13-10 Topic 5. ALRI

03/10/2013
ARI management training
TOPIC 5.
ALRI
1
03/10/2013
Contents
Acute lower respiratory infection
• Burden, the forgotten killer
• Pathogenesis & pathophysiology
• Diagnosis & treatment
• Community aqcuired pneumonia
• Hospital aqcuired pneumonia
• Bronchiolitis
• Primary care setting & prevention
Burden, the forgotten killer
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Pneumonia
is the no 1
killer of
children
Pneumonia, the leading killer
Unicef - WHO, Pneumonia the forgotten killer, 2006
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Magnitude of the problem in Indonesia

Pneumonia in children (<5 yr)
• Morbidity rate 10-20%
• Mortality rate 6/1000
• Pneumonia kills
– 50.000 children/year
– 12.500 children/month
– 416 children/day = passengers of 1 jumbo
jet plane !!!
Causes of death: infants

( 29 days-11 months)
Basic Health Research 2007 (Riskesdas)
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Causes of death: under-5 (1-4 years)
Basic Health Research 2007 (Riskesdas)
Garuda Indonesia
crash
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Pneumonia, the forgotten killer

• One among the major cause of mortality
• Pneumonia kills more children than any
other illness – more than AIDS, malaria &
measles combined
• Yet, no adequate concern
Pneumonia
the forgotten killer

of children
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Pathogenesis & pathophysiology
Acute upper
1 resp infection
2 Bacteremia
3 Adjacent org
Pneumonia pathogenesis
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External respiration - 3
to take place, gas exchange
ventilation (diffusion) from air to blood in
V alveolar capillary bed need an
optimal ratio between
VENTILATION & PERFUSION
V/Q = 4/5  VQ matching
perfusion Q V
Q Q V
Dyspnea pathophysiology
Clinically
V/Q = 4/5 DYSPNEA
CRUCIAL Resp system try to cope

POINT!
by increasing resp effort
V/Q mis-match,
V/Q ≠ 4/5
NOT optimal diffusion
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Dyspnea, two types

V - a VOLUME of air
FLOW VOLUME
FLOW in and out L/mnt
disturbance disturbance
the respiratory tract
Diffusion of O2 & CO2 between

DYSPNEA with DYSPNEA
alveoli & the blood  crucial with
point
EXPIRATORY INSPIRATORY
effort effort
Q - a VOLUME of blood
FLOW through L/mnt
e.g. Bronchiolitis, e.g. Pneumonia,
alveolar capillary
Asthma Pleural effusion
Sherwood L, The
Respiratory System, 2004
Diagnosis & treatment
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Spectrum of ARI  ‘ISPA’

AURI ALRI
Common
Bronchitis
cold
Rhino-
Bronchiolitis
sinusitis
Tonsilo-
Pneumonia
pharyngitis
Croup = laryngo-tracheo-bronchitis
Pneumonia
Inflammation of the lung parenchyme
parenchyme: alveoli & interstitial tisue
Infection, aspiration, radiation, ...
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Infection: Invasion & multiplication of microorganisms

such as bacteria, viruses, and parasites that are not
normally present within the body.
Infection: Invasion by & multiplication of pathogenic

microorganisms in a bodily part or tissue, which may
produce subsequent tissue injury and progress to overt
disease through a variety of cellular or toxic
mechanisms.
The Free Dictionary by Farlex
Symptomatology
Respiratory
Infection
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Pneumonia, symptomatology
symptom
• Preceeded by AURI: fever, rhinorrhea, & cough
• Fever: viral < bacterial - generally
pathophys • Tachypnea – most consistent
• Dyspnea -  Work of Breathing (WoB) -accessory
resp muscle: nasal flaring, retraction of
pathology
suprasternal, intercostal, arcus costal
(epigastrium)  chest indrawing
adaptive • Grunting - infants
response
• Head nodding – younger children
• Chest pain – older children
• Cyanosis
Insult
Pneumonia, pathophysiology
symptom Cough
 cough insults
pathophys  cough receptors – baro, chemo
 cough reflex
 cough mechanism
pathology
Dyspnea
adaptive
 respiratory physiology
response  ventilation – diffusion – perfussion
 ventilation perfusion missmatch
 Hypoxemia - hypoxia
  Work of Breathing
Insult
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Acute lower respiratory infection
Pneumonia  volume  V
 V/Q mismatch  diffusion
hypoxemia  hypoxia
 compensation  WoB
Dyspnea pathophysiology
Nasal flaring
symptom
pathophys
pathology
adaptive
response
Insult
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Chest indrawing  retraction

