acute respiratory in fection in children

Complete slide on acute repiratory infection children

1. TOPIC :Differential
Diagnosis in URTI & LRTI

2. What’s the Need
Magnitude of Problem
ARIisemergingasoneoftheleadingcausesof
morbidityandmortalityinthedevelopingworld.
Ofthe12milliondeathsoccurringannuallyunder5
yearsofage,ARIconstitutes19%ofthesedeaths.
20to25%ARIdeathsoccur<2months,50to60%
occurininfantsandveryfewdeathsoccurbetween1
to5years.
Nearly25%outpatientvisitsand15%ofallhospital
admissionsareofARI.
InurbansetupARIaccountsfor3-5episodes/child
/year,whileinruralareasitis1-3episodes/child/year.

3. Magnitude of Problem
WHOreport1999,estimates27%ofdisabled
adjustedlifeyears(DALY)duetoARI.
CFR(casefatalityrate)ofpneumoniaisthe
highestamongstARIviz10to15%.
ARI contributes to 15-30% of all under
five deaths in India and most of these
deaths are preventable

4. What constitutes ARI
•ARI is defined as acute invasion of any
part of respiratory tract starting from nose
to alveoli of lungs by micro-organisms
Upper
•Rhinitis (common
cold)
•Pharyngitis
•Tonsillitis
•Acute epiglottitis
Lower
•Laryngitis
•Tracheo-bronchitis
•Bronchiolitis
•Pneumonia

5. Definition
•Anupper respiratory tract infection(URTI) is an
illness caused by an infection, which involves
theupper respiratory tract, including the nose,
sinuses, pharynx, or larynx.

6. Risk factors for URIs
•Contact: Close contact with small children settings, such as school or daycare,
increases the risk of URI.
•Travel: , exposure to large numbers of individuals in closed settings. Increased
exposure to respiratory pathogens
•Environmental factors such as passive smoking and exposure to pollutants
•Immunocompromise that affects cellular or humoral immunity: Splenectomy, HIV
infection, corticosteroids, immunosuppressive treatment , familial predisposition with
immunological defects or anatomical and/or physiological features
•Malnutrition
•Lack of breast-feeding
•Cilia dyskinesia syndrome and cystic fibrosis
•Anatomic changes due to facial dysmorphisms
•Upper airway trauma, and nasal polyposis
•Anemia, rickets, malnutrition

7. Upper respiratory tract
infections
•Common cold
•Tonsillitis
•Sinusitis
•Ear infections

8. Common cold
•The common cold is an acute, self-limiting viral
infection of the upper respiratory tract involving the
nose, sinuses, pharynx and larynx.
Symptoms
•Runny or stuffy nose
•Sore throat
•Cough
•Congestion
•Slight body aches or a mild headache
•Sneezing
•Low-grade fever
•Generally feeling unwell (malaise)
https://www.mayoclinic.org/diseases

9. Conditions that may mimic
common cold

10. Influenza: biology & impact
•Single-stranded, enveloped, RNA virus
(orthomyxoviridae family)
•Influenza A
–Potentially severe illness; epidemic and pandemics
–Rapidly changing
•Influenza B
–Usually less severe illness; may cause epidemics
–More uniform
•Influenza C
–Usually mild or asymptomatic illness

11. Structure of the Influenza Virus
Polymerase (P) Proteins
Hemagglutinin (HA)
Neuraminidase (NA)
M2
Nucleoprotein (NP)
M1
Adapted from: Hayden FG et al. Clin Virol. 1997:911-42.

