Transcript LOWER RESPIRATORY TRACT INFECTIONS good

BRONCHIOLITIS
EPIDEMIOLOGY
 Annual incidence is 11.4% in children younger than 1 year
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and 6% in those aged 1-2 years.
Incidence peaks in those aged 2-8 months
95% have serologic evidence of past (RSV).; presence of
antibodies to RSV does not confer immunity.
Incidence of bronchiolitis winter months in temperate
climates and during the rainy season in tropical climates.
Hospitalization -2% of cases under 6 months
Mortality rate is 1-2% of all hospitalized patients and 3-4%
for patients with underlying cardiac or pulmonary disease.
EPIDEMIOLOGY
Accounts for 60% of all lower
respiratory tract illness in the
first year of life!
Bronchiolitis
 young infants, aged 2-24 months.
 viral infection of the small airways (bronchioles).
 increased mucus secretion, cell death followed by a
peribronchiolar lymphocytic infiltrate and submucosal
edema
 debris and edema produce narrowing and obstruction of
small airways.
 decreased ventilation in the lung causes
ventilation/perfusion mismatching and hypoxia.
 in expiratory phase of respiration, further dynamic
narrowing of the airways produces disproportionate airflow
decrease and resultant air trapping.
Pathophysiology
 The virus spreads from the upper respiratory tract to
the medium and small bronchi and bronchioles,
causing epithelial necrosis and initiating an
inflammatory response.
 The developing edema and exudate result in partial
obstruction, which is most pronounced on expiration
and leads to alveolar air trapping.
 Complete obstruction and absorption of the trapped
air may lead to multiple areas of atelectasis
lung hyperinflation
with a flattened
diaphragm and
bilateral atelectasis in
the right apical and left
basal regions
RISK FACTORS OF SEVERITY
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Prematurity
Low birth weight
Age less than 6-12 weeks
Chronic pulmonary disease
Hemodynamically significant cardiac disease
Immunodeficiency
Neurologic disease
Anatomical defects of the airways
Older siblings
Concurrent birth siblings
Passive smoke exposure
Household crowding
High altitude
ETIOLOGY
 Typically caused by viruses
 RSV-most common
 Parainfluenza
 Human Metapneumovirus
 Influenza
 Rhinovirus
 Coronavirus
 Human bocavirus
 Occasionally associated with Mycoplasma
pneumonia infection
Clinics
 Early symptoms are those of a viral URTI, including rhinorrhea,
cough, and sometimes low-grade fever.
 paroxysmal cough and dyspnea develop within 1-2 days.
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Fever
Increased work of breathing
Wheezing
Cyanosis
Grunting
Noisy breathing
Vomiting, especially post-tussive
Irritability
Poor feeding or anorexia
Clinics
Physical
 Tachypnea, over 50-60 breaths per minute (most common)
 Tachycardia
 Fever, usually in the range of 38.5-39°C
 Mild conjunctivitis, otitis, pharyngitis
 Diffuse expiratory wheezing
 Nasal flaring
 Intercostal retractions
 Cyanosis
 Inspiratory crackles
 Apnea, especially in infants younger than 6 weeks
 Palpable liver and spleen from hyperinflation of the lungs
and consequent depression of the diaphragm
DIFFERENTIAL DG
 Asthma
 Gastric reflux with aspiration of gastric contents also
may cause the clinical picture of bronchiolitis; multiple
episodes in an infant may be clues to this diagnosis.
Bronchitis
Congestive Heart Failure and Pulmonary Edema
Mycoplasma
Apnea
Pneumonia
 Cystic fibrosis
Vascular ring
Lobar emphysema
Foreign body
Cardiac disease
Reflux
Aspiration
LABORATORY AND IMAGISTICS
 Complete blood count (CBC) with white blood cell (WBC) count
within normal limits. 2/3 of the children have WBC counts of
10,000 to 15,000/μL. Most have 50 to 75% lymphocytes
 Serum chemistries may be affected in dehydration.
 Arterial blood gases (ABG) in severely ill patients, with
mechanical ventilation.
 Chest radiographs should include anterior-posterior (AP) and
lateral views.
