Pneumonia

DR NIMO ABDURAHMAN,
MD
Definition: Inflammation and
Infection of the lung parenchyma
Although most cases of pneumonia are
caused by microorganisms, noninfectious
causes include aspiration of food or
gastric acid, foreign bodies, hydrocarbons,
and lipoid substances, hypersensitivity
reactions, and drug- or radiation-induced
pneumonitis.
How big is the problem?
Nearly 4 million children die per
year worldwide.
It is the leading killer in
developing countries.
There has been a significant
reduction in mortality in the
developed world, WHY?
Affects younger ages more.
Etiology
InfectiousVs Non- infectious
Neonates and
immunocompromised vs
immunocompetent
The exact cause is difficult to
determine.
S. pneumoniae is the most
common bacterial pathogen,
followed by C. pneumoniae and M.
pneumoniae
Etiology
 Recurrent pneumonia
 is defined as 2 or more episodes in a single yr or 3 or more
episodes ever, with radiographic clearing between occurrences.
 An underlying disorder should be considered if a child experiences
recurrent bacterial pneumonia .
 Additional factors that promote pulmonary infection include
trauma, anesthesia, and aspiration.
RiskFactors for recurrent
pneumonia
◦ Host factors
 Immunity- primary vs secondary
 Anatomic abnormality
◦ Pathogen virulence
 More important for severity
◦ Socio-economic
 Crowding
 Smoke exposure
 Poverty
 Preceding viral infections
Pathogenesis
Pathologicprocess usually
depends on the etiologic agent.
Lobar Vs Bronchopneumonia
Lobar Pneumonia
 Congestion
 Red hepatization
 Grey hepatization
 Resolution
 Pathogenesis

Etiologic Agent vs Pathologic

Finding
S. pneumonia - lobar pneumonia
Viral and Mycoplasma - airway
obstruction
Group A streptococcus - more
diffuse interstitial pneumonia and
necrotizing pneumonia.
 S. aureus- confluent
bronchopneumonia
Clinical Presentation
Viral vs Bacterial pneumonia
Tachypnea is the most consistent
feature.
Usually preceded by viral URTI
Abrupt onset- bacterial pneumonia in
older children
Physical findings depend on the stage
of the disease.
Creptations, consolidation, decreased
air entry
Viral pneumonia is usually self limiting
 Increased respiratory rate:
 >/ 60 breath per minute infants younger than 2 months
old
 >/50 breaths per minute infants 2-12 months old
 >/ 40 breaths per minute children 1-5 years old
Severity of Pneumonia
Very severe pneumonia
Central cyanosis
Severe respiratory distress
Unable to drink or breast
feed/persistent vomiting
Convulsions, lethargy or
unconsciousness
Severe pneumonia

Chest wall indrawing or nasal flaring

Grunting (young infants)
Pneumonia
Fast breathing
Definite crackles on auscultation
No pneumonia
Cough or cold
No signs of pneumonia, severe or
very severe pneumonia
Classification
Clinical
◦ Community Aquired
◦ Nosocomial
◦ Chronic
◦ Typical vs atypical
◦ Aspiration pneumonia
Radiologic
◦ Lobar
◦ Interstitial
◦ Bronchopneumonia
Pneumonia in
Classification
Recurrent Pneumonia
◦ Two or more / year
◦ Three at any time
◦ Radiologic resolution between
episodes
Slowly resolving pneumonia
Diagnosis
CBC with differentials
Chest radiograph confirm the
diagnosis of pneumonia with clinical
features
◦ Also important for the detection of
complications of pneumonia
Etiologicdiagnosis difficult
Acute phase reactants
Cultures: blood, sputum; cold
agglutinin
Treatment
Indications for Hospitalization
Treatment
Stabilization
Supportive treatment
oOxygen
oAntipyretics
oNutrition
Antibiotics
 Treatments
 Antibiotic therapy
◦ Cotrimoxazole or Amoxicillin orally for 5days
 Admission: children with sever pneumonia
◦ IV Crystalline penicillin 1st line drug
◦ Ampicillin and Gentamicin i.e Neonatal Pneumonia
◦ Ceftriaxone and Vancomycin as second line
 Supportive care
◦ Oxygen therapy
◦ Hydration
 COMPLICATIONS
 Direct spread of bacterial infection within the thoracic cavity