12. Viral Nomenclature
1. CDC. Atkinson W, et al. Chapter 13: Influenza. In: Epidemiology and Prevention of Vaccine-Preventable Diseases, 4th ed. Department of Health
and Human Services, Public Health Service, 1998, 220
A / Sydney / 184 / 93 (H3N2)
Type of Nuclear
Material
Virus
type
Geographic
origin
Strain
number
Year of
isolation
Hemagglutinin
Virus
subtype
Neuraminidase

13. Bridges CB et al. Clin Infect Dis. 2003;37:1094-101. Heikkinen T et al. Lancet. 2003;361:51-9.
Pathogenesis of Influenza
•If not neutralized by mucosal antibodies, virus attacks
respiratory tract epithelium
•Infection of respiratory epithelial cells leads to cellular
dysfunction, viral replication, and release of viral progeny
•Release of inflammatory mediators contributes to
systemic manifestations of disease
•Influenza can be transmitted through small or large particle
•aerosols or through contact with contaminated surfaces

14. ACIP. MMWR. 2004,53(RR06)1-40. Kavet J. Am J Public Health. 1977;67:1063-70. Frank AL et al. J Infect Dis. 1981;144:433-441. Hayden FG et al. JAMA. 1999;282:1240-6.
•Sudden onset of symptoms, persist for
7+ days
•Incubation period: 1-4 days, average 2
days
•Infectious period of wild type virus:
–Adults shed virus typically from 1 day before
through 5 days after onset of symptoms
–Children shed higher titers for a longer
duration than adults
Clinical Features of Influenza

15. D/D For common cold

16. A Comparison of Common Cold
and Influenza Characteristic
Alternative Medicine Review Volume 12, Number 1 2007

17. Tonsillitis
•Tonsillitis is defined as an inflammation of
the tonsils and is a common upper RTI in
children
commonly encountered in primary care.
ages of 5 and 15 years
The prevalence of bacterial tonsillitis,
specifically group A beta hemolytic
streptococci (GABHS), is 15% to 30% of
children with sore throat and 5% to 15% of
adults with sore throat
InnovAiT · August 2017
Tonsillitis is usually viral; it is most
commonly caused by the rhinovirus,
followed by the coronavirus, and the
adenovirus

18. Clinical Signs and symptoms
•Frequent throat infections
•Breathing difficulties
•Dysphagia
•Redness of anterior
pillers
•Breathing through mouth
Dry mucous membrane
Oedema
•Local signs of tonsillitis
Unpleasant mouth odor
Unpleasant feeling in the
throat Lymph nodes are
small and dense Pus or
tonsil stones in lacunae

19. D/D of tonsillitis in children
•Scarlet fever
•Infectious mononucleosis
•HIV
•Herpes simplex virus infection

20. Scarlet fever
•Scarlet fever is caused by toxin-producing strains of
Streptococcus Pyogenes, a beta-haemolytic bacterium that is
classified as a Group A Streptococcus
•Highly contagious
•There is an exudative tonsillopharyngitis, and there may be
small red haemorrhagic spots on the hard and soft palate
InnovAiT · August 2017

21. Glandular fever
(infectious mononucleosis)
•EBV is the causative agent
•Patients typically presenting with a triad of sore
throat, fever and lymphadenopathy.
•There may be splenomegaly in up to 50% of patients
InnovAiT · August 2017

22. HIV
•HIV can cause ulcerative tonsillitis and pharyngitis
with fever. It occurs after an incubation period of
3–5 weeks with symptoms of myalgia, arthralgia,
lethargy, and in some people a non-itchy
maculopapular rash. Lymphadenopathydevelops a
week later (Caserta & Flores, 2010)
InnovAiT · August 2017

23. Herpes simplex virus
•Herpes simplex virus (HSV) pharyngitis presents with red,
swollen tonsils that may have aphthous ulcers on their
surfaces.
•Herpes simplex virus (HSV) pharyngitis presents
with red, swollen tonsils that may have aphthous
ulcers on their surfaces.
InnovAiT · August 2017

24. Complications of tonsillitis
•Peri-tonsillar abscess/quinsy
•Airway obstruction
•Post-Streptococcal glomerulonephritis
•Rheumatic fever
InnovAiT · August 2017

25. Sinusitis
•Sinusitis is one of the most common and
serious childhood infections
•It has been demonstrated that children have
upper respiratory tract infections 6-8 times per
year of which 5-10% are associated with
sinusitis.
Classification by duration of disease
•1. Acute
•2. Subacute
•3. Recurrent acute
•4. Chronic
Lieser, John D., and Craig S. Derkay. "Pediatric sinusitis: when do we operate?."Current opinion in otolaryngology & head and neck
surgery13.1 (2005): 60-66.