 Hyperinflation and patchy infiltrates ;these findings are
nonspecific and may be observed in asthma, viral or atypical
pneumonia, and aspiration.
 Focal atelectasis
 Air trapping
 Flattened diaphragm
 Increased anteroposterior diameter
 RSV rapid antigen testing done on a nasal swab or
washing is diagnostic but not generally necessary; it
may be reserved for patients with illness severe enough
to require hospitalization.
 A positive culture or direct fluorescent
antibody test result can confirm the diagnosis
of RSV infection
COURSE
 Depends on co-morbidities
 Usually self-limited
 Symptoms may last for weeks but generally back to
baseline by 28 days
 In infants > 6 months, average hospitalization
stays are 3-4 days, symptoms improve over 2-5 days
but wheezing often persists for over a week
 Disruption in feeding and sleeping patterns may
persist for 2-4 weeks
Prognosis
 Prognosis is excellent.
 Most children recover in 3 to 5 days without sequelae,
although wheezing and cough may continue for 2 to 4
wk.
 Mortality is < 1% when medical care is adequate.
Bronchiolitis has been identified as a risk factor for
asthma, but the association is controversial and the
incidence seems to decrease as children age.
Treatment
 Supportive therapy
 O2 supplementation as needed
 IV hydration as needed
 Indications for hospitalization include
 accelerating respiratory distress,
 ill appearance (eg, cyanosis, lethargy, fatigue),
 apnea by history, hypoxemia
 inadequate oral intake.
 children with underlying disorders such as cardiac disease,
immunodeficiency, or bronchopulmonary dysplasia, which
put them at high risk of severe or complicated disease, also
should be considered candidates for hospitalization
 In hospitalized children, 30 to 40% O2 by tent or face mask is
usually sufficient to maintain O2 saturation > 90%.
 Endotracheal intubation is indicated for severe recurrent
apnea, hypoxemia unresponsive to O2 therapy, or CO2
retention or if the child cannot clear bronchial secretions.
 Hydration maintained with frequent small feedings of clear
liquids. For sicker children, fluids should be given IV initially,
and the level of hydration should be monitored by urine
output and specific gravity and by serum electrolyte
determinations.
 There is little evidence that systemic corticosteroids are
beneficial
 Antibiotics should be withheld unless a secondary bacterial
infection (a rare sequela) occurs.
 Bronchodilators are not uniformly effective some children
may respond with short-term improvement. This is
particularly true of infants who have wheezed previously.
RIBAVIRIN
active in vitro against RSV, influenza, and measles, is toxic
 RSV immune globulin has been tried
 Prevention of RSV infection by passive immunoprophylaxis
with monoclonal antibody to RSV ( palivizumab )
SYNAGIS decreases the frequency of hospitalization but is
costly and is indicated primarily in high-risk infants
 RESPIRATORY PHYSIOTHERAPY
 NEBULISATIONS WITH: Epinephrine: 0.01 mL
(ie, 0.01 mL/kg of 1:1000 solution [1 mg/mL]) SC
q15-20min, not to exceed 0.3 mL/dose
Racemic epinephrine:
<2 years: 0.25 mL of 2.25% solution via nebulizer
diluted in 3 mL NS
>2 years: 0.5 mL of 2.25% solution via nebulizer
diluted in 3 mL NS
 ALBUTEROL, VENTOLINE 90 mcg; 4-8
inhalations q 20min up to 4 h, then q 1-4h prn;
use with a spacer device
NONSTANDARD THERAPIES
 Heliox
 Mixture of helium and oxygen that creates less turbulent
flow in airways to decrease work of breathing
 Only small benefit in limited patients
 Anti-RSV preparations RSV-IGIV or Palivizumab
 No improvement in outcomes
 Surfactant
 May decrease duration of mechanical ventilation or ICU
stay
COMPLICATIONS
 Highest in high-risk children
 Apnea
 Most in youngest children or those with previous apnea
 Respiratory failure
 Around 15% overall
 Secondary bacterial infection
 Uncommon, about 1%, most in children requiring
intubation
PNEUMONIA
•The WHO Child Health Epidemiology Reference Group estimated
an annual incidence of 150.7 million new cases, of which 11-20
million (7-13%) are severe enough to require hospital
admission.
