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DYSPNEA

SECOND MODUL
BY GROUP A-2

SCENARIO
A 13 months boy came to hospital with chief
complain of dyspnea since 3 days ago before
entered the hospital, there were also
complains of cough with sputum and fever.
The boy was born with 3 kgs weight, normal
birth. There wasnt history of dyspnea before.

KEYWORDS
A 13 MONTHS BOY
DYSPNEA 3 DAYS
COUGH WITH SPUTUM
FEVER
BORNNORMAL,WEIGHT=3 KGS
DYSPNEU BEFORE

QUESTIONS

What are the differential diagnosis (DD) and


the definition ?
What is the aetiology and epidemiology ?
What are the clinical signs of each DD ?
How is the patomechanism of each DD ?
What are the treatments of each DD ?
What are the examinations of each DD ?

QUESTIONS

What are the complications of each DD ?


What is the prognosis of each DD ?
What is the prenention of each DD ?

BRONCHIOLITIS

BRONCHIOLITIS
The inflamation of bronchiolus as
respons to injury because infection,
chemical contact such as smoke, that
oftenly happen to infant and children.

AETIOLOGY
RSV (Respiratory Sensitial Virus) 45 70%
from the bronchiolitis case in children
Para Influenza virus type I & III (10%)
Influenza Virus type A & B
Adenovirus
Rhinovirus
Enterovirus
Mycoplasma pneumoniae

RSV
Subfamily
: pneumovirinae
Genus
: pneumovirus
Not segmented
Plemorphic envelope
Nukleocapsid RNA helix linier
Lack neuraminidase activity
No hemagluttinin
Glycoprotein G receptor for cell attachmenut but
not to red blood cells. There F & Matrix (M)
Transmision by droplet and contaminated hand

EPIDEMIOLOGY
Most in age < 2 years old
Usually in age 26 month
man : woman = 1,5 : 1
Bronchiolitis winter

PREDISPOTITION FACTOR

Man
Premature
Overcrowding
Lack breast feeding
Comorbidity (congenital heart disease or
chronic pulmonal disease such as
bronchopulmonal displasia)

CLINICAL FEATURES

Rhinorrhea
Low grade fever/ sub febril
(38,5-39C)
Irritability
Letargy
Anorexia
Dyspnea
Wheezing
Tachycardy
Tachypneu

Cyanosis
Refraction of thorax wall
(intercostal &
suprasternal)
Side of the nose breathing
Vomit
Progressivity to
emergency if : paroxysmal
wheezing cough, dysnea,
irritability.

Sign happen for 3-7 days,


progessivity in beginning of 3-4 days
clinical resolution : 1-2 weeks

PATOGENESIS
Attachment of RSV (glycoprotein G)
Virus cleft
Sitonecrosis
Inflamation & oedema in bronchiolus terminalis
Narrowed lumen
Obstruction from epithel & inflamation cell
Obstruction of bronchiolus

Total obstruction
Atelectasis

partial obs.

air trapping

emphysema
hyperinflation
disturb. of ventilation & oxygenation
Irritability
Tachycardy
hipoxia dyspnea
Tachypnea
(hipoxemia)
Acidosis (CO2
retention)

INVESTIGATION

Anamnesa
Physical examination
Percussion hypersonor, heart dull <
Auscultation breath sound : bronchial
addition sound : ronchi, wheezing, crepitation
Rontgen ( thorax photo)
hyperinflation of the lung (hyperlusen)
elevation of the AP diameter (lateral photo)
depretion of diafragma
less of costophrenicus
the scattered of consolidation area (atelactasis)

Laboratory
peripherial blood image : normal
nasopharynx swab : normal flora
blood gas analyse : acidosis respiratory &
metabolic
Culture virus
3-7 days RSV is slowest & difficult to grow in
tissue culture
Serology test
immunoassay detection of protein G & F

MANAGEMENT

Humidified O2
Avoid sedative
Position of infant is sit 30-40
Fluid intake
Acidosis correction
Ribavirin (virazol) antivirus activity against RSV
Antibiotic for indication
corticosteroid
bronchodilator
Cor pulmonal digitalization

PROGNOSIS

Actually prognosis of bronchiolitis good


Self limiting disease 14 days
Prognosis is bad if : premature,
immunocompromizen person, child with
chronic cardiopulmonary disease
Mortality rate bronchilitis because RSV
0,5 1,5 %