26. Figure 1. The dynamics and changes over time in the microbiology of bacterial sinusitis.
Proc Am Thorac Soc,
http://www.atsjournals.org/doi/abs/10.1513/pats.201006-038RN
Published in: Itzhak Brook; Proc Am Thorac Soc2011, 8, 90-100.
© 2011 The American Thoracic Society

27. Diagnosis
•Diagnosis requires presence of two
major or one major-two minor symptoms
Major Symptoms
•Facial pain,
•Feeling of pressure and fullness
•Nasal congestion Nasal
•Postnasal purulent discharge
Lieser, John D., and Craig S. Derkay. "Pediatric sinusitis: when do we operate?."Current opinion in otolaryngology & head and neck
surgery13.1 (2005): 60-66.
Minor Symptoms
•Headache
•Cough
•Halitosis
•Fever Fatigue
•Dental pain
•Ear pain
•Feeling of pressure and fullness

28. Otitis media (OM).
in Children
•inflammation of middle ear that most often occur in
infant & young children but can occur at any age”
•but children get them more often than adults.
•Five out of six children will have at least one ear
infection by their third birthday.
Classification
•Acute otitis media
•Chronic otitis media
•Serous otitis media
•Secretory otitis media
•Suppurativeotitis media

29. Aetiology/ Risk factors
•The most common bacterial causes of
AOM areStreptococcus pneumoniae,
non-typeableHaemophilus influenzae,
andMoraxella catarrhalis.
•There is increasing evidence
that the predominant causative
pathogen in AOM is changing
fromStreptococcus
pneumoniaeto non-
typeableHaemophilus
influenzaesince the introduction
of pneumococcal conjugate
vaccines.

31. Clinical manifestation
•Otorrhea
•Otalgia
•Fever
•Rhinitis
•Tympanic membrane erythema,
may be perforated
•Hearing loss
•Irritability

32. Differential diagnosis
•Otitis externa
•Impacted cerumen or foreign body in ear
•Tympanosclerosis
•Otitis media with effusion
•Injury of the ear

33. Pathophysiology
Essentially,itisinflammationoftheairways/pulmonarytissue,
duetoviralorbacterialinfection,belowthelevelofthelarynx.
Gastro-oesophageal reflux may cause a chemical pneumonitis.
Smoke and chemical inhalation may cause pulmonary
inflammation

34. LRTI : infection below the level of
larynx
Larynogotracheobronchitis
Bronchitis
Bronchiolitis
Pneumonia

35. Clinical Manifestation of
Respiratory tract Infections
•Cough
•Fever
•Hoarseness of voice
•Stridor
•Fast breathing
•Breathing difficulties
•Cyanosis

36. Characteristics of Cough and their
etiological significance
Type of Cough Likely condition
Loose
(discontinuous),
productive
Bronchitis, asthmatic bronchitis
Brassy Tracheitis, habit cough
With stridor Laryngeal obstruction, pertussis
Paroxysmal Pertussis syndrome, F. body
Staccato Chlamydial pneumonia

37. Characteristics of Cough and their
etiological significance (contd…)
Type of Cough Likely condition
Nocturnal Upper or lower respiratory
tract allergic reaction.
With vigorous exercise Exercise induced asthma
Tight (wheezy) Reactive airway

38. Signs of significant respiratory
disease
•Fast Breathing (Tachypnoea)
–A proxy for hypoxia
–suggests significant respiratory disease.
Remember
•Normal RR vary with age
•Fever alone can increase the respiratory
distress

39. Signs of significant respiratory distress
Nasal flaring:
With inspiration, the side of the nostrils flares outwards

40. Signs of significant respiratory distress
Lower chest wall indrawing:
With inspiration, the lower chest wall moves in

41. P, 5 year old female
•Presents with an acute history of fever, cough
for 3 days
•She is irritable and has significant cough
•O/E She has arespiratory rate of 48/min and
chest indrawing.
•The parents are worried because the local
practitioner has told them that she has
pneumonia and should be admitted. They seek
your opinion.
How will you arrive at the diagnosis?

