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Lower Respiratory Infection

Agus Widiyatmoko
Lower Respiratory Tract

• Lower respiratory (tract) infection or

LTRI is a generic term for an acute
infection of the trachea (windpipe),
airways and lungs, which make up
the lower respiratory system.

• LTRIs include acute bronchitis,

AECB,and pneumonia.
Bacterial Diseases of the
Lower Respiratory
System (LRS)

Bacteria, viruses, and

fungi cause
• Bronchitis
• Bronchiolitis
• Pneumonia
Accute bronchitis
• Acute bronchitis is a shorter
illness that commonly follows a
cold or viral infection, such as
the flu
• Acute bronchitis usually lasts a
TYPES OF BRONCHITIS few days or weeks
Chronic bronchitis
• Chronic bronchitis is
characterized by a persistent,
mucus-producing cough on most
days of the month, three months
of a year for two successive
years in absence of a secondary
cause of the cough.
• Smokers
• People who are exposed to a lot of secondhand
Etiology & risk • People with weakened immune systems
factors • The elderly and infants
• People with gastroesophageal reflux disease
• People who are exposed to air pollution
 Inflammation or swelling of the
 Coughing
 Production of clear, white, yellow,
grey, or green mucus (sputum)
Signs & symptoms  Shortness of breath
of bronchitis  Wheezing
 Fatigue
 Fever and chills
 Chest pain or discomfort
 Blocked or runny nose
Diagnostic evaluation

• History collection
• Physical examination
• Chest x- rays
• Sputum cultures
• Pulmonary function test
• Spirometer excercises
• Bronchoscopy
Pharmacologic  Antibiotics - these are effective for
bacterial infections, but not for viral
management infections. They may also prevent
secondary infections.

Cough medicine - one must be careful not
to completely suppress the cough, for it is
an important way to bring up mucus and
remove irritants from the lungs.

Bronchodilators - these open the bronchial
tubes and clear out mucus.
Management, cont...

01 02 03
Mucolytics - these Anti-inflammatory Pulmonary
thin or loosen mucus medicines and rehabilitation
in the airways, glucocorticoid program - this
making it easier to steroids - these are includes work with a
cough up sputum. for more persistent respiratory therapist
symptoms. to help breathing.
Pneumonia - Definition
• Pneumonia is an
abnormal inflammatory condition of
the lung. It is often characterized as
including inflammation of
the parenchyma of the lung (that is,
the alveoli) and abnormal alveolar
filling with fluid
(consolidation and exudation)
• Community acquired PNA (CAP)
• Infection of lung parenchyma in pt who is not
hospitalized or living in a long-term care facility for
≥2 weeks

Definitions – • Hospital-acquired PNA (HAP)

• Occurs ≥48 hours after admission; not intubating on
Pneumonia admission

• Healthcare-associated PNA (HCAP)

• Non-hospitalized pt with extensive healthcare
contact and ≥1 criteria from below:
• IV therapy, wound care, or IV chemotherapy
within the prior 30 days
• Residence in a nursing home or other long-term
care facility
• Hospitalization in acute care hospital for ≥2
days within the prior 90 days
• Attendance at a hemodialysis clinic within the
prior 30 days

• Ventilator-associated PNA (VAP)

• Arises >48-72 hours after endotracheal intubation
Common Bacterial pneumonias

S. pneumoniae, typical pneumonia

H. influenza
Mycoplasma pneumoniae
Atypical pneumoniae
Legionella pneumophila
Chlamydophila psittaci
Community Acquired Pneumonia
• Definition:
Acute infection of the pulmonary parenchyma that is associated with at
least some symptoms of acute infection, accompanied by the presence
of an acute infiltrate on a chest radiograph, or auscultatory findings
consistent with pneumonia, in a patient not hospitalized or residing in a
long term care facility for > 14 days before onset of symptoms.

Bartlett. Clinical Infect Diseases 2000;31:347-82.