95% of all episodes of clinical pneumonia in
young children worldwide occur in developing
countries
PATHOPHISIOLOGY
 Inflammation of the alveolar space and may
compromise air exchange.
 Often complicating other lower respiratory infections
such as bronchiolitis or laryngotracheobronchitis,
pneumonia may also occur via hematogenous spread
or aspiration.
 Most commonly, this inflammation is the result of
invasion by bacteria, viruses, or fungi, but it can occur
as a result of chemical injury or may follow direct lung
injury
PATHOLOGY
 Bronchopneumonia is a patchy consolidation involving
one or more lobes. The neutrophilic exudate is centered
in bronchi and bronchioles, with centrifugal spread to the
adjacent alveoli.
 In interstitial pneumonia, patchy or diffuse inflammation
involving the interstitium is characterized by infiltration
of lymphocytes and macrophages. The alveoli do not
contain a significant exudate
 Bacterial superinfection of viral pneumonia can also
produce a mixed pattern of interstitial and alveolar
airspace inflammation.
Four stages of lobar pneumonia
In the first stage, within 24 hours of infection,
microscopically by vascular congestion and alveolar
edema. Many bacteria and few neutrophils are present.
2. The stage of red hepatization (2-3 d) similar to the
consistency of liver: presence of many erythrocytes,
neutrophils, desquamated epithelial cells, and fibrin
within the alveoli.
3. In the stage of gray hepatization (2-3 d), the lung is graybrown to yellow because of fibrinopurulent exudate,
disintegration of red cells, and hemosiderin.
4. The final stage of resolution :resorption and restoration
of the pulmonary architecture. Fibrinous
inflammation may extend into the pleural space, causing
a rub heard by auscultation, (resolution or to organization
and pleural adhesions)
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ETIOLOGY
 Bacteria accounted for 60%, of which 73% were due to
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Streptococcus pneumoniae; Mycoplasma pneumoniae and
Chlamydia pneumoniae were detected in 14% and 9%,
respectively.
S pneumoniae, S aureus H influenzae are by far the most
common bacterial pathogen in 1-3 years age group
Enterococci
Newborns: group B Streptococcus, gram-negative rods
(E.coli, Klebsiella pneumoniae), Lysteria monocytogenes
Chlamydia trachomatis, U urealyticum, Mycoplasma
hominis, Treponema pallidum Toxoplasma gondi
Viruses that cause acute pneumonia
adenovirus
coronavirus
influenza A and B viruses
parainfluenza virus
respiratory syncytial virus
coxsackievirus A21
rhinovirus
BACTERIA THAT CAUSE PNEUMONIA
 GRAM POSITIVE COCCI
1.Streptococcus Pneumoniae
the most common
2. Streptococcus Pyogenes
3. Streptococcus Agalactiae
ETIOLOGY OF BACTERIAL PNEUMONIA
 S- Pneumoniae generally resides in the nasopharynx
and is carried asymptomatic in approximately 50% of
healthy individuals. A strong association exists with
viral illnesses, such as influenza. Viral infections
increase Pneumococcal attachment to the receptors on
activated respiratory epithelium. Once aerosolized SP
go from the nasopharynx to the alveolus,
 Pneumococci infect type II alveolar cells,multiply in
the alveolus and invade alveolar epithelium.
Pneumococci spread from alveolus to alveolus through
the pores of Kohn, thereby producing inflammation
and consolidation along lobar compartments
 Patients with pneumococcal pneumonia may produce
bloody or rust-colored sputum
 Streptococcus agalactiae is a commensal organism in
the genital tract and it can cause pneumonia in newborns
which inhale fluid containing the bacteria during its
journey down the birth canal and develops pneumonia
soon after birth.
 Staphylococcus aureus is gram positive
organism,affecting children and old people. as well as
extreme ages.it can produce thin walled air filled cavities
("pneumatoceles")
 Staphylococcal pneumonia is diagnosed by finding
typical clusters of Gram-positive cocci by microscopy
and subsequently a growth of Staphylococcus aureus in
a purulent sputum that often appears creamy and
bloodstained.