42. TACHYPNEA –
Most consistent clinical sign of pneumonia
Age Respiratory rate
(breaths/min)
< 2 months 60 or more
2 months upto 12 mo 50 or more
12 months upto 5 years 40 or more
WHO recommends using these Respiratory rate cutoffs to
diagnose pneumonia at the community level
RR should be counted for full 60 secs.

43. P, has a respiratory rate of 48/min
•She has tachypnoea and a
RR higher than the age
specific cutoffs suggested by
WHO
•“Does this mean she has
pneumonia? This is simple
but is it good enough for me
to use for diagnosis in clinics
/hospital settings?”, wonders
your junior doctor.
Age Respiratoryrate
(breaths/min)
<2months 60ormore
2monthsupto
12months
50ormore
12monthsupto
5years
40ormore

44. Child with cough, rapid and difficult
breathing
Pneumonia-
Any cause
WALRI, Asthma,
LTB, Bronchiolitis
Non respiratory
causes

45. Tachypnoea
•A sensitive and specific tool –66% approx.
–as good or better than auscultation for pneumonia
•Any clinician therefore must use this merely as a
beginning step (Triage Sign).
•And then, use all their clinical skills for the final
conclusion.
•Remember several other clinical situations that
cause rapid breathing e.g.
–Respiratory causes: Asthma / Bronchiolitis/ WALRI
–Non-respiratory causes: metabolic acidosis, CHF,
raised ICT

46. What now?
•First rule out non –respiratory causes for
tachypnoea,
•You may have concluded that the focus of
infection is lower respiratory tract due to
presence of other chest signs,
•In this setting of child with cough, rapid and
difficult breathing, the likelihoods are:
–Pneumonia +complications
–Bronchiolitis
–Wheeze associated with Lower respiratory tract infxns
–Asthma
–Croup

47. Differentialdiagnosis
Asthma
Inhaled foreignbody
Pneumothorax
Cardiacdyspnoea
Pneumonitis from othercauses:
Extrinsic allergicalveolitis
Smokeinhalation
Gastro-oesophagealreflux

48. Child with Cough, Rapid, Difficult
breathing
•ConsiderBronchiolitisif:
–Age1mo-2yr
–1
st
episodeininfancy
–Presence of Upper
respiratorycatarrh
–Progressiveincreasein
respiratory distress
(tachypnoea,retractions)
–Wheeze+crackles
–Clinicalandradiological
evidenceofhyperinflation
•Consider Wheeze assoc with
LRTI (WALRI) if:
–Recurrentepisodes of
distressunder3yearsofage
–PresenceofUpperrespiratory
catarrh
–Progressive increase in resp
distress (tachypnoea,
retractions)
–Wheeze+crackles
–Clinicalandradiological
evidenceofhyperinflation
–Nofamilyorpersonalhistory
ofatopy

49. Child with Cough, Rapid,
Difficult breathing
•ConsiderAsthmaif:
–Recurrent episode, 3 or
more
–Wheeze
–Good response to
bronchodilator
–Hyperinflation
–H/o afebrile episodes
–Family/personal history of
atopy
•Consider Laryngo-
tracheo-bronchitis -
Croupif:
–Hoarseness of voice and
barking/ brassy cough
–Stridor
–Mild to marked respiratory
distress
–Sonorous rhonchi
–Fever usually mild or
spiking (tracheitis, rare)

50. Can viral LRTI or bacterial
pneumonia be clinically distinguished
•May be difficult as the investigations do not
confirm etiology
•Advantage of using the suggested
methodology-decreases the confounders to
viral pneumonia alone rather than broad ARI