Who Develops Community Acquired

• Community-acquired
pneumonia develops in people
with limited or no contact with
medical institutions or settings.
• CAP occurs throughout the
world and is a leading cause of
illness and death
• Risk Factors for pneumonia
• age
• alcoholism
Community • smoking
Acquired • asthma
• Immuno suppression
Pneumonia • institutionalization
• dementia
Several Microbes can
cause CAP
• The most commonly identified pathogens are
Streptococcus pneumoniae, Haemophilus
influenzae, and atypical organisms (i.e.,
Chlamydia pneumoniae, Mycoplasma
pneumoniae, Legionella sp).
• Typical pneumonia usually is caused by
bacteria such as Streptococcus pneumoniae.
Typical x • Atypical pneumonia usually is caused by the
influenza virus, mycoplasma, Chlamydia,
Atypical Legionella, adenovirus, or other unidentified
etiological • The patient's age is the main differentiating
agents factor between typical and atypical pneumonia;
young adults are more prone to atypical
causes, and very young and older persons are
more predisposed to typical causes.
• CAP is usually acquired via
inhalation or aspiration of
pulmonary pathogenic organisms
into a lung segment or lobe.
• Less commonly, CAP results from
Pathophysiology secondary bacteraemia from a
distant source, such as Escherichia
coli urinary tract infection and/or
• CAP due to aspiration of
Oropharyngeal contents is the
only form of CAP involving
multiple pathogens.
• Symptoms:
• Cough (typically productive)
• Fever with chills and sweats
• Shortness of breath
• Chest pain
Clinical Presentation • Signs:
• Fever, tachycardia,
• Crackles/rhonchi on lung
• Leukocytosis
• Infiltrate on Cxray (or other imaging) required
for the diagnosis of pneumonia
CAP: • If clinically suspect CAP, but negative Cxray
Diagnosis – consider:
• Chest CT
Imaging • Empiric treatment and repeat Cxray in 24-48
X ray chest gives the
leading clues in Diagnosis
Lobar Infiltrate Interstitial Infiltrate
CAP: Diagnosis – Sputum Gram Stain/Culture

• Optional for routine output evaluation

• Culture-positive rates range from 2-50%
• If require admission, obtain sputum Gram stain & culture and blood
• Ideally obtain sputum before antibiotic therapy, but do not delay
antibiotic waiting for a sputum sample
Diagnosis – Special Tests
• Urinary Legionella Antigen
• Serotype 1 only
• Accounts for 88% of USA isolates
• Sensitivity: 70%; specificity: >90%

• Urinary Pneumococcal Antigen

• Sensitivity: 60-90%, specificity: 100%
• Recent study found 10% of specimens from pts with non-pneumococcal
pneumonia were positive
Poor Prognostic Factors
• Age > 65 years
• Nursing home resident (HCAP)
• Presence of chronic lung disease
• High APACHE score
• Need for mechanical ventilation
Treatment Guidelines
• Where to treat:
• Many can be treated as an outpatient
• Must consider illness severity,
comorbidities, home support, adherence to
• Severity-of-illness scores can help guide
whether a pt needs hospital admission and
should always be supplemented with
clinical judgement

• CURB-65 criteria
• Confusion
• Urea >19 mg/dL
Severity of PNA • Respiratory rate ≥30
• Blood pressure (SBP <90 or DBP ≤60)
• ≥65 year old
• ≥2 criteria then needs hospital
admission and ≥3 criteria may need
ICU level of care

• Can also use Pneumonia Severity Index (PSI)

instead of CURB-65
Treatment Guidelines
• Pneumonia Severity Index (PSI)
• Prediction rule to stratify risk of death from CAP
• Assists in determining location of Rx for CAP
• Should not supercede clinical judgment
Fine, M. J. et al. N Engl J Med
• Then, add up
their risk points:

Risk Score
II < 70
III 71-90
IV 91-130
V > 130
PSI Index Mortality Rate
I 0.1-0.5%
II 0.4-0.9%
Outpt Tx
III 0-2.8%
IV 8.2-12.5% Needs Inpt
V 27-31% Tx

Fine, M. J. et al. N Engl J Med 1997;336:243-250


• CURB-65 criteria
• Confusion
• Uremia (BUN >20)
• Respiratory rate (RR >30)
• Blood pressure (SBP <90 or DBP < 60)
• Age 65 years or greater

