Lung Abscess, Bronchiectasis and Pleurisy

LUNG ABSCESS
Definition
 Lung abscess is defined as necrosis of the pulmonary tissue and formation of cavities
containing necrotic debris or fluid caused by microbial infection.
 The formation of multiple small (<2 cm) abscesses is occasionally referred to as necrotizing
pneumonia.
 Both lung abscess and necrotizing pneumonia are manifestations of a similar pathologic
process.
 Failure to recognize and treat lung abscess is associated with poor clinical outcome.

Classification of Lung Abscess

Lung abscesses can be classified based on the duration and the likely etiology:
 Acute abscesses are less than 4-6 weeks old
 Chronic abscesses are of longer duration
 Primary abscess is infectious in origin, caused by aspiration or pneumonia in the healthy host
 Secondary abscess is caused by:
o A preexisting condition (e.g. obstruction)
o Spread from an extrapulmonary site

o Bronchiectasis
o An immunocompromised state
 Lung abscesses can be further characterized by the responsible pathogen, such as:
o Staphylococcus lung abscess
o Anaerobic infections

o Aspergillus lung abscess

Pathophysiology
 Most frequently, the lung abscess arises as a complication of aspiration pneumonia caused by
mouth anaerobes.
 A bacterial inoculum from the gingival crevice reaches the lower airways, and infection is
initiated because the bacteria are not cleared by the patient's host defense mechanism.
 This results in aspiration pneumonitis and progression to tissue necrosis 7-14 days later,
resulting in formation of lung abscess
 Other mechanisms for lung abscess formation include bacteremia or tricuspid valve

causing
endocarditis,

septic(CONSISTS OF
BACTERIA
MOSTLY β
HEMOLYTIC
STREPTOCOCCI
VIRIDANS) emboli
multiple) to the lung.
(usually

 The oral anaerobe fusobacterium

necrophorum is the most common
pathogen.
Risks of Developing Lung Abscess
 Patients at the highest risk for developing lung abscess have the following risk factors:
o Periodontal disease
o Seizure disorder
o Alcohol abuse
o Dysphagia
o Other patients at high risk for developing lung abscess include individuals with an
inability to protect their airways from massive aspiration because of a diminished gag or
cough reflex, caused by a state of impaired consciousness (e.g. from alcohol or other
CNS depressants, general anesthesia, or encephalopathy)

Causes of Lung Abscess

 An abscess may develop as an infectious complication of a preexisting bulla or lung cyst.
 An abscess may develop secondary to carcinoma of the bronchus; the bronchial obstruction
causes post obstructive pneumonia, which may lead to abscess formation.
 Published reports since the beginning of the antibiotic area have established that anaerobic
bacteria are the most significant pathogens in lung abscess. The most common anaerobes are

o Peptostreptococcus species
o Bacteroides species
o Fusobacterium species
o Microaerophilic streptococci
 Aerobic bacteria that may infrequently cause lung abscess include

oStaphylococcus aureus
oStreptococcus pyogenes
oStreptococcus pneumoniae (rarely)
oKlebsiella pneumoniae
oHaemophilus influenzae
oPseudomonas aeruginosa
o Actinomyces species
 o Nocardia species
o Gram-negative bacilli
 Nonbacterial and atypical bacterial pathogens may also cause lung abscesses, usually in the
immunocompromised host these microorganisms include
o Parasites (Paragonimus and Entamoeba species)

o Fungi (e.g. Aspergillus,

Cryptococcus, Histoplasma,
Blastomyces, and
Coccidioides species)
COMMON
OPPORTUNISTIC
INFECTIONS IN HIV AID
3-4 STAGE
o Mycobacterium species

