DYSPNEA

GROUP A-6

MEMBERS OF GROUP A-6

Rahma
Chia
Ari
Olly
Fika
Nhida
Fitri
Sapril
Lelly
Yuyun
Ati
Natan
Hakim
Jo
Hema

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 ?

DIFFERENTIAL DIAGNOSES

Bronchiolitis
Acute Bronchitis
Bronkopneumonia
Pediatric pneumonia
Asthma bronchial

ACUTE BRONCHITIS
DEFINITION
Bronchitis an inflammation of the air passages
between the nose and the lungs, including the
windpipe or trachea and the bronchi.
Acute Bronchitis a bronchitic attack with a short,
severe course, due to exposure to cold, breathing of
irritants, or acute infection.

PRECIPITATING FACTORS
Usually caused by viral infection, but can also be caused by
bacterial infection & can heal without complications.
Like any upper airway inflammatory process, can increase a person
likelihood of developing pneumonia
Anyone can get acute bronchitis, but infants, young children,& the
elderly are more likely to get the disease
weaker immune systems
Smoker & people with heart or other lung diseases are also at
higher risk to developing acute bronchitis
Individual exposed to chemical fumes or high levels of air
pollution also have a greater chance

CLINICAL FEATURES
Cold
Cough
brings up a greenish yellow phlegm or sputum
Fever
Wheezing after coughing is common
Dyspnea
Tachypnea

PATHOGENESIS

Infection
Irritation of bronchial mucosal
Hypersecretion of bronchial mucus gland

Mucus production
Regular expectoration of sputum

Productive cough

Airway obstruction by mucous

Reduction of peripheral
airway caliber

Ventilation perfusion mismatch

V/Q mismatch

Prolonged turbulent airflow

during expiration

Hypoxia
Hypercapnea

Wheezing

Stimulate respiratory center

Dyspnea

DIAGNOSIS
Based on observing the patients symptoms &
health history
Listen to patients chest with stethoscope for
specific sounds that indicate lung inflammation
moist rales, crackling,
wheezing (indicates airway narrrowing)
Sputum culture may be performed

TREATMENT
When no secondary infection is present

treated in the same way as the common cold

Drinking plenty of fluids
Resting
For fever & pain, take acetaminophen (Datril,
Tylenol, Panadol)

 Cough suppressants are used only when the cough is

dry & produces no sputum
Expectorant cough medicines used to thin the
mucus in the lungs making it easier to cough up
If secondary bacterial infection is present

treated with antibiotic

PROGNOSIS
When treated, acute bronchitis normally resolves
in one to two weeks without complications,
although a cough may continue for several more
weeks.

BRONCHIOLITIS

BRONCHIOLITIS
Definition:An acute, infectious, inflammatory disease of
upper and lower respiratory tract resulting in
obstruction of small airways.
Etiology:Children through the first
2 yrs of life.
Causative organism:
RSV( most common)
Parainfluenza virus,
Adenovirus.

Clinical Features:

Dyspnoea
Fever
Cough
Wheezing
Tachypnea

Pathophysiology

Total

Viral infection

Destruction of ciliated respiratory epithelium

Impairs bronchial clearance

Accumulation of mucus and

debris in the bronchial tree

Obstruction
Partial

Atelectasis

Emphysema


Resistance to airflow in the small passages

Ventilation decreases

PO2 decreases

Stimulation of the peripheral chemoreceptor

Impulse to respiratory center

Respiratory effort

DYSPNOEAStimulation
of pulmonary
stretch receptor

TACHYPNOEA

Increased work of breathing

Subcostal recession and use

of accessory muscle of respiration

Patomechanism of fever
Infection Monocytes, macrophages

Endogenous pyrogenic cytokines:

IL-1,IL-2,TNFalfa & IFN

Hypothalamic regulatory center

Prostaglandin E2

Heat production

FEVER

Physical examination
Rise of the accessory muscle.
Liver and the spleen may be palpable below
the costal margins (as the result of depression
of the diaphragm due to emphysema).

Auscultation
Widespread rales heard at the end of
inspiration and early expiration.
Expiratory phase of breathing may be
prolonged and wheezes are audible.

Chest X-Ray
Reveals hyperinflation of the lung.
Scattered areas of consolidation are found due
to atelectasis secondary to obstruction or to
inflammation of alveoli.

Treatment
Depends on the severity of illness
Supplemental Oxygen is the mainstay of therapy.
If respiratory failure occurs, mechanical ventilation may
be required.
Aerolized bronchodilators Beta-agonist (albuterol)
most frequently used.
Nebulized epinephrin improving oxygenation
Aerolized ribavarin can be given to severe cases.

BRONKOPNEUMONIA

Bronkopneumonia
Defenition: an inflammation of lung parenchyme
(lobularies)
Aetiology
1. Streptococcus pneumoniae
2. Mycoplasma pneumoniae
3. Legionella pneumoniae

 Pathophysiology
Bacteria/mycoplasma/virus

Alveolar tissue

Trigger acute inflammation

Terminal bronchiles/lobes/interstitial

Congestion by neutrophils in capilaries

Red hepatisation confluent fibrinous exudates

Resolution fibrous adhesion between visceral and parietal layer

 Clinical symptoms
1. dyspnoea
2. fever
3. vomit
4. diarrhea
5. cough

 Supporting investigations
1. Chest radiogram
2. Sputum
3. Counter Cell (leucocyte)

Therapy
Oxygen therapy to solve hypoxia.
Peniccilin G to solve complication with pleural
effusion

