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BRONCHIECTASISAND

LUNG ABSCESS


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DEFINITION

Bronchiectasisrefers to an irreversible airway dilation that involves the lung

in either a focal or a diffuse manner.

TYPES

cylindrical or tubular- most common form

varicose

cystic.

Indian incidence -3 per 1000.


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TYPES According to macroscopic morphology, three types have been

described, which also represent a spectrum of severity 8:

cylindrical : bronchi have a uniform

calibre, do not taper and have parallel

walls (tram track sign and signet ring sign)

varicose : relatively uncommon,with a beaded appearances where

dilated bronchi have interspersed sites

of relative narrowing

cystic : severe form with cyst-likebronchi that extend to the pleural

surface; air-fluid levels are commonly

present


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PATTERN OF LUNG

INVOLVEMENT

ETIOLOGY BY CATEGORIES WORKUP

Focal Obstruction (e.g., aspirated foreign

body, tumor mass)

Chest imaging (chest x-ray and/or

chest CT); bronchoscopy

Diffuse Infection (e.g., bacterial,

nontuberculous mycobacterial)

Gram's stain/culture;

stains/cultures for acid-fast bacilli

and fungi. If no pathogen is

identified, consider bronchoscopywith bronchoalveolar lavage (BAL)

Immunodeficiency (e.g.,

hypogammaglobulinemia, HIV

infection, bronchiolitis obliterans

after lung transplantation)

Complete blood count with

differential; immunoglobulin

measurement; HIV testing

Genetic causes (e.g., cystic fibrosis,Kartagener's syndrome, alpha1antitrypsin deficiency)

Measurement of chloride levels insweat (for cystic fibrosis), 1antitrypsin levels; nasal or

respiratory tract brush/biopsy (for

dyskinetic/immotile cilia

syndrome); genetic testing

Major Etiologies of Bronchiectasis and Proposed Workup


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Autoimmune orrheumatologic

causes (e.g.,rheumatoidarthritis,Sjgren's syndrome,inflammatory

boweldisease)

Clinical examination withcareful

joint exam, serologic testing (e.g.,forrheumatoid factor).

Recurrent aspiration Test of swallowing function and

general neuromuscular strength

Miscellaneous (e.g., traction

bronchiectasis from postradiationfibrosis or idiopathic pulmonary

fibrosis)

Guided by clinical condition

Idiopathic Exclusion of other causes


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Pathophysiology

2 Prerequisites:

Infectious insult

Impairment ofdrainage,airway obstruction,and/or

adefect inhost defense.


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CLINICAL MANIFESTATIONS

Symptoms -

Cough (90 %)

Daily sputum production (76%)

Dyspnea (72%)

Hemoptysis (56%)

Recurrent pleurisy

Signs -

Clubbing of digits.

crackles n wheezing .


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DIAGNOSIS

persistent chronic cough and sputum production.

+

radiographic features - presence of "tram tracks" dilated airways.

Chest CT- choice ofinvestigation.CT findings include airway dilation(detected as parallel "tram tracks or as "signet-ring sign).

bronchial wall thickening in dilated airways, inspissated secretions(e.g., the "tree-in-bud" pattern)

cysts emanating from the bronchial wall (especially pronounced incystic bronchiectasis


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HRCT

Radiol Clin N Am 43(2005) 513-542


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4. Diagnosis Chest CT

dilated bronchi

bronchial wall

thickening

tree

in

budpattern

cysts

lack of tapering


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4 Goals:- 1. Eliminate cause.

2. Improve tracheo bronchial clearance.

3. Control active infection.

4. Reverse airflow obstruction.

No specific medical therapy exists for the treatment of bronchiectasis.

Pharmacologic therapy focuses on the treatment of infectious exacerbations

that these patients commonly experience.

Commonly used medications:

antibiotics,

beta-agonists,

inhaled corticosteroids, and

expectorants.

TREATMENT


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In acute exacerbations >> broad-spectrum antibacterial agents.

Sampling of respiratory secretions allows treatment with antibiotics based on

specific species identification.

Acceptable choices (mild to moderatelyill) :

Amoxicillin

Tetracycline

Trimethoprim-sulfamethoxazole

A newer macrolide (eg, azithromycin[83]or clarithromycin[84, 85])

A second-generation cephalosporin

A fluoroquinolone

Duration of antibiotic therapy : 7-10 days.

