Respiratory infections

By Bitseat W/gebriel (peds,PPCCM)

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Acute pharyngitis
• Inflammation of pharynx

• Recurrent Streptococcal Tonsillitis When an individual has seven

cultures proven episodes in 1 year, or five infections in 2 consecutive
years, or three infections each year for 3 years consecutively.

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Etiology
• Viruses constitute majority of causative agent (70–95%).
• Group A beta-hemolytic Streptococcus is most common pathogen
among bacteria.
• Group A Streptococcal Pharyngitis Common in children aged 5–11
years.
• Nearly 11–15% children aged ≥5 years act as asymptomatic carriers
of group A streptococcal (GAS). Mostly present during winter and
spring season.

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Clinical feature
• Hx
• Sudden onset of a sore throat ; Discomfort and pain while swallowing ,Fever
P/E
• Erythema, edema, exudates, or an enanthem (ulcers and vesicles) along with
lymphadenitis.
• If signs upper airway obstruction, assess for:
• Hydration status , Fever
• Oral/pharyngeal ulcers (coxsackie virus)
• Tonsillar exudates ;
• Tender anterior cervical lymphadenopathy ;
• Hepatosplenomegaly [Epstein–Barr virus (EBV)]
• Scarlet-fever type rash-blanching, sandpaper-like rash, usually more prominent in skin creases
• flushed face/cheeks with perioral pallor (GAS)
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Red flags
• Unwell/toxic appearance
• Respiratory distress
• Stridor
• Trismus
• Drooling
• “Hot potato” voice (muffled voice associated with
pharyngeal/peritonsillar pathology)
• Torticollis ; Neck stiffness/fullness

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Complications of GABHS
• Local suppurative complications:
• Parapharyngeal abscess, peritonsillar and retropharyngeal abscess, and
sepsis.
• Nonsuppurative illnesses:
• Acute rheumatic fever, acute post-streptococcal glomerulonephritis, post-
streptococcal reactive arthritis and possible pediatric autoimmune
neuropsychiatric disorders associated with S. pyogenes (PANDAS) or
childhood acute neuropsychiatric symptoms (CANS).

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Otitis media
• Over 80% of children will have experienced at least one episode of
otitis media (OM) by the age of 3 yrs
• Peak 1st 2 yrs of life
• 2 main categories: acute infection: suppurative or acute otitis media
(AOM); and inflammation accompanied by effusion, termed
nonsuppurative or secretory OM, or otitis media with effusion (OME)

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A diagnosis of AOM requires

(1) a history of acute onset of signs and symptoms,

(2) the presence of MEE, and
(3) signs and symptoms of middle-ear inflammation.
The definition of AOM includes:
Recent, usually abrupt, onset of signs and symptoms of middle-ear inflammation and MEE
The presence of MEE, indicated by any of the following:
Bulging of the TM
Limited or absent mobility of the TM
Air-fluid level behind the TM
Otorrhea
Signs or symptoms of middle-ear inflammation, indicated by either
Distinct erythema of the TM, or Distinct otalgia (discomfort clearly referable to the ear[s
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Risk factors
• age, 63-85% by 12 mo and 66-99% by 24 mo of age
• gender: M>F
• race,
• genetic background,
• socioeconomic status,
• type of milk used in infant feeding
• tobacco smoke exposure
• exposure to other children
• presence or absence of respiratory allergy,
• season of the year, and vaccination status
• congenital craniofacial anomalies
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Etiology
• Streptococcus pneumoniae:30-50%
• nontypeable Haemophilus influenzae
• Moraxella catarrhalis
• S. aureus and gram-negative organisms : in neonates and very young
infants who are hospitalized
• viruses: rhinovirus and respiratory syncytial virus (RSV)

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Pathogenesis
• Anatomic factor
• Host factor: IgG, IgA
• Viral infections
• Allergy

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Otoscopic findings

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Management
• Amoxacillin 80-90 mg/kg for 10
days
• 2nd line: : amoxicillin-clavulanate,
cefdinir, cefuroxime axetil, and
intramuscular ceftriaxone