CURB-65 Score Mortality Rate Tx Location

0 0.7% Outpatient
1 2.1% Outpatient
2 9.2% Inpatient
3 14.5% Inpatient - ?ICU
4 40.0% ICU
5 57.0% ICU
• Antibiotic initiated in the emergency department, ideally within 4 hours
• Quick administration has been associated with reduced mortality
• Use of empiric guidelines have reduced costs, mortality, LOS
• Based upon severity of illness and host immune status
• Target regimen based upon culture results
IDSA-ATS Treatment Guidelines

• Stratify empiric outpatient treatment based on

• Drug-resistant Streptococcus pneumoni risk
• > 25% resistance rate (e.g. Nashville, TN)
• Presence of co-morbidities
• Alcoholism/Aspiration risk
• Bronchiectasis/COPD
• Post-influenza
• Prior antibiotic use in the preceding 3 months
IDSA-ATS Treatment Guidelines

• Empiric Treatment – Outpatient:

• No confounding factors:
• macrolide (azithromycin 500mg x 1 day then 250mg Qday or
clarithromycin 500mg po Q12hrs or clarithro-ER 1000mg Qday)
• or
• doxycycline 100mg Q12hrs
IDSA-ATS Treatment Guidelines

• Empiric Treatment – Outpatient:

• Confounding factors present:
respiratory quinolone (levofloxacin 750mg Qday, moxifloxacin 400mg Qday)
beta-lactam (amoxicillin 1g Q8hrs, amox-clav-ER 2gm Q12hrs, cefpodoxime 200mg Q12hrs,
cefdinir 300mg Q12hrs, etc) + macrolide
beta-lactam + doxycycline
IDSA-ATS Treatment Guidelines

• Empiric Treatment – Hospitalized, non-ICU:

• Beta-lactam (ceftriaxone, cefotaxime, ampicillin, or ertapenem) + macrolide

or doxycycline
• Respiratory quinolone alone (levofloxacin, moxifloxacin, gemifloxacin)
IDSA-ATS Treatment Guidelines

• Empiric Treatment – Hospitalized, ICU:

• Beta-lactam (ceftriaxone, cefotaxime, or ampicillin/sulbactam) +

macrolide or respiratory quinolone

• PCN-allergic = resp quinolone + aztreonam

Risk Factors for Pseudomonas
• Structural lung diseases, such as
• Repeated exacerbations of severe COPD
leading to frequent steroid and/or antibiotic
• Health-Care Associated Pneumonia (HCAP)
• Hospitalized in acute care hospital two or more days within 90
days prior to infection
• Reside in long-term care facility
• Received IV abx, chemotx, or wound care in last 30 days
• Dialysis
• Beta-lactam (piperacillin-tazobactam,
cefepime, imipenem, or meropenem) +
ciprofloxacin or levofloxacin or
CAP: • Beta-lactam + aminoglycoside +
Pseudomonas azithromycin or
Coverage • Beta-lactam + aminoglycoside +
respiratory quinolone
• PCN-allergic = substitute aztreonam for
the beta-lactam
• Consider empiric coverage of MRSA
• Necrotizing pneumonia
• Post-influenza pneumonia
• History of MRSA or recurrent
skin abscesses

• Treat with vancomycin or linezolid

MRSA – Vancomycin vs. Linezolid
• Retrospective analysis of data from two separate, prospective trials (n = 1,019)
• Patients with nosocomial pneumonia
• Aztreonam + vancomycin or linezolid
• No difference in survival except in MRSA pneumonia subgroup (63.5% vs. 80%, p=0.03)
• Linezolid is an alternative to vancomycin in new IDSA/ATS guidelines

Wunderink, et al. Chest 2003

• Switch to po abx when…
CAP: • Hemodynamically stable
Oral Abx • Clinically improving
• Able to tolerate po
Therapy • Have normal GI tract fxn
• Rx for a minimum of 5 days
• Before discontinuation of therapy:
CAP: • Pt should be afebrile for 48–72 hrs
Length of • Pt should have no more than one CAP-
associated sign of clinical instability
Therapy • Longer duration usually indicated with
Legionella, Chlamydia, MRSA
CAP: • Temperature <37.8°C
• Heart rate <100 beats/min
Criteria for
• Respiratory rate <24 breaths/min
Clinical • Systolic blood pressure >90 mm Hg
Stability • Arterial oxygen saturation > 90% or pO2 > 60 mm Hg on
room air
• Ability to maintain oral intake
• Normal mental status
• HAP and VAP continue to be frequent
complications of hospital care. Together, they
Introduction are among the most common hospital-acquired
infections (HAIs), accounting for 22% of all
HAIs in a multistate point-prevalence survey.