51. Clinical differentiation of pneumonia
Feature Bacterial Viral
Onset Abrupt Gradual
Epidemic pattern - +
Course Progressive Self limiting
Temperature +++ ±
Toxemia +++ -
Respiratory
distress
++ + (infants)
Associated URTI+ +

52. Clinical differentiation of pneumonia
(contd…)
Feature Bacterial Viral
Auscultation
Crackles ++ ±
Wheeze ± ++
Radiological Confluent
infiltrates
(consolidation)
Diffuse infiltrates
in perihilar areas
Hyperinfiltration ± * (RSV infection)
Pleural
involvement
+ -
Pneumatocele + -

53. Differentiating features of typical and
atypical pneumonia
Features Typical Atypical
Onset Sudden Gradual
Fever +++ ±
Cough Productive Dry
Symptoms Pulmonary Systemic
Chest X-rayLocalized Diffuse

54. Let us focus on Community
aquired Pneumonia (CAP) now
•CAPisanacuteinfectionofthe
pulmonary parenchyma ina
previouslyhealthychild,acquired
outsideofahospitalsetting.
–nothavebeenhospitalizedwithin14
dayspriortotheonsetofsymptoms,or
–hasbeenhospitalizedlessthan4days
priortoonsetofsymptoms.
•Itexcludes
–Child with any immune-deficiency
•Severe Malnutrition
•Post measles state
–Ventilator assoc Pneum/ Nosocomial
spread
–Recurrent pneumonias

55. The doctor is now convinced. She says,
“Now I know that simple clinical tools used
judiciously can differentiate between
different causes for cough and rapid
breathing. And therefore help us be rational
in management.”
But Sir,
A. How do I confirm the diagnosis?
and if I have to use the correct antibiotics,
B. How can I suspect or confirm the
probable organisms?”

56. Investigations and their relevance
•CBC, ESR
•CRP
•Radiograph of chest
•Cultures:
–Throat swab
–Cough swab
–Sputum
–Lung tap
–Blood
CBC:
White cell count is often elevated.
Microbiological studies:
Blood cultures are seldom positive in
pneumonia (fewer than 10% are
bacteraemic in pneumococcal disease).
Sputum culture
Imaging:
Chest radiography (CXR) is not routinely
indicated inOPD .
CXR cannot differentiate reliably between
bacterial and viral infections.

57. Role of acute phase reactants,
etc. in pneumonia
•TLC, DLC, CRP are not diagnostic
•May be useful to monitor the
response to treatment.

58. Diagnosis-Radiological
•Do all patients require a chest radiograph?
•NO,
–Not all CAP, particularly if on domiciliary treatment
•Few -Yes,
–If severely ill
–If complication suspected (for example, pleural effusion)
–Ambiguous Diagnosis-tachypnoea without chest signs, etc.
•Does it differentiate between the etiological agents
•NO, Poor correlation

59. The Bronchovascular shadows are heavy, small patches of
increased density are scattered throughout both lung

60. Lobar consolidation right upper lobe

61. A guide to radiological diagnosis of
pneumonia
Acutelobarpneumonia–considerpneumococcal
pneumonia.
Rightupperlobepneumonia–suspectaspiration,
especiallyinneonatesandinfants.
Recurrentrightmiddlelobepneumonitis–consider
partialbronchialobstructionduetoglandsand
others.
Multiplesmallabscesses–staphylococcal
/Klebsiellapneumonia.
Severebilateralinterstitialpneumonia–virus

62. Microbiological Cultures
•Not recommended routinely
•Takes a long time and hence has limited
utility
•Sputum cultures / cough swabs have
relatively poor reliability
•Invasive methods can not be justified for
routine pneumonias.

63. QUESTIONS?????
•In the absence of a microbiological
diagnosis in most cases, How does one
know which bacteria is the offending
organism?
•Are there any other supportive evidences
for the probable etiology?