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Clinical feature
• irritability or a change in sleeping or eating habits and occasionally,
holding or tugging at the ear.in infants
• Fever
• Rupture of the tympanic membrane with purulent otorrhea is
uncommon.
• Systemic symptoms and symptoms associated with upper respiratory
tract infections also occur; occasionally there may be no symptoms,

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Croup
• Affects 2% of school age children
• 3:2 male-to-female ratio.
• spread by direct person-to-person contact through sneezing,
coughing, and droplets of contaminated nasopharyngeal secretions
on the hands.
• Etiologies- parainfluenza virus 1 and 3 ( commonest)
• Less common agents are parainfluenza 2 , influenza viruses A and B,
RSV, adenovirus, measles, and Mycoplasma pneumoniae

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Clinical presentation
• IP- 2-7 days
• Followed by coryza and a fever, which can be high or low,
• and in 24–48 hours the cxc signs appear:
barking cough and a stridor.
If the edema and narrowing of the airway increase, the breathing rate rises, the patient
becomes increasingly more agitated (to the extent that respiration is more difficult), and the
use of accessory musculature appears, with suprasternal drainage, intercostal and subcostal
retraction, and even cyanosis
P/E : hoarse voice, coryza, normal to moderately inflamed pharynx, and a slightly increased
respiratory rate.
Hypoxemia: imminent respiratory failure

Bacterial superinfection may occur 5-7 days in.

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Assessing severity
• Down Score
• Grade I—mild: stridor during crying or activity, absence of retraction
Grade II—moderate: inspiratory stridor at rest, suprasternal and
intercostal retraction at rest, but without agitation
• Grade III—severe: major inspiratory or biphasic stridor, with marked
suprasternal and intercostal retraction, and with agitation; signs of
respiratory difficulty
• Grade IV—imminent respiratory failure: weak cough, altered level of
consciousness, signs of hypoxemia

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Westley Score
• Stridor: – 0: absent – 1: during crying – 2: at rest
• Retraction: – 0: absent – 1: slight – 2: moderate – 3
• Entry of air: – 0: normal – 1: reduced but audible – 2: very reduced, hardly
audible
• Cyanosis (O2 saturation <92% on (FiO2) 0.21):
– 0: absent – 4: with agitation – 5: at rest
• Level of awareness: –
0: normal – 5: diminished
Total score: 0–1 = mild; 2–7 = moderate; ≥8 = severe
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• Radiographs of the neck can
show the typical subglottic
narrowing, or steeple sign, of
croup on the posteroanterior
view

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Management

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Epiglotitis
• Does not affect structures below the glottis
• Trachea and bronchi are healthy in epiglottitis
• Gas exchange is preserved in mild cases
• Hypoxemia only occurs as a result of hypercarbia in severe cases
• Signs of hypoxemia indicate ventilatory failure in most cases
• Etiology:Hib

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Epiglotitis
• Is dramatic, potentially lethal condition is characterized by an acute rapidly
progressive and potentially fulminating course of high fever, sore throat,
dyspnea, and rapidly progressing respiratory obstruction
• Usu. healthy child suddenly develops a sore throat and fever. Within a matter of
hours, the patient appears toxic, swallowing difficulty, and breathing is labored.
• Drooling is usually present and the neck is hyperextended in an attempt to
maintain the airway.
• The child may assume the tripod position, sitting upright and leaning forward
with the chin up and mouth open while bracing on the arms.
• A brief period of air hunger with restlessness may be followed by rapidly
increasing cyanosis and coma.
• Stridor is a late finding and suggests near complete airway obstruction
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• The diagnosis requires visualization of a large, cherry red, swollen
epiglottis by laryngoscopy
• Avoid anxiety provoking procedures
• Classic radiographic finding : thumb sign

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Management
• Broad spectrum antibiotics given initially after airway evaluated and
secured if needed
• Avoid racemic epinephrine
• More specific antibiotics can be given when cultures return
• Patient can usually be extubated in 2-3 days
• Pneumonia is a possible complication (25%)

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Management

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Bronchiolitis
• Bronchiolitis is an acute inflammatory condition of the bronchioles
that is a result of virus induced injury
• Respiratory syncytial virus (RSV) is the most common viral agent
isolated in about >50% .
Rhinovirus, parainfluenza, adenovirus, human metapneumovirus, and bocavirus
are the other viruses commonly causing the condition.
• Mycoplasma is more frequently implicated in older children with
bronchiolitis.