[Magill SS, Edwards JR, Fridkin SK; Emerging Infections Program Healthcare-Associated Infections
Antimicrobial Use Prevalence Survey Team. Survey of healthcare-associated infections. N Engl J Med
2014; 370:2542–3.]
2005 ATS/IDSA guidelines
Pneumonia* Definition
VAP Patients receiving mechanical ventilation for at least 24 h with first positive bacterial† respiratory
culture finding after ventilator start date.
HAP Patients with a first positive bacterial† respiratory culture finding >2 days from admission who do
not meet VAP definition.
HCAP Patients with a first positive bacterial† respiratory culture finding within 2 days of admission and
any of the following:
(1) admission source indicates a transfer from another health-care facility;
(2)receiving long-term hemodialysis (ICD-9-CMcodes); and
(3) prior hospitalization within 30 days who do not meet VAP definition
CAP Patients with a first positive bacterial† respiratory culture finding who do not meet VAP or HCAP

 All pneumonia cases with primary or secondary ICD-9-CM codes for pneumonia and positive respiratory culture finding treated in a hospital that collected at least 5 days
of culture data.†Eligible bacteria include: Acinetobacter, Bacillus, Bacteroides, Bordetella,Brucella, Chlamydia, Enterobacter, Escherichia, Haemophilus, Klebsiella,
Legionella, Listeria, MRSA, Mycoplasma, Proteus, Pseudomonas, Salmonella, Serratia, Shigella, S aureus, Streptobacillus, Streptococcus A, Streptococcus B,
Streptococcus C, Streptococcus D, Streptococcus F, Streptococcus G, Streptococcus nongroup, S pneumoniae, Yersinia.(2)
• Definition – not amended . Same as
2005 guidelines.
HAP/VAP ATS/IDSA • All recommendations were labeled as
2016 Practice either “strong” or “weak” (conditional)
guidelines according to the GRADE approach. The
words “we recommend” indicate strong
recommendations and “we suggest”
indicate weak recommendations.
Threshold values for cultured specimens used in the
diagnosis of pneumonia

Specimen collection/technique Values†

Lung tissue >104 CFU/g tissue
Bronchoscopically (B) obtained specimens
Bronchoalveolar lavage (B-BAL) >104 CFU/ml
Protected BAL (B-PBAL) >104 CFU/ml
Protected specimen brushing (B-PSB) >103 CFU/ml
Nonbronchoscopically (NB) obtained (blind) specimens
NB-BAL >104 CFU/ml
†CFU = colony forming units, g = gram, ml = milliliter >103 CFU/ml
CDC/NHSN Pneumonia (Ventilator-associated [VAP] and non-ventilator-associated Pneumonia [PNEU]) Event. January 2015, modified April 2015.
Should Selection of an Empiric Antibiotic Regimen for
VAP Be Guided by Local Antibiotic-Resistance Data?
• All hospitals regularly generate and disseminate a local antibiogram, ideally one
that is specific to their intensive care population(s) if possible
• Empiric treatment regimens be informed by the local distribution of pathogens
associated with VAP and their antimicrobial susceptibilities.

