1. Describe the respiratory system
• Essential components
of respi system :
– CNS
– Respi center
– Muscle
– Lung tissue

2. Depict signs of respiratory distress in a real
patient

3. Respiratory distress
• It is an abnormal physiologic condition identified by
increased work of breathing.
• The child in respiratory distress is effectively
compensating to preserve adequate gas exchange.

5. Signs of Respiratory distress
• Tachypnea
• Tachycardia
• Retractions
(supraclavicular, suprasternal, intercostal or
subcostal)
• Use of accessory neck muscles
• Nasal flaring and grunting
• Pallor or cyanosis
• Altered mental status
(restlessness, irritability, confusion, anxiety, inability
to recognize parents)

6. Positioning
• With an upper airway obstruction, the patient
characteristically assumes sniffing position (jaw thrust
forward) and may drool due to inability to swallow
secretions.
• A patient in severe respiratory distress may position
himself in the tripod position (seated and leaning
forward on outstretched arms), sitting upright and
leaning forward to maximize use of accessory
muscles.

7. Respiratory rate
• Abnormal respiratory rate is common finding in
respiratory distress.
• Although normal respiratory rate varies with age, a
rate greater than 60 breaths per minute is abnormal
in any child.
• A slow respiratory rate might arise concerns as it
may signifies respiratory fatigue and imminent
respiratory arrest in an exhausted child.

8. Retractions
• Subcostal, intercostal and suprasternal retractions
are manifestations of increased work of breathing as
well as use of accessory muscles of respiration.
• Paradoxic breathing (abdomen retracts upon
inspiration and expands upon expiration) may be
noted.

9. Nasal flaring and grunting
• Flaring of the nostrils with inspiration is also a sign of
respiratory distress.
• Grunting is a sound made by forceful expiration
against a partially closed glottis.
• Head bobbing may be seen in infants.

10. Lung Sounds and Auscultation
• Decreased breath sounds and diminished air entry in
the setting of increased respiratory effort suggest
worsening respiratory disease.

11. Heart Rate
• Tachycardia is a common finding in children in
respiratory distress and is not necessarily indicative
of cardiovascular instability.
• Bradycardia, for instance, is indicative of severe
hypoxemia and acidosis which require critical
interventions.
• Bradycardia in a child with history of respiratory
distress signifies imminent cardiopulmonary arrest.

12. Altered level of consciousness
• Some children might present with effortless
tachypnea resulting from an increased respiratory
drive caused by metabolic acidosis or central nervous
system disease.
• Therefore, mental status is evaluated as a gauge of
systemic oxygenation and critical management must
be done if the patient appears lethargic or agitated.

13. Normal Respiratory Rate
• Infant = 30 – 40 /min
• Toddler = 24 – 40 /min
• School age = 18 – 30 /min
• Adolescent = 12 – 16 / min

14. Define respiratory failure
• Respiratory failure is a syndrome of inadequate gas
exchange due to dysfunction of one or more essential
components of the respiratory system:
• Type I : Hypoxaemic respiratory failure. PaO2 < 60 mm Hg
with a normal or low PaCO2. This is caused by ventilation-
perfusion mismatch with either/both:
– Under-ventilated alveoli (eg pulmonary oedema, pneumonia or
acute asthma).
– Venous blood bypasses ventilated alveoli (eg right to left cardiac
shunts).
• Type II : Hypercapnic respiratory failure. PaCO2 > 50 mm Hg
and indicates inadequate alveolar ventilation. Any
ventilation-perfusion mismatch will affect PaO2 and
therefore hypoxaemia is also common.

15. • Common causes of type • Common causes of type
I respiratory failure II respiratory failure
– COPD. – Drug
– Pneumonia. overdose, poisoning.
– Pulmonary oedema. – Myasthenia gravis.
– Pulmonary fibrosis. – Polyneuropathy.
– Asthma. – Poliomyelitis.
– Pneumothorax. – Muscle disorders.
– Pulmonary embolism. – Head injuries and neck
– Pulmonary hypertension. injuries.
– Cyanotic congenital heart – Hypothyroidism.
disease.
– Bronchiectasis.
– Acute respiratory distress
syndrome.

16. Ix :
• Arterial blood gas analysis: confirmation of the diagnosis.
• CXR: often identifies the cause of respiratory failure.
• FBC: anaemia can contribute to tissue hypoxia; polycythaemia may
indicate chronic hypoxaemic respiratory failure.
• Renal function tests and LFTs: may provide clues to the aetiology or
identify complications associated with respiratory failure. Abnormalities in
electrolytes such as potassium, magnesium, and phosphate may
aggravate respiratory failure and other organ dysfunction.
• Serum creatine kinase and troponin I: to help exclude recent myocardial
infarction. Elevated creatine kinase may also indicate myositis.
• TFTs (hypothyroidism may cause chronic hypercapnic respiratory failure).
• Spirometry: useful in the evaluation of chronic respiratory failure.
• Echocardiography: if a cardiac cause of acute respiratory failure is
suspected.
• Pulmonary function tests are useful in the evaluation of chronic
respiratory failure.
• ECG: to evaluate a cardiovascular cause; it may also detect dysrhythmias
resulting from severe hypoxaemia or acidosis.

