39.

21 Pneumonia
Swati Dublish, Varinder Singh
Pneumonia is an inflammation of the parenchyma of the lungs. radiological services may not be easily available, a more pragmatic
Usually pneumonia is caused by microorganisms; however, non
infectious causes include aspiration of food or gastric acid, foreign term lower respiratory tract infection (LRTI) is used wherein the
bodies, hydrocarbons, and lipoid substances, hypersensitivity diagnosis is made on the basis of simple clinical signs (e.g., fast
breathing). This simple definition cannot and does not make any
reactions, and drug-or radiation-induced pneumonitis. The present distinction between viral bronchiolitis, croup, wheeze associated
chapter focuses on pneumonia resulting from infections. lower respiratory tract infection (WALRI), asthma, and pneumonia.
EPIDEMIOLOGY CLASSIFICATION OF PNEUMONIA
Acute respiratory infections (ARIs) encompass viral and bacterial Pneumonia may be classified as simple and complicated pneumonia.
infections of the respiratory tract. NFHS-3 data suggests that as Simple pneumonia can be bronchopneumoniapatchy involvement
many as 6% children under age 5 years in India showed symptoms of the lung, which can be uni- or bilateral; and, lobar
of ARI at some time in the 2 weeks preceding the survey. While which involves almost wholeofa single lobe. Complicatedpneumonia
upper respiratory infections are often self-limiting, lower respiratory refers to a situation where the pulmonary parenchymal pneumonia
infection is
infections, in particular, pneumonias, pose a potentially life complicated by parapneumonic effusions, empyema, necroizing
threatening situation. Most pneumonia deaths are caused by pneumonia abscesses or cavities, pneumothorax or bronchopleural
bacteria. Pneumonias are the number one cause of under 5 child fistula.
mortality, responsible for nearly 400,000 deaths in India annually. Given the difficulties in making an
These deaths can be prevented by appropriate treatment with monia etiology is often inferred frometiological diagnosis, pneu
epidemiology. Therefore
antibiotics. Pneumonia can be distinguished from upper respiratory another reasonable classification is
tract infections by the use of simple clinical signs such as respiratory community-acquired
(CAP) and hospital-acquired pneumonia (HAP). CAP is pneumonid
rate and lower chest indrawing. the presence of signs and symptoms of pneumonia in a defined as
healthy child due to an infection contracted outside of thepreviously
i.e., child hospital,
should not have been hospitalized within 14 days prior
DEFINITIONS
to the onset of symptoms, or has been
There are several ways in which pneumonia can be defined. From hospitalized <4 days prior to
onset of symptoms. Hospital-acquired pneumonia
pathological viewpoint, pneumonia results from inflammation of can be early-onset
and late-onset. Early HAP is a pneumonia
lungs due to an infectious agent which may start an inflammatory 4 days of hospitalization and is more likely occurring within the hrst
response and ensuing damage may involve airways, alveoli, due to antibiotic sensitive
bacteria. It usually carries a better prognosis,
connective tissue, visceral pleura and vascular structures. While a
more practical definition of pneumonia will include fever, respiratory (occurring 5 days or more after admission) iswhile late-onset HAP
more likely due to
symptoms, and evidence of parenchymal involvement by either polymicrobial and multidrug-resistant pathogens, and associated
physical examination or the presence of air space opacities on with increased patient mortality and
chest radiography. Most experts define pneumonia as association Atypical pneumonia occurs morbidity.
with acute onset of fever, cougn, a
of clinical findings with radiographic evidence of infiltrates. rapid breathing while few can have associated
in many developing countries and also in many
Since with low-grade fever or no fever, a more gradual onset
peripheral settings, and malaise which is headache, nonproductive cou5
referred to as atypical pneumonia.
 SECTION 39 | Respiratory Diseases 2203
TABLE 1:1Risk factors for
Definiteriskfactors
development of pneumonia,
. Malnutrition Likely risk factors Possible risk factors
Low birth weight " Parental smoking
. Maternal illiteracy
Iack of excusive breastfeeding during first Zinc deficiency " Daycare attendance
4 months " Maternal inexperience
. Rainfall (humidity)
" Underlying comorbid conditions:
L2ck of measles immunization High altitude (cold air)
Indoor air pollution Congenital heart disease Vitamin Adeficiency
Overcrowding Esophageal obstruction or dysmotility, e.g.. Higher birth order
vascular rings, tracheoesophageal fistula Outdoor air pollution
Gastroesophageal reflux disease
Mucociliary dysfunction,e.g., cystic fibrosis,
primary ciliary dyskinesla
Neuromuscular
Asthma
disorders
Immunodeficiency
Diabetes mellitus
(congenitalor acquired)
Bronchopulmonary
lung disease
dysplasia and chronic
Sickle cell disease

PATHOGENESIS
Most pulmonary pathogens are transmitted from BOX 1: Risk factors of mortality in children with severe pneumonia.
hur droplet infection. Bacteria may be person-to-person Age <6 months
of microaspiration. Droplet particles transmitted by inhalation Head nodding
larger than 10 are usually
large enough to be deposited in the pharynx, Altered sensorium
may lodge in the larger airways while particleswhereas those 3-10 u
between 0.5 and 3 u
Inability to feed
Pallor
reach the alveolar surface. Viruses are among the
of pneumonia in early infancy. Many children are common causes
Severe malnutrition
infected with the Concomitant diarrhea or other underlying comorbid ilnesses such as
respiratory viruses but only few develop pneumonia. congenital heart disease
Any breach in the normal defense mechanisms
nia in the body like altered mucociliary clearance oragainst pneumo
cough reflex or
bumoral andcellular immunity; or an obstructed airway Flowchart 1: Pathogenesis of lobar pneumonia.
to pneumonia. The risk factors predisposing to predisposes
pneumonia
detailed Table 1 while Box 1 details risk factors associated with
in are Bacteria enters alveolus
increased mortality due to pneumonia.