Epidemiology of Lung Abscess

 Frequency
o The frequency of lung abscess in the general population is not known.
 Sex
o A male predominance for lung abscess is reported in published case series.
 Age

o Lung abscesses likely occur more commonly in elderly patients

because of the increased incidence of periodontal disease and the increased prevalence of
dysphagia and aspiration.
Mortality/Morbidity
 Most patients with primary lung abscess improve with antibiotics, with cure rates
documented at 90-95%
 Host factors associated with a poor prognosis include advanced age, debilitation,
malnutrition, human immunodeficiency virus infection or other forms of
immunosuppression, malignancy, and duration of symptoms greater than 8 weeks.
 The mortality rate for patients with underlying immunocompromised status or bronchial
obstruction who develop lung abscess may be as high as 75%.
 Frequently hospital acquired aerobic organisms are associated with poor outcomes

Clinical Features of Lung Abscess

History
Symptoms depend on whether the abscess is caused by anaerobic or other bacterial infection.
 Anaerobic infection in lung abscess
o Patients often present with indolent symptoms that evolve over a period of weeks to
months.
o The usual symptoms are fever, cough with
purulent and copious sputum production, night
sweats, anorexia, and weight loss.
o The expectorated sputum
characteristically is foul smelling and
bad tasting.
o Patients may develop hemoptysis or pleurisy .
 Other pathogens in lung abscess
o These patients generally present with conditions that are more emergent in nature and are
usually treated while they have bacterial pneumonia.
o Cavitation occurs subsequently as parenchymal necrosis ensues.
o Abscesses from fungi, Nocardia species, and Mycobacteria species tend to have an
indolent course and gradually progressive symptoms.

Physical Examination
 The findings on physical examination of a patient with lung abscess are variable.
 Physical findings may be secondary to associated conditions such as underlying

pneumonia or pleural effusion.

 Patients with lung abscesses may have low-grade fever in anaerobic
infections and temperatures higher than 38.5°C in other infections.
 Generally, patients with in lung abscess have evidence of gingival disease.

 present (e.g.
Clinical findings of concomitant consolidation may be

dullness to percussion, bronchial breath

sounds, course inspiratory crackles)
 Evidence of pleural friction rub and signs of associated pleural effusion, empyema, and
pyopneumothorax may be present. Signs include contra-lateral shift of the mediastinum,
dullness to percussion, and absent breath sounds over the effusion.
 Digital clubbing may develop rapidly

Diagnosis and Management of Lung Abscess

Differential Diagnosis
 Pulmonary tuberculosis
 Empyema thoracis
 Lung cancer
 Pneumonia
 Pulmonary embolism
 Infective Endocarditis
 Pneumocystis Jirovecii Pneumonia (Pneumocystis Carinii Pneumonia)
 Wegener Granulomatosis
 Hydatid Cysts (ECHINOCCCUS GRANULOSIS, ECHINOCOCCUS MULTICULARIS
GROUP OF TAPE WORMS0

Diagnosis of Lung Abscess

 Refer the patient to higher centre for laboratory studies and imaging studies
 CBC (FULL BLOOD PICTURE, CXRAY, SPUTUM FO CULTURE AND
SENSITIVITY)

Treatment
 Perform pre referral treatment
o IV fluids
o Antibiotics (START WITH PENICILLINC 5 MU IV 6HOURLY FOR AT
LEAST 4 DAYS , THEN ORAL GIVE TAB AUGUMENTIN (CLAVULENIC
+ AMOXYCILLIN) THIS MEDICATION IS GOOD FOR BACTERIAS
WHICH PRODUCE β LACTAMASE ANTAGONISM. and analgesics
o Monitor vital signs
o ALSO ADD TAB METRONIDAZOLE (FLAGYL) 400MG ORALLY TDS 7
DAYS
 Refer the patient to higher centre (hospital) for proper management

Prevention
 Prevention of aspiration is important to minimize the risk of lung abscess.
 Early intubation in patients who have diminished ability to protect the airway from massive
aspiration (cough, gag reflexes), should be considered.
 Positioning patient in the supine position at a 30° reclined angle minimizes the risk of
aspiration. Vomiting patients should be placed on their sides.
 Improving oral hygiene and dental care in elderly and debilitated patients may decrease the
risk of anaerobic lung abscess.