• Values and preferences: Targeting the specific pathogens and to assure adequate
• Remarks: The frequency with which the distribution of pathogens and their
antimicrobial susceptibilities are updated should be determined by the institution.
Considerations should include their rate of change, resources, and the amount of
data available for analysis.
What Antibiotics Are Recommended for Empiric
Treatment of Clinically Suspected VAP?
• Coverage for S. aureus, Pseudomonas aeruginosa, and other gram-negative bacilli in all empiric regimens (strong
recommendation, low-quality evidence).
• i. We suggest including an agent active against MRSA for the empiric treatment of suspected VAP only in patients
with any of the following:
• a risk factor for antimicrobial resistance (Table 2),
• patients being treated in units where >10%–20% of S. aureus isolates are methicillin resistant, and
• patients in units where the prevalence of MRSA is not known (weak recommendation, very low-quality evidence).
• ii. We suggest including an agent active against methicillin sensitive S. aureus (MSSA) (and not MRSA) for the
empiric treatment of suspected VAP in patients without risk factors for antimicrobial resistance, who are being
treated in ICUs where <10%–20% of S. aureus isolates are methicillin resistant (weak recommendation, very low-
quality evidence).
• 2. If empiric coverage for MRSA - vancomycin or linezolid (strong recommendation, moderate-quality evidence).
• 3. empiric coverage for MSSA (and not MRSA) - piperacillin-tazobactam, cefepime, levofloxacin, imipenem, or
meropenem (weak recommendation, very low-quality evidence). Oxacillin, nafcillin, or cefazolin are preferred
agents for treatment of proven MSSA, but are not necessary for the empiric treatment of VAP if one of the above
agents is used.
• 4. Two antipseudomonal antibiotics from different classes for the empiric treatment of
suspected VAP only in patients with any of the following:
• a risk factor for antimicrobial resistance,
• patients in units where >10% of gram-negative isolates are resistant to an agent being
considered for monotherapy, and
• patients in an ICU where local antimicrobial susceptibility rates are not available (weak
recommendation, low-quality evidence).

• 5. We suggest prescribing one antibiotic active against P. aeruginosa for the empiric
treatment of suspected VAP in patients without risk factors for antimicrobial resistance
who are being treated in ICUs where ≤10% of gram-negative isolates are resistant to the
agent being considered for monotherapy (weak recommendation, low-quality evidence).
• 6. In patients with suspected VAP, we suggest avoiding Colistin / aminoglycosides if alternative agents
with adequate gram-negative activity are available (weak recommendation, low-quality evidence).

• Values and Preferences: These recommendations are a compromise between the competing goals of
providing early appropriate antibiotic coverage and avoiding superfluous treatment that may lead to
adverse drug effects, Clostridium difficile infections, antibiotic resistance, and increased cost.

• Remarks: The 10%–20% threshold for deciding whether or not to target MRSA and the 10% threshold
for deciding whether or not to prescribe 1 antipseudomonal agent or 2 were chosen by the panel with a
goal of trying to assure that ≥95% of patient receive empiric therapy active against their likely
pathogens; when implementing these recommendations, individual ICUs may elect to modify these
• If patient has structural lung disease increasing the risk of gram-negative infection (ie, bronchiectasis or
cystic fibrosis), 2 antipseudomonal agents are recommended.
Should Patients With VAP Receive 7 Days or
8–15 Days of Antibiotic Therapy?

• 1. For patients with VAP, we recommend a 7-day course of

antimicrobial therapy rather than a longer duration (strong
recommendation, moderate-quality evidence).

• Remarks: There exist situations in which a shorter or longer duration

of antibiotics may be indicated, depending upon the rate of
improvement of clinical, radiologic, and laboratory parameters.
What Is the Optimal Duration of Antibiotic
Therapy for HAP (Non-VAP)?

• 7-day course of antimicrobial therapy (strong recommendation, very

low quality evidence).

• Remarks: There exist situations in which a shorter or longer duration

of antibiotics may be indicated, depending upon the rate of
improvement of clinical, radiologic, and laboratory parameters.
Should Antibiotic Therapy Be De-escalated
or Fixed in Patients With HAP/VAP?

• Antibiotic therapy be de-escalated rather than fixed (weak recommendation,

very low-quality evidence).

• Remarks: De-escalation refers to changing an empiric broad-spectrum

antibiotic regimen to a narrower antibiotic regimen by changing the
antimicrobial agent or changing from combination therapy to monotherapy.
• In contrast, fixed antibiotic therapy refers to maintaining a broad-spectrum
antibiotic regimen until therapy is completed.
Should Discontinuation of Antibiotic Therapy Be Based Upon
PCT Levels Plus Clinical Criteria or Clinical Criteria Alone in
Patients With HAP/VAP?