Pediatric
Pneumonia

Pneumonia
inflammation
of the
parenchyma of
the lungs

Epidemiology
* More than 4 million deaths annually in
children less than 5 years primarily in
developing countries
* Major cause of morbidity and one of the
most common causes of medical
intervention and hospitalization

Adapted from Klein M, Pediatric Infect Dis J. 1995; Campbell PW III, Curr Opin Pediatr. 1995

Etiology
* >
* Nonbacterial:
* Viral (majority of
pediatric pneumonias)
* Mycoplasma,
Chlamydia
* Bacterial
* dependent on age

Common Pathogens in Infants

<3 months
Group B
streptococcus
Chlamydia
Staph aureus
Gram negative
organisms

Common Pathogens in
Children
3 months to 5 years of age
* S. pneumoniae
* H. influenzae
* Less Common
* M. catarrhalis
* S. aureus
* Group A
streptococcus

Common Pathogens in
Children
>5 years
* M.
pneumoniae
* C.
pneumoniae

Pathophysiology
congestion (vascular congestion and
alveolar edema)
red hepatization (erythrocytes, neutrophils,
desquamated epithelial cells, and fibrin
within the alveoli)
gray hepatization (fibrinopurulent exudate,
disintegration of red cells, and
hemosiderin)

Clinical Features
A history of an upper respiratory illness before the
onset of symptoms is common
cough
post tussive vomiting
fever
chest pain
abdominal pain
In severe cases: Tachypnea grunting retractions
cyanosis

The Pathognomic Sign of

Pneumonia

the presence of crackles (also called as

crepitations).
Localized crepts in a febrile child without
underlying lung disease is pneumonia until
proven otherwise.
not all children with pneumonia have
crepitations. Decreased breath sounds with
dull note on percussion and presence of
bronchial breathing are also suggestive of
pneumonia.

Diagnosis of Pneumonia
* History
* Clinical Presentation
* Diagnostic studies

Investigations
*
*
*
*

Non invasive
Chest x-ray PA view
Complete blood count
Sputum cultures and gram
stain

Diagnostic Difficulties in
Pediatric Pneumonia
* Sputum samples are often unobtainable
* Some common pathogens are not
easily cultured: C. pneumoniae and M.
pneumoniae
* Nasopharyngeal samples are unreliable
due to high asymptomatic carriage
rates

Investigations continued
*
*
*
*
*

Invasive
Pleurocentesis
Bronchoalveolar lavage
Transbronchial biopsy
Open lung biopsy

X-ray Findings
* Viral: hyperinflation, segmental
atelectasis, interstitial infiltrates
* Mycoplasma : usually lobar
* Bacterial: Lobar consolidation,
more common in the older child,
diffuse infiltrates

Treatment
*
*
*
*
*

Oxygen if indicated
Antibiotics
Analgesics and antipyretics
Chest physiotherapy
Expectorants

Anti-microbial Therapy
* Empiric therapy is justified as initial
management as the specific
bacteriological etiology is unknown and
delaying therapy while trying to find a
diagnosis may be injurious to the
patient

Antimicrobial selection in
children 3 months to 5 years
* S. pneumoniae, H. influenzae
most common
* Beta-lactams : Amoxicillin,
amoxicillin-clavulanic acid,
cephalosporins
* Macrolides : erythromycinsulfisoxazole
* Trimethoprim-sulfamethoxazole

Indications for hospitalization

*
*
*
*
*

Severe disease at the onset

Younger age
Underlying disease (pulmonary or cardiac)
Toxemia, sepsis or sepsis syndrome
Respiratory distress or need for assisted
ventilation or hypoxia
* Socioeconomics (problems with
compliance or access to medications)
* Failure to respond to oral antibiotics

Complications

Pleural effusions
Bronchiectasis
Empyema
Pneumothorax

ASMA
BRONCHIAL

DEFENISI
Asthma is the clinical result of a
chronic eosinofil rich inflammation
of the bronchial tree.

ETIOLOGY

ALLERGENS
WEATHER
EXERCISE
EMOTIONS

EPIDEMIOLOGY

Its attack children and

adults
Man > women

PATOPHYSIOLOGY
Inhalled allergen
Response to extrinsic
IgE production by plasma cell ( B cell ) & lymphoid tissue
IgE binds to mast cell (on bronchial wall)
Desensitization/ degranulation of mast cell after binding antigen on IgE
Secretion of mediators in mast cell (histamine, leucotrine, prostaglandin)
React at specific reseptor sites on membrane of smooth muscle
(bronchial smooth mucles)

cAMP
Bronchoconstrictor of smooth muscle

Capillary permeability
Mucosa Edema

Narrowing airway

Wheezing
Breathlessness
Cough

CLINICAL FEATURES

Breathlessness
Cough usually dry
Wheezing
Cyanosis
Unconciousness
Fatigue
Tachycardi

chronic asthma

EXAMINATION
- Radiology examination
1. hyperlusent
2. dilatation of intercostal
3. lower diaphragma
- Laboratorium examinations
1. skin test
2. blood test ; IgE, eosinophil
3. blood gas analyze
4. sputum evaluation

TREATMENT
1. Anti-inflammatory agonis
- steroid.
- non steroidal anti-inflammatory drugs
2. Bronchodilators
- Beta 2-adrenergic agonis
- metil santin
- anticholinergic drugs

PREVENTION

Avoidance of exacerbation factors

Stopping smoking
Limitation of exercise

PROGNOSIS

RECOVER IN ADOLESCENS
BAD MANAGEMENT
WORSE

COMPLICATIONS

PNEUMOTHORAKS
ATELEKTASIS
BRONCHITIS

Thank
You