Staphylococcal pneumonia and
bronchopneumonia ( cont’)
 Commonly following influenza in debilitated patients
and in those with cystic fibrosis.
 Abcess formation is very common.
 The abcesses are thin walled,multiple and commonly
bilateral giving rise to patchy bronchopneumonia.
 Some strains of staphylococcal bacteria produce toxins
(poisons) when they grow and reproduce on food.
 Contaminated food with staphylococcal bacteria and
these toxins can cause staphylococcal food poisoning.
The toxins can also cause scalded skin syndrome and,
very occasionally, toxic shock
syndrome
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Bacteria gram positive rods
1.
Bacillus anthracis
Nocardia sp
3. Actinomyces sp.
 Bacteria Gram Negative cocci
1. Neisseria meningitidis
2. Moraxella catarrhalis
 Bacteria gram negative rods
1. Klebsiella pneumoniae
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Bacillus anthracis is Anthrax or Wool-Sorters disease
Associated with wool sorting, with animal handlers, and
veterinarians,produces eschar
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Nocardia sp
Beaded filamentous rod shaped bacteria, Pleura
and chest wall involvment
Actinomyces sp.
Beaded filamentous rod shaped bacteria, causing
rib destruction, cutaneous sinuses, cavitation,
spreads to pleura and chest wall.
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 Neisseria meningitidis (meningococci) cause
epidemics in schools,adolescents .
 Klebsiella pneumoniae produces Current Jelly
sputum, more commonly seen in patients with cronic
cardiopulmonary ilness, immunocompromised. Also
called (friedlanders bacillus)
 Severe form of pneumonia with high mortality
 Upper lobes being most affected with massive lobar
consolidation
 Sputum is jelly like and blood stained producing
(current jelly sputum).
2.Pseudomonas aeruginosa produces green sputum, abscess
formation, Common cause of pneumonia in cystic fibrosis
and those with severely compromised respiratory defenses.
3. Acinetobacter sp. often found on respiratory therapy
equipment and on human skin
very difficult to treat due to multiple drug resistance.
4. Burkholderia pseudomallei exposure with contaminated
soil
Francisella tularensis ,Tularemia Infection is via tick
bite or contact with contaminated rabbits.
6. Hemophilus influenzae more commonly seen in
patients with COPD, alcoholics, and the elderly.
7. Bordetella pertussis Whooping cough
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ANAEROBIC BACTERIA
 •Bacteroides
 •Fusobacterium
 •Porphyromonas
 •Prevotella
 •Actinomyces
 •Bifidobacterium
 •Clostridium
 •Peptostreptococcus
 •Propionibacterium
Gram-Negative Bacteria
 E-coli, Salmonella, Pseudomonas, Moraxella,
Helicobacter, Stenotrophomonas, Legionella,
 Along with the above mentioned bacteria, there are
several other type of Gram-Negative bacteria such as
Hemophilus influenzae (also known as Bacillus
influenzae), Neisseria Meningitidis, Moraxella
Catarrhalis, Neisseria Gonorrhoeae,
Acinetobacter Baumanii (which comes under
Nosocomical Gram-Negative bacteria group).
Fungal Pneumonia
 Endemic fungi
 Histoplasmosis
 Blastomycosis
 Cryptococcosis
 Sporotrichosis - primarily a lymphocutaneous disease,
but can involve the lungs as well
 Aspergillus
 Candida
 Coccidiodomycosis
 Histoplasmosis All Chickens, bats, river valleys
 Coccidioidomycos All California, Southwest USA
 Coccidioides immitis: Pneumonia may develop after
travel to the southwestern United States and after
exposure to a wind or rain storm in an endemic area.
 Blastomyces dermatitidis: Patients may have traveled
to the midwestern United States or the Canadian
Shield.
Protozoal Pneumonia
 Parasites causing pneumonia are
 1.Toxoplasma gondii
2.Strongyloides stercoralis
3.Ascariasis.