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Clinical presentation
• Persistent cough, following a prodrome of coryza lasting 1–3 days,
with tachypnea with or without chest recessions and wheeze +/-
crackles
• Associated fever, usually below 39°C,
• in around 30% cases and poor feeding, vomiting usually after 3–5
days of illness.
• Apnea may be the only presenting feature, particularly below 6
weeks of age.
• The chest may appear hyperexpanded and may be hyper-resonant to
percussion.
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Management

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Management
• SABA
• Ipratropium bromide
• Inhaled steroids
• ???

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Pneumonia in children
Pneumonia is an inflammation of the parenchyma of the
lungs.
Infectious vs. Non infectious
Epidemiology
Is a substantial cause of morbidity and mortality in childhood
throughout the world.
Leading cause of under 5 mortality
Contributes to 28% of under 5 mortality
Accounts for ¾ of ARI deaths
The incidence of pneumonia is more than 10-fold higher and
the number of childhood-related deaths due to pneumonia
≈2000-fold higher, in developing than in developed countries. 36
The introduction of Haemophilus influenzae vaccine and
heptavalent pneumococcal conjugate vaccine has reduced
the overall incidence of pneumonia in infants and children in
areas of the world with good coverage.

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Risk factors
Lung diseases-asthma, cystic fibrosis
Anatomic abnormalities-TEF, cleft palate
GERD-recurrent aspiration
Neurologic disorders- loss of consciousness, neuromuscular
disorders
Poverty, indoor cooking, over crowding
Bottle feeding
Immunodeficiency states- HIV, malnutrition, steroid
therapy…
CHF-VSD, AV canal defect
Viral respiratory tract infection 38
Etiologies
S. pneumoniae, H. influenzae, and S. aureus are the major causes of
hospitalization and death from bacterial pneumonia among children in
developing countries.
Viruses are responsible for 45% of the episodes of pneumonia
The highest frequency occurs between the ages of 2 and 3 yr, decreasing
slowly thereafter.
Influenza virus and respiratory syncytial virus (RSV) are the major
pathogens, especially in children <3 yr of age.
 Others: parainfluenza viruses, adenoviruses, rhinoviruses, and
metapneumovirus.

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Common Pathogens
Age Group Common Pathogens (in Order of Frequency)

Newborn Group B Streptococci

Gram-negative bacilli
Listeria monocytogenes
Herpes Simplex
Cytomegalovirus
Rubella

1-3 months Chlamydia trachomatis

Respiratory Syncytial virus
Other respiratory viruses

3-12 months Respiratory Syncytial virus

Other respiratory viruses
Streptococcus pneumoniae
Haemophilus influenzae
Chlamydia trachomatis
Mycoplasma pneumoniae

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Pneumonia - Common Pathogens
Age Group Common Pathogens (in Order of Frequency)

2-5 years Respiratory Viruses

Streptococcus pneumoniae
Haemophilus influenzae
Mycoplasma pneumoniae
Chlamydia pneumoniae

5-18 years Mycoplasma pneumoniae

Streptococcus pneumoniae
Chlamydia pneumoniae
Haemophilus influenzae
Influenza viruses A and B
Adenoviruses
Other respiratory viruses

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Noninfectious causes include;
Aspiration of food or gastric acid,
Foreign bodies,
Hydrocarbons, and lipoid substances,
Hypersensitivity reactions, and
Drug- or radiation-induced pneumonitis.