symptom
pathophys
pathology
adaptive
response
Insult
Pneumonia, pathology
symptom
Insulst  adaptive response (esp. immune
response)  inflammation, pathology
pathophys  Red Hepatization stage
alveoli consist of : leucocyte,
fibrine,erythrocyte, bacteria
pathology
 Grey Hepatization stage
adaptive fibrine deposition, phagocytosis
response  Resolution stage
neutrophil degeneration, loose of fibrine,
bacterial phagocytosis
Insult
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Pneumonia, pathology
www.medicsindex.ning.com
Normal CXR
symptom
pathophys
pathology
adaptive
response
Insult
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Pneumonia, pathology imaging

symptom
pathophys
pathology
adaptive
response
Insult
Pneumonia, adaptive response

symptom
pathophys
pathology
• Leucocytosis
adaptive • Neutrophyl domination
response • CRP – C-reactive protein – inflammation
• Procalcitonin – bacterial
Insult
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Pneumonia, etiology
symptom
 Virus
 Bacteria
pathophys  Fungi
 Atypical pathogen
pathology
Depends on age
adaptive
response
Insult
CAP pathogen accoding to age

Neonates 1-2 months 3-12 months 1-5 years >5 years
Streptococcus Chlamydia Viruses Viruses S pneumoniae
group B trachomatis
Enteric gram Ureaplasma Streptococcus S pneumoniae M pneumoniae
negative urealyticum pneumoniae
Viruses H influenzae Mycoplasma C pneumoniae
pneumoniae
Bordetella Staphylococcu Chlamydia
pertussis s aureus pneumoniae
Moraxella
catharrhalis
Disorders of resp tract in children, Kendig’s, 2012
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Pneumonia, DIAGNOSIS
symptom
Combination of all aspects
• Clinical course
pathophys • Symptomatology
• Pathophysiology: hypoxemia – BGA, pulse
oxymetry
pathology
• Pathology – imaging
• Adaptive response – blood, inflammation marker
adaptive
response • Insults – definitive, but dificult, specimen
availability. Blood culture – not a representative
specimen
Insult
Oxygen saturation
• Blood gas analysis
• Pulse oxymetry
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Classification
• Source of infection
o Community acquired pneumonia (CAP)
o Hospital acquired pneumonia (HAP)
o Ventilator associated pneumonia (VAP)
• Diagnosis
o Clinical -- mostly
o Radiological -- supporting
o Etiology – difficult, specimen
• Severity – WHO classification
Community aqcuired pneumonia
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Pneumonia, TREATMENT
Severe Pneumonia
• Hospitalization
• Antibiotic administration
o Pennicilline, Chloramphenicol
o Amoxycillin + Clavulanic Acid
o Cephalosporine
• Intra Venous Fluid Drip
• Oxygen
• Detection & management of complications
Indication for hospitalization

Should be considered for
• Infants <6 months, unless a viral etiology or Chlamydia trachomatis is

suspected and they are relatively asymptomatic
• A child of any age whose family cannot provide appropriate care and
assure compliance with the therapeutic plan
Additional indications
• Hypoxemia (O2 sat <92%)