The pathogenesis of pneumonia is variable. The classical stages Enmeshed in epithelial lining fluid containing opsonins and lgG
of lobar pneumonia (especially pneumococcal) include congestion,
red hepatization, gray hepatization, and resolution (Flowchart 1). In
viral pneumonia, there is infection of the perialveolar cells leading Ingestion by alveolar macrophages (type ll alveolar cells), e.g.
to thickening of alveolar walls. This leads to occlusion of alveolar encapsulated bacteria like S. pneumoniae
space with exudates, slough, and activated macrophages, leading Or
to poor gas exchange. In many cases, there may be inflammation
of the bronchioles leading to air trapping and contributing to Complement-mediated bacterial lysis
poor gas exchange. Alveolar consolidative pneumonias can be
further subclassified into two groups-airspace pneumonia and
Failure of this mechanism
bronchopneumonia. Airspace pneumonia starts in the peripheral
parenchyma and is acquired by the inhalation of small particles,
e.g. pneumonia caused by Streptococcus pneumoniae, Legionella, Recruitment of polymorphonuclear leukocytes (PMNS) with
and Klebsiella pneumoniae. Consolidation spreads concentrically phagocytic functions with cytokine release and inflammatory reaction
because of the production of exudate and results in a spherical
nntrate (round pneumonia). Bronchopneumonia starts adjacent to
Cenrally located bronchi and is acquired by the aspiration of infective Vascular congestion with fluid and PMNs in
particles. alveoli-Congestionwithin 24 hours
Ininterstitial pneumonia. the walls of the alveoli and interstitial
eptae are involved,and the alveolar space is spared. The interstitial Fibrin deposition in the alveolar spaces, with
rate predominantdy includes lymphocytes, macrophages, and crossing pores of Kohn and edema and clusters strands of fibrin
plasma cells. purulent exudates in alveoli containing fibrin, PMNsofand
RBCS and
Red Hepatization bacteria

ETIIn pediatrica
OLOGYage group,the developingimmune systemaand age-related Active phagocytosis of
exposuresandresultviralinpathogens.
infection caused by varied yet consistent set of cell wall proteins and bacteria by PMNs and release of bacterial
bacterial The potential pathogens are, therefore, plugs and blurring ofpneumolysin
cellular
leading to contracting fibrinous
defined separately for each age group (Table 2). The pneumonia in architecture-Gray Hepatization
neonatal period is mostly caused by group B streptococci or gram- Appearance of anticapsular
iegative enteric bacteria. antibodies-Resolution-within 7 days
2204 PART VIil | Systemic Pediatrics

TABLE 2: Common etiological agents causing community-acquired y TABLE3: Age-specific respiratory rates as per WHo for cut offfor LRTI.
pneumonia at different age groups. Age Respiratory rate
Newborns and young <2 months >60/min
infants <3 months 3 months to 5 years Older than S years
2 months-12 months >50/min
Group B " Adenoviruses S. pneumoniae
>40/mín
StreptocOCcus Bocavirus S. aureues >12 months-5 years
Mycoplasma
Enteric gram Human
pneumoniae (LTRI: lower respiratory tract infection; WHO: World Health Organization)
negative bacilli metapneumovirus
. Influenza A
and B
Streptococcus
viruses with
seen in younger children though may be more often associated
pneumoniae
. Parainfluenza
Hoemophilus
a nonbacterial pathogen. Tachypnea (Table 3) is a simple yet fairly
influenzae viruses
Chiamydia " Coronaviruses specificand sensitive sign for pneumonia if asthma and bronchiolitis
trachomatis . Rhinovirus have been excluded. In infants with pneumonia, tachypnea may
Group Dstreptococci " Streptococcus correlate with hypoxemia. Other causes of tachypnea could be fever.
pneumoniae dehydration,or metabolic acidosis.
" Listeriasp.
Anaerobes " Haemophilus Intercostal, suprasternal, or subcostal retractions indicate
also been
influenzae severe pneumonia. Nasal flaring and head bobbing have
" Staphylococcus statistically associated with hypoxemia. Fever is the most sensitive
signs
aureus sign while grunting and retractions are the most specific
. Bordetella pertussis corresponding to presence of alveolar infiltrates onchest radiograph.
(<0.5%).