Moderate-to-severe symptoms : parenteral antibiotics, such as an

aminoglycoside (gentamicin, tobramycin) and antipseudomonal synthetic

penicillin, a third-generation cephalosporin, or a fluoroquinolone, may be

indicated.

ANTIBIOTICTREATMENT


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Patients with bronchiectasis from CF are often infected with mucoid

Pseudomonas species, and, as such, tobramycinis often the drug of choice

for acute exacerbation.

NTM infections > 2 sputum samples +ve

> 1 BAL fluid sample +ve

> a biopsy sample h/p features(eg. granuloma or a +ve stain- AFB)+

1+VE sputum culture or a pleural fluid +ve on culture .

Treatment ofMAC in the setting of bronchiectasis, theA

merican ThoracicSociety recommends a 3- to 4-drug treatment regimen with clarithromycin,

rifampin, ethambutol, and possibly streptomycin that is continued until the

patient's culture results are negative for 1 year. The typical duration of therapy

may be 18-24 months.


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BRONCHIAL HYGIENE - to enhance secretion clearance hydration and mucolytic administration,

aerosolization of bronchodilators and hyperosmolar agents (e.g., hypertonicsaline)

chest physiotherapy

ANTI-INFLAMMATORY THERAPY-

dyspnea,

decreased need for inhaled beta-agonists,

reduced sputum production with inhaled glucocorticoids.

REFRACTORY CASES

select cases, surgery can be considered, with resection of a focal area of

suppuration. In advanced cases, lung transplantation can be considered.


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Pneumonia

Recurrent fibrinous pleurisy

Pleural effusion/empyema Haemoptysis-fatal

Brain abscess

Secondary amyloidosis.

COMPLICATIONS


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PREVENTION

gamma-globulin Ig deficient.

Vaccination resp.infection- (influenza n pnemococcal vaccines). suppressive antibiotic treatments

(1) administration of an oral antibiotic- (e.g.ciprofloxacin) daily for 12 weeksper month;

(2) rotating schedule- oral antibiotics- minimize the risk of drug resistance);

(3) macrolide antibiotic daily or three times per week ;

(4) inhalation of aerosolized antibiotics - [e.g., tobramycin inhalation solution(TOBI)] on a rotating schedule (e.g., 30 days on, 30 days off) decreasing the

microbial load.(5) intermittent administration ofIV antibiotics (e.g., "clean-outs") for

patients with more severe bronchiectasis and/or resistant pathogens.


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A

AFC

RB

EDAPM

B

C

Necrotizing pneumonia or lung gangrene refers to multiple small

pulmonary abscesses in contiguous areas of the lung, usually

resulting from a more virulent infection.

lung abscess refers to a microbial infection of the lung that results in

necrosis of the pulmonary parenchyma.

LUNG

ABSCESS


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Depending onduration ofinfection

acute - 6 wks

Depending on presence orabsence of underlying pulmonarylesion.

Primary= abscess in previously healthy patient or in a patient at risk for

aspiration

Secondary= associated bronchogenic neoplasm or immunocompromised patient.

.

CLASSIFICATION

nonspecific lung abscess refers to cases in which no likely pathogen is recovered from

expectorated sputum.

Putrid lung abscess is a term applied to anaerobic bacterial lung abscesses, which are

characterized by distinctive foul-smelling breath, sputum, or empyema fluid.


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ETIOLOGY Microbial Pathogens Causing Cavitary Lung Infection

Aspiration-Prone Host -

Anaerobic bacteria plus microaerophilic and/or anaerobic streptococci, Gemella spp.

Embolic (endovascular) lesions: usually Staphylococcus aureus, Pseudomonas aeruginosa,Fusobacterium necrophoruma

Endemic fungi: Histoplasma, Blastomyces, Coccidioides spp.

Mycobacteria: M. tuberculosis,M. kansasii, M. avium

Immunocompromised Host-

M.tuberculosis,

Nocardia asteroides, Rhodococcus equi, Legionella spp., P

.aeruginosa,Enterobacteriaceae (especially Klebsiella pneumoniae),Aspergillus spp., Cryptococcus spp.

Previously Healthy Host-

Bacteria: S. aureus,bS.milleri, K. pneumoniae, group AStreptococcus;Gemella, Legionella,

andActinomyces spp.

Parasites:

Entamoeba histolytica, Paragonimus westermani,

Strongyloides stercoralis


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MECHANISMS OFINFECTION

Commonest cause Aspiration of oropharyngeal contents.

