Management of childhood pneumonia

1. MANAGEMENT OF CHILDHOOD
PNEUMONIA
DR ADEDEJI O.N

2. OUTLINE
• INTRODUCTION
• EPIDEMIOLOGY
• AETIOLOGY
• CLASSIFICATION
• PATHOGENESIS
• CLINICAL FEATURES
• MANAGEMENT
• COMPLICATIONS
• PREVENTION
• PROGNOSIS
• REFERENCES

3. INTRODUCTION
• Pneumonia refers to an acute pathogen driven inflammation of the lung
parenchyma.
• Clinically, it is also defined as a condition typically associated with fever,
respiratory symptoms and evidence of parenchymal involvement, either by
physical examination or by presence of infiltrates on chest radiograph.
• Anatomic/radiologic definition is the presence of pulmonary infiltrates on the
chest radiograph

4. INTRODUCTION
• The World Health Organization (WHO) defines pneumonia as the presence of easily
recognizable clinical parameters like chest wall in-drawing, tachypnoea in a child with
cough and or difficulty in breathing of < 28 days.
• This is to facilitate early recognition, adequate treatment and prompt referral if the
need arises.

5. EPIDEMIOLOGY
• Pneumonia is recognized as one of the leading cause of death among children
under five globally. (UNICEF 2019).
• It kills about 2500 children every day and accounted for 15% of all under five
deaths .
• The incidence of pneumonia is more than 10 fold higher and number of childhood
related deaths from pneumonia is about 2000 fold higher in developing than in
developed countries.

6. S. pneumoniae is
estimated to cause up to
1 million child deaths per
year worldwide3
Childhood pneumonia is the leading cause of mortality in
children < 5 years
• 156 million new cases per year worldwide1
• More than 2 million deaths/year due to pneumonia in children < 5 years1
• S. pneumoniae may account for 30–50% of all pneumonia cases in children2,3
Childhood incidence of pneumonia by country

7. EPIDEMIOLOGY
• Regional disparities still occur in the percentage of under 5 deaths with 5%
occurring in developed nations as opposed to 16% occurring in sub Saharan
Africa.
• Nigeria is one of the five countries with more than half of the world’s annual
incident cases of pneumonia.
• In 2019, 162,000 under fives died from pneumonia related events in Nigeria.

9. EPIDEMIOLOGY
• Abdulkarim et al in 2013 found that pneumonia accounted for 13.3% of the total
admission in the university of Ilorin teaching hospital (UITH) with a case fatality
of 6.6% with a male preponderance of 1.5:1.
• Ibraheem and Aderemi et al in 2018 with a similar report of 13.8% of total
admission in UITH with a case fatality of 8.3%.

11. CLASSIFICATION
• BASED ON PROBABLE ORIGIN
• TYPE OF INFECTING ORGANISM
• PATTERN OF INVOLVEMENT/ ANATOMICAL DISTRIBUTION/ RADIOLOGIC
• BASED ON SEVERITY

12. CLASSIFICATION
. Area of probable origin
 community acquired pneumonia which is disease acquired outside hospital setting
or within 48hrs of admission.
 hospital acquired pneumonia( nosocomial/ health care facility associated
infection) – pneumonia which has its onset during a stay in the hospital or up to a
week after discharge.
Ventilator acquired pneumonia: pneumonia acquired within 48 hours of
endotracheal intubation. It is a form of hospital acquired pneumonia.

13. CLASSIFICATION
• Pattern of involvement/ anatomical distribution
Lobar pneumonia- affectation of the parenchyma within an anatomic lobe sparing
the airways.
Positive air bronchogram sign.
Bronchopneumonia- characterized by multiple patchy opacities and usually
bilateral.
Interstitial pneumonia- presence of streaky opacities with an interstitial
distribution on chest radiograph.