Complications of Pulmonary Abscess

 Rupture into pleural space causing empyema
 Pleural fibrosis
 Trapped lung
 Respiratory failure
 Bronchopleural fistula
 Pleural cutaneous fistula
 In a patient with coexisting empyema and lung abscess, draining the empyema while
continuing prolonged antibiotic therapy is often necessary
Prognosis
 The prognosis for lung abscess following antibiotic treatment is generally favorable.
 Over 90% of lung abscesses are cured with medical management alone, unless caused by
bronchial obstruction secondary to carcinoma.

BRONCHOECTASIS
Definition, Causes and Epidemiology of Bronchiectasis Bronchiectasis is an
abnormal and permanent dilatation of bronchi, most often secondary to an infectious process.
 It may be either focal, involving airways supplying a limited region of pulmonary
parenchyma, or diffuse, involving airways in a more widespread distribution.
 Although this definition is based on pathologic changes in the bronchi, diagnosis is often
suggested by the clinical consequences of chronic or recurrent infection in the dilated
airways and the associated secretions that pool within these airways.

Aetiology and Pathogenesis

 Bronchiectasis is a consequence of inflammation and destruction of the structural
components of the bronchial wall. Infection is the usual cause of the inflammation.

Infectious Causes
 Adenovirus and Influenza virus are the main viruses that cause bronchiectasis in association
with lower respiratory tract involvement.
 Virulent bacterial infections, especially with potentially necrotizing organisms such as
Staphylococcus aureus, Klebsiella, and anaerobes, remain important causes of bronchiectasis
when antibiotic treatment of pneumonia is not given or is significantly delayed.
 Bronchiectasis has been reported in patients with HIV infection, perhaps at least partly due
to recurrent bacterial infection.
 Tuberculosis can produce bronchiectasis by a necrotizing effect on pulmonary parenchyma
and airways and indirectly as a consequence of airway obstruction from bronchostenosis or
extrinsic compression by lymph nodes.
 Others causes include
o Non Tuberculous mycobacteria
o Mycoplasmal (rare)
o Fungal infections (rare)

Predisposing Factors (to Recurrent/Chronic Infections and hence Bronchiectasis)

 Endobronchial obstruction leads to local impairment of host defense mechanisms
predisposing to recurrent infections.
o Slowly growing endobronchial neoplasms
o Foreign-body aspiration
o Bronchostenosis, from impacted secretions, or from extrinsic compression by enlarged
lymph nodes.

 Generalized impairment of
pulmonary defense mechanisms
occurs with
o Immunoglobulin deficiency

o Primary ciliary disorders

o Cystic fibrosis
Non-infectious Causes

 Exposure to a toxic substance that incites a severe inflammatory

response. Examples include inhalation of a toxic gas such as ammonia or aspiration of acidic
gastric contents
 An immune response in the airway may also trigger inflammation, destructive changes, and
bronchial dilatation.

Epidemiology of Bronchiectasis
 Frequency
o No systematic data are available to detail the incidence or prevalence of bronchiectasis.
o Bronchiectasis remains a major cause of morbidity in less-developed countries,
especially in countries with limited access to medical care and antibiotic therapy.
 Race
o No racial predilection exists other than those that may be associated with socioeconomic
status.
 Sex
o Evidence suggests that non – Cystic Fibrosis-related bronchiectasis is more common and
more virulent in women, particularly slender white women older than 60 years.
o In these patients, bronchiectasis is often caused by primary Mycobacterium avium
complex (MAC) infection
 Age
o In the pre antibiotic era and in today's less-developed countries, symptoms usually began
in the first decade of life.
o Today, the age of onset, except for those with Cystic Fibrosis, has moved into adulthood.
o The differences in prevalence between age groups are a direct reflection of the
differences in prevalence of the underlying causes of bronchiectasis, lung disease, and/or
chronic infections