17. Management
• A patient with acute respiratory failure
generally needs prompt hospital admission in
an intensive care unit.
• Many patients with chronic respiratory failure
can be treated at home, depending on the
severity of respiratory failure, underlying
cause, comorbidities and social circumstances.
• Immediate resuscitation may be required.
• Appropriate management of the underlying
cause.

18. Describe obstructive and restrictive
respiratory conditions

19. Obstructive disorders
• These are respiratory disease which make it more
difficult to get air out of the lungs.
• This group of disorders is characterized by obstruction
of normal airflow due to airway narrowing and
includes: Asthma, COPD, bronchiectasis, cystic
fibrosis and tumors.
• Mechanisms causing airway narrowing differ and may
include obstruction by a mucus plug, airway
compression and smooth muscle constriction.

20. Obstructive disorders
• In general, obstructive disorders lead to hyperinflation
of the lungs as air is trapped behind closed airways.
• Residual volume is increased as in the ratio of RV:
TLC. Functional residual capacity also increased.
• In patients with severe obstruction, air trapping is so
extensive that vital capacity is decreased.

21. • In addition, dynamic compression of the airway
prolongs the FEV1, as well as the forced expiratory
flow rate measured over the middle half of expiration
(FEF 25-75%)
• Both FEV1 and FVC are reduced, but the reduction in
FEV1 is greater (airway narrowing reduces the speed
of forced expiration such that FEV1 is reduced to an
abnormally low fraction of FVC, perhaps to 40% or
lower).
• Result: low FEV1 / FVC.

22. Obstructive disorders
• Extrathoracic- stridor
• Intrathoracic- wheezing, best heard during expiration
• Long deep breaths
• Hyperinflated and tympanitic to percussion

23. Bronchoconstriction causes obstructive
airway problems

26. Restrictive disorders
• These are respiratory disease which makes it more
difficult to get air into the lungs.
• They “restrict” inspiration.
• Examples include:
Fibrosis, sarcoidosis, silicosis, asbestosis, muscular
diseases and chest wall deformities.

27. Restrictive disorders
• In fibrosis or alveolar wall thickening, the increased
connective tissue reduces lung compliance, making it
difficult to expand the lung during inspiration.
• In condition such as alveolar edema, respiratory distress
syndrome, or infiltrative interstitial lung diseases, the lungs
are stiff decreasing its compliance.
• Extrapulmonary factors that can contribute to decrease
vital capacity include limited thoracic expansion (Pleural
fibrosis, Kyphoscoliosis) and nerve or muscular
dysfunction.

28. • As a result, all lung volumes are reduced. In
particular, there can be marked decreases in total lung
capacity and functional vital capacity.
• FEV1 and FVC are reduced proportionately but the normal
ratio is preserve.
• The patient might demonstrate rapid shallow breathing.
He/she might also shows grunting.
• Percussion of the respiratory system demonstrate dull/
hyper-resonance?

32. Differentiate clinical presentation of
obstructive airway
Upper airways obstruction Lower airways obstruction
Stridor Wheezing
• harsh sound •Continuous expiratory sound
•Produced near larynx by the vibration of •Due to turbulence airflow
upper airway structures •Musical
•Inspiratory ( expiratory – less common) •Partial obstruction produces wheezing
•hoarseness – effect vocal chord sound at later phase of expiration
•Supraglottic etiology – moves with child’s •Harsh, monophonic and low pitch (usually
head from large, central airways)
•Decreases while sleep – inspiration at lower • high pitched and musical (from small and
rate during sleeping peripheral airways)
Suprasternal retraction Rhonchi
•Pressure gradient between trachea and •Secretion in intrathoracic airways, resulting
atmosphere in irregular sound
Rales or crackles
•Sound characterized by of crumpling
celophane due to fluid or secretion in small
airways

33. Describe conditions presented with
wheezing in children and infants
• Acute wheezing :
– Infection
– Foreign body aspiration (FBA)
• Chronic/ recurrent wheezing
– Anomalies of the tracheobronchial tree (ie Congenital
tracheomalacia and bronchomalacia)
– Cardiovascular disease (pulmonary artery dilation
and/or left atrial enlargement, including large left to
right shunts, can compress large airways and cause
wheezing)
– Mediastinal masses (ie tumors, cyst, LN enlargement)

34. Upper respiratory tract conditions -
to be presented in tabulated manner
• common cold
• acute pharyngitis
• acute otitis media
• acute sinusitis