14. CLASSIFICATION
• Type of infecting organism
Bacterial – pneumococcal, staphylococcal
Viral: measles virus, respiratory syncytial virus
Fungal : pneumocystis jiroveci
Protozoan- Toxoplasma gondi

15. BASED ON SEVERITY
• Very severe pneumonia :
• Severe pneumonia:
• Pneumonia:
•
• No pneumonia
• Central cyanosis, severe respiratory
distress, inability to drink.
•
Chest wall indrawing
• Fast breathing, definite crackles on
auscultation
cough and cold only

16. RISK FACTORS
• Six Definite Risk Factors
– malnutrition (weight–for–age <–2z)
– low birth weight (≤2500 g)
– non–exclusive breastfeeding
– Lack of measles immunization
– household air pollution(HAP)
– overcrowding (7 or more persons sharing the same household)

17. Likely risk factors:
•Zinc deficiency
•Mother’s experience as a caregiver
•Concomitant disease, e.g. heart disease, sickle cell disease, immunodeficiency states
RISK FACTORS CONTD.

18. RISK FACTORS CONTD.
Possible risk factors:
•Mother’s education
•Day care attendance
•Outdoor air pollution
18

19. RISK FACTORS FOR PNEUMONIA IN NEONATES
• Premature rupture of membranes
• Low birth weight
• Preterm delivery
• Concomitant disease e.g. heart disease
19

20. RISK FACTORS
SOCIO-
DEMOGRA
PHIC
Nutritional environmental Comorbid/ intercurrent
illness
Age
Gender
Low family
income
Low birth weight
Non exclusive
breastfeeding
Malnutrition
Vitamin A
deficiency
Zinc deficiency
Parental smoking,
exposure to combustible
product of biomass burning
such as firewood.
Daycare attendance
Upperrespiratory infections
in household contacts,
Rainy/harmattan seasons
Non immunization for
vaccine preventable
diseases like measles,
pertussis, diphtheria.
Diarrhoeal disease
Sickle cell anaemia
HIV/ AIDS
Underlying chronic
broncho-pulmonary
diseases.

21. AETIOLOGY
• Can be viral, bacterial, fungal.
• Viral pathogens are the commonest causes outside the neonatal period up to age 5
years.
• Bacterial pathogens are associated with significant morbidity and mortality.
• Atypical organisms are commoner amongst children 5 years and above

22. AETIOLOGIC AGENTS BASED ON AGE GROUPS
AGE GROUPS FREQUENT PATHOGENS
NEONATES Group B Streptococcus, E. coli and other Gram negative bacilli, S. pneumonia, H.
influenzae.
3WEEKS- 3 MONTHS Respiratory syncytial virus, other respiratory viruses (rhinoviruses, parainfluenza
viruses, influenza viruses, adenovirus), S. pneumoniae, H. influenzae
4MONTHS – 4 YEARS Respiratory syncytial virus, other respiratory viruses (rhinoviruses, parainfluenza
viruses, influenza viruses, adenovirus), S. pneumonia, H. influenzae, Mycoplasma
pneumoniae group A Streptococcus
>5 YEARS M. pneumoniae, S. pneumoniae, Chlamydophila pneumoniae, H. influenzae, influenza
viruses, adenovirus, other respiratory viruses, Legionella pneumophila

23. PATHOGENESIS
• Possible access routes include :
• inhalation of infected droplet nuclei,
• Aspiration,
• bronchogenic spread of infected oropharyngeal secretions,
• haematogenous source,
• spread from contiguous chest locations.

24. PATHOGENESIS
• The respiratory tract has both specific and non specific protective mechanisms that act
in concert to prevent microbial invasion of the airways.
• The non specific defence mechanisms include the nasal hairs , turbinates , vocal cords,
glottis, the cough reflex., humidification, neutrophils and resident alveolar
macrophages.

25. PATHOGENESIS
• The specific defence mechanisms includes the action of the B and T lymphocytes
resulting in activation of cytotoxic T cells and production of specific antibodies.
• Pneumonia results from damage caused by access by pathologic organisms to the
otherwise sterile distal segments.

26. PATHOGENESIS OF BACTERIAL PNEUMONIA
• Bacterial invasion of the distal part of the alveoli provokes immune response which
leads to the release of inflammatory cytokines and endotoxins: leukotriene B4, C4 D4
and E 4, IL 1,8 TNF α
• Resulting in chemotaxis, vasodilatation and increased endothelial
permeability,causing fluid to gravitate from the vascular space into the alveoli.
• This is leads to congestion which is seen as consolidation on chest x-ray.