Clinical Manifestations of Bronchiectasis

History
 Patients typically present with persistent or recurrent cough and purulent sputum production
which is postural related.
 Hemoptysis occurs in 50 to 70% of cases
 When a specific infectious episode initiates bronchiectasis, patients may describe a severe
pneumonia followed by chronic cough and sputum production.
 Alternatively, patients without a dramatic initiating event often describe the insidious onset
of symptoms.
 Dyspnea or wheezing generally reflects either widespread bronchiectasis or underlying
chronic obstructive pulmonary disease.
 With exacerbations of infection, the amount of sputum increases, it becomes more purulent
and often more bloody, and patients may become febrile.

Physical Examination
 Variable
 Any combination of crackles, rhonchi, and wheezes may be heard, all of which reflect the
damaged airways containing significant secretions.
 As with other types of chronic intrathoracic infection, clubbing may be present.
 Cyanosis and plethora
 Wasting and weight loss
 Patients with severe, diffuse disease, particularly those with chronic hypoxemia, may have
associated cor pulmonale and right ventricular failure.

Diagnosis and Management of Bronchiectasis

Differential Diagnosis of Bronchiectasis

 Bronchial asthma
 Chronic Bronchitis
 Acute Bronchitis
 Emphysema
 Aspiration Pneumonia/ Bacterial Pneumonia
 Pulmonary Tuberculosis

Investigations
Refer the patient to higher centre for laboratory studies and radiographic studies.

Treatment
 Pre referral resuscitation
o IV fluids
o Antibiotics, and analgesics
o Monitor vital signs
 Referral
o Practitioner skilled in caring for patients with bronchiectasis should be consulted.
o Give initial treatment and refer the patient.

Pleurisy [Pleuritis, Pleurodynia]

Definition, Causes and Epidemiology of Pleurisy [Pleuritis, Pleurodynia]

Introduction and Definition

 The pleura are a two layered sac that holds the lungs and separates them from the chest wall,
diaphragm, and heart.
 The pleura that lines the inside of the chest is called the parietal pleura and that covering the
lungs are called the visceral pleura.
 If you are healthy, the pleura are separated by a thin layer of fluid.
 This lets the lungs expand and contract easily during breathing.
 Pleurisy results from an inflammation of this sac.
 The inflammation that occurs with pleurisy can cause pain with breathing and may even
cause a large amount of fluid to collect in the pleural sac.
 Pleurisy can go away on its own or worsen so that fluid has to be drained from around the
lungs.
 Some people develop scar tissue called adhesions after they have pleurisy. They then have
chronic pain or shortness of breath.

Types of Pleurisy

 There are two types of pleurisy , dry and wet

pleurisy.
 In dry pleurisy, the more common condition, the inflamed pleurae rub directly against
each other.
 In wet pleurisy, fluid oozes from the inflamed tissue into the space between the lungs and the
chest wall. This fluid may compress the lungs, making breathing difficult.
 Both types of pleurisy often occur as complications of respiratory tract infections, such as
pneumonia, viral infections, and tuberculosis, and are more likely to develop in persons who
are highly susceptible to such infections.

Causes of Pleurisy
There are many causes of pleurisy, these include:
 Infectious disease caused by virus, bacteria, fungus, tuberculosis, or parasites

Cancer such as
mesothelioma or spread
from other areas
 Collagen vascular disease such as lupus erythematosus, rheumatoid arthritis, sarcoid disease,
or scleroderma
 Trauma from bruised or broken ribs
 for example
Gastrointestinal disease,

pancreatitis, peritonitis, or a
collection of pus under the
diaphragm
 Reaction to drugs such as methotrexate and penicillin

Other Causes

 Uremia (AZOTEMIA) COLLECTION AMMONIA FROM THE LIVER IN

THE UREA- URINE CYCLE) IF UREA IS EXCESS NOT EXCRETED TIMELY BY
THE KIDNEY.
 Blood clot in lung
 Radiation therapy
 Chemotherapy drugs
 Asbestos
 HIV

Clinical Features of Pleurisy

Chest Pain
 This is the most common symptom.