35. common cold acute pharyngitis acute otitis media acute sinusitis
Fever Inflamed pharynx and fever, Cough
Nasal discharge soft palate irritability, Nasal symptoms
Loss of appetite Enlarged and tender headache, Fever
Difficulty sleeping. LN apathy, Headache
anorexia, Facial pain and
vomiting, swelling
diarrhea Sore throat
Rhinovirus, Adenovirus RSV, rhinovirus, Rhinovirus,
coronavirus, RSV Enterovirus Pneumococcus, adenovirus, influenza,
Rhinovirus H. influenzae or parainfluenza
Gp A β-hemolytic
strepto
Treat fever and pain Paracetamol Paracetamol Nebulized anti-
with paracetamol or Penicillin (bact only) Ibuprofen microbials
ibuprofen

36. Pnuemococal Staphylococcus Mycoplasma Viral pneumonia
pneumonia pneumonia pneumonia
S. Pneumoniae Staphylococcus Mycoplasma Influenza virus
aureus pnuemoniae Parainfluenza virus
Community
acquires
Presentation Presentation Presentation
•Skin infection •Fever •Fever
•Soft tissue •Malaise •Chills
infection – •Headche •Non productive
pyomyositis, septic •Persistent slowly cough
bursitis worsening dry •Rhinitis
•Toxic shock cough •Myalgias
syndrome •Chills •Headache
•Endocarditis •Sore throat •fatigue
•Osteromyelitis •Pluertictic chest
•Pneumonia pain
•Food poisoning
•UTI
Tx Tx Antibiotics amantindine,
Antibiotics Antimicrobial Macrolides, rimantidine,
therapy doxycyline acylovir

37. Pertussis – whooping cough
Etiology
Caused by Bordetella pertussis
Infect among human through respiratory droplets (coughing)
Clinical presentation
Infants beyond neonatal period through school age
Catarrhal stage – injection, increased nasal secretion and low grade fever 1-2 weeks
Paroxysmal stage – coughing (expiration) to dislodge plugs of necrotic bronchial
epithelial tissues and thick mucus. Lasted 2-4 weeks
Followed by forceful inhalation against narrowed glottis – whoop characteristic
Convalescent stage – symptom gradually resolve 1-2 weeks, coughing less severe,
whooping cough dissapear.
CNS damage due to hypoxia, bacterial pnuemonia,
Adult – starts with broncholitis illness.
Tx
Erythromycin – early coarse, eradicates nasopharyngeal carriage within 3-4days,
ameliorate the effects of infection, ineffective at paroxysmal stage, , ass with pyloric
stenosis if given to neonates <4 weeks old
Azithromycin & clarithromycin – shorter duration, ass with gastrointestinal adverse
effects
Pertussis-specific immunoglobin – effectivelt reduced symptoms at paroxysmal stage
TMP-SMZ (trimethoprim/sulfamethozxazole)

38. Pulmonary tuberculosis
Etiology
Caused by Mycobacterium tuberculosis
Spread via respiratory droplets – become respiratory nuclei, <10um can reach alveoli
Clincal manifestation
•Asymptomatic in older and infants patient
•+ve tuberculin skin test
•Minimal abnormalities on CXR infiltration with hilar lymphadenopathy (Ghon complex)
•Malaise, low grade fever, erythema nodosum, lympahadenopathy symptoms.
Investigation
Tuberculin skin test (TST)
•T-cell-mediated hypersensitivity, 2-6 weeks
Mantoux test
•Intradermal injection of 5TU on volar surface of forearm, screen high-risk population and for
diagnosis in all ill patients or contacts.
•False –ve at early phase of illness or immunosuppression
Culture
Tissue, sputum, fluid
Treatment
Antibiotics – RIPES, 9-months of isoniazid&rifampin 98% case cured
Prevention - BCG

39. • Acute viral bronchiolitis
• transient infant wheeze
• chronic lung diseases of prematurity
• bronchiectasis.

40. Acute viral bronchiolitis
• lower respiratory tract infection (LRTI) that
primarily affects the small airways
(bronchioles)
– RSV is the most common cause, followed by
rhinovirus
– Less common causes include parainfluenza
virus, human metapneumovirus, influenza
virus, adenovirus, coronavirus,

41. • S/s : fever (usually ≤38.3ºC), cough, mild
respiratory distress, preceded by a one- to three-
day history of upper respiratory tract
symptoms, such as nasal congestion and/or
discharge.
• PE :
– tachypnea
– intercostal and subcostal retractions, often with
expiratory wheezing.
– The chest may appear hyperexpanded with increased
anteroposterior (AP) diameter and may be
hyperresonant to percussion.
– Findings on auscultation include any combination of
expiratory wheeze, prolonged expiratory phase, and
both coarse and fine crackles.
• Ix : Mild hypoxemia (oxygen saturation <95
percent) commonly is detected by pulse
oximetry, even without clinical signs of desaturation

42. • Mx :
– SEVERITY ASSESSMENT — Severe bronchiolitis is
indicated by persistently increased respiratory
effort (tachypnea; nasal flaring;
intercostal, subcostal, or suprasternal retractions;
accessory muscle use;
grunting), hypoxemia, apnea, or acute respiratory
failure
– In healthy infants and young
children, bronchiolitis usually is a self-limited
disease.
– Maintain oxygenation and hydration.
– Bronchodilator therapy may be beneficial in a
subset of patients

43. Transient infant wheeze
• The successful transition from fetal to
neonatal life at delivery requires a series of
rapid physiologic changes of the
cardiorespiratory system. These changes result
in redirection of gas exchange from the
placenta to the lung and comprise:
– Replacement of alveolar fluid with air
– Onset of regular breathing
– Increase in pulmonary blood flow as a result of
increased systemic vascular resistance and
decreased pulmonary vascular resistance (PVR)

44. • difficulty may be a consequence of :
– impaired lung function due to fluid retention,
– airway obstruction associated with congenital
anomalies,
– persistent pulmonary hypertension,
– apnea associated with lack of respiratory effort.