28. PATHOGENESIS OF VIRAL PNEUMONIA
• Virus usually spreads down the airways, infecting respiratory cells causing replication and
damages respiratory epithelium, with consequent release of inflammatory cytokines, increa
sing vascular permeability.
• With progression , sloughed cellular debris, mucus and inflammatory cells cause airway ob
struction.
• There is also predisposition to secondary bacterial infection.

29. PATHOGENESIS OF FUNGAL PNEUMONIA
• Fungal pneumonia is different as inhaled spores travel down the alveoli , residing there
in to grow into a fungal ball.
• This can subsequently spread to the vasculature causing life threatening systemic
effects.

31. PATHOGENESIS
• The increased alveolar diffusion barrier may cause ventilation perfusion mismatch
which can cause impaired gas exchange leading to hypoxaemia.
• Increased pulmonary vascular resistance coupled with the increased myocardial
oxygen requirement may cause heart failure.
• Septicaemia may result from seeding of bacteria to the blood.

32. PATHOLOGY
• Congestion
• Occurs within 24 hours of infection.
• alveoli filled with fluid with few neutrophils and numerous bacteria.
• Lung appears heavy and red.
• Red hepatization
• Vascular congestion persists, with extravasation of red cells into alveolar spaces, along
with increased numbers of neutrophils and fibrin.
The filling of airspaces by exudates leads to a gross appearance of solidification of the
alveolar parenchyma.

33. PATHOLOGY
Grey hepatization
Red cells disintegrate with persistence of neutrophils and fibrin.
The alveoli still appears consolidated but grossly the colour is paler.
Resolution
Lysis and removal of fibrin via sputum or lymphatics
Begins after 9 days without antibiotics
Sudden improvement of patient’s condition

35. CLINICAL FEATURES
• The cardinal features of pneumonia in children are cough and or difficulty in breathing
with tachypnoea.
• age < 2 month : > 60 breaths/min
• age 2 up to 12 months : > 50 breaths/min
• Age > 1 up to 5 year : > 40 breaths/min
• age > 5-10 years : ≥ 28 breath / min
• age > 10 years : ≥25 breath/min

36. CLINICAL FEATURES OF PNEUMONIA IN CHILDREN
Fever (temperature ≥37.5 oC)
They may in addition have vomiting, poor feeding, diarrhoea or convulsion.
• Older children may complain of chest pain (due to pleuritis), have cream coloured or
brownish sputum•

37. CLINICAL SIGNS
• Respiratory distress (evidenced by grunting , nasal flaring , in-drawing of the lower
chest wall, intercostal recession)
• • Crepitations (crackling sound similar to that produced by squeezing a sheet of paper
or dry leaves) in one or more lung zones.
• Area of dull percussion note and bronchial breath sound (suggests lobar pneumonia)
•

38. DEFINITION OF CLINICAL SIGNS
• Flaring alae nasi
• Widening of nostrils; Occurs in pneumonia complicated by pleuritis.
• Intercostal indrawing;
• Retraction of the soft tissue between the ribs during inspiration. It is a sign of
hyperinflation and a flattened diaphragm due to small airway obstruction

39. DEFINITION OF SIMPLE CLINICAL SIGNS
• Lower chest wall indrawing ;
• Inward movement of the lower chest wall during inspiration (sometimes the
xiphisternum is also pulled in.
• Occurs when the intrathoracic pressure is lowered

40. NEWBORNS WITH PNEUMONIA
• In the neonatal period children with pneumonia have the general features of neonatal
sepsis:
• Temperature instability
• Tachypnoea, tachycardia
• poor feeding, vomiting
• lethargy or irritability
• Convulsion

41. RECURRENT PNEUMONIA
• • Defined as occurrence of 2 episodes of pneumonia in a year or 3 or more episodes
ever, with evidence of radiographic clearing in between episodes.
• • An underlying disorder should be investigated in such scenarios.