64. Etiology
Viral infections :e.g
InfluenzaA
Respiratory syncytial virus(RSV)
Human metapneumovirus(hMPV)
Varicella-zoster virus(VZV)
Chickenpox
Covid19
Bacterial infection :
Streptococcus pneumoniae majority
H. influenzae
Staphylococcus aureus
Klebsiella pneumoniae
Enterobacteria -eg, Escherichia coli
Anaerobes
Atypicalorganisms
Mycoplasmapneumoniae
Legionellapneumophila,
Chlamydophilapneumoniae
Secondary bacterial
infection
relatively common following viral
upper respiratory tract infection
(URTI)
orLRTI.

65. 0-3 months
Gram Negative, E. Coli, Klebsiella
St pyogenes,
Chlamydia
Viruses-CMV, Herpes
3mo-5yrs
Str pneumoniae
H Influenzae
Staph aureus
Viruses –CMV, RSV, Influenza,
Parainfluenza
Mycoplasma pneum
>5 yrs
Str pneumoniae
Staph aureus
Viruses –Influenza, Varicella
Mycoplasma pneum
St pyogenes
Age related Pathogens involved in
Community Aq Pneumonia

66. Reliability of predicting a specific
etiological agent based on clinical
features and/or radiography
•Generally POOR
•ONE EXCEPTION -STAPH
–More likely if
•Very rapid progression
•Skin Lesions, infected scabies
•Pleural Effusion or Empyema/ Pneumothorax
•post measles

67. Treatment of CAP
•Out patient
•In patient
Out Patient
•Supportive Care
•Withhold antibiotics (if not sick and viral etiology)
•Features of atypical pneumonia –Start Macrolides
•Reassess the child after 48 hr.

68. Indications for admission to hospital
(in patients)
–Marked tachypnea
–difficulty in breathing
–marked chest indrawing
–intermittent apnea, grunting
–not feeding/ dehydrated
–family not able to provide appropriate
observation or supervision.
–Failure of OPD treatment
–Presence of high risk factors

69. Inpatient management of pneumonia
Specific Supportive
Antimicrobial Hydration
Nutrition
Oxygen
Antipyretics
Physiotherapy
Adjuvants

70. Treatment of CAP
•Antibiotic Treatment shall be discussed in
the following slides in this manner
–Pneumonia (non-severe disease)
–Severe –very severe pneumonia
–Suspected Staphylococcal disease
•It gives the first and second line options
as per IAP-RTI consensus guidelines.

71. *Use Separately in 1:2 ratio as
combinations available are not
scientifically correct
# Second line domicillary therapy is for
patients who show inadequate or no
response to first line treatment after
48hrs, though have no deterioration or
increase in severity.
Disease Pneumonia
Setting Domicilliary
AGE First LineSecond Line#Suspected Staphylococcal ds
Upto 3mo Usually Severe, treated as inpatients
3mo-
5yrs of
age
AmoxycillinCo-amoxy
clavulinic acid
OR
Chloremphenicol
Cefuroxime
OR
Co-amoxy clavulinic acid OR
Amoxycillin+ Cloxacillin*
5 yrs plusAmoxycillinMacrolide
OR
Co-amoxy-
clavulinic acid
Cefuroxime
OR
Co-amoxy clavulinic acid
OR
Amoxycillin+ Cloxacillin*

72. Severe –Very Severe Pneumonia
Treat as In-patient
Age First Line Second Line
0-3 mo Inj 3
rd
Gen Cephalosporins:
Cefotaxime/Ceftriaxone
+
Aminoglycoside (Gent/Amika)
Inj Co-amoxy clavulinic acid
+
Aminoglycoside (Gent/Amika)
3mo-5 years Inj Ampicillin
OR
Inj Chloremphenicol
OR
Inj Ampicillin +
Inj Chloremphenicol (<2 years of age)
OR
Inj Co-amoxyclavulinic acid
Inj Co-amoxy clavulinic acid
OR
Inj 3
rd
Gen Cephalosporins:
Cefotaxime/Ceftriaxone
5 years +
Inj Ampicillin
OR
Inj Co-amoxyclavulinic acid
OR
Macrolides (if Mycoplasma
suspected)
Inj Co-amoxy clavulinic acid
OR
Inj 3
rd
Gen Cephalosporins:
Cefotaxime/Ceftriaxone
AND
Macrolides