45. Respiratory distress syndrome
• Respiratory distress (ie, tachypnea and labored
breathing) and cyanosis occur at or soon after birth.
• Typical signs include
– grunting (which prevents end-expiratory alveolar collapse),
– nasal flaring (which reduces nasal resistance and reflects
increased use of accessory muscles of respiration),
– and intercostal and subcostal retractions (due to decreased
lung compliance and the highly compliant chest wall).
• Surfactant deficient
• inability to clear lung fluid from air spaces

46. Bronchiectasis
• Abnormal dilation and distortion of the
bronchial tree, resulting in chronic obstructive
lung disease.
• End result of a variety of pathophysiologic
processes that render the bronchial walls
weakened, easily collapsible, chronically
inflamed, and plugged with mucus secretions.
• Associated findings include atelectasis,
emphysema, fibrosis, and hypertrophy of the
bronchial vasculature.

47. • S/s : productive cough, purulent sputum,
fever, pleuritic chest pain, and dyspnea
• PE :
– Crackles (inspiratory popping sounds) and rhonchi
(coarse expiratory breath sounds),
– Wheezing (less common)
– Clubbing of the nailbed
– Chest wall deformity, which can be seen in
obstructive lung diseases (eg, cystic fibrosis)

48. • Ix :
– CXR - linear atelectasis and dilated and thickened airways,
HRCT
– sweat chloride or DNA testing
– blood count with differential, immunoglobulins, and IgG
subclasses
• Mx : aimed at treating the underlying cause, improving
mucocilliary clearance, treating and preventing
infection, and controlling inflammation
– Antibiotic therapy
– Chest physiotherapy
– Mucolytic agents and airway hydration
– Bronchodilators
– Anti-inflammatory drugs
– Immunization

49. Laryngotracheobronchitis (Croup)
• It is a viral infection of the middle respiratory tract
occurs from 6 months to 6 years of age with peak
incidence in the 2nd year of life.
• There is mucosal inflammation and increased
secretions affecting the airway, but it is the edema of
the subglottic area that is potentially dangerous as it
may result in critical narrowing of the trachea.

50. Laryngotracheobronchitis (Croup)
• A small decrease in diameter secondary to mucosal
edema and inflammation exponentially increases
airway resistance and significantly increases work of
breathing.
• During inspiration, walls of the subglottic space are
drawn together, aggravating the obstruction and
producing stridor characteristic of croup.

51. Laryngotracheobronchitis (Croup)
• Symptoms are
 Low grade fever, cough and coryza for 12-72 hours followed
by
 Stridor that may occur when excited, at rest or both
(Harsh, high-pitched respiratory sound produced by
turbulent airflow; usually inspiratory, but may be biphasic
and is a sign of upper airway obstruction)
 hoarse voice, brassy or “barking” cough
 Respiratory distress of varying degree
• Onset of symptoms is usually over several days and often start
and worse at night.
• Symptomatic reinfection is common but usually mild.

52. Laryngotracheobronchitis (Croup)
• Parainfluenza viruses (type 1,2,3) are the
commonest cause but other viruses such as human
metapneumovirus, RSV and influenza virus type A
and B, adenovirus, enterovirus, measles, mumps
and rhinoviruses can produce similar clinical picture.
• Chest X-ray reveals a characteristic narrowing of the
subglottic region known as the “steeple sign”.

54. Assessment of severity
• a

55. Laryngotracheobronchitis (Croup)
• When the upper airway obstruction is mild, the
stridor and chest recession disappear when the child
is at rest.
• The child can usually be managed at home and
need to be closely monitored for signs of increasing
severity.
• Most cases of croup are mild and resolve within 1 to
2 days.

56. Laryngotracheobronchitis (Croup)
• Indication for hospital admission
Moderate and severe viral croup
Poor oral intake
Family lives a long distance from hospital, lacks
reliable transport
Toxic looking
Age less than 6 months
Unreliable caregivers at home

57. Management of Croup

58. Management of Croup
• Oxygen therapy indication include severe viral croup
and percutaneous SaO2 <93%.
• Steroids are helpful in moderate to severe cases.
• Antibiotics may be indicated if the child fails to
improve or if purulent secretions are present where
coverage should be directed towards
Staphylococcus and H.influenzae.