4.Cryptosporidia
5.Hookworms
A variety of parasites can affect the lungs. These parasites
enter the body through the skin or by being swallowed, they
travel to the lungs, usually through the blood. The
eosinophils, responds hihgy to parasite infection. Eosinophils
in the lungs can lead to eosinophilic pneumonia.
Rickettsial Pneumonia
 Typhus fevers (epidemic and endemic)
 Rocky mountain spotted fever,scrub typhus,
rickettsialpox
 Louse-borne
 flea-borne through rats and mouse fleas
Rickettsial Pneumonia
 Q fever ranging from multiple segmental opacities to
pleural effusion, lobar consolidation, or linear
atelectasis.
 Hepatosplenomegaly is a common finding; it usually is
accompanied with elevation of liver enzymes
 Rickettsia pneumonia cannot be distinguished
clinically, radiologically, or histologically from atypical
pneumonia.
ATYPICAL BACTERIA
 These are the bacteria's that will be called as atypical bacteria and
causing also atypical pneumonias like other viral agents etc.and
constitute following organisms
 Legionella
 Mycoplasma pneumoniae
 Chlamydia trachomatis an afebrile pneumonia,
usually seen in 2 wk to 6 months of age
 Chlamydia psittaci
 Chlamydia pneumoniae , Chlamydia trachomatis
 This is a sexually transmitted disease that may also cause pneumonia
and bronchitis. It usually is a subacute infection of early infancy
producing a sudden cough and eosinophilia without fever that lasts
from 1-3 weeks, but it may occur in adults too.
Etiology of Pneumonia in
Hospitalized Children
 – Streptococcus pneumoniae 73%
 – Mycoplasma pneumoniae 23%
 – Chlamydia pneumoniae 13%
 – Mycobacterium tuberculosis 2%
Features of viral Pneumonia
 Strikes primarily in the fall and winter and tends to be more serious in people
with cardiovascular or lung disease.
 Usually starts with a dry (nonproductive) cough fever ,headache, sore
throat,dry cough, malaise,running nose,common cold, aches and pains
precedes several days before viral pneumonia ;
 In viral pneumonia onset is less abrupt
 Leucocyte count is usually normal or low
• On x ray may show features of interstitial or of atypical pneumonia
• Course is mild and self limiting and resolves by 7-10 days time
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Diagnosis confirmed by isolation of virus and serological tests
Features of Bacterial
Pneumonia
 Onset is often sudden
 High grade fever
 Rigors and chills
 Sputum is rusty coloured or blood stained
CLINICS
 Neonates
 The infant may present with tachypnea; grunting, flaring,
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and retractions; lethargy; poor feeding; or irritability.
Fever may not be present in newborns; however,
hypothermia and temperature instability may be
observed.
Cyanosis may be present in severe cases.
Nonspecific complaints, such as irritability or poor
feeding, may be the presenting symptoms.
Cough may be absent in the newborn period.
Early-onset group B streptococci infection usually
presents via ascending perinatal infection as sepsis or
pneumonia within the first 24 hours of life. Chlamydia
trachomatis pneumonia should be considered in infants
aged 2-4 weeks and is often associated with conjunctivitis.
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Infants
 After the first month of life, cough is the most common
presenting symptom.
 Infants may have a history of antecedent upper
respiratory symptoms.
 Depending upon the degree of illness, tachypnea,
grunting, and retractions may be noted. Vomiting, poor
feeding, and irritability are also common.
 Infants with bacterial pneumonia often are febrile, but
those with viral pneumonia or pneumonia caused by
atypical organisms may have a low-grade fever or may be
afebrile. The child's caretakers may complain that the
child is wheezing or has noisy breathing.
Toddlers and preschool
children
 A history of antecedent upper respiratory illness is
common.
 Cough is the most common presenting symptom.
 Vomiting, particularly post-tussive emesis, may be
present. Chest pain may be observed with
inflammation of or near the pleura. Abdominal pain
or tenderness is often seen in children with lower
lobe pneumonia and replaces chest pain!
 The presence and degree of fever is dependent upon
the organism involved.
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Older children and adolescents
 Atypical organisms, such as Mycoplasma, are more
common in this age group.