42. RECURRENT PNEUMONIA
• • Causes
• • Hereditary disorders
• Sickle cell disease
• Cystic fibrosis
• • Disorders of cilia
• Immotile cilia syndrome
• Kartagener syndrome

43. RECURRENT PNEUMONIA
• • Anatomic disorders
• Pulmonary sequestration
• Gastroesophageal reflux
• Tracheoesophageal fistula
• Foreign body
• Bronchiectasis

44. RECURRENT PNEUMONIA
• Disorders of immunity
• HIV/AIDS
• Bruton agammaglobulinemia
• Severe combined immunodeficiency syndrome
• Chronic granulomatous disease
• Leucocyte adhesion defect

45. MANAGEMENT
• History
Risk factors
comorbidities
Preceding upper respiratory tract illness
Fever
Cardinal features- tachypnoea, difficulty with breathing and or cough.
Chest pain
Vomiting, diarrhoea, upper abdominal pain

46. MANAGEMENT
• Physical examination
Toxic appearance
Consciousness level- restless, lethargic, unconscious
Febrile
Cyanosed
Hydration status
Respiratory distress- dyspneic, tachpneic, nasal flaring, recession
• Cardiovascular examination- tachycardia, third heart sound
• Abdominal examination- tender hepatomegaly

47. MANAGEMENT
• RESPIRATORY SYSTEM EXAMINATION
Signs Lobar pneumonia Bronchopneumonia
Chest deformity None None
Chest movement Diminished or absent Normal
Mediastinal shift None None
Tactile fremitus Increased Normal
Percussion note Dull Resonant
Vocal resonance Increased Normal
Breath sound Bronchial or vesicular Vesicular
Added sound Crepitation (crackles) Crepitation (crackles)

48. MANAGEMENT
• Investigations
• The goals are to
• Confirm diagnosis
• Determine the severity of the disease and associated complications
• Identify causative organism
• Monitor treatment

49. INVESTIGATION
• Chest radiograph
• Remains the most frequently requested investigation in pneumonia
• Usually PA view with or without a lateral view
• Identifies the presence and anatomic patterns of the parenchymal lesions
including location, extent and complications.
• May also suggest the possibility of certain aetiologies.

50. CHEST RADIOGRAPHS

51. CHEST RADIOGRAPH

52. CHEST RADIOGRAPHS

54. CHEST RADIOGRAPHS

55. CHEST RADIOGRAPHS

56. CHEST RADIOGRAPHS

57. CHEST RADIOGRAPH

58. Lung ultrasound
• This has been proposed as the alternative first line imaging modality to diagnosing
Pneumonia in children.
• It is radiation free, cheaper and with immediate bedside availability of results.

59. LUNG ULTRASOUND

60. LUNG ULTRASOUND

61. LUNG ULTRASOUND

62. LUNG ULTRASOUND

63. INVESTIGATION
• Blood culture- positive yield in 20 – 33% of cases.
• Sputum culture
• Bronchoscopic fluid or broncho-alveolar lavage washings.
• Nasal washings or nasopharyngeal swab specimens
• Pleural fluid culture- In cases of pleural effusion
• Lung aspirate studies
• Serology

64. INVESTIGATIONS
• Full blood count-
• Acute phase reactants- raised ESR and CRP levels.
• Electrolyte profile : to identify SIADH

65. INVESTIGATIONS
• IFA using immunofluorescence microscopy on NPA – Rapid diagnosis +/- viral culture
• PCR – for viruses, Chlamydia, Mycoplasma & some bacterial agents
- Rapid diagnostic test
- Very sensitive
-
• NPA culture for viral agents using specific cell lines

66. DIFFERENTIAL DIAGNOSIS
• Acute bronchiolitis
• Congestive heart failure
• Bronchial asthma
• Lung abscess
• Pulmonary oedema
• Aspiration pneumonitis
• Atelectasis

67. TREATMENT
• Can be
1. Specific
2. Supportive
3. Addressed to complications

68. TREATMENT
• Specific treatment would be targeted at the likely offending organism.
• Empirical antibiotics for bacterial pneumonia.
• Change antibiotics depending on response and results of sensitivity patterns.

69. TREATMENT
• Common antibiotic combination
• Beta lactamase agents or 2nd generation cephalosporin plus an aminoglycoside-
amoxicillin clavulanate or cefuroxime plus gentamicin.
• For MRSA strains- vancomycin or quinolones.
• Macrolides for atypical pneumonia and sickle cell co-mobidity.
• Cotrimoxazole for HIV co infected children.