75% abscesses - posterior segment Rt. upperlobe or Apical

segments of either lowerlobe - aspirated material - gravitatein the supine subject.

The development of lung abscess favoured by conditions that

prevent normal clearance of pulmonary secretions lung

tumours, bronchiectasis , inhaled foreign bodies.

Secondary infection in cong. abn like bronchopulmonary

sequestration & lung cysts .


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. Symptoms - fatigue cough

sputum production- putrid-smelling sputum indicative of the

presence of anaerobes.

while the foul odor - organisms' production of short-chain fatty

acids such as butyric or succinic acid.

fever Chills are uncommon.

pleurisydue to pleural involvement by contiguous spread or by a

bronchopleural fistula.

Signs - no signs specific for lung abscess

Digitalclubbing within a few wks. d/t inadequate t/t.

Dullness to percussion

Diminished breath sounds - abscess - too large

- near the surface of lung.

bronchialbreath sounds

CLINICAL MANIFESTATION


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DIAGNOSIS

1. IMAGING CXR PA VIEW, CT CHEST.

2. MICROBIOLOGICAL STUDIES stains ncultures.

Difficult to isolate anaerobic bacteria m/c cause.

if symptoms and clinical setting right for anaerobic

infection, generally treat empirically.

Gram stain: both+ve & -ve,mixed

AFB & Anaerobicculture

Transtrachealaspirates (TTA), transthoracicneedle aspirates

(TTNA), BAL, pleural fluid, or bloodcultures allow uncontaminated

specimens.

3. Bronchoscopy


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RADIOLOGICAL FINDINGS

Chest radiograph-

Increased density

Cavity formation Cavity with air-fluid levels

Fibrosis

Pleural effusion


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Manifests radiologically as a

cavity

With air fluid levels.


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Figure 16Figure 16--2. Reactivation tuberculosis withalarge cavitarylesioncontaining anair2. Reactivation tuberculosis withalarge cavitarylesioncontaining anair--fluidlevelin the right lowerfluidlevelin the right lowerlobe. Smallercavitarylesions are seenin otherlobes. (From Armstrong P et al:lobe. Smallercavitarylesions are seenin otherlobes. (From Armstrong P et al:Imaging of diseases of theImaging of diseases of the

chest,chest, ed2, St. Louis,1995, Mosby.)ed2, St. Louis,1995, Mosby.)


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TREATMENT ANTIBIOTIC THERAPY

Depending on presumed or established etiology.

ANAEROBIC BACTERIA

CLINDAMYCIN initially 600 mg i/v qid

followed by 300 mg qid orally.

any beta -lactam/beta-lactamase inhibitor combination; parenteral

treatment may be followed by orally administered amoxicillin/clavulanate.

Penicillin was previously regarded as a preferred drug for these infections,but many oral anaerobes produce -lactamases and clindamycin proved

superior to penicillin G.

Metronidazoleanaerobes.


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FAILURE OF THERAPY

Persistence of fever beyond57days.

progression of the infiltrate .

exclude factors such as - obstruction, complicating

empyema and involvement of antibiotic-resistant

bacteria.

bronchoscopy and/or CT to detect a possible associated

anatomic lesion, such as a tumor, or a foreign body.


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S. aureus

vancomycin =trough serum level of 1520 micro g/mL.

alternative linezolid.

Daptomycin should not be used for pulmonary infections

AEROBIC gram-negative bacteria antibiotic senstivity test

common pathogens - K. pneumoniae and P. aeruginosa

prolonged courses of parenteral antibiotics.

Carbapenems or beta -lactams are frequently combined with

aminoglycosides; oral fluoroquinolones are often effective initially,but resistance is common with prolonged use.

Aerosolized colistin and aminoglycosides .


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SURGICAL INTERVENTION

1. Surgery rarely required 10 -12 % cases.

2. Indications: failure of medical management, suspected

neoplasm, or hemorrhage.

3. Predictors of poorresponse to antibiotic therapyalone:

abscesses associated-with an obstructed bronchus, large

abscess (>6 cm in diameter), relatively resistant organisms

such as P. aeruginosa.

4. The usual procedure in such cases is a lobectomy.

5. Alt. intervention percutaneous drainage under CT

guidance.


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RESPONSE TO THERAPY

Usually show clinicalimprovement with fever within3-

5 days of initiation ofantibiotic therapy.