• Dehydration, or inability to maintain hydration orally
• Moderate to severe respiratory distress
• Toxic appearance
• Underlying conditions: CVS dis, metabolic dis, immunocompromised
• Presence of complications (effusion, empyema, ... )
• Failure of outpatient therapy (worsening - no response in 24-72 hrs)
Renato T. Community acquired pneumonia.
Kendig’s disorders of the respiratory tract in children. Philadelphia. 2006.
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Antibiotic consideration
• Bacterial pneumonia should be considered in
children when tere is persistent or repetitive
fever >38.5o C with dyspnea & tachypnea
• All children with a clear clinical diagnosis of

pneumonia should receive antibiotics as
bacterial and viral pneumonia cannot reliably
be distinguished from each other
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Pneumonia, complications
• Direct, thoracic cavity
o Pleural effusion
o Pneumothorax
o Empyema
o Pericarditis
• Bacteremia & hematologic spread
o Meningitis
o Suppuratie arthritis
o Osteomyelitis Nelson textbook, 19th, 2011
Hospital aqcuired pneumonia
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Lack of HAP guideline

• HAP problem is usually faced in large / referral hospital
• Only few guideline about HAP, mostly for adults
• HAP guideline for children - almost none!
• 2 fundamental problems with assessing the literature

relating to HAP.
• The first is that most publications deal with VAP, whereas
most HAP occurs in non-ventilated and nonintubated
patients
• The second problem is that there are no universally
accepted ‘gold’ or reference standard diagnostic criteria for
HAP or VAP
Journal of Antimicrobial Chemotherapy (2008) 62, 5–34
Definition & epidemiology

• Hospital-Acquired Pneumonia (HAP) or Nosocomial
Pneumonia (NP) is defined as pneumonia developing 48 h
after hosp admission that was not incubating at the time of
admission
• HAP affects 0.5% to 1.0% of inpatients and is the most
common HealthCare-Associated Infection (HCAI)
contributing to death
• It is increase hospital stay by 7–9 days
• HAP is associated with mechanical ventilation, in which
case it is termed Ventilator-Associated Pneumonia (VAP)
• In patients with VAP, there is a 24% to 50% mortality rate,
which increases to 76% if infection is caused by multidrug-
resistant pathogens
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HAP classification
HAP can be divided into early- and late-onset
• Early-onset occurs within 4–5 days of admission and
tends to be caused by antibiotic-susceptible
community-type pathogens,
• Late-onset infections tend to be caused by antibiotic-
resistant hospital opportunists
• Increasing frequency of early-onset HAP caused by
pathogens more commonly associated with
nosocomial disease
HAP clinical diagnostic - 1

• difficult, no universally accepted clinical criteria
• overlap of clinical signs & symptoms between pneumonia
and other forms of sepsis, and the diagnosis of HAP often
cannot be made on clinical criteria alone
• with these reservations, the clinical diagnosis of HAP can
be based on:
o the presence of fever (38.3°C),
o increase O2 requirement
o leucocytosis (10 000/uL) or leucopenia (4000/uL),
o purulent tracheal secretions and
o the presence of a new and/or persistent infiltrate on CXR, which
is otherwise unexplained
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HAP clinical diagnostic - 2

• An European consensus group believed that a
diagnosis of pneumonia could be based on
pulmonary infiltrates plus 2 of the other criteria
• in some patients, increasing severity of pneumonia
may be associated with increasing evidence of
circulatory collapse (shock, tachycardia,
hypotension and elevated blood urea
concentrations)
• considerable variation in the clinical presentation of
HAP and that distinction from other forms of sepsis
is difficult.
HAP radiological diagnostic

• when a diagnosis of HAP is being considered, a
good quality CXR should be obtained and
compared with previous CXRs if available.
• CT scanning may assist in the differential

diagnosis of HAP and may guide management
in patients who are not responding to
treatment and who have a complex CXR.
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HAP microbiological diagnostic