 In addition to the symptoms observed in younger
children, adolescents may have other constitutional
symptoms, such as headache, pleuritic chest pain, and
vague abdominal pain. Vomiting, diarrhea, pharyngitis,
and otalgia/otitis are other common symptoms.
PHISICAL EXAM
 respiratory distress, hypoxemia, and hypercarbia
 grunting, flaring, severe tachypnea, and retractions
 assessment of oxygen saturation by pulse oximetry
 Visual inspection - respiratory effort and count the
respirations – tachypnea
 Auscultation -crackles or rales
 Percussion -identify an area of consolidation.
 rashes and pharyngitis
IMAGERY
 The typical radiological finding is a homogenous, non-
segmental, circumscribed consolidation of lung tissue.
The opacities are situated anywhere in the lungs,
although they are located most often in the basal
segments, and are unifocal or multifocal. An air
bronchogram is often seen and is considered to be
characteristic of pneumococcal pneumonia. The
affected segments of the lung are not reduced in
volume. Pleural involvement (pleural effusion) is not
usual
CLINICAL FORMS Broncho-Pneumonia
 Common cause is staphylococcal infection.
 Bronchopneumonia is characterized by patchy exudative
consolidation of lung parenchyma due to terminal
bronchiolitis with consolidation of peribronchial alveoli.
 Bilateral (less often unilateral), patchy consolidation with
intervening normal lung tissue.
Lesion is more extensive at the base of the lung and often
fuses together resembling lobar pneumonia (confluent
bronchopneumonia).
Transverse thin-section CT scan at the level of the carina in a patient with measles infection
shows multiple centrilobular nodules (arrowhead) and bilateral areas of lobular consolidation
(arrows).
Franquet T Radiology 2011;260:18-39
©2011 by Radiological Society of North America
Staphylococcal Pneumonia in
Children
 • Pneumonia caused by S. aureus associated with high
 rate of complications (e.g., pleural effusion or
 empyema in 55-80%; pneumothorax,
 pyopneumothorax, and pneumatoceles frequently
observed)
 • Very high mortality rates reported in primary
 staphylococcal pneumonia
CLINICS
 TOXIC SYMPTOMS:
 Toxic shock syndrome is caused by toxins secreted by
Staph aureus. Toxic shock syndrome is characterized
by the sudden onset of high fever, vomiting, diarrhea,
and muscle aches, followed by low blood pressure
which can lead to shock and death. There may be a
rash with peeling of skin.
 FUNCTIONAL:
 Dyspnea
 Chest discomfort
 Pleuritic pain
 Chest splinting
 Cough productive of purulent or blood-tinged sputum
 Tachypnea
 Tachycardia
 In advanced cases you may see:
 Cyanosis
 Confusion
 Pain referral to the abdominal region due to
diaphragmatic inflammation
PHYSICAL SIGNS
 respiratory distress, hypoxemia, and hypercarbia
 grunting, flaring, severe tachypnea, and retractions
 assessment of oxygen saturation by pulse oximetry
 Visual inspection - respiratory effort and count the
respirations – tachypnea
 Auscultation -crackles or rales
 Percussion -identify an area of consolidation.
 rashes and pharyngitis
IMAGERY
 INTERSTITIAL
 CONDENSATIONS
 CONFLUATION
 PROGRESSION TO ABCESS, EMPIEMA
 Restitutio ad integrum or pneumatocelae
Gram negative infections
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Gram negative infections are caused by Klebsiella
pneumoniae, Escherichia coli, Pseudomonas aeruginosa,
Haemophilus influenzae, and Proteus.
The radiological picture is identical, and it is not possible to
differentiate between bacteria.
Gram negative lung infections are seen in chronically ill
patients , chronic lung diseases, diabetes, or different types of
cancer.
Aspiration to the respiratory tract is the commonest
single cause of Gram negative pneumonia.
Opacities caused by Gram negative bacteria are usually
localized in the basal lung segments. It is not possible to
differentiate these opacities from those caused by
staphylococcus aureus.