DEFERVESCENCE expected within

5

-10

days. Persistent fever beyond this time indicates DELAYED

RESPONSE.

such patients should undergo bronchoscopy or furtherdiagnostic tests to define the underlying anatomyand

microbiology of the infection.


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COMPLICATIONS

1. Empyema

2. Bronchopleural fistula

3. Pneumothorax , pyoneumothorax

4. Metastatic cerebral abscess

5. Sepsis

6. Fibrosis,bronchiectasis,amyloidosis


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There are three primary types of bronchiectasis. These types aredescribed by their anatomical appearance.

Cylindricalbronchiectasis is the mildest form and reflects the loss of thenormal tapering of the airways. The symptoms may be quite mild, like achronic cough, and usually are discovered on CT scans of the chest.

Saccular bronchiectasis is more severe, with further distortion of theairway wall and symptomatically, affected persons produce more sputum.

Cystic bronchiectasis is the most severe form of bronchiectasis, and

fortunately it is the least common form. This often occurred in the pre-antibiotic era when an infection would run its course and the patientwould survive with residual lung damage. These patients often would havea chronic productive cough, bringing up a cup or more of discolored mucuseach day.


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Supportive Treatment

The following general measures are recommended:

Smoking cessation

Avoidance of second-hand smoke

Adequate nutritional intake with supplementation, if necessary Immunizations for influenza and pneumococcal pneumonia[81, 82]

Confirmation of immunizations for measles, rubeola, and pertussis

Oxygen therapy is reserved for patients who are hypoxemic withsevere disease and end-stage complications, such as cor pulmonale.


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Antibiotic Therapy

Antibiotics have been the mainstay of treatment for more than 40 years. Oral,parenteral, and aerosolized antibiotics are used, depending on the clinical situation.

In acute exacerbations, broad-spectrum antibacterial agents are generally preferred.However, if time and the clinical situation allows, sampling of respiratory secretions

during an acute exacerbation may allow treatment with antibiotics based on specificspecies identification.

Acceptable choices for the outpatient who is mild to moderately ill include any of thefollowing:

Amoxicillin

Tetracycline

Trimethoprim-sulfamethoxazole

A newer macrolide (eg, azithromycin[83]or clarithromycin[84, 85])

A second-generation cephalosporin

A fluoroquinolone

In general, the duration of antibiotic therapy for mild to moderate illness is 7-10 days.

For patients with moderate-to-severe symptoms, parenteral antibiotics, such as anaminoglycoside (gentamicin, tobramycin) and an antipseudomonal synthetic penicillin, a

third-generation cephalosporin, or a fluoroquinolone, may be indicated. Patients withbronchiectasis from CF are often infected with mucoid Pseudomonas species, and, assuch, tobramycin is often the drug of choice for acute exacerbation.

Infection with Mycobacterium avium complex (MAC) provides special treatmentchallenges. For the treatment of MAC in the setting of bronchiectasis, the AmericanThoracic Society recommends a 3- to 4-drug treatment regimen with clarithromycin,rifampin, ethambutol, and possibly streptomycin that is continued until the patient's

culture results are negative for 1 year. The typical duration of therapy may be 18-24

months.


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Regularantibioticregimens

Some patients with chronic bronchial infections may need regular antibiotictreatment to control the infectious process. Some clinicians prefer to prescribeantibiotics on a regular basis or for a set number of weeks each month.

The oral antibiotics of choice are the same as those mentioned previously.Potential regimens include daily antibiotics for 7-14 days of each month,alternating antibiotics for 7-10 days with antibiotic-free periods of 7-10 days,or a long-term daily dose of antibiotics. For patients with severe CF andbronchiectasis, intermittent courses of intravenous antibiotics are sometimesused.[86, 87]

Aerosolizedantibiotics

In the past several years, the nebulized route of antibiotic administration hasreceived more attention because it is capable of delivering relatively highconcentrations of drugs locally with relatively few systemic adverse effects.[88]

This is particularly beneficial in treating patients with chronic infection from Paeruginosa. Currently, inhaled tobramycin is the most widely used nebulizedtreatment for patients with bronchiectasis from either CF or non-CF causes ofbronchiectasis.[89, 90, 91, 92, 93]Gentamicin[94]and colistin[95]have also been used.

No significant studies have examined the long-term use of inhaled antibioticsin patients with non-CF bronchiectasis. A study by Govan et al found sustainedlong-term benefit (12 mo) of inhaled gentamicin in this subgroup, along withan acceptable side effect profile.[96]Optimal dosing regimen of inhaledgentamicin still needs to be elucidated.