In absence of cough, possibility of pneumonia is low
The clinical presentation of viral pneumonia may include
younger subcostal) with
Viruses are among the frequent pathogens in children (RSV) tachypnea, retractions (supracostal, intercostal or
pathogens, respiratory syncytial virus
or without nasal flaring. Although low to moderate grade fever is
than 2 years. Of the viral The presence of
2 years. Other diagnostic marker.
is detected in up to 40% of children younger than common, yet fever is a poor
sneezing or
influenza A and B viruses, concomitant upper respiratory infection (rhinorrhea,
viruses detected are adenoviruses,
bocavirus, human metapneumovirus, parainfluenza viruses, corona viral etiology though may
otitis media) supports a probability of ainfection.
commonly Mild to moderate
viruses, and rhinovirus. RSV and Influenza virus infections be associated with secondary bacterial losses and
predispose infants and young children to bacterial
infections. dehydration may be present due to increased insensible common
is less
human
Rhinovirus is usually associated with a mild disease while poor oral intake in sick babies. Systemic toxicity
with though influenza may lead to high fever and toxic and appearance.
metapneumovirus infection in younger children may present sinusitis, bacterial
is an important nonviral develop acute otitis media,
severe disease. Chlamydia trachomatis Children can
encephalopathy, myositis,
pathogen in infants between 3 and 19 weeks of age. tracheitis, febrile seizures,encephalitis or influenza
Among the bacterial causes of pneumonia in young
children, myocarditis, or Reyes syndrome during an episode of
(30-50% cases), followed by
S. pneumoniae is most common
pneumonia.
aureus, and initial manifestation
Haemophilus influenzae (10-30% cases),Staphylococcus In atypical pneumonia due to mycoplasma,
pneumnoniae are present with of voice. Fever, usually
K. pneumoniae. Multiple serotypes ofS. is pharyngitis followed by hoarseness
serotyping study done in vomiting and
different prevalence rates. According to a low grade, and cough are predominant symptoms; less common.
from invasive and life-threatening be seen in up to 20% patients. Rhinitis is
India, among 150 clinical isolates diarrhea may
The mean
pneumococcal infections 59.3% belonged to serotypes
1, 6, 19, 5, 23, Crepitations or wheezing may be audible on auscultation.
isolate in meningitis and 2 weeks although cough may persist for
and 7. Serotype lwas the most common duration of illness is around
among 42 pneumococcal Mycoplasma infection may be associated with
empyema. According to another study,nearly half in adults were
more than a month.
mucocutaneous
strains, over one-third in children and sinusitis, otitis media, myocarditis, pericarditis,
and
serotypes 5, 6, and 7.The remainingll of 14
strains in children and 20 eruptions, hemolytic anemia, arthritis, glomerulonephritis,
encephalitis, cerebellar
3, 4, 10, nervous system disease (aseptic meningitis,
of 28strains in adults belonged to 8 serogroups/types, namely psychosis, and
11, 12, 13, 19, and 20. Prevalence of penicillin
resistance is currently ataxia, transverse myelitis, peripheral neuropathy,
reported to be low in most of the country. Guillain-Barré syndrome).
bacterial
Among severely malnourished children, K.
pneumoniae, S. Streptococcus pneumoniae is the most common more than
and H. influenzae are the pneumonia in children, responsible for
aureus, S. pneumoniae, Escherichia coli, Bordetella
pathogen causing upper respiratory
common organisms. Other bacterial infections such as 50% cases. The onset may be preceded by a mild otitis media. In
also be considered conjunctivitis, or
pertussis and Mycobacterium tuberculosis should tract infection, purulent unilateral
in differential diagnosis. infants, a sudden high-grade fever accompanied by a seizure, and
Blasto manifestations. Irritabilit,
Fungal pneumonia (due to Histoplasma, Coccidioides, diarrhea or vomiting may be the earliest
grunting, abdominal
normal immunocompetent hosts is nasal flaring, rapid and shallow respirations, unilateral diminished
myces, and Cryptococcus) in
uncoimon. distention, perioral cyanosis, tachycardia, and
course of the illness.
swabs and
A recent study which collected nasopharyngeal commonly respiratory excursion may be seen during the receptors. In the
aspirates showed that S. pneumoniae and RSV were most Cough may be absent as alveoli have few cough patient
isolated from children with severe disease. older child and the adolescents, the onset is abrupt and the rigors,
along with chills or
may appear ill with high grade-fever Sputum
CLINICAL FEATURES fever, headache, dyspnea, pleuritic pain, and cough. years of age.
production may be apparent in children older than 8-10
Children with pneumonia usually present with fever, tachypnea, pneumonia
productive cough, abdominal and/or chest pain. In pneumonia Occasionally, signs and symptoms suggestive of bacterial
caused by atypical pathogens, a more gradual onset associated with may be absent; fever may be the only sign. H. influenzae Bpneumonia
particulariy
low-grade fever or no fever, headache, nonproductive cough and 0s more common in children younger than 5 years of age,
malaise may be present. The presence of wheezing is more often in children under 2 years. Staphylococcus aureus pneumoita
 SECTION 39 | Respiratory Diseases 2205
presents as an acute and:
severe rapidly
50% oof cases pneumatocele
formation progressive
may illness. In almost nicrobiome limits its utility. The isolate may reflect the colonizing
air trapping. 0ccur dueto destruction
of bronchial walls leading to bacteriarather than the invading bacteria. It is worth mentioning that
vOpncumothorax Empyema, can
metastatic lesion in thecomplications. Itpneumothorax,
ati aand
are common many acommon bacterial and viral pathogens may be present in the
also lead respiratory passages of the normal population as well. Their presence
0rains of pericardium, joint, muscles,
communty-associated methicillin-resistant
(CA-MRSA)Ccarryingthe gene ffor S. aureus
might be attributed toeither persistence or prolonged excretion after
an infection.
