Bronchiectasis and Lung Abscess

Bronchiectasis
An irreversible airway dilation that involves the lung
in either a focal or a diffuse manner
An abnormal and permanent dilatation of bronchi
Categorized as cylindrical or tubular (the most common
form), varicose, or cystic.

Etiology

Infectious or noninfectious causes

Focal bronchiectasis;
compression by adjacent lymphadenopathy or
parenchymal tumor mass
airway tumor or aspirated foreign body
Diffuse bronchiectasis;
an underlying systemic or infectious disease process.
Immunodeficiency
Genetic causes (e.g., cystic fibrosis, , 1 antitrypsin
deficiency)
Autoimmune or rheumatologic causes (e.g.,
rheumatoid arthritis)
Recurrent aspiration

More pronounced involvement of the upper lung fields is

most common in cystic fibrosis (CF) and is also observed
in postradiation fibrosis.
Bronchiectasis with predominant involvement of the
lower lung fields usually has its source in chronic
recurrent aspiration .
Nontuberculous mycobacteria often preferentially affects
the midlung fields. Finally, predominant involvement of
the central airways is reported in association with allergic
bronchopulmonary aspergillosis (ABPA)
In many cases, the etiology of bronchiectasis is not
determined.
As many as 25–50% of patients referred for
bronchiectasis have idiopathic disease.

Epidemiology

Varies greatly with the underlying etiology.

For example, CF,in late adolescence or early adulthood In
contrast, MAC infection; nonsmoking women older than
age 50 years.
In general, the incidence of bronchiectasis increases
with age. Bronchiectasis is more common among women
than among men.
In areas where tuberculosis is prevalent, bronchiectasis
more frequently occurs as a sequela of granulomatous
infection.
High incidence of malnutrition in certain areas may
predispose to immune dysfunction and development of
bronchiectasis.

Pathogenesis and Pathology

The most widely cited mechanism of infectious

bronchiectasis is the "vicious cycle hypothesis," in which
susceptibility to infection and poor mucociliary clearance
result in microbial colonization of the bronchial tree.
Pseudomonas aeruginosa, colonizing damaged airways
and evading host defense mechanisms. Impaired
mucociliary clearance can result from inherited
conditions such as CF
pneumonia caused by Bordetella pertussis or
Mycoplasma pneumoniae) can result in significant airway
damage and poor secretion clearance.
The presence of the microbes incites continued chronic
inflammation, with consequent damage to the airway
wall, continued impairment of secretion and microbial
clearance, and ongoing propagation of the
infectious/inflammatory cycle.

Small-airway wall inflammation and larger-airway wall

destruction as well as dilation, with loss of elastin,
smooth muscle, and cartilage.
Inflammatory cells in the small airways release proteases
and other mediators, such as reactive oxygen species and
proinflammatory cytokines, that damage the larger-
airway walls.
In addition to emphysema, bronchiectasis has been
observed in patients with 1 antitrypsin deficiency.

Proposed mechanisms for noninfectious bronchiectasis

include immune-mediated reactions that damage the
bronchial wall
Clinical Manifestations

The most common clinical presentation is a persistent

productive cough with ongoing production of thick,
tenacious sputum.
Crackles and wheezing on lung auscultation, and some
patients exhibit clubbing of the digits.
Acute exacerbations of bronchiectasis are usually
characterized by changes in the nature of sputum
production, with increased volume and purulence.
However, typical signs and symptoms of lung infection,
such as fever and new infiltrates, may not be present.

The classic manifestation

Cough with production mucopurulent or tenacious
sputum lasting for months to years
Can be dry
Dyspnea, wheezing, & pleuritic chest pain.
Recurrent “bronchitis” requiring antibiotics
Past history of repeated RTI
Hemoptysis
P/E - Audible rals over the involved lung .
- Pulm. Osteoarthropathy, marked clubbing and
cyanosis
Diagnosis
Laboratory Tests.
CBC
Immunoglobulin quantitative- IgG,IgM,IgA
Sputum culture & smear for bacteria, mycobacterium &
fungi.
CXR
Abnormal but non diagnostic in 90%
Common finding
Increased bronchovascular markings
Dilated & thickened airways (tram or parallel line)
Air fluid level or cystic spaces
Pleural Rxn & displaced fissure
usually based on presentation with a persistent chronic
cough and sputum production accompanied by
consistent radiographic features.
The presence of "tram tracks" indicating dilated airways
is consistent with bronchiectasis. Chest CT is choice for
confirming the diagnosis.
CT findings include airway dilation (detected as parallel
"tram tracks" or as the "signet-ring sign, lack of
bronchial tapering, bronchial wall thickening in dilated
airways, inspissated secretions, or cysts emanating from
the bronchial wall.
Approach to the Patient: Bronchiectasis
Elicitation of a clinical history, chest imaging, and a
workup to determine the underlying etiology.
Evaluation of focal bronchiectasis almost always requires
bronchoscopy to exclude airway obstruction by an
underlying mass or foreign body.
A workup for diffuse bronchiectasis includes analysis for
the major etiologies. Pulmonary function testing is an
important component of a functional assessment of the
patient.