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Classification of pneumonia
Clinically
1. Community acquired pneumonia
Typical/’’Classic’’ Pneumonia
 S. pneumonia,
 HIB, S.aureus
Atypical pneumonia
 Afebrile, clear chest, CXR-extensive infiltration
 Viruses and mycoplasma
Aspiration pneumonia-rare

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2. Hospital acquired pneumonia
 After 72 hours of admission or
 After 5 days of hospital discharge
 60% aerobic gram negative
 mostly enterobactericae (klebseilla,E.coli
and enterobacter)
 Less commonly-Pseudomonas
 10-15% -S. aureus

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Anatomic/Radiologic classification
Alveolar/Air space Pneumonia
Air brnchogram is characteristic
 Lobar type of consolidation
 S.pneumonia, Klebseilla, HIB
 Bronchopneumonia
Patchy and segmental distribution
Staph. aureus, strep. pyogens, HIB
Interstitial /Peribronchovascular pneumonia
Reticular or reticulonodular infiltrates
Patchy or homogenous opacity
Atypical pneumonia agents, Non infectious Pneumonia

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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

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Underlying causes
Hereditary disorders
Cystic fibrosis
Disorders of immunity
Primary – like CVIDS, SCIDS
Secondary – like HIV/AIDS
Anatomic disorders
Pulmonary sequestration
Lobar emphysema
Gastroesophageal reflux
Foreign body
Tracheoesophageal fistula (H-type)
Disorders of cilia
Immotile cilia syndrome 47
Pathogenesis
• The lower respiratory tract is normally kept sterile by
physiologic defense mechanisms like;
• Mucociliary clearance,
• Secretory immunoglobulin A (IGA)
• Clearing of the airway by coughing
• Macrophages

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Viral pneumonia
Usually results from spread of infection along the airways,
accompanied by direct injury of the respiratory epithelium.
→Airway obstruction from swelling, abnormal secretions, and
cellular debris.
→Atelectasis, interstitial edema, and ventilation-perfusion
mismatch causing significant hypoxemia.

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Bacterial pneumonia
Most often occurs when respiratory tract organisms colonize the
trachea and subsequently gain access to the lungs.
Also result from direct seeding of lung tissue after bacteremia.
M. Pneumoniae
Attaches to the respiratory epithelium, inhibits ciliary action, and
leads to cellular destruction and an inflammatory response in the
submucosa.
As the infection progresses, sloughed cellular debris,
inflammatory cells, and mucus cause airway obstruction, with
spread of infection occurring along the bronchial tree, as it does
in viral pneumonia.

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S. Pneumoniae
Produces local edema that aids in the proliferation of
organisms and their spread into adjacent portions of lung,
often resulting in the characteristic focal lobar involvement.
Group a streptococcus
Results in more diffuse infection with interstitial pneumonia
Necrosis of tracheobronchial mucosa;
Formation of large amounts of exudate, edema, and local
hemorrhage, with extension into the interalveolar septa;
and
Involvement of lymphatic vessels and the increased
likelihood of pleural involvement.

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S.Aureus pneumonia
Manifests in confluent bronchopneumonia, which is often
unilateral and characterized by the presence of
Extensive areas of hemorrhagic necrosis and irregular areas
of cavitation of the lung parenchyma, resulting in
pneumatoceles, empyema, or, at times, bronchopulmonary
fistulas.

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CLINICAL MANIFESTATIONS
Often preceded by several days of symptoms of an URTI
typically rhinitis and cough.
In viral pneumonia, fever is usually present but lower than
in bacterial pneumonia.
Tachypnea is the most consistent clinical manifestation of
pneumonia.
Severe infection may be accompanied by cyanosis and
respiratory fatigue, especially in infants.

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Intercostal, subcostal, and suprasternal retractions, grunting,
nasal flaring, and use of accessory muscles is common in severe
cases.

P/E
Early in the course of illness, diminished breath sounds,
scattered crackles, and rhonchi .
Consolidation or complications (effusion, empyema, or
pyopneumothorax) dullness and breath sounds may be
diminished.
Abdominal distention may be prominent because of gastric
dilation from swallowed air or ileus.