Complications such as empyema and lung abscess are
frequently seen
Atypical or Interstitial or viral
Pneumonia
 Causes
 Mycoplasma
 Legionella
 Chlamydia
 Pneumocystis carinni
. Coxiella
 Fungi
 Histoplasma capsulatum (histoplasmosis)
 Coccidioides immitis (coccidioidomycosis
Atypical or Interstitial or viral
Pneumonia
 In atypical pneumonia the x ray finding usually do
not show lobar type of picture but meaning that
the affection is restricted to small areas that is
interstitial spaces between alveoli, rather than
involving a whole lobe. As the disease progresses,
however, the look can tend to be lobar pneumonia.
 There is also absence of leukocytosis.
 Extrapulmonary symptoms, give some clue to the
causing organism.
Atypical or Interstitial or viral
Pneumonia
 In atypical pneumonia :x ray chest infiltration,
commonly begins in the perihilar region (where
the bronchus begins) and spreads in a wedge- or
fan-shaped fashion toward the periphery of the
lung field.
 Reticular shadows as small linear striations
running in all directions on which may be small
white nodular appearance.
Transverse thin-section CT scan at the level of the carina in a patient with measles infection
shows multiple centrilobular nodules (arrowhead) and bilateral areas of lobular consolidation
(arrows).
Franquet T Radiology 2011;260:18-39
©2011 by Radiological Society of North America
Atypical or Interstitial or viral
Pneumonia
 The most common pathogen of this group is Mycoplasma
pneumoniae. It ranks second only to S. pneumoniae.
 onset is usually more insidious.
 Mycoplasma pneumoniae can be communicated through close
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personal contact via respiratory droplets or contact with poultry
or birds chicken etc.
EXTRAPULMONARY MANIFESTATIONS:
gastrointestinal
musculoskeletal
dermatologic
cardiac
neurologic symptoms
hematological
Complications of Pneumonia
1. Pulmonary fibrosis.
2. Bronchiectasis
3. Lung abscess
4. Empyema
5. Bacteremia with abscess in other organs
6.ARDS
7.Bacteremia
8.Collapse of lung
9.Hemoptysis
Complications of Pneumonia
 Parapneumonic effusions
 Septic arthritis
 Endocarditis
 Pericarditis
 Respiratory failure
 Mental symptoms
Differential Diagnoses
 Acute Respiratory Distress Syndrome
Asthma
Bronchiolitis
Empyema and Abscess
Bronchitis
Foreign Body Aspiration
Pertussis
Investigations of Pneumonia
 Total and differential count
 PBF
 Blood ,urine,sputum culture/sensitivity
 Gram staining/stain for AFB
 Fiberoptic bronchoscopy with bronchial washing/
brushing /biopsy
 Inflamatory tests: ESR, Fg, CRP, alpha 2 globulin
 Pulse oximetry
 Urine latex agglutination test: antigen detection assays
for S pneumoniae
 Blood and sputum cultures
 Fluid recovered from the pleural space should be sent for
Gram stain and culture, along with pH, glucose, protein,
and lactate dehydrogenase (LDH).
IMAGERY
Anteroposterior radiograph of a
child with a bacterial pneumonia
parahilar peribronchial infiltrates
hilar adenopathy
History of Empiric Therapy
 Bacterial Pneumonia in Children:
 • Early 1900’s Serum therapy
 • 1950’s Penicillin, the miracle drug
 • 1960’s Ampicillin improves Haemophilus coverage;
 semisynthetic penicillins (oxacillin, nafcillin)
provide Staph coverage
 • 1980’s 2nd and 3rd generation cephalosporins
provide excellent coverage for the “usual suspects”
 • 2010Are beta-lactams still reliable?