COMPLICATION

Dehydration
Secondary infection (bacterial pneumoni,
otitis media)
Pneumothorax
Pneumomediastinum
Cor pulmonal

PREVENTION
Avoid contact with person that have
respiratory infection
The patient isolated to prevent
nosocomial spread
Maintain the body clean washing hand

PNEUMONIA

DEFINITION
Inflammation located at lung parenchyma,
distal from bronchiolus terminalis including
bronchiolus respiratorius & alveoli, and
causing consolidation of the lung tissue
and localized gas exchange.

buku interna, 3rd edition

aEtiology
Most
strp.pneumoniae
Gram positive shape, with ovoid/lancet shape cocci
Virulence factors
polysaccharide
capsule & IgA protease
Leading cause for adults and children
Human pathogen, no animal reservoir
Transmission: person to person contact
inhalation of contaminated droplet

HAEMOPHILUS INFLUENZA
Small, coccobacillus and pleomorphic
Capsular polysaccharide, membrane
lipooligosaccharides & IgA protease as a virulence
factors.
Transmission: inhalation of infected droplet
Strictly human pathogen.

KLEBSIELLA PNEUMONIAE
Specific sign
purulent sputum( red current jelly )
Most
men in middle/old age [ alcoholic or having
chronic disease ]

PSEUDOMONAS
Generally for patient at RS/ having suppression in
defense system { leukemia/ renal transplantation that
consumed immunosuppressive drugs in high dose.
Beside antimicrobial therapy
change in normal
flora in respiratory tract & possibly cause increasing
quantity of that microbes.
Mostly because contamination of ventilation tools.

STAPH. AUREUS
Secondary infection for hospitalization patient that
having low defense mechanism system.

Consider for causing bronchopneumonia


Usually bad prognosis although using antibiotic.
complication: lung abses and emphysema

MYCOPLASMA PNEUMONIAE
Infection ( pharyngitis / bronchitis ) but only 10% from
patient
Usually young adult infected
Clinical manifestation is similar like viruses but
followed by interstitial pneumonitis
Positive response to tetracycline/erythromycin
Also causing primer atypical pneumonia/ walking
pneumonia

LEGIONELLA PNEUMOPHILLA
Resource
AC, shower
Sporadic
After incubation (2-10 days) symptom appear
(malaise, dry cough, fever, headache, muscle pain, anorexia,
diarrhea)
Usually infect adult, smokers and who have lower lung
defense system.

P.Carinii (parasite protozoa)


AIDS patient

VIRUS
Usually infect upper respiratory tract
Children is main target ( adult
10%)
Symptoms ( headache, fever, muscle pain, malaise and dry
cough)
Generally not chronic (reversible and did not need ICU
attention)
Influenza type A&B and adenovirus
Antibiotic not effective against virus

Predisposition Factors
Patient after operation
Smokers
Alcoholic
Patient with chronic respiratory tract
disease/infection
AIDS
- Baby usually susceptible.

Division of Pneumonia
1.

Lobar Pneumonia
- lobes have a consolidation, exudates
especially intra alveolar
- aetiology: pneumococci & Klebsiella

2.

Necrotisation pneumonia
- granuloma can morph to caseosa necrosis &
develop cavity
- aetiology: fungi & tubercle

3. Lobular pneumonia
-

Spreading of pores, exudation of fibrinosa at bronchioles


Etiology: strp & staph type

4. Interstitial pneumonia
-

Perivascular exudation & edema between alveoli


Etiology: virus & mycoplasma

Patomechanism
Infection in the alveoli

Pulmonary membrane become inflamed & highly porous


Fluid & erythrocyte and leukocyte leak out of the blood into the
alveoli
Infected alveoli become progressively filled with fluid & blood cells
Infection spreads by extension of bacteria from alveolus to alveolus

Large areas of the lung (whole lobes @ lung) become consolidated


(filled with fluid and cellular debris ( foreign matter)

So what happen to the lungs functional?


The gas exchange functions of the lungs change in different stages
of the disease
Early stage
hypoventilation
Ventilation not susceptible,
Cannot balancing Co2 development

lack of O2 that can


enter alveoli

So what happen again if hypoventilation occur?


2 major pulmonary abnormalities:
Reduction in the total available surface area of the respiratory
membrane
Decreased ventilation-perfusion ratio

Both of that abnormality will cause:


Hypoxemia (low blood O2) Pco2
Hypercapni (high blood co2)

Clinical examination
1.