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DIAGNOSIS
CXR- confirms the diagnosis of pneumonia and may indicate
a complication such as a pleural effusion or empyema.
Viral pneumonia is usually characterized by hyperinflation with
bilateral interstitial infiltrates and peribronchial cuffing .
Confluent lobar consolidation is typically seen with pneumococcal
pneumonia
 pneumatocele in S.aureus

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The white blood cell (WBC) count can be useful in
differentiating viral from bacterial pneumonia.
In viral pneumonia: normal or elevated but is usually not higher
than 20,000/mm3, with a lymphocyte predominance.
Bacterial pneumonia: elevated WBC count in the range of 15,000-
40,000/mm3 and a predominance of granulocytes.

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The definitive diagnosis of a viral infection rests on the isolation of
a virus or detection of the viral genome or antigen in respiratory
tract secretions.
The definitive diagnosis of a bacterial infection requires isolation
of an organism from the blood, pleural fluid, or lung.
Blood cultures are positive in only 10% of children with
pneumococcal pneumonia

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Treatment

Indications for admission

Age <6 mo
Sickle cell anemia with acute chest syndrome
Multiple lobe involvement
Immunocompromised state
Toxic appearance
Moderate to severe respiratory distress
Requirement for supplemental oxygen
Dehydration
Vomiting or inability to tolerate oral fluids or medications
No response to appropriate oral antibiotic therapy
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• Outpatient Rx
• Cotrimoxazole
• Ampicillin
• Amoxycillin
• Augmentin
• oral cephalosporin

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Inpatient Rx
Fluid and nutrition
Oxygen
Antipyretics
Antibiotics
 Neonate - Ampicillin +Gentamycine
Children - Crystalline penicillin +/- CAF
 3rd gene. Cephalosporins
 macrolides

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Prognosis
If uncomplicated CAP: response to therapy, with
improvement in clinical symptoms (fever, cough, tachypnea,
chest pain), within 48-96 hr of initiation of antibiotics.
Radiographic evidence of improvement lags substantially
behind clinical improvement.
Pneumococcal pneumonias and chlamydial pneumonia - 1-3
mo for complete radiographic clearing.
Mycoplasma pneumoniae - radiographic improvement
occurring within 2 wk to 2 mo.
staphylococcal, Legionella, and enteric gram-negative
pneumonias can take as long as 3-6 mo to resolve
radiographically.

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No improvement with appropriate antibiotic therapy, consider:
 complications, such as empyema
Bacterial resistance
Nonbacterial etiologies such as viruses and aspiration of
foreign bodies or food
Bronchial obstruction from endobronchial lesions, foreign
body, or mucous plugs;
Pre-existing diseases such as immunodeficiencies, ciliary
dyskinesia, cystic fibrosis, pulmonary sequestration, or cystic
adenomatoid malformation
Other noninfectious causes
A repeat chest radiograph is the 1st step.

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Complications
Direct spread of bacterial infection within the thoracic
cavity
Pleural effusion,
Empyema,
Lung abscess
Pericarditis
Bacteremia and hematologic spread:
Meningitis, suppurative arthritis, and osteomyelitis are rare
complications.

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 Purulent Pleurisy or Empyema
Empyema is an accumulation of pus in the pleural space.
Mostly in pneumonia due to Streptococcus pneumoniae,
Staphylococcus aureus and Haemophilus influenzae (incidence
has decreased since the introduction of the Hib vaccination).
Group A streptococcus, gram-negative organisms, tuberculosis,
fungi, and malignancy are less common causes.
May result from rupture of a lung abscess into the pleural
space, by contamination introduced from trauma or thoracic
surgery, or, rarely, by mediastinitis or the extension of intra-
abdominal abscesses.

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Epidemiology
Empyema is most frequently encountered in infants and
preschool children.
It occurs in 5-10% of children with bacterial pneumonia and
in up to 86% of children with necrotizing pneumonia.

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Pathology
Empyema has 3 stages:
Exudative stage: fibrinous exudate forms on the pleural
surfaces.
Fibrinopurulent stage: fibrinous septa form, causing
loculation of the fluid and thickening of the parietal pleura.