 The pain is generally a sharp, stabbing pain, but may also

be a dull ache or a burning sensation.

 It is usually worse when you take a deep breath, cough, or

move around.
 The pain is usually better if you take shallow breaths or lie on the side that hurts.
 Chest pain is what usually causes people with pleurisy to seek medical attention.

Cough
 Patient may get a cough, depending on the cause of the pleurisy.

Cough may be dry or productive of sputum

or blood
Management of Pleurisy

Refer patients with pleurisy to higher level (hospital) for diagnosis and treatment but make sure a
patient is given pre referral treatment.

Diagnosis
 Pleurisy is frequently diagnosed only when other more serious causes have been ruled out
 Diagnostic pleural tap
 A tuberculin test may be done to learn whether tuberculosis is a factor
 Chest X-ray to detect the presence of pleural fluid
 Electrocardiogram (ECG)

Treatment
 Treat the underlying infection or disease, often with antibiotics.
 The symptoms of pleurisy can be relieved somewhat by resting.

 Anti-inflammatory medications and even cortisone drugs are very effective in relieving the
inflammation and pain, particularly in dry pleurisy. DICLOFENIC, DICLOPAR,
PARACETAMOL (CHOOSE ONE)

 Anti-inflammatory drugs, such as ibuprofen or aspirin , to reduce

the pain and inflammation.
 Patient may have less pain if lie on the side that hurts.
 Patient should avoid exerting herself/himself or doing anything that would cause him/her to
breathe hard.

 If there is huge pleural effusion, it

may need to be drained.
Prevention
Most pleurisy is caused by infection and is unavoidable. You can avoid severe pleuritic chest
pain by early diagnosis and treatment with anti-inflammatory drugs.
 Diagnosis and Treatment of
Lung Abscess
Diagnosis of Lung Abscess

Laboratory studies
 A complete white blood cell count with differential may reveal leukocytosis and a left shift.
 Obtain sputum for Gram stain, culture, and sensitivity, acid-fast bacilli stain and
Mycobacterial culture.
 Blood culture may be helpful in establishing the etiology.
 Obtain sputum for ova and parasite whenever a parasitic cause for lung abscess is suspected.

Imaging Studies
 Chest radiography
o A typical chest radiographic appearance of a lung abscess is an irregularly shaped cavity
with an air-fluid level inside.
o Anaerobic infection may be suggested by cavitation within a dense segmental
consolidation in the dependent lung zones.
o Up to one third of lung abscesses may be accompanied by an empyema.
 Computed tomography
o CT scanning of the lungs may help visualize the anatomy better than chest radiography.
o CT scanning is very useful in the identification of concomitant empyema or lung
infarction.
 Ultrasonography
o Peripheral lung abscesses with pleural contact or included inside a lung consolidation are
detectable using lung ultrasonography at the bedside.
o Lung abscess appears as a rounded hypoechoic lesion with an outer margin.

Treatment Can be Medical or Surgical

 Medical care
o Empiric antimicrobial therapy must be comprehensive and should cover all likely
pathogens suspected in this clinical setting.
o Treatment of lung abscess is guided by the available microbiology and knowledge of the
underlying or associated conditions.
 Antibiotic therapy
Treatment options available include:
o Standard treatment of an anaerobic lung infection is clindamycin (0.6 – 2.7g/day IV in 2-
4 divided doses followed by 150-300 mg PO qid).
o Ampicillin plus sulbactam (3g IV q6h) is well tolerated and as effective as clindamycin
with or without a cephalosporin in the treatment of aspiration pneumonia and lung
abscess.
 o Moxifloxacin is clinically effective and as safe as Ampicillin plus sulbactam in the
treatment of aspiration pneumonia and lung abscess
o Although Metronidazole is an effective drug against anaerobic bacteria, the experience
with Metronidazole in treating lung abscess has been rather disappointing, because these
infections are generally polymicrobial. Not standard practice to use Metronidazole alone
because some anaerobic cocci and most microaerophilic streptococci are resistant. Use it
in combination with Ampicillin.
 Loading dose: 800mg to start with, then
 Maintenance dose: 400mg 8 hourly PO. IV infusion 500mg every 6-8 hours not to
exceed 4 g/d.
o In hospitalized patients who have aspirated and developed a lung abscess, antibiotic
therapy should include coverage against S aureus and Enterobacter and Pseudomonas
species.
 