Physical examination:

fever, tachycardia and tachypnea mostly found


Rales and crackles sound in auscultation (25%)
Dullness to percussion (33%)

2.

Imaging x-rays

Consolidation, homogen/inhomogen
Sharp border
Lung volume not changed
Silhouette sign positive

Air Bronchogram Sign (ABS)

3. Sputum evaluation
4.

Blood evaluation

5.

Other test:
Serum electrolyte
Blood urea nitrogen(BUN)/creatinin
Arterial oxygen saturation

TREATMENT

Penicillin & erythromycin

Erythromycin, ciprofloxacin &


Nifampicine
Erythromycin & tetracycline
Amphyciline
Cephalosporin

P.pneumococcus

P. legionella
P. mycoplasma

( for bacteria that not produce B-lactamase)


Haemophilus Influenzae

Nofsilin, oxacyline,
Vancomycin (for MRSA infection)
( penicillin resistant )

P.staphylococcus

Penicillin

P.streptococcus

Prevention
Vaccination exchange between
country
Quarantine to foreigner/tourist
Healthy lifestyle

Revision

20 common disorder (RESPIRATORY


DISORDER), William J. Hueston, international
edition
Radiology lecture notes
Buku ajar ilmu penyakit dalam, third edition,
Slamet Hayuno and friend.

BRONCHIALE
ASMA

definition
Bronchial asthma is a disease in which
inflammation of the airways causes
airflow into and out of the lungs to be
restricted.

aEtiology
Extrinsic : atopy/allergy
Intrinsic : tractus respiratory infection
exercise
drugs
psicogen

Epidemiology
Child ; women : man = 1:1,5
Adult ; women = man
Indonesia : 5-7%

Symptoms:

Dyspnea
Wheezing
Cough with sputum
Chest pain
Nostril respiration
Takipneu

Patomechanism

Antigen enter to the upper respiratory tract

Antigen combines with specific Ig E on mast cell in the respiratory mucosal


These cell relase performed mediators that open thight junction between epithelial cells
Then, antigen enter the mucosal to activate mucosal mast cell and eusinophils
Release additional mediators (directly or via neuronal reflex)

Other mediators

Chemotaxis of
Neutrophils &
Eusinophils

Histamine and bradykinin

Mediators

1. Contraction of bronchial
1. Platelet aggregating factors
smooth muscles
2. Leucotrienes
2. Hyperemia
3. Prostaglandin E2
3. Edema
4. Netrophils & eosinophils
5. Mucus retention
Vasodilatation
Vascular permeability
BRONCHIAL ASTHMA

Examination

1.
2.

Anamnese
Physical examination
Radiologhy
Allergy testing by skin testing
Pulmonary function tests
Laboratory
Blood
Sputum

Treatment

1.
2.

Non pharmacology
Retire the allergen
Give information to
the people

Pharmacology
Bronchodilators
1. Metil xantin
2. Aminofilin
3. Adregenic agonis
4. Anti-colinergic
Anti-inflamation
1. Corticosteroid
2. Natrium cromolin

Complications

Bronchitis
Pneumonia
Emfisema
Cor pulmonal

Expectations (prognosis):
There is no cure for asthma, though
symptoms sometimes decrease over time.
With proper self management and medical
treatment, most people with asthma can
lead normal lives.

BRONCHOPNEU
MONIA

INTRODUCTION
Secondary disease
Insidens : infant or toddlers

CLINICAL FEATURE
HISTORY:

SUBFEBRIL
DYSPNEA
COUGH
RHINITIS

CLINICAL EXAMINATION
PHYSICAL

INSPECTION :
MODERATE DISEASE,GENERAL CONDITION
NORMAL,RETRACTION,BREATHING RATE> 50X/MINUTE
PALPATION : N
PERCUSION : N
AUSCULTATION : HIGH FREC & DIFFUSE RONCHI IN ONE OR BOTH
OF THE LUNG

OTHER TESTS

RADIOLOGY
NORMAL OR INFILTRAT usually bilateral
and widespread, but not always
symmetrical

MEDICATION

AB POLIFRAGMATION
STREP,AMPIC+CHLORAMPHENICOL
< 2 MONTH : AMP+GENTAMICIN
O2
SEDATIVA
CORTICOSTEROID
LIQUID INTAKE OBTAIN

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