• the assessment of the causal pathogens of HAP and
their therapy should be guided by local surveillance
data and results of microbiological investigations in
the individual patient
• not all organisms isolated from respiratory

specimens should be regarded as pathogens that
necessarily require therapy; they should be
interpreted and treated in the light of the full
clinical picture, if necessary after consultation
between microbiologists and clinicians
HAP microbiological diagnostic
• when probable (universally accepted)

pathogens such as pneumococci are isolated
from respiratory specimens in patients with
suspected HAP, they should be treated
• the significance of blood isolates should be

reviewed in the light of the patient’s clinical
condition during consultations between
clinicians and microbiologists
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HAP treatment - 1
• the use of systemic AB alone or in conjunction with
topically applied non-absorbable antibiotics as part of a
selective decontamination of the digestive tract (SDD)
regimen has been investigated for the prevention of HAP,
particularly VAP
• the Cochrane review reported that a combination of
topical and systemic prophylactic antibiotics reduces
respiratory tract infections & overall mortality in adult
patients receiving intensive care
• SDD regimens should include topical and parenteral
agents with activity against Gram-negative bacilli and
that the choice of treatment should depend on local
pathogen antimicrobial susceptibility profiles
HAP treatment - 2
• the choice of empirical antibiotic therapy should be
based on:
o the knowledge of the nature & susceptibility patterns
of the pathogens that are prevalent on that unit,
o early- or late-onset infection),
o recent administration of antibiotic therapy and
o co-morbidities
• Similarly, definitive therapy should be determined
by culture and susceptibility test results.
Recommendation Grade A
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HAP treatment - 3
• For patients with early-onset infections who have
not previously received antibiotics and in the
absence of other risk factors, the use of co-
amoxiclav or cefuroxime would be appropriate
• For patients with early-onset infections who have

recently received antibiotics and/or who have other
risk factors, a third-generation cephalosporin
(cefotaxime or ceftriaxone), a fluoroquinolone or
piperacillin/tazobactam would be appropriate.
HAP treatment - 4
• where patients respond to therapy, the routine
duration of empirical therapy should be no longer
than 8 days. Recommendation Grade C
• in order to reduce mortality and morbidity in
patients with VAP, treatment with an appropriate
antibiotic should be started as soon as possible.
Recommendation Grade C
• there is no proven optimal antibiotic regimen for
patients with HAP suspected or proven to be caused
by P. aeruginosa. Treatment options include
ceftazidime, ciprofloxacin, meropenem and
piperacillin/tazobactam
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HAP treatment - 5
• wherever possible, antimicrobial monotherapy is used
for the management of bacterial HAP.
Recommendation Grade A
• no firm conclusion can be reached on the use of