Natoxin lethal to leukocytes Panton-Valentine leukocidin
can lead to tissue (PVL), Gram stain and culture of induced or expectorated sputum
necrosis,
necrotizing pneunmonia, and necrotizing fascütis. skin can be attempted in older children (>8 years old) and adolescents.
streptococCUs and srepococcUs Pyogenes are Group Specimen produced by cough and containing excess squamous
of pneumonia, usually presenting with infrequent causes rather than epithelial cells indicates an upper tract origin. Specimens
fever. Infection with measles,
varicella, and bacteremia
infection from group A streptococcus influenza
and Scarlet
predispose ofto
with >25 squamous cells per low-power field are not considered
because of impairment adequate. Other useful parameters are the presence of neutrophils
host immunity. and a monotonous or relatively monotonous morphology of the
Chlamydophila pneumoniae infection usually occurs in children bacteria in the specimen. However, it is still difficult to differentiate
between the ages of 5and 15 years and the usual route of the colonizing bacteria from the real culprit.
ie via respiratory secretions and transmission
tomites. The illness begins with In adults, urinary antigen tests for the detection of S. pneumoniae
a nonspecific prodrome of loW-grade correlate well with sputum culture and therefore are routinely used to
headache and cough. Patients may fever, malaise, sore throat. diagnose pneumococcal pneumonia in adults. However, in
initially show signs of upper positive result of pneumococcal urinary antigen test does notchildren,
rospiratorytract intections such as pharyngitis, reliably
later progressing to pneumonia or laryngitis or sinusitis distinguish infection from mere
10 an lgE-mediated bronchial bronchitis. pneumoniae leads recommended.
C. colonization and therefore, 15 not
of patients may show reactivity. The physical examination Testing for viral pathogens can be done using nasopharyngeal
Gne or coarse crepitations. nonexudative pharyngitis, wheezes, and aspirate for RT-PCR,viral antigen detection or acute and convalescent
adolescents. Complications suchPneumonia
is more common in
as pleural effusion, sera for serology.
pneumatocele,
pneumothorax, interstitial fibrosis, and lung abscess can occur The diagnostic tests utilized for M. pneumoniae infections include
other complications include erythema
nodosum, reactive arthritis, serology, cold agglutinating antibodies, culture, and molecular-based
methods such as PCR assays. Serologic tests include complement
Guillain-Barré syndrome, meningoencephalitis, myocarditis, and fixation, enzyme-linked immunosorbent assays (ELISAs), and rapid
endocarditis. Chest radiographs
lesion of only one lobe is the mostshowing
a single subsegmental enzyme immunoassay cards. Cold agglutinin titers >1:64 are present
common lesion though alveolar at the time of acute illness adults but the test is less well studied in
infltrates or subsegmental pneumonitis without consolidation may children. Serology is the primary means of diagnostic testing for
also be seen. Pleural effusion is uncommon.
It is difficult to distinguish viral from C. pneumoniae. Confirmation of primary acute infection requires
the basis of clinical features, radiology, or bacterial pneumonia on documenting an immunoglobulin M(IgM) titer of 1:16 or greater or
laboratory
but presence of an upper respiratory catarrh, ainvestigations a fourfold rise in IgG titer between acute and convalescent serum
Dredominance in leukocyte count is more commonly seen lymphocytic specimens. In case of reinfection, IgM antibody may not appear, and
in viral
pneumonia. The chest X-ray showing lobar, segmental, or rounded the level of IgG antibody titer may rise quickly within 1-2 weeks of
well-defined consolidation affecting a single lobe, large pleural means of The organism or its DNA can also be directly identified by
infection.
effusion, abscess, bullae or pneumatoceles point to a possible or throat swabs, culture or PCR testing in specimens from nasopharyngeal
sputum, blood, or tissue.
bacterial etiology. Bacterial superinfection of a viral pneumonia In children with severe or life-threatening
can be suspected when there is an abruptchange in symptoms with pneumonia, invasive
samples like bronchoscopy with bronchoalveolar lavage or brush
appearanceof generalized toxicity, marked and changed leukocytosis
and new X-ray findings of parenchymal consolidation or pleural biopsy or percutaneous lung aspiration (blind or CT guided) may
be necessitated. In children who are mnechanically ventilated
effusion.
endotracheal aspirates for gram stain and culture can be done.
Ancillary tests like complete blood count with WBC differential
COMPLICATIONS may help to guide therapy and also may give an inication regarding
The complications of pneumonia include parapneumonic effusions, anemia or thrombocytopenia heralding hemolytic-uremic syndrome
empyerr a, necrotizing pneumonia, pneumatoceles, lung abscess, associated with pneumococcal infection. Acute phase reactants
and pr1eumothorax. The complications are to be clinically suspected such as C-reactive protein (CRP), erythrocyte sedimentation rate
In cases not responding to treatment or showing deterioration. (ESR), and procalcitonin do not clearly distinguish bacterial from
viral infection when used in isolation. Low values may be helpful in
DIAGNOSIS distinguishing viral pneumonia from bacterial pneumonia associated
with bacteremia. Declining values of CRP or procalcitonin may
Etiological Diagnosis correlate with improvement in clinical symptoms. Oxygern saturation
measurements through pulse oximetry provide a noninvasive
Larly lcntification of the etiologic agent is important for all
niectios disease to provide a target oriented and narrow spectrum
estimate of arterial oxygenation and are usefful for monitoring the
severity of respiratory dysfunction, but have no role as an etiological
eamerit to rationalize the usage of antibiotics and minimize the tool.