• Using PCT levels plus clinical criteria to guide the discontinuation of

antibiotic therapy, rather than clinical criteria alone (weak
recommendation, low-quality evidence).

• Remarks: It is not known if the benefits of using PCT levels to

determine whether or not to discontinue antibiotic therapy exist in
settings where standard antimicrobial therapy for VAP is already 7
days or less.
Should Discontinuation of Antibiotic Therapy Be Based Upon
the CPIS Plus Clinical Criteria or Clinical Criteria Alone in
Patients With Suspected HAP/VAP?

Not using the CPIS to guide the discontinuation of antibiotic therapy

(weak recommendation, low-quality evidence).
Atypical Pneumonia
Mycoplasmal Pneumonia – also known as
Primary Atypical Pneumonia or Walking Pneumonia
• Mycoplasma pneumoniae, pleomorphic, wall-less
• Mycoplasma produce small “fried-egg” colonies
after two weeks’ incubation on enriched media
containing horse serum and yeast extract
• Common in children and young adults – often mild
enough to go undiagnosed for long periods of time
• Diagnosis: PCR or serological tests (IgM antibodies)
Legionellosis or Legionnaires’ disease

• Legionella pneumophila, Gram– rod

• First discovered in 1976 among a group of elderly men attending an American Legion Convention
in Philadelphia
• The bacteria grow in water (pools, lakes, water systems of buildings, air conditioning units, etc.)
then disseminated in the air
• Transmission by inhaling aerosols; no person to person transmission
• Diagnosis: Bacterial culture, FA tests, DNA probes
• Pneumonia and pleurisy (15 - 20% mortality rate when hospitalized)
• Treatment: Erythromycin
Viral Diseases of the
Lower Respiratory System (LRS)
Several viruses can cause pneumonia as a complication of infections such as influenza, measles,
or chickenpox
Etiologies are not usually identified in a clinical laboratory because of the difficulty in isolating and
identifying viruses.
Viral etiology suspected if no cause determined.

Respiratory Syncytial Virus:

• Most common cause of pneumonia in infants – 4,500 deaths annually
• Causes cell fusion (syncytium) in cell culture
• Symptoms: Coughing
• Diagnosis by serologic test for viruses and antibodies
• Treatment: Ribavirin
• Influenzavirus, ssRNA, 8 segments
• Symptoms: Chills, fever,
headache, muscle aches
(no intestinal symptoms)
• Viral strains identified by antigenic
differences in the H and N spikes
• Also divided by antigenic
differences in protein coats:
• Type A → mammals and birds (most severe and
extensive); currently most common antigenic variants
of influenza A virus: H1N1 and H3N2
• Types B and C → humans only
• Viral isolates identified by HI and IF testing with
monoclonal antibodies
Hemagglutinin (H) spikes used for
attachment to host cells
Neuraminidase (N) spikes used to
release virus from cell
H and N are virulence factors and
Mutations in H and N leads to
antigenic shifts (major changes
only for type A) or antigenic drifts
(minor changes for all types)
 natural immunity and
vaccination obsolete
H antigen
N antigen