linezolid or a glycopeptide as optimal treatment of
patients with HAP or VAP caused by MRSA
• there is no established evidence upon which to base
the conversion of intravenous to oral treatment in the
management of HAP, these decisions must be taken on
a case by case basis according to the therapeutic clinical
response to treatment
HAP treatment - 6
• Chest physiotherapy cannot be recommended for
the direct management of patients with HAP due
to lack of evidence demonstrating improved
outcomes. Recommendation Grade B
• in the absence of clear evidence of its benefit, the
routine use of steroids in the management of
cases of HAP cannot be promoted
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Bronchiolitis
Background
• Bronchiolitis is an acute inflammatory injury of the
bronchioles that is usually caused by a viral infection.
• it may occur in persons of any age, severe symptoms
are usually only evident in young infants; the larger
airways of older children and adults better
accommodate mucosal edema.
• usually affects children <2 years, a peak in aged 3-6
months.
• Acute bronchiolitis is the most common cause of lower
respiratory tract infection in the first year of life.
• It is generally a self-limiting condition and is most
commonly associated with RSV
emedicine.medscape.com/article/961963
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Epidemiology
• Bronchiolitis is a significant cause of resp dis worldwide.
• WHO: 150 million new cases occur annually; 11-20
million (7-13%) of these cases are severe enough to
require hospital admission. Worldwide, 95% of all cases
occur in developing countries.
• The frequency of bronchiolitis in developed countries
appears to be similar to that in the United States.
• Epidemiologic data for underdeveloped countries are
incomplete.
• Morbidity and mortality may be higher in less-
developed countries because of poor nutrition and lack
of resources for supportive medical care.
Risk factors
• Low birth weight, particularly premature infants
• Lower socioeconomic group
• Crowded living conditions, daycare, or both
• Parental smoking
• Chronic lung disease, particularly BPD
• Severe congenital or acquired neurologic disease
• Congenital heart disease (CHD) with PH
• Congenital or acquired immune deficiency diseases
• Age less than 3 months
• Airway anomalies
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Symptomatology - 1
Because bronchiolitis primarily affects young infants,
clinical manifestations are initially subtle, such as
the following:
• fussy and have difficulty feeding during the 2 to 5-
day incubation period
• Low-grade fever (usually < 101.5°F); possible
hypothermia in infants younger than 1 month[4]
• Increasing coryza and congestion
• Apnea: May be the presenting symptom in early
disease
Symptomatology - 2
• Fever (38-39°C)
• Tachycardia
• Tachypnea
• Dyspnea due to flow disturbances
o Retractions, expiratory effort
o Diffuse, fine wheezing
• Cyanosis
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Pathophysiology
• Bronchioles are small airways (< 2 mm in diameter)
and lack cartilage and submucosal glands.
• Bronchiolar injury and the consequent interplay
between inflammatory and mesenchymal cells can
lead to diverse pathophysiologic condition:
o Increased mucus secretion
o Bronchial obstruction and constriction
o Alveolar cell death, mucus debris, viral invasion
o Air trapping
o Atelectasis
o Reduced ventilation that leads to V/Q mismatch
Pathology
• small bronchiole epithelium was circumferentially infected but
basal cells were spared. Both type 1 and type 2 alveolar
pneumocytes were also infected.
• airway obstruction was due to epithelial and inflammatory cell
debris mixed with fibrin, mucus, and edema fluid but not to
bronchial smooth muscle constriction
• neutrophil inflammation, but not eosinophil inflammation, is
related to the severity of a first infection in infants
• the inflammation, edema, and debris result in obstruction of
bronchioles, leading to hyperinflation, increased airway
resistance, atelectasis, and V/Q mismatching.
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Insults - etiology
• Most cases of bronchiolitis result from a viral
pathogen, such as RSV, parainfluenza virus,
influenza virus, or adenovirus.
• Bronchiolitis is highly contagious. The virus that
causes it is spread from person to person through
direct contact with nasal secretions, airborne
droplets, and fomites.
• RSV is the most commonly isolated agent in 75%
of children younger than 2 years who are
hospitalized for bronchiolitis.
Diagnosis
• The history and the physical examination form the
primary basis for the diagnosis
• Over a period of 2-5 days, RSV infection progresses
from the upper to the lower respiratory tract, and
this progression leads to the development of cough,
dyspnea, wheezing, and feeding difficulties.
• When the patient is brought to medical attention,
the fever has usually resolved.
• Infants younger than 1 month may present as
hypothermic
• Hypoxia is the best predictor of severe illness and
correlates best with the degree of tachypnea
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Treatment - 1
• Because no definitive treatment for the
specific virus exists, therapy is directed toward
symptomatic relief and maintenance of
hydration and oxygenation.
• Medical therapies used to treat bronchiolitis
in infants and young children are controversial
• Although numerous medications and
interventions have been used to treat
bronchiolitis, at present, only oxygen
appreciably improves the condition of young
children with bronchiolitis
Treatment - 2
• Bronchodilator therapy to relax bronchial smooth
muscle, is not supported as routine practice by
convincing evidence. If bronchodilator therapy is
started, it may be continued in patients who
demonstrate clinical improvement.
• Corticosteroids have not proved beneficial in improving
the clinical status of patients with bronchiolitis
• Beta-agonists and ipratropium bromide, an aerosolized
anticholinergic agent, have not shown effectiveness in
the management of infants with respiratory syncytial
virus (RSV) and wheezing
• Essential update: On-demand inhaled adrenaline
superior to fixed-schedule inhaled adrenaline
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Primary care setting &