70. Antibiotic therapy
Category of child
ren
Outpatients Inpatients
FIRST LINE ALTERNATIVES* FIRST LINE ALTERNATIVES*
< 2 Months Admit and treat as neonatal sepsis
≥ 2 Months
Dosages
2–11mons:
250mgBD
1 -2 yrs: 500 mg B
D
3 – 4 yrs :750 mg
BD
High dose Oral A
moxicillin (90mg/k
g/day in 2 divided
doses ) for at leas
t 5 days
Oral Amoxicillin
-Clavulanic acid
(amoxicilllin co
mponent 90mg/
kg/day in 2 divi
ded doses )
OR………
IV/IM genticin (5-7.
5mg/kg once daily)
AND ONE OF THE
SE:
a)IV amoxicillin (15
0mg/kg/day in 3 div
ided doses) ;
b)IV ampicillin (40
mg/kg/dose 6 hourl
y);
…………..
IV Ceftriaxone (50-
100mg/kg/
day every 12-24ho
urs) OR IV Cefotaxi
me (100-200mg/kg/
day in 4 divided do
ses ) OR IV/IM Gen
ticin (5-7.5mg/kg o
nce daily) AND IV
Cloxacillin (100-20
0mg/kg in 4 divide
d doses) OR……

71. Antibiotic therapy contd.
Category of child
ren
Outpatients Inpatients
FIRST LINE ALTERNATIVES* FIRST LINE ALTERNATIVES*
< 2 Months Admit and treat as neonatal sepsis
≥ 2 Months High dose Oral A
moxicillin (90mg/k
g/day in 2 divided
doses ) for at leas
t 5 days
OR Oral Cefpodo
xime (10mg/kg/
day in 2 divided d
oses)
OR Oral Cefuroxi
me (20-30 mg/kg/
day in 2 divided d
oses ) for at least
5 days
c) IV benzyl penic
illin (50,000 units/
kg/dose 6 hourly)
for at least 5 days
OR IV Cefuroxime (
150mg/kg/day in 3
divided doses) AN
D IV/IM Genticin (5-
7.5mg/kg once dail
y) for at least 5 day
s.

72. Antibiotic therapy contd.
Category of childre
n
Outpatients Inpatients
FIRST LINE ALTERNATIVES* FIRST LINE ALTERNATIVES*
HIV-Infected Childre
n
High dose Oral
Amoxicillin (90m
g/kg/day in 2 div
ided doses ) for
at least 10 days
Oral Amoxicillin
-Clavulanic aci
d (amoxicilllin c
omponent 90m
g/kg/day in 2 di
vided doses )
OR……….
IV/IM genticin (5-7.
5mg/kg once daily)
AND ONE OF THE
SE:
a)IV amoxicillin (15
0mg/kg/day in 3 div
ided doses) ;
b)IV ampicillin (40
mg/kg/dose 6 hourl
y);
………….
IV Ceftriaxone ( 50-10
0mg/kg/day every 12-
24hours) OR IV Cefot
axime (100-200mg/kg/
day in 4 divided dose
s ) OR
IV Cefuroxime (150m
g/kg/day in 3 divided
doses) AND IV/IM Ge
nticin (5-7.5mg/kg on
ce daily)
……….

73. Antibiotic therapy contd.
Category of child
ren
Outpatients Inpatients
FIRST LINE ALTERNATIVES* FIRST LINE ALTERNATIVES*
HIV-Infected Chil
dren
High dose Oral
Amoxicillin (90m
g/kg/day in 2 div
ided doses ) for
at least 10 days
….OR Oral Cefp
odoxime (10mg/k
g/day in 2 divided
doses ) OR Oral
Cefuroxime (20-3
0 mg/kg/day in 2
divided doses ) f
or at least 10 day
s
c)IV benzyl penicilli
n (50,000 units/kg/
dose 6 hourly)
PLUS high dose co
-trimoxazole (20mg
/kg/day of trimetho
prim) for at least 10
days
…… PLUS
High dose Co-trim
oxazole (20mg/kg/
day of Trimethopri
m in 4 divided dos
es) for at least 10 d
ays

