Chronic Lower Respiratory Tract Infections

8/14/2019 Chronic Lower Respiratory Tract Infections

1/32

CHRONIC LOWERCHRONIC LOWER

RESPIRATORY TRACTRESPIRATORY TRACT

INFECTIONSINFECTIONS


2/32


3/32

BRONCHIECTASISBRONCHIECTASIS

LUNG ABSCESSLUNG ABSCESS


4/32

BronchiectasisBronchiectasis

DefinitionDefinition

Dilation of bronchi.Dilation of bronchi.

EpidemiologyEpidemiology

Incidence low(


5/32

Bronchiectasis contd.Bronchiectasis contd.

PathogenesisPathogenesis

Exact process obscure. Most likelyExact process obscure. Most likely

multifactorial, with the different factorsmultifactorial, with the different factorstaking on different degrees of importance intaking on different degrees of importance in

each patient.each patient.


6/32

Bronchiectasis contd.Bronchiectasis contd.

Mechanistic TheoriesMechanistic Theories

There are 4:There are 4:

i) Pressure of secretion theoryi) Pressure of secretion theory

ii) Atelectasis theoryii) Atelectasis theory

iii)Traction theoryiii)Traction theory

iv)Infection theoryiv)Infection theory


7/32

Pressure of secretion theoryPressure of secretion theory

Thick secretions obstruct, then mechanicallyThick secretions obstruct, then mechanically

distend the airway and the dilation persistsdistend the airway and the dilation persistseven after clearance of the obstruction.even after clearance of the obstruction.


8/32

Atelectasis theoryAtelectasis theory

Collapse of lung parenchyma leads toCollapse of lung parenchyma leads to

increasingly negative intrapleural pressureincreasingly negative intrapleural pressureand later dilation of the bronchus inand later dilation of the bronchus in

question.question.


9/32

Traction theoryTraction theory

Fibrosis and scarring from parenchymalFibrosis and scarring from parenchymal

disease exert traction on the bronchial walls.disease exert traction on the bronchial walls.


10/32

Infection theoryInfection theory

Infection and the inflammatory responseInfection and the inflammatory response

damage the supportive structures of thedamage the supportive structures of thebronchial wall and subsequentbronchial wall and subsequent

bronchiectasis.bronchiectasis.


11/32

SummarySummary

Only the Infection Theory is supported by animal models ofOnly the Infection Theory is supported by animal models ofthis disease. Atelectasis and traction play minimal, if anythis disease. Atelectasis and traction play minimal, if anyroles, in the pathogenesis of bronchiectasis.roles, in the pathogenesis of bronchiectasis.

Bronchial obstruction and poor drainage i.e. retention ofBronchial obstruction and poor drainage i.e. retention ofsecretions (from such cases as foreign bodies) along withsecretions (from such cases as foreign bodies) along withinfection appear to be the major factors in most cases.infection appear to be the major factors in most cases.

Infection or obstruction occurring alone is unlikely to lead toInfection or obstruction occurring alone is unlikely to lead tothe more severe forms of bronchiectasis.the more severe forms of bronchiectasis.


12/32

ClassificationClassification

a) Cylindrical bronchiectasis (Group I)a) Cylindrical bronchiectasis (Group I)

Dilation regular, with the airway continuing to have aDilation regular, with the airway continuing to have aregular outline.regular outline.

b) Varicose bronchiectasis (Group II)b) Varicose bronchiectasis (Group II)

Dilation irregular, with areas of dilation and constriction.Dilation irregular, with areas of dilation and constriction.

c) Saccular bronchiectasis (Group III)c) Saccular bronchiectasis (Group III)

Dilation marked, with destruction of structural componentsDilation marked, with destruction of structural componentsof the airway wall.of the airway wall.


13/32


14/32

AETIOLOGYAETIOLOGY

a) Infectiona) Infection

The most common:The most common:

i)Tuberculosisi)Tuberculosisii)Histoplasmosisii)Histoplasmosis

iii)Pertussis, measles(complicated by pneumonia)iii)Pertussis, measles(complicated by pneumonia)

iv)Adenovirus (types 1,3,4,7, and 21) 20 to 64 per centiv)Adenovirus (types 1,3,4,7, and 21) 20 to 64 per centdevelop bronchiectasisdevelop bronchiectasis

v) Herpesvirusv) Herpesvirus

vi)vi)Aspergillus fumigatusAspergillus fumigatus

vii)vii) Mycoplasma pneumoniaeMycoplasma pneumoniae


15/32

b) Congenital and genetic disordersb) Congenital and genetic disorders

i) Cystic fibrosisi) Cystic fibrosis

ii) Williams-Campbell syndromeii) Williams-Campbell syndrome iii) Tracheobronchomegalyiii) Tracheobronchomegaly

iv) Marfan syndromeiv) Marfan syndrome

v)Alpha-1-antiproteinase deficiency[v)Alpha-1-antiproteinase deficiency[-1--1-antitrypsin deficiency]antitrypsin deficiency]

vi) Congenital bronchiectasisvi) Congenital bronchiectasis


16/32

c) Ciliary Abnormalitiesc) Ciliary Abnormalities

i) Congenital : Kartagener syndrome [triad ofi) Congenital : Kartagener syndrome [triad of

situs inversus,sinusitis & bronchiectasis].situs inversus,sinusitis & bronchiectasis].There is an underlying congenital abnormalThere is an underlying congenital abnormal

ciliary function.ciliary function.

ii)Acquired : occurs as a result of infection.ii)Acquired : occurs as a result of infection.