73. Severe-Very Severe Disease
SUSPECTED STAPHYLOCOCCAL DS
Inj 3rd Gen Cephalosporins: Cefotaxime/Ceftriaxone
+ Cloxacillin
OR
Inj Cefuroxime +Aminoglycoside
OR
Inj Co-amoxyclavulinic acid + Aminoglycoside
Second line: Vancomycin/ Teicoplanin/ Linezolid
+
Inj 3rd Gen Cephalosporins

74. When to switch to the second line
therapy
Second line domiciliary therapy (non-
severe) is for patients who show
inadequate or no response to first line
treatment after 48hrs, though have no
deterioration or increase in severity.
In case of severe disease, once again the
second line treatment is started if there is
any increase in severity in 48 hours or
clinical non response in 72-96 hours

75. Supportive therapy for CAP
•Oxygen :
–as indicated by pulse oxymetry and/ or ,
–clinical signs of hypoxia like rapid breathing as well as retractions
•IV Fluids:
–If dehydrated,
–Tachypnoea severe enough to make the child unable to drink, or
–impending respiratory failure.
•Fever management
–Important as fever increase oxygen requirement
–Paracetamol and sponging are useful in most situations.
•Bronchodilators,where indicated
–should be used to decrease the work of breathing.

76. Duration and mode of therapy
•Domiciliary 5-7 days, Oral
•If on second line, then treat for
7-10days
•If admitted:
–All antibiotics by parenteral
route (i.v.) to begin with
–Switch to oral after 48-72
hrs or earlier if can accept
–Step-down/ switch therapy
for Inj 3
rd
generation
Cephalosporins
•3
rd
generation oral like
Cefpodoxime
•NOT Cefixime because it
lacks action against Strep.
Pneumoniae
•Fluoroquinolones are not
recommended
–Total 5-7 days more
IfStaphylococcal disease:
•2 weeks if no complication; Else 4-6 weeks

77. Presence of comorbidity:
congenital heartdisease,
chronic lung disease ofprematurity,
chronic respiratory conditions suchas
-cysticfibrosis,
-bronchiectasisor
-immunedeficiency
Admission should also be consideredfor
All children under the age of 6 months
Children in whom treatment with antibiotics has failed (most
children improve after 48 hours of oral, outpatient antibiotics)
Patients with troublesome pleuritic pain

78. Be sure to offer the patient and parents general support, explanation and reassurance.
Respiratory support as required, including oxygen
Pulse oximetry to guide management
Severerespiratorydistresswith↓levelofconsciousnessandfailuretomaintain
oxygenationindicatesaneedforintubation
complication &prognosis
Complete resolution after treatment should be expected in
the vast majority of cases.
Bacterial invasion of the lung tissue can cause pneumonic
consolidation, septicemia, empyema, lung abscess
(especially S. aureus) and pleural effusion.
Respiratory failure, hypoxia and death are rare unless
there is previous lung disease or the patient is
immunocompromised.

79. Prevention
Prevention of pneumococcal pneumonia and influenza by
vaccination, for high-risk individuals with pre-existing
heart or lung disease.
Smoking in the home is a major risk factor for all
childhood respiratory infection.

80. Conclusion
•URI are common during the winter season and for the most part, are benign, but
they can seriously affect the quality of life for a few weeks.
•Complications of upper respiratory tract infections are relatively rare,
except with influenza.
•Its important to timely diagnose and treat with appropriate treatment to
prevent further complications
Understanding the pathophysiology ofLRTI
Conducting properHistory
Performing careful physicalExamination
Comprehensionthe Impact of the disease on thefamily
Close follow up afterdischarge

81. 12 -References
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