74. Antibiotic therapy contd.
Category of childre
n
Outpatients Inpatients
FIRST LINE ALTERNATIVES* FIRST LINE ALTERNATIVES*
Children with si
ckle cell diseas
e
High dose Oral
Amoxicillin (90
mg/kg/day in 2
divided doses
) for at least 5
days
Oral Amoxicillin
-Clavulanic aci
d (amoxicilllin c
omponent 90m
g/kg/day in 2 di
vided doses )
OR…….
IV/IM genticin (5-
7.5mg/kg once d
aily) AND ONE O
F THESE:
a)IV amoxicillin (
150mg/kg/day in
3 divided doses) ;
b)IV ampicillin (4
0mg/kg/dose 6 h
ourly);
…………..
IV Ceftriaxone ( 5
0-100mg/kg/day
every 12-24hours
) OR IV Cefotaxi
me (100-200mg/k
g/
day in 4 divided
doses )
OR IV Cefuroxim
e (150mg/kg/day
in 3 divided dose
s) AND IV/IM Gen
ticin (5-7.5mg/kg
once daily) PLUS
…..

75. Antibiotic therapy contd.
Category of child
ren
Outpatients Inpatients
FIRST LINE ALTERNATIVES* FIRST LINE ALTERNATIVES*
Children with si
ckle cell diseas
e
High dose Oral
Amoxicillin (90
mg/kg/day in 2
divided doses
) for at least 5
days
……OR
Oral Cefpodoxi
me (10mg/kg/da
y in 2 divided d
oses ) OR Oral
Cefuroxime (20-
30 mg/kg/day in
2 divided doses
) for at least 5d
ays
c) IV benzyl peni
cillin (50,000 unit
s/kg/dose 6 hourl
y)
PLUS oral erythr
omycin (60-100m
g/kg/day in 4 divi
ded doses)
…..PLUS
ORAL Azithromy
cin
(10mg/kg) daily d
ose for 3 days

76. SUPPORTIVE CARE
• Ensure patent airway
• If oxygen saturation is < 95% in room air or signs of severe respiratory distress
are present, give supplemental oxygen.
• Allow small frequent feeds/fluids if tolerated.
• If there is in severe respiratory distress, give intravenous isotonic fluid.

77. SUPPORTIVE CARE
• For high grade fever (temperature ≥ 39⁰C), give paracetamol, ibuprofen can also be
given. Avoid tepid sponging.
• Nursing care should be provided at least 3hourly: check vital signs including oxygen
saturation
• Monitoring is key.

78. COMPLICATIONS
• RESPIRATORY COMPLICATIONS
Pleural effusion
Pneumothorax
Broncho-pleural fistula
Pyo-pneumothorax
Interstitial or subcutaneous emphysema
Lung abscess
Respiratory failure

79. COMPLICATIONS
• SYSTEMIC COMPLICATIONS
Cardiac failure
Pericarditis
Endocarditis
Septicaemia
• Metabolic
SIADH
Respiratory acidosis

80. TREATMENT OF COMPLICATIONS
• Treat associated congestive cardiac failure
• Treat anaemia
• Drain empyema/ effusion (closed thoracostomy tube drainage)
• Relieve pneumothorax

81. PROGNOSIS
• Depends on factors such as:
• Age of patient
• Type of organism
• Duration between onset of symptom and initiation of treatment
• Nutritional status
• Presence of comorbidities
• Presence of complication

82. PROGNOSIS
• Patients with uncomplicated pneumonias show response to treatment, with
improvement in clinical symptoms within 48 to 96hr of initiation of antibiotics.
• Radiographic evidence of improvement lags substantially behind clinical
improvement.

83. PREVENTION
 General health promotion
Good housing unit- prevent overcrowding.
Environmental sanitation
Adequate nutrition
Emphasizing benefits of exclusive breastfeeding
Minimize exposure to pollutants
Good personal hygiene

84. PREVENTION
 Specific protection
Childhood immunization- Hib, pneumococcal conjugate vaccine, measles vaccine.
Zinc and vitamin A supplementation.