nergerice of drug resistance. However, the bacteriological diagnosis
pneumonia is neither routinely feasible nor useful as the yield is
very low. Imaging
Dlood culture positivity in children being treated as severe Chest radiographs are less reliable in
Pieumonia is around 8%.It is more likely to be positive in presence
distinguishing viral from bac
terial pneumonia and also do not reliably
of sepsis or organ dysfunction. The culture of respiratory specimens distinguish among the
various possible bacterial pathogens. The usual
can be done but have major drawbacks. Their utility for any clinical chest radiograph in a bacterial patterns seen on a
Papose is limited. Younger children are unable to expectorate and
pneumonia are alveolar or airspace
processes, and interstitial patterns usually reflect other
en When sputum is ayailable. its contamination by the upper airway however an overlap is possible. Alarge lobar or diffuse etiologies;
consolidation,
2206 PART VIIH Systemic Pediatrics

a bulging fissure indicating extensive exudate or occult abscess in a
lobar pneumonia, and associated pleural effusion are some findings
highly suggestive of bacterial pneumonia. Adiffuse, bilateral, uffy
infiltrate extending into the periphery also suggests abacterial proces,
central peribronchial infiltrate with or without atelectasis suggests a
viral or Mycoplasma infection. Aperibronchial infiltrate with or with
outperipheral patchy alveolar opacification suggests a viral process; ultrasound is similar to X-ray for detecting consolidation, effusion and
a reticulonodular infiltrate confined to one lobe suggests Mycoplas
ma pneumonia. Bronchopneumonia associated with lung necrosis,
cavitation, pneumatoceles, and abscesses is more likely to be due to
S. aureus. Less commonly, S. pneumoniae, H. influenzae, and enteric
gram-negative bacilli such as K. pneu moniae and hydrocarbon aspi
ration can also result in necrotizing pneumonia.
Chest X-rays are not routinely necessary in patients being treated
on OPD basis with a strong clinical suspicion of pneumonia. How
ever, frontal view chest radiographs should be performed in patients
with suspected or documented hypoxemia or significant respiratory
distress; and, in patients with failed initial antibiotic therapy to verify
the presence or absence of complications of pneumonia, including
pneumothorax, parapneumonic efusions and necrotizing pneumo
nia. Chest radiography for the diagnosis of pneumonia is not routinely
recommended in patients with wheezing in the absence of fever or
hypoxemia. It may, however, be obtained in those with severe disease
requiring admission to document the presence, size, and character
of parenchymal infiltrates and identify complications that may
require other therapy. Lateral radiographs are not routinely required
in pediatric age group and lead to unnecessary radiation exposure.
Routine follow-up chest radiographs are also not warranted in case of
uneventful recovery. Indications of repeat chest radiograph are:
No clinical improvement or progressive symptoms or clinical
deterioration any time after initiation of antibiotic therapy
Recurrent pneumonia involving the same lobe
Lobar collapse on initial chest radiography with suspicion of an
anatomic anomaly,chest mass, or foreign body aspiration
Ultrasonography of chest is an operator dependent modality
which is now upcoming as a bedside modality for ICU settings, It
has the advantage of no radiation exposure and availability at point
of care as compared to chest X-ray. A recent study suggests that lung
interstitial disease. It can be done at bedside and ICUs in nonrespon
sive cases to look for any complications.
CT chest, due to its high radiation, has no role in routine cases of
pneumonia.
TREATMENT Community-acquired Pneumonia
An effort should be made to identify the possible etiologic agent based
on the clinical and laboratory criteria so that the use of antibiotics can be
minimized and the danger of antibiotic resistance curtailed (Table 4).
Outpatient Treatment
In previously healthy children with suspected bacterial pneumonia being
treated on OPD basis, amoxicillin is the first-line antibiotic in a dose of
50 mg/kg/day, given in two or three divided doses. If epidemiology is
suggestive of resistant pneumococci (currently this is not the usual status
in India), higher doses (90 mg/kg/day) with 8 hourly dose interval may be
used. No oral cephalosporin at doses studied in children provides activity
against resistant pneumococci at the site of infection that equals high
dose amoxicillin. S. pneumoniae and H. influenzae strains are often resistant
macrolides (estimated to be about 35% of isolates in our country)
and therefore, macrolides are not recommended as empiric therapy.
In case of nonserious allergy to B-lactams, trial of amoxicillin or oral
cephalosporin (cefuroxime or cefpodoxime) under medical supervision

&TABLE 4: Antimicrobial treatment as per suspected or documented etiology.

Disease Pneumonia

Setting Domiciliary
Age First line Second line Suspected staphylococcal disease
Up to 2 mon ths Usually severe, always treated as inpatients
Above 2 monthst Amoxicillin or cotrimoxazole* Co-amoxiclav OR Amoxicillin + Cloxacillin (1:2)
Cefuroxime OR
Cefuroxime
OR
Co-amoxiclay

*In case the diagnosis is made in community by a peripheral health worker.

