before routine use of nebulized

intravenous gentamicin in these patients. Inhaledaztreonam Aztreonam is a monobactam with a monocyclicbeta-lactam structure. As inhalation of the intravenous preparation ofaztreonam induces airway inflammation, a lysine salt formulation wasdeveloped for inhalation. In patients with cystic fibrosisand Pseudomonasairway colonization, inhaled aztreonam 75 mg 3 timesdaily (at least 4 hours apart) for 28 days improved FEV1, decreasedsputum Pseudomonasdensity, and delayed time to need for intravenousor other inhaled antipseudomonal antibiotics compared with placebo. Allof the studies have used a particular mesh nebulizer for administration ofaztreonam, called the Altera eFlow. Preliminary evidence suggests that

inhaled aztreonam is not beneficial in noncystic fibrosis bronchiectasis.(See"Cystic fibrosis: Antibiotic therapy for lung disease", section on
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'Inhaled aztreonam lysine'and"Delivery of inhaled medication in adults",section on 'Mesh nebulizers'.)

All of the inhaled antibiotics have the potential to cause bronchospasm, so the first treatment isgenerally administered in a supervised setting with spirometry before and 15 and 30 minutes

after the test dose [2]. If a patient is going to develop bronchospasm, it will usually occur duringthe first treatment.Albuterolshould be immediately available for inhalation shouldbronchospasm develop. Subsequently, pretreatment with an inhaled beta-agonistbronchodilator can be given to those patients who develop mild bronchoconstriction. For thosewhose FEV1decreases by >15 percent or >200mL after antibiotic inhalation, we generally donot administer further doses [2].

Patients treated with inhaled antibiotics should be assessed for medication-related adverseeffects (eg, throat irritation or pain, abnormal taste sensation, cough, chest discomfort) anddevelopment of resistant organisms.

Other inhaled antibiotics are under investigation for noncystic fibrosis bronchiectasis,

includingcolistinand both dry powder and dual-release (contains free and liposomal drug)preparations ofciprofloxacin[24,25]. (See"Cystic fibrosis: Antibiotic therapy for lung disease",section on 'Inhaled colistin'.)

Intermittent intravenous antibioticsIntermittent intravenous antibiotics are not part ofroutine care of patients with stable bronchiectasis. In the absence of an acute exacerbation,administration of intravenous antibiotics should be reserved for patients with resistantorganisms (such as Pseudomonas) being prepared for major surgery, such as resection of abronchiectatic region of lung or another procedure during which pulmonary function may becompromised.

Mucolytic agents and airway hydrationA variety of agents, such as nebulized hypertonic

saline solution,mannitol,and mucolytic agents, have been developed to help patients clear theirairways of secretions. Among these therapies, some evidence favors hypertonic saline, but theother therapies have not been proven to be beneficial in noncystic fibrosis bronchiectasis. Incontrast, nebulized hypertonic saline anddornase alfaare beneficial in cystic fibrosis.Avoidance of dehydration is logical, but of unproven benefit. (See"Role of mucoactive agents inthe treatment of COPD"and"Cystic fibrosis: Overview of the treatment of lung disease", sectionon 'Agents to promote airway secretion clearance'.)

Nebulized hypertonic saline Nebulized hyperosmolar agents,including hypertonic (6 to 7 percent) saline andmannitol,have beenstudied as mucokinetic therapies [26]. Their mechanism of action is

thought to be related to improved mucus rheology, increased ciliarymotility, and enhanced cough clearance. Another possibility, suggestedby in vitro data, is that low mucus salinity rather than under hydrationcontributes to mucus retention, which is counteracted by hypertonicsaline [27]. We use hypertonic saline in patients with tenacious orcopious phlegm to augment expectoration, based on clinical experience.

The efficacy of nebulized hypertonic saline (6 percent) was examined in40 patients with noncystic fibrosis bronchiectasis who were randomlyassigned to treatments with hypertonic saline or isotonic saline daily for12 months [28]. No between group differences were found inexacerbation rates, quality of life, FEV1, or sputum colonization.
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inhaled glucocorticoid use [42]. Adverse effects of inhaled glucocorticoids are discussedseparately. (See"Major side effects of inhaled glucocorticoids".)

Oralibuprofenis occasionally used to reduce airway inflammation in children aged 6 to 13 withcystic fibrosis, but data are insufficient to support a role for nonsteroidal anti-inflammatoryagents (NSAIDs) in adult noncystic fibrosis bronchiectasis [43]. (See"Cystic fibrosis: Overview

of the treatment of lung disease", section on 'Ibuprofen'.)