If the pus is not drained, it may dissect through the pleura

into lung parenchyma, producing bronchopleural fistulas and
pyopneumothorax, or into the abdominal cavity.

Rarely, the pus dissects through the chest wall (empyema

necessitatis).

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Organizational stage
There is fibroblast proliferation;
Pockets of loculated pus may develop into thick-walled abscess
cavities or the lung may collapse and become surrounded by a
thick, inelastic envelope (peel).

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CF
Most patients are febrile, develop increased work of breathing or
respiratory distress, and often appear more ill.

Lab

Radiographically, all pleural effusions appear similar, but the

absence of a shift of the fluid with a change of position indicates a
loculated empyema.
 Septa may be confirmed by ultrasonography or CT.
The maximal amount of fluid obtainable should be withdrawn by
thoracentesis and studied.
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The effusion is empyema if bacteria are present on Gram
staining, the pH is <7.20, and there are >100,000 neutrophils/?L.
In pneumococcal empyema, the culture is positive in 58% of
cases.
pneumococcal PCR analysis if culture is negative.
Blood cultures have a high yield, possibly higher than cultures of
the pleural fluid.
Leukocytosis and an elevated sedimentation rate may be found.

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Complications
With staphylococcal infections, bronchopleural fistulas and
pyopneumothorax commonly develop.
purulent pericarditis, pulmonary abscesses, peritonitis from
extension through the diaphragm, and osteomyelitis of the ribs.
Septic complications such as meningitis, arthritis, and osteomyelitis
may also occur.
Septicemia is often encountered in H. influenzae and
pneumococcal infections.

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Treatment
Treatment includes systemic antibiotics and thoracentesis
and possibly chest tube drainage with or without a
fibrinolytic agent, video-assisted thorascopic surgery (VATS),
or open decortication.
If empyema is diagnosed early, antibiotic treatment plus
thoracentesis achieves a complete cure.
The selection of antibiotic should be based on the in vitro
sensitivities of the responsible organism.

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Clinical response in empyema is slow; even with optimal
treatment, there may be little improvement for as long as 2 wk.
With staphylococcal infections, resolution is very slow, and
systemic antibiotic therapy is required for 3-4 wk.
Instillation of antibiotics into the pleural cavity does not
improve results.
 Multiple aspirations of the pleural cavity should not be
attempted.
If pleural fluid septa are detected on ultrasound, immediate
VATS can be associated with a shortened hospital course.
Closed chest-tube drainage is usually continued for about 1 wk.

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Instillation of fibrinolytic agents into the pleural cavity via
the chest tube may promote drainage, decrease fever,
lessen need for surgical intervention, and shorten
hospitalization.
Streptokinase 15,000 U/kg in 50 mL of 0.9% saline daily for
3-5 days and urokinase 40,000 U in 40 mL saline every 12 hr
for 6 doses have been evaluated in randomized trials in
children.
There is a risk of anaphylaxis with streptokinase, and both
drugs can be associated with hemorrhage and other
complications.

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In the child who remains febrile and dyspneic >72 hr after
initiation of therapy with intravenous antibiotics and
thoracostomy tube drainage, surgical decortication via VATS or,
less often, open thoracotomy may speed recovery.

The long-term clinical prognosis for adequately treated

empyema is excellent, and follow-up pulmonary function
studies suggest that residual restrictive disease is uncommon,
with or without surgical intervention.

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Pulmonary Abscess
Are localized areas composed of thick-walled purulent
material formed as a result of lung infection that lead to
destruction of lung parenchyma, cavitation, and central
necrosis.
 Lung abscesses are much less common in children than in
adults.
A primary lung abscess occurs in a previously healthy
patient with no underlying medical disorders.
A secondary lung abscess occurs in a patient with
underlying or predisposing conditions.

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Pathology and pathogens
Risk factors
Aspiration,
Pneumonia,
Cystic fibrosis,
Gastroesophageal reflux,
Tracheoesophageal fistula,
Immunodeficiencies,
Postoperative complications of tonsillectomy and
adenoidectomy,
Seizures, and
A variety of neurologic diseases.
In children, aspiration of infected materials or a foreign body
is the predominant source of the organisms causing 78
If recumbent : right and left upper lobes and apical segment of
the right lower lobes are the dependent areas most likely to be
affected.
In a child who was upright, the posterior segments of the upper
lobes were dependent and therefore are most likely to be
affected.