Disease Severe pneumonia

Setting In-patient
Age First line Second line Suspected staphylococcal disease
Up to 2 months Inj ampicilin and gentamicin. Inj third-generation cephalosporins:
If there is suspicion of sepsis/ Inj piperacillin-tazobactam + (Cefotaxime/Ceftriaxone)+ Cloxacilin
meningitis: Inj vancomycin added if severe OR InjClindamycin
third-generation cephalosporins sepsis or septic shock t Aminoglycoside
(cefotaxime/ceftriaxone) + OR
aminoglycoside (Genta/amika) InjCo-amoxiclav + Aminoglycoside
Second line: Vancomycin/Teicoplanin +Inj third generation
cephalosporins
Above 2 months Inj Ampicillin Inj Ampicillin + InjGentamicin Injthird-generation cephalosporins:
of age OR InjCo-amoxiclav (Cefotaxime/Ceftriaxone) + (Cloxacillin/Clindamycin)
OR OR
Inj 3rd Gen. Cephalosporin Inj or oral Co-amoxyclav
(Cefotaxime/Ceftriaxone) Second line: Vancomycin/Teicoplanin/Linezolid +
Injthird-generation cephalosporins
Can be changed to oral amox when improvement seen
'Can be changed to oral cefpodoxime/cefdinir once improvement seen

R BOX 2:| ndications forhospitalization in children with pneumonia.
Aderate to severe pneumonia defined by respiratory distress
nchypnea >70/min, retrections, grunting. nasal flaring or head
hobbing) and hypoxemia (SpO, <90%)
ron 6 months of age with
suspected bacterial pneumonia
Dehydration,vomiting or inability to take oral medication
Oesence of comorbid conditions, e.g., immunologic disorders.
Kertatologic, cardiaC, and chronic pulmonary conditions, genetic
mdromes, neurocognitive disorders, reactive airway disease
3den or infants with concerns regarding
therapy or follow-up compliancewith proper
be done. Cefixine is not
recommended as a
bac noorer action against pneumococCus as respiratory antibiotic as
compared to
d third-generation oral cephalosporins. If there is history other second
ious allergy including anaphylaxis, other options such assuggestive of
macrolide,
Auuotoouinolone or linezolid can be tried.
indications of Hospitalization (Box 2)
The children with severe should be hospitalized for
management. WHO
defines severe pneumonia as "cough or difficulty breathing plus one
af the following: lower chest indrawing, nasal
flaring, or grunting. Very
seyere pneumonia is defined as "cough or difficulty breathing plus one
of the foilowing: cyanosis, severe respiratory distress, inability to drink or
vomiting everything, or lethargy/unconsciousness/convulsions. Infants
under 3 months have nonspecific signs and often can have associated
sepsis/meningitis and are therefore almost always be hospitalized and
treated as severe disease with a combination therapy. Arecent randomized
controlled trial (1SPOT) and meta-analysis has shown that children with
2chypnea with chest indrawing without any evidence of severe disease
may be managed at home with oral antibiotics with good monitoring by
healthcare workers.
Indications of Starting Macrolides
. Children with a subacute presentation with prolonged low-grade fever,
persistent cough, chest signs out of proportion to the radiographic
abnormality (usually showing perihilar streaky infiltrates).
Children with acute pneumonia like presentation with radiological
evidence of patchy or lobar consolidation who also have or develop
extrapuimonary manifestations like myocarditis, hemolytic anemias,
glomerulonephritis, aseptic arthritis, CNS problems (aseptic meningitis,
encephalitis, ataxia), etc.
Nonresponse to first-line antibiotics in children who are immunized with
Hib/PCV and have no suppurative complications of CAPs.
Inpatient Supportive Therapy
Patients vwhose oxygen saturation is <92% while breathing air should be
treated with oxygen given by nasal cannulae, high-flow delivery device,
head box or face mask to maintain oxygen saturation >92%. Nasogastric
tubes may compromise breathing and should therefore be avoided in
severely ill children. Intravenous fluids should be used judiciously and
serum electrolytes monitored. Antipyretics should be used to control fever
and it helps in decreasing the oxygen demand in such cases.
Antibiotic Therapy
Children with severe and life-threatening bacterial pneumonia should
be started on parenteral antibiotics to achieve optimal blood and tissue
Concentrations. Around 1% of children with pneumococcal pneumonia
may have meningitis as well; therefore, the antibiotics are required in
nigher doses. The empiric antimicrobials being recommended are for
ne bacterial pathogens most likely to cause pneumonia, especially
.pneumonioe. Routine use of antibiotics is not indicated in preschoolers as
nany cases of pneumonia are due to a viral etiology. Clinical expertise and
decision and level of facility and good follow-up in such cases can be useruI
In rationalizing antibioticusage.
ntants and school aged children with severe pneumonia requiring
If
umission should be started on iniection ampicillin or penicllin G.
Pencilin resistance in S. pneumonige is suspected or in infants and
chldren with life-threatening infection where H. influenzae Bcould be
parenteral third-
Organisn, patients should be started on Intravenous co-
offending ceftriaxone).
generation cephalosporins (cefotaxime or
ornoxyclavulanate is as efective as third-generation cephalospom.
SECTION 39 | Respiratory Diseases 2207
antibiotic in children whom
A macrol1de can be added to a 6-lactarm
M.pneumoniae or Cpneumonige is sUspected
can be
If there is a suspicion of infection due to S. aureus, cloxacillin
added to the B-lactam therapy or else co-amoxyclavulanate can be used. in
failure or resistant cases, vancomycin or clindamycin can be added to the
p-lactarn therapy.