1. Pleural effusion,

2. empyema, Lung Abscess and Atelectiasis

3. pericarditis
 Bacteremia and hematologic spread:
◦ Meningitis, suppurative arthritis, and osteomyelitis are rare
complications of hematologic spread of pneumococcal or H.
influenza type b infection.
Complications

Parapneumonic Effusion
Common causes : S. aureus, S.
pneumoniae, and S. pyogenes
Treatment is based on the effusion
Antibiotics and tube
thoracotomy(Chest tube)
Fibrinolytic therapy
Differentiation of the pleural
fluid
Bronchiolitis
Bronchiolitis
Itis a lower respiratory tract
infection that predominantly affects
the smaller airways (bronchioles).
Commonly affects infants and
young children
Predominantly viral in origin
No bacterial etiology established
Rarely followed by a super-infection
RSV accounts for over 50% of
cases.
Other agents include; para-
influenza, adenoviruses,
mycoplasma and occasionally
human metapneumovirus
Risk Factors
Young age (< 6 months)
Not breast fed
Crowding
Having older family members in
the family
Prematurity, Low birth weight
Being male
Anatomic Defects
Pathogenesis
IgE antibody production and
eosinophilic degranulation results
in epithelial injury
Airways undergo obstruction with
edema, mucus, and cellular debris.
Airway narrowing is significant in
infants
Eventually lead to hyperinflation
and atelectasis
Clinical Manifestation
History of preceding upper
respiratory tract symptoms one-
to three-day prior: nasal
congestion and/or discharge and
mild cough.
Fever (usually ≤ 38.3ºC)
Apnea may occur in infants
Dehydration
Restlessness or lethargy
P/E
Tachypnea, intercostal and
subcostal retractions
Hyper-inflated chest, hyper-resonant
to percussion
Coarse and fine crackles
Hypoxemia
Cyanosis
Expiratory wheeze(may not be
audible if the airways are profoundly
narrowed)
Diagnostic Approach

Detailed history and physical

examination
Respiratory distress and
wheezing
CBC
CXR
Bronchodilator challenge
Viral tests: PCR, culture
Differential Diagnosis
Allergy and Asthma
Congenital Malformations
Foreign Body Aspiration
Gastroesophageal Reflux
Cystic Fibrosis
Pneumonia
Pulmonary Edema
Treatment
Main Treatment is supportive
Bronchodilator trial
Prognosis and Prevention
Mean median of disease is 12
days
Case fatality is <1%
Hand washing
Apnea, uncompensated
respiratory acidosis, or
severe dehydration are poor
prognostic signs.
Bronchial Asthma
Bronchial Asthma
 It is a chronic inflammatory condition
of the air ways leading to episodic
airflow obstruction & hyper
responsiveness to provocative
exposures
 Symptoms are associated with
widespread but variable airflow
obstruction
 All children with early childhood
wheezing might not develop bronchial
asthma
Etiology
Not generally definitely known
But researches suggested the
interplay between genetic &
environmental factors
 Childhood risk factors for
persistent Asthma
 Parental asthma
 Allergy-atopic dermatitis, rhinitis,
food allergy
 Severe lower respiratory tract
infections (pneumonia, bronchiolitis
or wheezing apart from colds)
 Male gender, low birth weight
 Environmental tobacco exposure
 Clinical Manifestation
 Chronic symptoms are the core
manifestation of asthma
 Dry cough(intermittent) &/or
expiratory wheeze are the most
common chronic symptoms
 Older children - SOB & chest tightness
 Younger children - non-focal chest pain
 Respiratory symptoms are
characteristically worse at night.
 Decreased physical activity,
general fatigue, difficulty in
keeping up with peers
 Symptoms are typically provoked
by numerous common events or
exposures like; exertion, hyper
ventilation(laughing), cold/dry air,
irritants and allergic conditions like
rhinitis, conjunctivitis, atopic
dermatitis & food allergies
Types of Childhood
Asthma
• Recurrent Wheezing- triggered
by common viral infections
• Chronic asthma – associated
with allergy and progresses to
later age
Differential Diagnosis for Wheeze
Investigation
 Lung function tests - expiratory
airflow measurements are helpful in
diagnosing & monitoring asthma
 Spirometry
 FEV1
 FEV1/FVC
 Broncho-provocative tests -
inhaled methacholine, histamine &
cold/dry air. It is rarely practiced.
 Exercise challenge
 Spirometry
- Airflow obstruction is defined as FEV1
reduced to less than 80 %predicted and
an FEV1/FVC ratio of less than 0.8 (80 %)