Primary abscesses are found most often on the right side,

whereas secondary lung abscesses, particularly in
immunocompromised patients, have a predilection for the left
side.

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Both anaerobic and aerobic organisms can cause lung
abscesses.
Common anaerobic bacteria include
Bacteroides spp,
Fusobacterium spp, and
Peptostreptococcus spp.
Common aerobic organisms include
 Streptococcus spp,
Staphylococcus aureus,
Escherichia coli,
Klebsiella pneumoniae, and
Pseudomonas aeruginosa.
Fungi can also cause lung abscesses, particularly in
immunocompromised patients. 80
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Clinical Manifestations
The most common symptoms are cough, fever, tachypnea,
dyspnea, chest pain, vomiting, sputum production, weight
loss, and hemoptysis.
On P/E retractions with accessory muscle use, decreased
breath sounds, and dullness to percussion in the affected
area.
Diagnosis
CXR - parenchymal inflammation with a cavity containing
an air-fluid level.
A chest CT scan can provide better anatomic definition of an
abscess, including location and size.

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An abscess is usually a thick-walled lesion with a low-
density center progressing to an air-fluid level.
Abscesses should be distinguished from pneumatoceles,
which often complicate severe bacterial pneumonias.
Pneumatoceles are characterized by;
Thin- and smooth-walled, localized air collections with or
without air-fluid level.
Often resolve spontaneously with the treatment of the
specific cause of the pneumonia in short period.

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Although gram stain of sputum can provide an early clue as
to the class of bacteria involved, sputum cultures typically
yield mixed bacteria and are therefore not always reliable.
To avoid contamination from oral flora methods include
direct lung puncture, percutaneous aspiration aided by ct or
transtracheal aspiration, and bronchoalveolar lavage
specimens obtained bronchoscopically.
To avoid invasive procedures in previously normal hosts,
empiric therapy can be initiated in the absence of culturable
material.

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Treatment
Conservative management is recommended for pulmonary
abscess.
Most experts advocate a 2- to 3-wk course of parenteral
antibiotics for uncomplicated cases, followed by a course of
oral antibiotics to complete a total of 4-6 wk.
Antibiotic choice should be guided by results of gram stain
and culture but initially should include agents with aerobic
and anaerobic coverage.
Penicillinase-resistant agent active against S. Aureus and
anaerobic coverage, typically with clindamycin or
ticarcillin/clavulanic acid.
If gram-negative bacteria are suspected or isolated, an
aminoglycoside should be added.
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Early CT-guided percutaneous drainage has been advocated
as it can hasten the recovery and shorten the course of
parenteral antibiotic therapy needed.
For severely ill patients or those whose status fails to
improve after 7-10 days of appropriate antimicrobial therapy,
surgical intervention should be considered.
Minimally invasive percutaneous aspiration techniques,
often with CT guidance, are the initial and, often, only
intervention required.
In rare complicated cases, thoracotomy with surgical
drainage or lobectomy and/or decortication may be
necessary.

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Complications
If ruptured
Empyema
Pyothrax
Pneumothorax
Bronchpleural fistula
DDx
Empyema
Necrotising pneumonia
Sequestration
Pneumatocele
Bronchogenic cyst

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Prognosis
Overall, prognosis for children with primary pulmonary
abscesses is excellent.
The presence of aerobic organisms may be a negative
prognostic indicator, particularly in those with secondary
lung abscesses.
Most children become asymptomatic within 7-10 days,
although the fever can persist for as long as 3 wk.
Radiologic abnormalities usually resolve in 1-3 mo but can
persist for years.

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References
• Nelson Textbook of pediatrics
• ERS handbook of pediatric Respiratory medicine 2nd ed
• IAP pediatric standard treatment guidelines 2022
• Pediatric respiratory diseases comprehensive textbook

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