Worldwide Trends in
Pneumococcal Resistance
ATB
 Amoxicillin 80 mg/kg/d PO divided 2-3
 Penicillin 100 ooo units/kg/d iv divided qid or orally
 Cefuroxime (Zinacef) IV: 150-200 mg/kg/d IV
divided q8h
 Ceftriaxone (Rocephin) 50-75 mg/kg/d IV/IM qd;
not to exceed 1 g
 Cefotaxime (Claforan) 100-200 mg/kg/d IV/IM
divided q6-8h
Erythromycin 30-50 mg/kg/d (base and
ethylsuccinate) PO divided q6-8h
 Clarithromycin 15 mg/kg/d PO divided q12h
 carbapenems,
 fluoroquinolones,
 aminoglycosides,
 vancomycin
 Methicillin-resistant Staphylococcus aureus, known as
MRSA, is a type of Staphylococcus aureus that is
resistant to the antibiotic methicillin and other drugs
in the same class, including penicillin, amoxicillin, and
oxacillin
 Therapeutic choice: vancomycin, targocid
( teicoplanin), linezolid ( zyvoxid)

Empiric Therapy of Children with Pneumonia
(I)
 • Cefotaxime/Ceftriaxone reasonable empiric
 therapy for pneumococcus, Haemophilus,
 Moraxella, MSSA
 • Add macrolide for coverage of Mycoplasma
 and Chlamydia in older patients (? ≥ 2-3 yrs)
 • Add clindamycin or vancomycin in patients
 with severe or complicated pneumonia
 (clindamycin in most cases if low rates of R;
 vancomycin if life-threatening)
 Need to establish specific etiologic
 diagnosis when possible (e.g.,
 thoracentesis, culture, molecular
 diagnostics)
 • Consider aggressive management of
 empyema (e.g., video-assisted
 thoracoscopic surgery: VATS)
Pneumocystis carinii pneumonitis (PCP) is a common
opportunistic disease that occurs almost exclusively
in persons who have profound immunodeficiency.
PCP was and still is the most common life-threatening
opportunistic infection occurring in patients with HIV
disease.
PCP: Clinical Features
 Cough
 Usually nonproductive, occasionally whitish sputum.
 Dyspnea
 Fever
 May be accompanied by night sweats, but not
rigors.

Rales
 May be present, but are often absent.
Tachypnea and fever
Diffuse bilateral alveolar disease can be observed by
radiography.
Diagnosis requires the identification of P carinii in
pulmonary tissue or lower airway fluids.
Lung biopsy, inducement of sputum, bronchoalveolar
lavage, or needle aspiration of the lung.
The Gomori, Giemsa, fluorescence-labelled antibody,
or toluidine blue O stains may be used to identify the
organism.
PCP: CXR Findings
 90-95% have pulmonary infiltrates.
 Combined interstitial & alveolar infiltrates.
 Predominantly at bases and centrally.
 Pneumothorax can be present.
 Lace like appearance.
PA Chest Radiograph
Demonstrates
bilateral, perihilar,
R > L, ground glass
opacities
PA Chest Radiograph
 Progressive
disease showing
extensive ground
glass opacification
with consolidation
PA Chest Radiograph
 Progressive
disease showing
extensive ground
glass opacification
with consolidation
Histologic Diagnosis
 Sputum (induced if necessary):
 Diagnostic
 Flexible Bronchoscopy with Bronchoalveolar lavage to
find pnuemocytis carinii in sputum and secretions.
.
Diagnosis continued
 Gomori methenamine silver (GMS) stain from BAL
specimen showing “crushed ping-pong ball”
appearance of cyst wall
 Calcofluor white stains the fungal cyst wall for rapid
diagnosis
Diagnosis continued
 Immunofluorescence showing trophozoites
(arrowheads) and cysts (arrows)
•Four drugs currently available for therapy of P
carinii pneumonitis are:
 Pentamidine isethionate
 Trimethoprim-Sulfamethoxazole
 atovaquone
 trimetrevate
Trimethoprim-sulfamethoxazole is
preferred because of its low toxicity and
greater efficacy.
BACTRIM-DS
 Bactrim DS tablet contains. 160 mg of trimethoprim
and 800 mg of Sulfamethoxazole.
 21 days course
 Prednisolone 40 mg bid x 5 days, then 40 mg/day x 5
days, then 20 mg/day to completion of treatment
 Alternative Treatments:
 TMP 15 mg/kg/day PO + dapsone 100 mg/day x
21 days
 Pentamidine 4 mg/kg/day IV x 21 days
-Atovaquone 750 mg PO bid with meal x 21 days
PCP is the most frequently identified serious in
HIV disease