59. Acute epiglottitis (Supraglottitis)
• It is less common than croup, typically presents with
a greater degree of airway compromise.
• H.influenzae type B is the major etiologic organism.
• The incidence of epiglottitis has decreased with the
administration of H. influenzae vaccine.
• It is most common in children aged 1-6 years but
affect all age groups.

60. Clinical manifestations of Acute epiglottitis
• Patients typically present with acute onset (over several hours)
of
 High fever in an ill, toxic-looking child
 An intensely painful throat preventing child from speaking or
swallowing with saliva drools down the chin
 Marked dysphagia
 Soft inspiratory stridor and rapidly increasing respiratory
difficulty over hours
 Patients are often encountered leaning forward in a “tripod”
position (Immobile, upright with an open mouth)
• Unlike croup, cough is frequently absent.

61. Acute epiglottitis (Supraglottitis)
• Attempts to lie the child down or examine the throat
with a spatula or perform a lateral neck X-ray must
not be undertaken as this may precipitate total
obstruction and death.
• Instrumentation of the throat with tongue depressors
is not advisable as this can precipitate a fatal
laryngospasm.

62. Acute epiglottitis (Supraglottitis)
• If the diagnosis of epiglottitis is suspected, urgent hospital
admission and treatment are required.
• The child should be intubated under controlled conditions
with a general anesthetic.
• Rarely, this is impossible and urgent tracheostomy is life-
saving.
• Only after securing the airway, blood is taken for culture
and broad-spectrum IV antibiotics such as cefuroxime
directed against H.influenzae and gram-positive
organisms started.
• Tracheal tube can usually be removed after 24 hours and
antibiotics given for 2-3 days.
• Prophylaxis with rifampicin is offered to close household
contacts.

63. Clinical features of croup and epiglottitis
Croup Epiglottitis
Onset Over days Over hours
Preceding coryza Yes No
Cough Severe, barking Absent or slight
Able to drink Yes No
Drooling saliva No Yes
Appearance Unwell Toxic, very ill
Fever <38.5 Celsius >38.5 Celsius
Stridor Harsh, rasping Soft, whispering
Voice, cry Hoarse Muffled, reluctant to
speak

64. Laryngomalacia
• It is the most common congenital anomaly of the
larynx, accounting for up to 60% of all anomalies.
• Inspiratory stridor is the hallmark of the condition.
• Symptoms are typically aggravated when the child is
supine or crying.
• Examination reveals partial collapse of a flaccid
supraglottic airway with inspiration.
• The condition is generally benign and self-limited, as
most cases resolve by 18 months of age.
• Severe cases may require surgical intervention if the
distress prevents adequate feeding.

68. Congenital subglottic stenosis
Etiology
•Can be iatrogenic
•Intubation and mechanical ventilation – residual damage to the larynx
•Down’s syndrome infants more susceptible due to smaller larynx
Clinical manifestation
•Subglottic obstruction produces stridor and frequently biphasic (expiration and
inspiration)
•Worsen with respiratory effort
•Viral infection exacerbate subglottic stenosis
Diagnostic studies
•Requires endoscopic evaluation
Treatment
•Tracheostomy and reconstructive surgery may be necessary
•Some improve with age as larynx grow and require no intervention

69. Retropharyngeal abscess & Peritonsilar abcess
Retropharyngeal abscess Comparison Peritonsilar abscess
<6 years Age >10 years
Posterior pharynx Location Oropharynx
S. aureus, anaerobes Etiology Group A streptococci, anaerobes
Insidious to sudden Prodrome onset Biphasic with sudden worsening
None Stridor No
Yes Retraction No
Muffled Voice “Hot potato” muffled
Arching of neck or normal Position and appearance Normal
Drooling Swallowing (dysphagia) Drooling, trismus
No Barking cough None
Severe Toxicity Dyspnea
>101 F Fever >101 F
Thickened retropharyngeal space X Ray None needed
Leukocytosis with left shift WBC count Leukocytosis with left shift
Antibiotics, surgical drain - abscess Therapy Antibiotics, aspiration
None Prevention Treat Group A streptococci early

70. Diphtheria
Etiology
Caused by bacteria Corynebacterium diphtheriae
spread through respiratory droplets from infected person or carrier
Infects nose, throat causes gray to black, thick fiber like covering airway
Infects skin - Skin lesions
Produces toxins – spread via bloodstream to other organs
Signs and symptom
Mild fever, sore throat, chills – few days after infection
Breathing problems, croup-like (barking cough), drooling, hoarseness
Nasal discharge, fatigue
Dysphagia, paralysis, heart failure – serious
Tx
Antitoxin IV/IM
Antibiotics – penicillin and erythromycin
Diphtheria vaccine – lasted for 10 years (if in contact with infected person)

71. Chronic lung disease of prematurity
• Infants who still have an oxygen requirement at a
post-menstrual age of 36 weeks are described as
having bronchopulmonary dysplasia (BPD) or chronic
lung disease.
• Criteria for diagnosis are oxygen requirement beyond
36 weeks post conceptional age or beyond 28 days of
life.