85. PREVENTION
 Early diagnosis and prompt treatment
High index of suspicion
Make early diagnosis (clinical, culture and radiography)
Treat with appropriate antibiotics

86. PREVENTION
 Limitation of disability
Treat congestive cardiac failure
Fluid restriction for cases with SIADH
Drain empyema
Relieve pneumothorax
 Rehabilitation
Chest physiotherapy

87. GAPPD
The Integrated Global Action Plan for Pneu
monia and Diarrhoea (GAPPD)

88. Integrated Global Action Plan for Prevention and Control of Pn
eumonia & Diarrhoea (GAPPD)
• Action plan formulated by WHO and UNICEF in 2009
 Pneumonia and diarrhoea similar determinants , best addressed in a coordi
nated fashion
 Components: PROTECTION, PREVENTION, TREATMENT
 Target 2013 -2015/2030
 Country level assessment by IVAC, Johns Hopkins Bloomberg School of Pub
lic Health across 10 indicators in 9 African and 6 Asian Pacific countries (72
% burden in 2014 and 2016, 55% of under-5s world population)
1
1

89. Fig. 9: 10 Selected GAPPD Indicators

90. The Integrated Global Action Plan for Pneumonia andDiarrho
ea (GAPPD)
• Pneumonia Goals by 2025
– Reduce mortality from pneumonia in children less than 5 years of age
to fewer than 3 per 1000 live births
– Reduce the incidence of severe pneumonia by 75% in children less th
an 5 years of age compared to 2010 levels

91. The Integrated Global Action Plan for Pneumonia andDiarrho
ea (GAPPD)
• Pneumonia Coverage Targets
– 90% full dose coverage of each relevant vaccine (80% coverage in eve
ry district)
– 90% access to appropriate pneumonia case management (80% cover
age in every district)
– At least 50% coverage of exclusive breastfeeding during the first 6 mo
nths of life.

92. Overlap of Pneumonia & Diarrhoea Treatment

93. GAPPD performance

94. CONCLUSION
• Pneumonia remains a killer of children especially in under 5yrs.
• Early diagnosis and prompt treatment can prevent its attending morbidity and
mortality.
• Childhood survival strategies like exclusive breastfeeding, immunization can help to
reduce the burden of this menace.

95. questions
• 1.the following statements are true except
• A. globally, respiratory syncytial virus is the commonest cause of childhood
pneumonia
• B. staphylococcus spp is associated with anaemia
• C . Pneumatocoeles are commonly caused by klebsiella
• D. AP Chest xray view is preferred.

96. questions
• The following statements are true
A. Lung aspirate studies should be routinely done in children with symptoms of
pneumonia and preconsultation antibiotic use
B. Blood culture is a non invasive and most specific microbiologic investigation
C. FBC may show eosinophilia in chlamydial pneumonia
D. Blood culture yield is about 5%

97. REFERENCES
•
• Pneumonia and other lower respiratory infections. Abdul-Wahab B.R
Johnson, Rasheedat M, Ibraheem , Aisha A. Gobir & Wilson I.Aderele.
• Paediatric and child health in a tropical region. 3rd edition, Azubuike and
Nkanginieme.
• Nelson textbook of paediatrics. 20th edition.
• Childhood pneumonia at the University of Ilorin Teaching Hospital, Ilorin
Nigeria. Abdulkarim A.A, Ibraheem R.M, Adegboye A.O, Johnson WBR,
Adeboye MAN. Niger J Paed 2013; 40 (3): 284-289.

98. REFERENCES
• Leung, D. T., Chisti, M. J., & Pavia, A. T. (2016). Prevention and Control of
Childhood Pneumonia and Diarrhoea. Paediatric clinics of North America,
63(1), 67-79.
• Liu, L., Oza, S., Hogan, D., Chu, Y., Perin, J., Zhu, J., and Black, R. E.
(2016). Global, regional and national causes of under-5 mortality in 2000-
15: an updated systematic analysis with implications for the Sustainable
Development Goals. The Lance, 388(10063), 3027-3035.

99. REFERENCES
• UNICEF (2016). UNICEF Nigeria – The children – Maternal and child
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