Mutation Mutation
#1 #2

Mutation #1
of Mutation #2
Antigenic drift

Human influenza
Influenza virion virion
from an animal

of genome

Host cell

ANTIGENIC SHIFT shift Only for A
Prevention and Treatment

• Wide spread epidemics due to antigenic shifts 

• Symptoms and Diagnosis
• Complications often due to bacterial secondary
infections (??)  50,000 – 70,000 deaths/year in
US - also Guillain-Barré and Reye’s syndrome
• Vaccine produced in chicken embryos: flu shot and
nasal spray (LAIV)
• Four antiviral drugs currently approved by FDA to
treat acute, uncomplicated influenza
• Fungal spores are easily inhaled; they may
Fungal germinate in the lower respiratory tract
Diseases of • The incidence of fungal diseases has been
increasing in recent years
the • Mycoses in the sections below can be treated
Lower with amphotericin B
• Coccidioidomycosis
• Pneumocystis Pneumonia
System (LRS)
Coccidioidomycosis =
Valley Fever
• Coccidioides immitis, dimorphic
• Airborne transmission
• Most cases are subclinical, some get
respiratory infection with flu-like symptoms
• In < 1% of cases (due to predisposing factors,
such as fatigue, poor nutrition, etc.):
progressive, disseminated disease form
resembling TB
• Diagnosis: serological tests
• 97% of reported cases are from California and
Pneumonia (PCP)
Pneumocystis jiroveci
(P. carinii), tiny fungus
Commonly found in nature,
healthy human lungs and animals 
Aerosol transmission
Illness and death in newly infected infants
and immunosuppressed individuals
Used to be leading cause of death in AIDS
patients – now preventive drug therapy
Diagnosis: detection of cysts in sputum

• Bronchiectasis is defined as the

irreversible dilatation of the
cartilage-containing airways
bronchi or bronchioles.
• The airways are dilated up to 4 times the
normal size
• Bronchi and bronchioles are so dilated they
can be followed out to the pleural surfaces•
Mechanisms of
development of
• Bronchiectasis may result
from one of three main

• A.Bronchial wall injury

• Desquamation of the
epithelium and necrotising
Mechanisms of
development of
• B. Bronchial lumen
• Focal Congenital bronchial
• Foreign body
• Broncholithiasis
• Endobronchial neoplasm
• Rt mid lobe synd
Mechanisms of
development of

• C. Traction from
adjacent fibrosis
• Many conditions may lead to bronchial wall
injury.These include infections like
Mechanisms • Recurrent infections
of • Impaired host defense leading to infection
• Exaggerated immune response
development • Congenital structural defects of the
of bronchial wall
• And extrinsic insults damaging the airway
Bronchiectasis wall
• Symptoms
1. Persistent and recurrent cough with purulent
and sputum production.
2. Repeated respiratory tract infection.
Clinical 3. Haemoptysis 50-70% of cases.

Features 4. Systemic symptoms like : fatigue, weight loss

and myalgia
5. Pneumonia type- chronic cough and sputum
6. Few patients give an history of insidious onset of symptoms.
7. Some remain asymptomatic.
8. Some give history of non-productive cough termed as ‘Dry-bronchiectasis’.
9. Dyspnea in around 72% cases.
10. Wheezing
11. Pleuretic chest pain
• In past the severity of the bronchiectasis was classified according the amount of
sputum production.
<10ml – Mild bronciectasis
10-150ml- Moderate Bronchiectasis
>150ml – Sever Bronchiectasis.
• At present it is classified accorrding to the radiological findings

1. Many a times combination of

crackles(73%), wheeze and ronchi
are heard.
2. Clubbing(2-3%) may be present.
3. In severe cases with hypoxemia it
may be associated with cor-
pulmonale and features of right
ventricular failure.
4. Cyanosis and plethora are a rare
finding secondary to polycythemia
from chronic hypoxia.
1 2 3
Patient history Physical examination Laboratory tests
• Childhood infections, exposure to • Auscultation for focal wheezes or other • Routine hematology is non specific but
pulmonary pathogens, aspiration of adventitial sounds, examination of may show anaemia and increased
foreign bodies, pulmonary symptoms in nares and upper respiratory tract for white blood count. It may also show
siblings polyps or evidence of chronic sinusitis polycythemia as a response to chronic
• Quantitative immunoglobulin levels of IgG, IgM and IgA are useful to exclude
• Quantitative serum alpha 1 anti trypsin levels used to rule out AAT deficiency

• Sputum analysis
when sputum is allowed to settle may reveal Dittrich plugs, small, white or yellow concretions.
Gram’s stain may reveal Pseudomonas and E-coli suggestive of CF but not diagnostic.
Presence of non-mucoid sputum is suggestive of pseudomonas aeruginosa, while presence of
eosinophilia and golden plugs containing hyphae is suggestive of aspergillous species.
• Routine bacterial, fungal, and mycobacterial cultures may reveal other organisms.