Gastroesophageal refluxThere is emerging concern that gastroesophageal reflux (GER)and bronchiectasis are associated [44]. Among patients with advanced lung disease awaitinglung transplantation, patients with bronchiectasis had the highest prevalence of GER (50percent) [45]. As a result, gastric acid suppression (eg, H2 blocker, proton pump inhibitor) isused in patients with symptomatic GER or those with two or more exacerbations in a year. Therole of diagnostic testing (eg, esophageal pH monitoring, manometry, esophagram, or upperendoscopy) is uncertain. We typically pursue diagnostic testing or additional anti-refluxmeasures in patients with persistent symptoms or frequent, unexplained exacerbations.(See"Clinical manifestations and diagnosis of gastroesophageal reflux in adults"and"Medical

management of gastroesophageal reflux disease in adults".)

ImmunizationsData are limited regarding immunization guidelines for individuals withchronic respiratory diseases. Seasonal influenza vaccine is typically administered annually topatients with bronchiectasis, as for other chronic respiratory diseases. (See"Seasonal influenzavaccination in adults".)

Despite limited data in bronchiectasis, pneumococcal vaccine is typically given to patients withbronchiectasis, as is recommended for patients with other chronic respiratory diseases [46]. In aprospective randomized study of 167 adults with chronic respiratory diseases including 20 withprobable bronchiectasis, the group receiving both influenza and pneumococcal vaccines hadsignificantly reduced numbers of acute infectious exacerbations during the first, but not second

year of the study as compared to the group receiving the influenza vaccine alone [47].(See"Pneumococcal vaccination in adults", section on 'Approach to vaccination'.)

PULMONARY REHABILITATIONPulmonary rehabilitation is efficacious in COPD, and afew small studies support a benefit in patients with bronchiectasis. In a trial that randomlyassigned 30 patients with bronchiectasis to pulmonary rehabilitation plus chest physiotherapy orchest physiotherapy alone, the pulmonary rehabilitation group had greater improvements inexercise tolerance and health related quality of life [48]. In a trial of 32 patients withbronchiectasis, an eight week exercise rehabilitation program improved the distance traveledduring a walk test and endurance capacity, compared to a control group [49]. The addition ofspecific inspiratory muscle training extended the improvement in exercise capacity another

three months.We generally offer participation in pulmonary rehabilitation to patients with moderate-to-severeairflow limitation on pulmonary function testing, similar to the guidelines for COPD.(See"Pulmonary rehabilitation in COPD".)

SURGERYThe combination of impaired defense mechanisms and recurrent infection oftenresults in diffuse bronchiectasis affecting multiple lobes of the lung. In the setting of diffusebronchiectasis, there is little opportunity for surgical cure, other than bilateral lungtransplantation. Nevertheless, there is a role for surgery in some patients to remove particularlydiseased segments or to control massive hemoptysis. Goals are conservative, aiming to controlspecific disease manifestations rather than cure or elimination of all areas of bronchiectasis.

Resection of bronchiectatic lungThe immediate goal of surgical extirpation includesremoval of the most involved segments or lobes with preservation of nonsuppurative or
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nonbleeding areas. Middle and lower lobe resections are most often performed. The superiorsegment of the lower lobe may be involved to a lesser extent and can frequently be salvagedwhen considering lower lobe resection. Surgical intervention is often combined with anaggressive antibiotic and bronchial hygiene regimen to reduce bacterial infection and improvedrainage.

Major indicationsThe major indications and goals for resectional surgery in bronchiectasisinclude:

Removal of destroyed lung partially obstructed by a tumor or the residueof a foreign body

Reduction in acute infective episodes in patients with frequentexacerbations due to localized bronchiectasis

Reduction in overwhelming purulent and viscid sputum production inpatients with bronchiectasis confined to one or two lobes andunresponsive to medical therapy

Elimination of bronchiectatic airways subject to uncontrolled hemorrhagewhen other measures fail (see'Management of hemoptysis'below)

Removal of an area suspected of harboring resistant organisms such asMAC [50]or multidrug resistant tuberculosis [51](see"Treatment ofnontuberculous mycobacterial infections of the lung in HIV-negativepatients", section on 'Surgical management'and"Diagnosis, treatment,and prevention of drug-resistant tuberculosis", section on 'Surgery')

OutcomesSurgical case series have shown low operative mortality (600 mL/day) due to bronchiectasis that cannot be controlled with less invasivemeasures. The evaluation and management of massive hemoptysis is discussed separately.(See"Overview of massive hemoptysis"and"Massive hemoptysis: Initial management".)
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