- FEV1/FVC appears to be a more sensitive

measure of impairment than FEV1,
whereas FEV1 may be a more useful
measure of risk for future exacerbations
 Peak Expiratory Flow rates-
declines only when airflow obstruction
is severe
 Radiography
 Hyperinflation (flattening of diaphragm
& peribronchial thickening)
 Complications ( collapse,
pneumothorax)
 To rule out asthma masqueraders
(pneumonia, bronchiolitis, FBA)
• CT scan
Management
• Goals of treatment
 Maintain normal activity
 Prevent sleep disturbances
 Prevent chronic asthma
symptoms
 Minimize severe exacerbations
 Maintain normal lung function
 Minimize adverse effects of drugs
Management Approach
SYMPTOM
CLASSIFICATION
Severe Persistent Step 4 FEV1/FVC <60%
◦ Day: continual PEF Variability >30%
◦ Night: frequent
Moderate Persistent Step 3 FEV1/FVC 60-80%
◦ Day: daily PEF Variability >30%
◦ Night: >1/week
Mild Persistent Step 2 FEV1/ FVC>80%
◦ Day: >2/week (<1/day) [3-6/week] PEF Variability 20-30%
◦ Night: >2/month
Mild Intermittent Step 1 FEV1/ FVC >80%
◦ Day: <2/week PEF Variability <20%
◦ Night: <2/month
DAILY MEDICATIONS
Preferred Treatment:
Step 4
◦ High-dose inhaled corticosteroids, AND
◦ Long-acting beta2-agonists
Step 3
◦ Low-to-medium dose inhaled
corticosteroids, AND
◦ Long-acting beta2-agonists
Step 2
◦ Low-dose inhaled corticosteroids
Step 1
◦ No daily medication needed
 Standard Therapy

Standard asthma treatment should include

short-acting beta 2-agonists, systemic
glucocorticoids, and supplemental oxygen
1.Short-acting beta 2-agonists
- inhaled short-acting beta 2-agonists (SABA,
eg albuterol, salbutamol
-can be administered continuously or
intermittently (via nebulizer or metered dose-
inhaler [MDI] with spacer)
2.Glucocorticoids
Systemic — to decrease airway inflammation
and secretions
may be given as prednisone, prednisolone, or
methylprednisolone. Dose-1 mg/kg every 12
hours for a total of five days
Route — Oral is preferred to IV administration
since it is less invasive and equally
efficacious.
Taper in patients a course longer than 10 days
and may be tapered by decreasing the dose
by 50 % every two to three days
 Inhaled— are not as effective as systemic
glucocorticoids for severe asthma
exacerbations and should not be used as a
substitute for systemic glucocorticoids.
3.Supplemental oxygen
It should be provided by nasal cannula or face
mask as needed to maintain an oxygen
saturation of ≥ 92 %.
All nebulized medications should be delivered
with oxygen, generally at a flow rate of 6 to
8 L/min.
Prognosis
Recurrent coughing and wheezing occurs in 35% of
pre–school-age children.
⅓ - persistent asthma into later
childhood,
⅔ -improve on their own
Asthma severity by the ages of 7–10 yr of age is
predictive of asthma persistence in adulthood.
Children with moderate to severe asthma and with
lower lung function measures are likely to have
persistent asthma as adults.
Children with milder asthma and normal lung
function are likely to improve over time, with
some becoming periodic (disease-free mo to yr);
however, complete remission for 5 yr in
childhood is uncommon
Thank You