• Pilocarpine ionophoresis (Sweat test)

for the evaluation of CF
• Skin test*
Aspergillus antigen
• Aspergillus Precipitin test
Diagnostic criteria 1000 IU/ml or a greater than 2 folds increase from the
• Auto-immune screening test
For RA and other auto-immune diseases. For ex ANA antibody assay.
• Computerized tomography
the HRCT is has almost completely replaced bronchography. The sensitivity and
specificity are 84-89% and 82-99% respectively.
additional advantages include non invasiveness, avoidance of possible allergen to
contrast media and information regarding other pulmonary processes.
Reid’s classification
Depending on the findings of the CT scan it is classified as :
1.Cylindical bronchiectasis has a tram track lines in longitudinal section or
signet ring in case of a horizontal section and the adjacent pulmonary artery
representing the stone.
2.Varicose bronchiectasis : has irregular or beaded bronchi with alternating
dilatation and constriction.
3.Cystic bronchiectasis has large cystic spaces and a honey comb
appearance. This contrasts with blebs of emphysema.
Types of

Cylindrical Varicose Cystic

Types of bronchiectasis
Cylindrical bronchiectasis
Varicose bronchiectasis
Cystic bronchiectasis
Supportive Treatment

• Cessation of smoking
• Avoidance of second-hand smoking
• Adequate nutritional intake
• Immunizations for influenza and pneumococcal pneumonia
• Conformation of immunizations for measles, rubella and pertusis
• Oxygen therapy is reserved for patients with hypoxemia and end stage complications such as cor-
1. Treatment of infection
2. Clearance of the secretion
3. Reduction of the inflammation
4. Treatment of the underlying problem
• Antibiotics- Initially during the acute phase amoxicillin,TMP or levofloxacin
should be started and later proper antibiotic should be chosen accordingly to the
Sputum culture and Gram’s stain.
• When pseudomonas is the organism oral Quinolone or parentral therapy with
aminoglycosides, carbapenam or third generation cephalosporins should be
• There is no firm guidelines for therapy and hence should be continued for 10-14
• Aerosolized antibiotics
It delivers relatively high concentration of drugs with relatively lesser
systemic side-effects.
It is beneficial in treating Pseudomonas infection.
Currently, inhaled Tobramycin is most widely used. Gentamycin and Colistin
have also been used
• Bronchial hygiene
Proper mechanical and devices with proper positioning of the patient can
help the patients with copious secretions.
Postural drainage with percussion and vibration helps in effective clearance.
Devices like Flutter device, Intrapulmonic percussive ventilation device and
incentive spirometry are available.
Newest device is the ‘Vest’ system wherein a pneumatic compression vest is
worn by the patient periodically throughout the day.
Tapping of the chest wall to
dislodge the secretions
Positional drainage and
Use of mucolytics can help thinning out the thick mucous secretions.
Use of recombinant DNAse which help in the destruction of the DNA released by
the neutrophiles has shown improvement in the PF in case of CF.
Bronchodilators help in the obstruction and clearance e of the bronchus.
Use of nebulizations concentrated with 7% NaCl have shown beneficial in
CF-related Bronchiectasis.
• Anti-inflammatory therapy
Reduce the inflammation caused by the organisms and subsequently reduce the
tissue damage.
Inhaled corticosteroids, Leucotriene inhibitors and NSAID can be given.
Studies have shown use of inhaled corticosteroids have shown qualitative
improvement in the quality of life.
Azithromycin has known anti-inflammatory properties and its long term use has
shown ,marked improvement in CF and non-CF bronchiectasis.
• Surgical resection
Helpful in advanced or complicated disease.
Indications :
1.Patients who have focal disease that is poorly controlled by anti-biotics.
2.Reduction of acute infective episodes
3.Massive haemoptysis(Alternatively bronchial artery embolization may be
4. Foreign body or tumor removal
5. Consideration in the treatment of MAC or Aspergillus specific infections
• Complications :
empyema, haemmorrhage, prolonged air leak and persistent atelectasis.
Mortality is <1 %.
• Lung transplantation
Single or double lung transplantation for severe bronchiectasis,
predominantly related to CF. FEV1 < 30
and in younger patients it may be considered.