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Bronchodilator Therapy

Bronchodilators, including beta-agonists andanticholinergics, may help some patients with

bronchiectasis, presumably reversingbronchospasm associated with airwayhyperreactivity and improving mucociliaryclearance.[107, 108, 109]High-quality, large,

randomized clinical trials of bronchodilatortreatment in bronchiectasis have not beenperformed, however.


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ANTI INFLAMMATORY THERAPY

Azithromycin has known anti-inflammatory properties and long-term use has been studied in patients with both CF and non-CFbronchiectasis. In non-CF patients, azithromycin has been shown todecrease exacerbations and improve spirometry and microbiologicprofiles.[115]In CF patients a meta-analysis suggests that it improves

lung function, especially in those patients colonized withPseudomonas.[103]

A practical approach is to use tapering oral corticosteroids andantibiotics for acute exacerbations and to consider inhaledcorticosteroids for daily use in patients with significant obstructivephysiology on pulmonary function testing and evidence of

reversibility suggesting airway hyperreactivity. However, Kapur et alreported that the evidence supporting the use of inhaled steroids inadults with stable bronchiectasis is insufficient.[116]


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Medication Summary

No specific medical therapy exists for the treatment ofbronchiectasis. Pharmacologic therapy focuses on thetreatment of infectious exacerbations that these patients

commonly experience, most often in the form of an acutebronchitis-type syndrome.

The most widely accepted and commonly used medicationsin the treatment of acute infectious processes associatedwith bronchiectasis include antibiotics, beta-agonists,inhaled corticosteroids, and expectorants. Other morecontroversial medications have been previously mentionedin this article for completeness but are not discussed here.


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Antibiotics

Class Summary

These are the mainstays of treatment of patients with bronchiectasis andinfectious exacerbations. The route of antibiotic administration varies withthe overall clinical condition, with most patients doing well on outpatient

regimens. Some patients benefit from a set regimen of antibiotic therapy,such as therapy for 1 week of every month.

The choice of antibiotic is provider dependent, but, in general, theantibiotic chosen should have a reasonable spectrum of coverage,including the most common gram-positive and gram-negative organisms.Treatment of the patient who is more ill or the patient with CF oftenrequires intravenous anti-Pseudomonas species coverage with an

aminoglycoside, most often in combination with an antipseudomonalsynthetic penicillin or cephalosporin.Aerosolized tobramycin has beenfound effective in patients with cystic fibrosis (CF).


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Inhaled Beta Agonist

Class Summary

Although no long-term studies have been performed with inhaled beta-agonists, these medications are routinely used in patients withbronchiectasis for multiple reasons. Bronchiectasis may cause an

obstructive defect on pulmonary function testing that may respond toinhaled beta-agonists. Many older patients with bronchiectasis often havea concomitant illness, such as chronic obstructive pulmonary disease, thatresponds to inhaled beta-agonists.

Finally, in the acute infectious bronchitic exacerbation that occurs inpatients with bronchiectasis, patients may develop transient obstructiveairway physiology that may improve with an inhaled beta-agonist. Along

these same lines, many patients are started on inhaled steroids for long-term airway stabilization, but the efficacy of these medications inbronchiectasis is questionable, and any effect simply may be secondary tothe treatment of other concomitant obstructive airway diseases.


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Inhaled Corticosteroids

Class Summary

Studies suggest a benefit of inhaledcorticosteroids in bronchiectasis, although the

optimal dosing remains to be determined. No

significant studies of oral steroid therapy in

patients with bronchiectasis have been

performed.


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Expectorants

Class Summary

One of the hallmarks of bronchiectasis is a chronic, thick, viscidsputum production. In bronchiectasis, it is extremely difficult for thebody's natural mucociliary clearance mechanisms to adequately

clear the sputum produced. Although definitive evidence is lacking,expectorants are expected to increase respiratory tract fluidsecretions and to help loosen phlegm and bronchial secretions.

By reducing the viscosity of secretions, expectorants increase theefficacy of the mucociliary clearance system. Expectorants are oftenmarketed in combination with decongestants, which may provide

some patients additional relief. View full drug information

Guaifenesin (Mucinex)


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Cylindrical bronchiectasis



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Varicose bronchiectasis



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Cystis / saccular bronchiectasis


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