 Duration of therapy
o Although the duration of therapy is not well established, most clinicians generally
prescribe antibiotic therapy for 4-6 weeks.
o Expert opinion suggests that antibiotic treatment should be continued until the chest
radiograph has shown either the resolution of lung abscess or the presence of a small
stable lesion.
o The rationale for extended treatment maintains that risk of relapse exists with a shorter
antibiotic regimen.

 Response to therapy
o Patients with lung abscesses usually show clinical improvement, with improvement of
fever, within 3-4 days after initiating the antibiotic therapy.
o Defervescence is expected in 7-10 days.
o Persistent fever beyond this time indicates therapeutic failure, and these patients should
undergo further diagnostic studies to determine the cause of failure.
o Considerations in patients with poor response to antibiotic therapy include bronchial
obstruction with a foreign body or neoplasm or infection with a resistant bacteria,
mycobacteria, or fungi.
o Large cavity size (ie, > 6 cm in diameter) usually requires prolonged therapy.
o Because empyema with an air-fluid level could be mistaken for parenchymal abscess, a
CT scan may be used to differentiate this process from lung abscess.
o A nonbacterial cause of cavitary lung disease may be present, such as lung infarction,
cavitating neoplasm, and vasculitis.
o The infection of a preexisting sequestration, cyst, or bulla may be the cause of delayed
response to antibiotics.

Surgical Care
 Surgery is very rarely required for patients with uncomplicated lung abscesses.
 : Diagnosis and Treatment of
Bronchiectasis
Radiographic and Laboratory Findings

Chest Radiograph
 Is important but the findings are often nonspecific
 The radiograph may be normal with mild disease

Computed tomography (CT)-in advanced centres

 Provides an excellent view of dilated airways as seen in cross-sectional images

Sputum Examination
 Often reveals an abundance of neutrophils and colonization or infection with a variety of
possible organisms.
 Appropriate staining and culturing of sputum often provide a guide to antibiotic therapy.

Other investigation (to determine the cause) in advanced centres

 Fiberoptic bronchoscopy for endobronchial obstruction
 Measurement of sweat chloride levels for cystic fibrosis
 Skin testing, serology, and sputum culture for Aspergillus
 Pulmonary function tests may demonstrate airflow obstruction associated with chronic
obstructive lung disease.

Treatment
 No specific medical therapy exists for the treatment of bronchiectasis.
 Therapy is focused on the treatment of infectious exacerbations that the patient commonly
experiences, most commonly in the form of an acute bronchitis-type syndrome.
 Aggressively pursue and treat any associated or known causal condition of the
bronchiectasis.

Therapy has four major goals

 Elimination of an identifiable underlying problem
 Improved clearance of tracheobronchial secretions
 Control of infection, particularly during acute exacerbations
 Reversal of airflow obstruction