17/32

d) Immunodeficiencyd) Immunodeficiency

e) Foreign body aspiratione) Foreign body aspiration

g) Right middle lobe syndromeg) Right middle lobe syndrome

h) Asthmah) Asthma

i) Others:

-heroin intoxication-heroin intoxication

-intralobar pulmonary sequestration-intralobar pulmonary sequestration-bronchogenic cyst-bronchogenic cyst

-chronic sinusitis-chronic sinusitis


18/32

-recurrent aspiration e.g. tracheo--recurrent aspiration e.g. tracheo-

oesophageal fistula, cerebral palsyoesophageal fistula, cerebral palsy

-inhaltion of noxious gases-inhaltion of noxious gases -racial predilections-racial predilections


19/32

PresentationPresentation

Age: mainly preschool and early school ageAge: mainly preschool and early school age

years.years. Symptoms: manifestations range fromSymptoms: manifestations range from

chronic cough with early morning sputumchronic cough with early morning sputum

production in an overtly healthy child toproduction in an overtly healthy child torecurrent pneumonia with or withoutrecurrent pneumonia with or without

haemoptysis in a chronically ill one.haemoptysis in a chronically ill one.


20/32

Chronic cough worse in the morning.Chronic cough worse in the morning.

Purulent , foul smelling sputum. Halithosis.Purulent , foul smelling sputum. Halithosis.

HaemoptysisHaemoptysis

Others: weight loss, intermittent fever,Others: weight loss, intermittent fever,

wheezing, dyspnoea, chest pain.wheezing, dyspnoea, chest pain.


21/32

Clinical signsClinical signs

Harrisons sulciHarrisons sulci

Finger clubbingFinger clubbingCyanosisCyanosis


22/32

Dullness to percussion, crepitationsDullness to percussion, crepitations

(crackles), rhonchi, decreased air entry,(crackles), rhonchi, decreased air entry,

bronchial breath sounds- usually localizedbronchial breath sounds- usually localized

over the bronchiectatic area when saccularover the bronchiectatic area when saccular

changes are present except in diffusechanges are present except in diffuse

disease.disease.


23/32

DiagnosisDiagnosis

CXray findings not diagnostic but can beCXray findings not diagnostic but can be

suggestivesuggestive In mild cases: segmental accentuation, lossIn mild cases: segmental accentuation, loss

of definition of lung markings.of definition of lung markings.

In severe cases: honeycomb pattern ofIn severe cases: honeycomb pattern ofcystic changes.cystic changes.


24/32

BronchographyBronchography

Flexible fibreoptic bronchoscopyFlexible fibreoptic bronchoscopy

CT ScanCT Scan Magnetic resonance imagingMagnetic resonance imaging

Lung scintigraphyLung scintigraphy


25/32

Differential diagnosesDifferential diagnoses

All underlying causesAll underlying causes


26/32

Evaluation of patients withEvaluation of patients with

bronchiectasisbronchiectasis

Identify cause and predisposing factorsIdentify cause and predisposing factors

Infection:Infection: Sputum or BALF for M/C/SSputum or BALF for M/C/S

Mycobacterial/fungal culturesMycobacterial/fungal culturesViral cultureViral culture

Skin tests (PPD, fungal)Skin tests (PPD, fungal)

Serological studiesSerological studies


27/32

ImmunodeficiencyImmunodeficiency

FBCFBC

Quantitative immunoglobulinsQuantitative immunoglobulins

IgG subclassesIgG subclasses

WBC function (nitroblue tetrazolium dyeWBC function (nitroblue tetrazolium dyetest, chemotactictest, chemotactic assays,assays,

etc.)etc.)

Total haemolytic complementTotal haemolytic complement


28/32

AspirationAspiration

Barium swallowBarium swallow

Extended oesophageal pH monitoringExtended oesophageal pH monitoring


29/32

Ciliary dysfunctionCiliary dysfunction

Nasal/tracheal epithelium: light and electronNasal/tracheal epithelium: light and electron

microscopymicroscopy

Cystic fibrosisCystic fibrosis

Sweat testSweat test


30/32

ComplicationsComplications

Brain and lung abscessBrain and lung abscess

Empyema & pyopneumothoraxEmpyema & pyopneumothorax

Bronchopleural fistulaBronchopleural fistula

Severe atypical pneumoniaSevere atypical pneumonia

HaemoptysisHaemoptysis

AmyloidisisAmyloidisis

Cor pulmonale in advanced diseaseCor pulmonale in advanced disease


31/32

TreatmentTreatment

MedicalMedical

Chest physiotherapyChest physiotherapy

AntibioticsAntibiotics BronchodilatorBronchodilator

Good nutritionGood nutrition

Bronchoscopy: to remove foreign body orBronchoscopy: to remove foreign body orthick secretionthick secretion


32/32

Treatment (contd.)Treatment (contd.)

SurgicalSurgical

Failure of medical treatment, if disease isFailure of medical treatment, if disease is

localizedlocalized

PrognosisPrognosis

Depends on causative factorsDepends on causative factors

Documents

Chronic Lower Respiratory Tract Infections