72. Pathophysiology of BPD
• The lung damage (alveolar cells, interstitium and
blood vessels) comes from pressure and volume
trauma from artificial ventilation, oxygen toxicity and
infection.
• Oxygen concentration greater than 40% are toxic to
the neonatal lung.
• Oxygen-mediated lung injury results from the
generation of superoxides, hydrogen peroxide and
oxygen free radicals which disrupt membrane lipids.

73. Pathophysiology of BPD
• Assisted ventilation with high peak pressures produces
barotrauma, compounding the damaging effects of highly
inspired oxygen levels.
• Inflammatory mediators are released and causing increase
permeability of blood vessels leading to leakage of water
and protein.
• In later stages, there is fibrosis and cellular hyperplasia.
• Severe lung damage can leads to respiratory failure.

75. Risk factors of BPD
• In most patients, BPD develops after ventilation for RDS
that may have been complicated by PDA (Patent ductus
arteriosus) or pulmonary interstitial emphysema.
• Inflammation from prolonged assisted ventilation and
repeated systemic and pulmonary infections may play a
major role.
• Failure of RDS to improve after 2 weeks, the need for
prolonged mechanical ventilation and oxygen therapy
required at 36 weeks’ postconceptional age are
characteristics of patients with RDS in whom BPD
develops.

76. Risk factors of BPD
• BPD also may develop in infants weighing less than
1000g who require mechanical ventilation for poor
respiratory drive in the absence of RDS.
• 50% of infants of 24 to 26 weeks’ gestational age
require oxygen at 36 weeks’ corrected age.

77. Chest X-Ray of BPD
• The chest X-ray characteristically shows widespread
areas of opacification, sometimes with cystic changes
accompanied by areas of over-distention and
atelectasis, giving the lung a sponge like appearance.
• Histopathology of BPD reveals interstitial
edema, atelectasis, mucosal metaplasia, interstitial
fibrosis, necrotizing obliterative bronchiolitis and
overdistended alveoli.

80. Clinical manifestations of BPD
• The clinical manifestations of BPD are oxygen dependence,
hypercapnia, compensatory metabolic alkalosis, pulmonary
hypertension, poor growth and development of right-sided heart
failure.
• Increased airway resistance with reactive airway
bronchoconstriction also is noted and is treated with
bronchodilating agents.
• Severe chest retractions produce negative interstitial pressure
that draws fluid into the interstitial space.
• Together with cor pulmonale, these chest retractions cause fluid
retention, necessitating fluid restriction and the administration of
diuretics.

81. Management of BPD
• Some infants need prolonged artificial ventilation, but most are
weaned onto continuous positive airways pressure (CPAP)
followed by additional ambient oxygen, sometimes over several
months.
• To reduce risk of subglottic stenosis, a tracheotomy may be
indicated.
• To reduce oxygen toxicity and barotrauma, ventilator settings
are reduced to maintain blood gases with slightly lower PaO2
(50mmHg) and higher PaCO2 (50 to 75 mmHg) levels than for
infants during the acute phase of RDS.

82. Management of BPD
• Dexamethasone therapy may reduce inflammation,
improve pulmonary function and enhance weaning of
patients from assisted ventilation.
• However, corticosteroid therapy may increase risk of
abnormal neuro-development including cerebral palsy,
thus limits use to those at highest risk and only short
courses are given.

83. Management of BPD
• Some babies go home while still receiving additional
oxygen.
• A few infants with severe disease may die of intercurrent
infection or pulmonary hypertension.
• Some survivors of BPD have hyperinflation, reactive
airways and developmental delay.
• Subsequent pertussis and RSV (Respiratory syncytial
virus) infection may cause respiratory failure necessitating
intensive care and thus prophylaxis against RSV should
be given.

84. Inhaled foreign body
Epidemiology
•Common, 4 y/o
•Main right bronchus (direct continous with trachea
•May migrate on larynx (coughing) causes occlusing of airway
Clinical manifestation
•Cough, localized wheezing, unilateral absence of breath sounds, stridor, blood sputum (rare)
•fever, cough, sputum production, or chest pain – need medical attention
•Persistence wheezing unresponsive to bronchodilator therapy, persistent atelectasis, recurrent
or persistence pneumonia, persistent cough without other explanation – suspect foreign body
inhalation.
•Lodge in esophagus and compress trachea – produce respiratory symptoms
Diagnostic studies
•Radiographic studies – presence of radiopaque object or eveidence of air trapping
Prevention
•Education to parent and caregiver
•Small toys should kept away

85. Pneumothorax
• defined as a collection of air
that is located within the thoracic
cage between the visceral and
parietal pleura
– Primary : no underlying lung disease
– Secondary : complication of underlying lung disease
(ie asthma, cystic fibrosis, necrotizing pneumonia, and
interstitial lung disease)

86. • S/s : dyspnea and pleuritic chest pain that is
described as sharp or stabbing. The pain
typically is diffuse on the affected side with
radiation to the ipsilateral shoulder. A dry or
non-productive cough
• PE :
– deviation of the trachea towards the contralateral
side
– diminished breath sounds
– hyperresonant percussion
– decreased vocal fremitus on the affected side.
– Other signs : tachypnea, increased work of
breathing, and cyanosis.