General Therapy
 Patients should stop smoking
 Patients should avoid second-hand smoke
 Patients should have adequate nutritional intake with supplementation, if necessary
 Immunizations for influenza and pneumococcal pneumonia are recommended
 Immunizations for measles, rubeola, and pertussis should be confirmed
 Oxygen therapy is reserved for patients who are hypoxemic with severe disease and end-
stage complications, such as cor pulmonale
Bronchial Hygiene
 With its tenacious sputum and defects in clearance of mucus, good bronchial hygiene is
paramount in the treatment of bronchiectasis.
 Postural drainage with percussion and vibration is used to loosen and mobilize secretions.
.
Antibiotics
 Antibiotics are the mainstay of treatment.
 The route of antibiotic administration varies with the 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 1week of
every month.
 The choice of antibiotic is provider dependent, but in general the antibiotic 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 Cystic Fibrosis often requires
intravenous anti-Pseudomonas species coverage with an aminoglycoside, most often in
combination with an antipseudomonal synthetic penicillin or cephalosporin
 In acute exacerbation, broad-spectrum antibacterial agents are generally preferred.
 However, if time and the clinical situation allows, then sampling respiratory secretions
during an acute exacerbation may allow treatment with antibiotics based on specific species
identification.

Acceptable choices for the outpatient who is mild to moderately ill include
 Amoxicillin: 500 mg PO 8 hourly for 10 days
 Doxycycline: 100 mg PO every 12 hours for 10 days
 Trimethoprim-sulfamethoxazole 960mg PO 12 hourly for 10 days
 A newer macrolide
o Azithromycin: Day 1: 500 mg PO; Days 2-5: 250 mg/d PO
o Clarithromycin 500 mg PO bid for 7-14 days
 A second-generation cephalosporin
 One of the fluoroquinolones e.g. Levofloxacin 500 mg PO/IV once daily
 In general, the duration is 7-10 days

For patients with moderate-to-severe symptoms, parenteral antibiotics are indicated

 An aminoglycoside
o Gentamicin: 3 mg/kg/d IV divided tid in normal renal function; once-a-day dosing also
effective
o Amikacin: 10-15 mg/kg/d IV/IM divided bid/tid; not to exceed 1.5 g/d regardless of
higher Body Weight
 An antipseudomonal synthetic penicillin
 A third-generation cephalosporin
o Ceftriaxone: IV 1-2g bid
 A fluoroquinolone
o Ciprofloxacin IV 200 mg bid
Bronchodilators
 Bronchodilators, including beta-agonists and anti-cholinergics, may help some patients with
bronchiectasis, presumably reversing bronchospasm associated with airway hyperreactivity
and improving mucociliary clearance
 Salbutamol (short acting beta 2 agonist)
o Acute symptoms: 2 inhalations repeated q4-6h
 Salmeterol (Long acting beta 2 agonist)
o 1 inhalation (50 mcg) bid at least 12 h apart

Anti-inflammatory Medication
 The rationale is to modify the inflammatory response caused by the microorganisms
associated with bronchiectasis and subsequently reduce the amount of tissue damage.
 A practical approach is to use tapering oral corticosteroids (e.g. prednisolone) and antibiotics
in the acute exacerbation and to consider inhaled corticosteroids for daily use in patients with
significant obstructive physiology on pulmonary function testing and evidence of
reversibility suggesting airway hyperreactivity.
 Beclomethasone dipropionate
o 200 mcg (4puffs) twice daily or 100mcg (2 puffs) 3 – 4 times daily by aerosol inhalation

Surgical Therapy
When bronchiectasis is localized and the morbidity is substantial despite adequate medical
therapy, surgical resection of the involved region of lung should be considered.

Complications
 Recurrent pneumonia requiring hospitalization
 Empyema
 Lung abscess
 Hemoptysis
 Progressive respiratory failure
 Cor pulmonale
 Progressive respiratory failure and cor pulmonale are the most common causes of
pulmonary-related mortality in bronchiectasis.

Prognosis
 Overall, the prognosis is good, but it varies with the underlying or predisposing condition.
 Bronchiectasis associated with Cystic Fibrosis may carry a worsened prognosis.
 In general, patients do well if they are compliant with all treatment regimens and practice
routine preventive medicine strategies.
 Overall, the prognosis is good, but it varies with the underlying or predisposing condition.