Treatment: Bronchiectasis

Control of active infection and improvements in

secretion clearance and bronchial hygiene

Antibiotic Treatment
Antibiotics targeting Haemophilus influenzae and P.
aeruginosa should be administered in acute
exacerbations, usually for a minimum of 7–10 days.
Bronchial Hygiene

include hydration and mucolytic administration,

aerosolization of bronchodilators and hyperosmolar
agents
Anti-Inflammatory Therapy
reduced sputum production with inhaled glucocorticoids.
Risks of immunosuppression and adrenal suppression
must be carefully considered with use of anti-
inflammatory therapy in infectious bronchiectasis.
Refractory Cases

In select cases, surgery can be considered, with resection

of a focal area of suppuration.
Complications
recurrent infections
Recurrent infections can result in injury to superficial
mucosal vessels, with bleeding and, in severe cases, life-
threatening hemoptysis.
Prognosis
The decline of lung function in patients with non-CF
bronchiectasis was similar to that in patients with COPD,
with the forced expiratory volume in 1 s (FEV1) declining
by 50–55 mL per year.

Lung Abscess
Refers to a microbial infection of the lung that results in
necrosis of the pulmonary parenchyma.
Necrotizing pneumonia or lung gangrene refers to
multiple small pulmonary abscesses in contiguous areas
of the lung, usually resulting from a more virulent
infection.

Classification
Classified by clinical and pathologic features including the
tempo of progression, the presence or absence of an
associated underlying lesion, and the microbial pathogen
responsible.
Duration defines the infection as acute versus chronic,
with the dividing line usually at 4–6 weeks.

Abscesses occurring in the presence of underlying

pulmonary lesions, including tumors or systemic
conditions (e.g., HIV infection), are referred to as
secondary; those that occur in the absence of underlying
pulmonary lesions are considered primary.
Nonspecific lung abscess -no likely pathogen is recovered
from expectorated sputum; presumed to be due to
anaerobic bacteria.
Putrid lung abscess -anaerobic bacterial lung abscesses,
ized by distinctive foul-smelling breath, sputum, or
empyema fluid.

Etiology
Anaerobic bacteria.
Mycobacteria, especially M. tuberculosis.
Fungi and some parasites also cause lung abscess.

An acute lung abscess developing in a young, previously

healthy patient, especially in conjunction with influenza,
is likely to involve Staphylococcus aureus
In an immunocompromised host, enteric gram-negative
bacilli—especially Klebsiella.
Microbial Pathogens Causing Cavitary Lung Infection
Aspiration-Prone Host
Anaerobic bacteria
Embolic (endovascular) lesions: usually Staphylococcus
aureus, Pseudomonas aeruginosa
Immunocompromised Host
M. tuberculosis, P. aeruginosa, Enterobacteriaceae
(especially Klebsiella pneumoniae), Aspergillus spp.,
Cryptococcus spp.
Previously Healthy Host
Bacteria: S. aureus, K. pneumoniae, group A
Streptococcus;
Parasites: Entamoeba histolytica, Strongyloides
stercoralis

Multiple pulmonary lesions that are not caused by

microbes may resemble lung abscess.
In some cases, multiple lung abscesses result from septic
emboli, most commonly in association with tricuspid
valve endocarditis.

Clinical Features

Nonspecific lung abscess -indolent infection that evolves

over several days or weeks, usually in a host who has a
predisposition to aspiration. A common feature is
periodontal infection with pyorrhea or gingivitis.
The usual symptoms are fatigue, cough, sputum
production, and fever. Chills are uncommon. weight loss
and anemia. Some patients have putrid-smelling sputum

Diagnosis

Imaging, including chest x-ray and CT

Lymphadenopathy is not associated with bacterial lung
abscess; thus this finding suggests an alternative
diagnosis.

Microbiologic studies include stains and cultures of

expectorated sputum to detect aerobic bacterial
pathogens.
In most cases, the etiology of anaerobic lung abscess is
clear: the host is prone to aspiration and has an abscess
in a dependent pulmonary segment, with no other likely
cause. As stated above, putrid breath, sputum, or
empyema fluid indicates anaerobic infection.

Treatment: Lung Abscess

Antibiotic Selection
Infections caused by anaerobic bacteria should usually
be treated with clindamycin; the initial IV dosage of 600
mg four times daily can be changed to an oral dosage of
300 mg four times daily once the patient becomes
afebrile and improves clinically. until imaging shows that
chest lesions have cleared or have left a small, stable
scar.
Miesso(MD)