87. • Ix : ABG, CXR
• Mx : depends on the size of the
pneumothorax, the extent of respiratory
distress, and the presence or absence of
underlying lung disease. The goals of
treatment are to remove air from the pleural
space and to prevent recurrence.
– Supplemental oxygen
– Needle aspiration
– Thoracostomy tube

88. Empyema
• Early in the course of parapneumonic
effusion, the pleura becomes inflamed;
leakage of proteins, fluid, and leukocytes.
At the time of formation, the pleural effusion is usually
sterile with a low leukocyte count.
With time, bacteria invade the fluid, resulting in
empyema, which is defined as the presence of grossly
purulent fluid in the pleural cavity.
• S/s : persistent fever, cough, malaise, decreased
appetite, chest pain, and dyspnea
• PE : tachypneic, but breaths may be shallow to minimize
pain, mediastinal shift and tension
hydrothorax, Hypoalbuminemia

89. • Ix : Pulse oximetry , Blood and sputum culture,
CXR
• Management:
– Main goals : sterilization of the pleural cavity,
resolution of pleural fluid, and reexpansion of the
lung
– Antibiotics
– Thoracocentesis
– Chest tubes
– Surgical (for symptoms for more than one week
only)

90. Pneumatocele
• A pneumatocele is a cavity in the lung
parenchyma filled with air (cyst) that may
result from pulmonary trauma during
mechanical ventilation
• Ddx : Lung ca, TB
• Mx : palliative care

91. Lung abscess
• Result from lung tissue necrosis from an
infection (ie pneumonia)
• Conditions contributing to lung abscess
– Aspiration of oropharyngeal or gastric secretion
– Septic emboli
– Vasculitis: Wegener's granulomatosis
– Necrotizing tumors:

92. Congenital diaphragmatic hernia Congenital lobar emphysema (congenital
lobar over distention)
Etiology Over inflation of one lobe during neonatal
Improper joining of structure during fetal dev. period – left upper lobe (often)
Stomach, small intestine, spleen appear in
chest cavity,
Lung tissue not completely develop
Left side – common
Increase risk with +ve family hx
Symptom •Produces respiratory distress because
Breathing difficulty after born due to surrounding lung tissue has compressed
ineffective movement of diaphragm and •Mediastinal shift
crowding of lung tissue, which causes collapse
Cyanosis, tachypnea, tachycardia
Irregular chest movement
Absence of breath sound on both side
Bowel sound heard in the chest
Palpation – abd feels less full
Xray – abd organs in chest cavity
Surgery - place abd organs back n repair Lobectomy – if RDS is severe and progressive
diapgrmatic opening
Breathing support until recvers from surgery

93. H type- tracheoesophageal fistula -

94. • S/s : if the defect is large, with coughing and
choking associated with feeding.
• Diagnosis — attempt to pass a catheter into
the stomach. This finding can be confirmed
with an anterior-posterior chest radiograph
that demonstrates the catheter curled in the
upper esophageal pouch
• Mx : surgical ligation of the fistula.
– if the distance between esophageal segments is
large, staged procedures are performed that
include elongation of the esophagus.

96. Gastroesophageal reflux (GER)
 It is defined as the effortless retrograde movement of
gastric contents into the esophagus.
 In infancy, GER is not always an abnormality.
 Distinction between physiologic GER and pathologic
GER in infancy and childhood is determined by
presence of reflux-related complications.

97. Physiologic GER
 Physiologic GER (Spitting up) is normal in infants
younger than 8 to 12 months of age.
 Nearly half of all infants are reported to spit up at 2
months of age.
 It is caused by inappropriate relaxation of the lower
esophageal sphincter as result of functional
immaturity.
 Infants who regurgitate stomach contents meet the
criteria for physiologic GER, as long as they maintain
adequate nutrition and have no signs of respiratory
complications or esophagitis.

98. Clinical manifestations
 Presence of GER is easy to observe in an infant who spits up.
 In older children, the refluxate is usually kept down by
reswallowing, but GER may be suspected by associated
symptoms, such as:
• Heartburn
• Cough
• Dysphagia
• Wheezing
• Aspiration pneumonia
• Hoarse voice
• Failure to thrive
• Recurrent otitis media/ Sinusitis

99. Clinical manifestations
 GER can have both esophageal and extraesophageal
manifestations.
 The esophageal manifestations are those caused
directly by contact between refluxed gastric juice and
the esophageal mucosa.
 The extra-esophageal manifestations are caused by
contact between refluxed gastric juice and
extraesophageal organs or by reflexes triggered by
acid in the esophagus that affects other organs.