Durotion of Treotment
Totalcourse of therapy depends on severity, rapidity of response and likely
organism. Most CAP will need treatment for 5 days while severe admitted
cases shali need 7-10 days of therapy. In the presence of complications
or infection with S. Jureus, duration of therapy might be prolonged to
4-6 weeks. In the absence of bacteremia, or in children with bacteremia
in whom secondary foci of infection have not been found, transition to
oral therapy can take place as early as 2-3 days after the start of parenteral
therapy as soon as the patient is stable and able to take orally.
Response to Therapy
Children receiving adequate therapy should demonstrate clinical and
laboratory signs of improvement within 48-72 hours. If there is no
response to medical management, further investigations should be carried
out to look for any evidence of complications or presence of resistant
pathogens. Criteria for terming nonresponse to treatment at 48-72 hours
are as follows:
" Vital signs and parameters:
Persistence or increase in the general fever pattern with other causes
like thrombophlebitis ruled out
Increased respiratory rate, grunting, chest retractions, cyanosis
Persisting increased heart rate
Oxygen saturation <90% with room air, need for supplemental
oxygen or ventilation
Systemic or focal symptoms or signs:
Clinically defined "toxicity" based on clinical judgment or change in
mental status
Chest pain, splinting of the chest
Inability to maintain oral intake and hydration
Change in the extent of abnormal or absent breath sounds at
auscultation or dullness in response to percussion
. Laboratory and/or radiologic results:
Increasing WBC count, with total count and percentage of immature
forms of neutrophils
Levels of inflammatory markers (e.g., procalcitonin, CRP)
Isolation of a pathogen by culture: increased parenchymal involve
ment, presence of or increase in pleural fluid, or development of
pulmonary abscess or necrotizing pneumonia as documented on
imaging
CRITERIA FORDISCHARGE
Improvement in general condition, activity and appetite and
stable or baseline mental status
Pulse oximetry >90% at room air for at least 12-24 hours
No evidence of increased work of breathing in form of tachypnea,
tachycardia, retractions, and nasal flare
Patients are able to tolerate oral medications
No social issues regarding observation at home, compliance to
therapy or regular follow-up by parents/caregivers
NEWER THERAPEUTIC STRATEGIES
Vitamin D: Vitamin D simulates the production of cathelicidin
and defensins (antibacterial proteins), reduces the inflammatory
response and increases Th2 lymphocytes. Arecent RCT evaluating
the effect of single oral mega dose of vitamin D, in children between
6months and 5 years of age with pneumonia did not show any
biological benefit either for therapy or prevention.
Zinc: Zinc has a role in immunomodulation and
integrity of immune function and its role in managementmaintaining
of diarrhea
is well known. There are conflicting reports about the role of
treatment of pneumonia. Recent studies have shown no benefit.
zinc in
2208 PART VI|Systemic Pediatrics
Corticosteroids: They are potent inhibitors of recruitment of cells to
site of infection. They may be used inseverely ill, hyperinflammatory
patients (proin•lammatory phenotype with CRP > 150 mg/L) to
shorten the course of illness. But their role is controversial and
currentlynot a standard of care.
The other modalities like toll-like receptors, complement inhibi
tors,GM-CSE adrenomedullin, angiopoietin, and stem cells are still
under enquiry.
BPREVENTION
Primary Prevention
Key primary measures to reduce deaths due to ARI inciudes pro
moting adequate nutrition, increasing immunization coverage
rate, reducing indoor air pollution and imparting health education.
Preventing childhood pneumonia is critical to millennium develop
mentalgoal-4 target of reducing child deaths.
Promotion of exclusive breastfeeding till 6 months of age, and
appropriate initiation of complementary feeds can reduce mortality
due to ARI. Similarly, improving maternal nutrition status and
micronutrient (vitamin/mineral) supplementation reduces the risk
of low birth weight infants which in turn improves the overall survival
associated with ARI in infants and children.
Immunization: Effective implementation of Expanded Program
on Immunization (EPI) would in turn strengthen the ARI control
program. Vaccines against diphtheria, pertussis, and measles when
given appropriate coverage can drastically decrease the mortality
associated with ARI. Vaccination against pneumococcus, and
H. influenzae type B may decrease the incidence and deaths
associated with pneumonia in children.
Health education about ARI begins from parents who need
to learn to recognize severe forms, understand when to take their
child to healthcare center and make use of appropriate healthcare
facilities. They need tobe sensitized for promotion of breastfeeding,
cessation of parental smoking, and reducing indoor air pollution.
It needs to be extended to PHC worker to identify which children
require home care, and which cases need to be referred. Education
needs to be imparted to hospital/ first referral unit (FRU) staff to
manage complicated cases.
Secondary Prevention
Early diagnosis and treatment with antibiotics can prevent large
proportion of deaths due to ARI. Case management of ARI essentially
consists of (1) differentiation or identification of clinical condition
by degree of severity, (2) initiation of appropriate antibiotics, and
(3) timely and appropriate referral monitoring and follow-up.
ACUTE RESPIRATORY INFECTION CONTROL
PROGRAM
Acute respiratory infection control program was initiated officially
by WHO in the year 1978 with the main objective of reducing
the mortality from childhood pneumonia. It sought to introduce
scientific protocols for case management with rational and judicious
use of antibiotics.
The main objective of ARI program is to reduce high mortality
from ARI in children under 5 years through health education,
effective case management and immunization against diphtheria/
pertussis/measles which contribute substantially to overall ARI
morbidity and mortality. WHO-ARI treatment guidelines provide a
simple classification for use by community health workers. ARI has
been covered under the integrated management of neonatal and
childhood illness (IMNCI). Based on selected clinical signs, the child
0splaced in a classification and treated accordingly (see Chapter 51 ).
Global Action Plan for Pneumonia
Integrated Global Action Plan for Prevention and Controlof
Pneumonia and Diarrhea
Global plan to simultaneously tackle pneumonia and diarrhea, two
of the leading killers,of children, was released by WHO and UNICEF
in 2013. The goal is to end preventable childhood deaths due to
pneumoniaand diarrhea by 2025. The objectives of the plan include:
Protect children with good health practices from birth:
Breastfeed exclusively for 6 months
Provide adequate complementary feeding
Supplement diet with nutrients like vitamin A
Prevent children frombecoming ill:
Vaccinate against pertussis, measles, Hib, pneumococcal
disease, and rotavirus
Wash handswith soap
Improve access to safe drinking water and sanitation
Reduce household air pollution
HIV prevention
Provide cotrimoxazole prophylaxis for HIV-infected and
exposed children
Treat children who are ill:
Improve care-seeking behavior and referral to health facilities
Leverage case management at the health facility and
community levels
Use amoxicillin and oxygen to treat pneumonia; low osmolar
ity oral rehydration solution (ORS), and zinc to treat diarrhea
Continue feeding (including breastfeeding)
The plan's integrated approach is designed to be far more effec
tive and efficient than previous single disease focused approaches
because many of the solutions needed to fight pneumonia and
diarrhea are complementary.
IN A NUTSHELL
1. Pneumonia may be classified as simple and complicated
pneumonia. Simple pneumonia can be bronchopneumonia and
lobar pneumonia. Complicated pneumonia refers to effusions,
empyema, necrotizing pneumonia abscesses or cavities,
pneumothorax or bronchopleural fistula.
2. Viruses are the among frequent pathogens in children younger
than 2 years. RSV is most commonly implicated virus.
3. Among the bacterial causes of pneumonia in young children,
Streptococcus pneumoniae and Haemophilus influenzae are the
most common.
4. Malnutrition, low birth weight, and lack of exclusive breastfeeding,
predispose to pneumonia. Maternal education and awareness in
fluence the care seeking behavior for children with pneumonia.
5. Tachypnea is a simple yet fairly specific andsensitive sign for
pneumoniaif asthma and bronchiolitis have been excluded.
6. Children with pneumonia usually present with fever, tachypnea,
productive cough, and chest pain. In pneumoniacaused by
atypical pathogens, a more gradual onset associated with low
grade fever or no fever, headache, nonproductive cough and
malaise may be present.
7. Chest X-rays are not routinely necessary in patients being treated
on OPD basis with astrong clinical suspicion of pneumonia.
8. In previously healthy children with suspected bacterial pneumo
niabeing treated on OPD basis, amoxicillin is the first-line antibiot
ic in a dose of 50 mg/kg/day,given in two or three divided doses.
9. Children with severe or very severe pneumonia (as per WHO
definitions) should be hospitalized for management.
10. Children with severe and life-threatening bacterial pneumonia
should be started on parenteral antibiotics and offered support
ive therapy.

MORE ON THIS TOPIC
uioale f Cappiello AR, Mastrototaro MF, et al.
Community-acquired
pneumonia in children. Early Hum Dev. 2013;89(Suppl 3):S49-52.
NoSchejterY, Cohen-Cymberknoh M, Tenenbaum A. Antibiotic treatment of
chidren with conmmunity-acquired pneumonia:comparison of
or penicillin
ampicitin versus cefuroxime. Pediatr Pulmonol. 2013:48: 52-8
nt2 Pnewan P Shah D, et al. Vitamin D
supplementation for treatment
and orevention of pneumonia in under-five children: A randomized
oeolind placebo controlled trial. indian Pediatr. 2016:53(1 1):967-76.
läisal NSngh M, Thumburu KK, et al. Burden of invasive pneumococcal
a.s22se in children aged 1month to 12 years living in South Asia: a
Svste 3tic review. PLoS One. 2014,9:e96282
Korpp MDiagnosis and treatment of community-acquired pneumonia in
children. Acta Paediatr. 2012;101:702-4.
SECTION 39 Respiratory Diseases 2209
Mathew JL, Patwari AK, Gupta Pet al. Acute respiratory infection and
pneumonia in India: a systematic review of literature for advocacy and
action: UNICEF-PHFI series on newborn and child health, India. ndian
Pediatr. 2011;48:191-218.
Nascimento-Carvalho CM. Pharmacotherapy of childhood pneumonia.
Expert Opin Pharmacother. 2010:1 1:225-31
Smith MJ, Kong M, Cambon A, et al. Effectiveness of antimicrobial quidelines
for community-acquired pneumonia in children. Pediatrics.
2012:129:e1326-33.
WHO. Pocket Book of Hospital Care for Children: Guidelines for the
Management of Common Childhood ilIlnesses, 2nd edition. Geneva:
World Health Organization; 2013.
Zimmerman DR, Kovalski N, Fields S, et al. Diagnosis of childhood pneumonia:
clinical assessment without radiological confirmation may lead to
overtreatment. Pediatr Emerg Care. 2012:28.646-9.