100. Extraesophageal complications
 Cardiac: Atypical chest pain, ischemia
 Vocal cords: Laryngitis, granuloma, polyps, ulcers,
neoplasm
 Respiratory: asthma, recurrent bronchitis, aspiration
or chronic interstitial pneumonia, sleep apnea,
chronic or recurrent cough
 Pharyngeal: pharyngitis, hoarseness
 Oral: Erosions, burning mouth syndrome
 Other: sudden infant death syndrome, otitis media

101. Investigations
1. Barium upper gastrointestinal series
2. 24-hour esophageal pH probe monitoring
3. Esophageal impedance monitoring
4. Endoscopy

102. Relation to respiratory symptoms
 GER has been associated with significant respiratory
symptoms in infants and children.
 The infant’s proximal airway and esophagus are lined
with receptors that are activated by water, acid or
distention.
 Activation of these receptors can increase airway
resistance, leading to development of reactive airway
disease.

103. Relation to respiratory symptoms
 One postulated mechanism for gastroesophageal reflux-
mediated airway disease involves micro-aspiration of
gastric contents that leads to inflammation and
bronchospasm.
 However, experimental evidence also supports the
involvement of esophageal acid-induced reflex
bronchospasm in the absence of frank aspiration.
 Therapy using histamine 2 blockers or proton pump
inhibitors has been shown to benefits patients with
steroid-dependent asthma, nocturnal cough and reflux
symptoms.

104. Asthma and GER
 In 1892, Sir William Osler first postulated a
relationship between asthma and gastroesophageal
reflux, manifested by a bi-directional cause-and-effect
presentation.
 Prevalence of GER is more common in asthmatics
compared to control populations ranging from 47 to
75%.
 Severe studies suggest that severe nocturnal asthma
is more likely to be associated with GER than daytime
asthma.

106. Asthma and GER
 Not all asthmatics with GER will have esophageal
symptoms.
 The mechanism of esophageal acid induced
bronchoconstriction includes a vagally mediated
esophageal bronchial reflex, airway hyper
responsiveness and microaspiration.

109. Asthma and GER
 It has been suggested that a vagally mediated reflex exists
whereby acid reflux into the lower esophagus initiates
bronchoconstriction via a shared autonomic innervation
between esophagus and bronchi based on their common
embryonic origin.
 Support is based on this two lines of evidence:
• Acid infusion of the esophagus in asthmatic children results
in increased airway resistance, which can be reversed with
antacids.
• Infusion of antacids into the distal esophagus of asthmatic
children during sleep induces bronchoconstriction,
suggesting presence of a protective mechanism.

110. Asthma and GER
 Esophageal acidification has also been associated with
heightened non-specific hyperresponsivity of the airways to
bronchoconstrictors contributed by increased vagal
tone, “priming” the airways to other triggers.

111. Asthma and GER
 Asthmatics have significant decreased lower esophageal sphincter
pressures, greater esophageal acid exposure times, more frequent
episodes of GER and longer esophageal acid clearance times.
 There may be increase in transient lower esophageal sphincter
(LES) relaxations, LES hypotonia and esophageal due to autonomic
dysfunction in asthmatics patient.
 Furthermore, LES pressure augmented by diaphragm normally
prevents GER but it can be prevented by hyperinflation and hiatal
hernia.
 LES pressure can also be overcome by increased negative
intrathoracic pressures (bronchospasm, cough, upper airway
resistance syndrome and obstructive apnea).

112. Asthma and GER
 Anti-reflux therapy results in improvement in asthma in
approximately 70% of patients.
 Acid-suppression medication such as histamine 2 receptor
antagonists (ranitidine) or proton pump inhibitors (omeprazole)
are helpful in reducing volume of gastric contents.
(Therapeutic trial)

115. Chronic cough and GER
 GER can potentially stimulate sensory limb of cough
reflex in multiple ways.
 It can irritate upper respiratory tract without aspiration
(such as larynx) and the lower respiratory tract by
either macro-microaspiration.
 It can also cause cough by stimulating an esophagus
bronchial cough reflex whereby refluxate into distal
esophagus alone is a sufficient stimulus.

116. Chronic cough and GER
 GER related cough occurs predominantly during the
day and in the upright position whereby some
patients may have nocturnal symptoms.
 Cough may be the sole manifestation of GER and is
often long standing.
 Diagnosis can be made with certainty only when
cough are resolved with specific anti-reflux therapy.

117. Senario 3
 Samy, a 2 days old premature infant who was
born at 30 weeks gestational age was noted
to be cyanosed by a nurse. There was
absence of chest movement.
 What is Samy’s clinical condition?
 Respiratory distress syndrome (RDS)
 What is your immediate action?
 surfactant replacement therapy
 IV glucocorticoid administration
 What is the mechanism of his respiratory
failure?
 Immature lung  lack surfactant  atelectasis

118. Senario 5
 Aminah a 2 year old toddler has been having
mild cough and rhinorrhea for the past 2
days. It was associated with low grade fever.
Suddenly her mother noticed that she breath
noisily with fast breathing.
 What is Aminah’s clinical condition?
 Common cold
 What are the relevant physical finding that
you would like to look for?
 Signs of respiratory distress
 Outline the principle management.
 Symptomatic therapy