prevention
Primary care setting

• Limited
o Knowledge
o Human resources
o Facilities
o Fund
• Should be
o Simple
o Affordable
o Mass oriented
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03/10/2013
Strategy, advocation
Pneumonia, DIAGNOSIS
symptom Highest standard Practical approach
Clinical setting of all aspects Field setting
Combination
• Clinical course
pathophys • Symptomatology
• Pathophysiology: hypoxemia – BGA, pulse
oxymetry
pathology
• Pathology – imaging
• Adaptive response – blood, inflammation marker
adaptive
response • Insults – definitive, but dificult, specimen
availability. Blood culture – not a representative
specimen
Insult
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03/10/2013
Simple clinical manifestation

• Fast breathing
Age respiratory rate
< 2 mo 60
2 - 12 mo 50
1 - 5 yr 40
• Chest indrawing
WHO pneumonia classification

Signs Classification
• Fast breathing Severe pneumonia
• Chest indrawing
• Stridor in calm child
• Fast breathing Non-severe pneumonia
• No fast breathing Other respiratory illness
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Treatment, primary care setting

• Prompt treatment of pneumonia with a full
course of appropriate antibiotics is lifesaving.
• UNICEF & WHO have published guidelines for
diagnosing and treating pneumonia in
community settings in the developing world
• This approach is proven, affordable and
relatively straightforward to implement
• Cotrimoxazole & amoxicillin are effective drugs
against bacterial pathogens and are often used to
treat children with pneumonia in developing
countries.
Risk factors
Low birth weight
Not breastfed Malnutrition
Incomplete Vit A deficiency

immunization
PNEUMONIA
Young age Cold weather
High prevalence
‘Kumis pa joko’ pathogen carrier
Exposure to indoor
& outdoor pollution
ETS, biomass fuel, vehicle &
industry pollution
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03/10/2013
Framework of pneumonia control
THANK YOU
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03/10/2013

ARI management training

Burden, the forgotten killer

Pneumonia, the leading killer

Unicef - WHO, Pneumonia the forgotten killer, 2006

Magnitude of the problem in Indonesia

Causes of death: infants

Basic Health Research 2007 (Riskesdas)

Causes of death: under-5 (1-4 years)

Basic Health Research 2007 (Riskesdas)

Pneumonia, the forgotten killer

the forgotten killer

Pathogenesis & pathophysiology

V/Q = 4/5  VQ matching

CRUCIAL Resp system try to cope

Dyspnea, two types

Diffusion of O2 & CO2 between

Diagnosis & treatment

Spectrum of ARI  ‘ISPA’

parenchyme: alveoli & interstitial tisue

Infection, aspiration, radiation, ...

Infection: Invasion & multiplication of microorganisms

Infection: Invasion by & multiplication of pathogenic

Acute lower respiratory infection

Chest indrawing  retraction

Pneumonia, pathology imaging

Pneumonia, adaptive response

CAP pathogen accoding to age

Disorders of resp tract in children, Kendig’s, 2012

Community aqcuired pneumonia

Indication for hospitalization

• Infants <6 months, unless a viral etiology or Chlamydia trachomatis is

• Hypoxemia (O2 sat <92%)

• All children with a clear clinical diagnosis of

Hospital aqcuired pneumonia

Lack of HAP guideline

• 2 fundamental problems with assessing the literature

Journal of Antimicrobial Chemotherapy (2008) 62, 5–34

Definition & epidemiology

Journal of Antimicrobial Chemotherapy (2008) 62, 5–34

HAP clinical diagnostic - 1

Journal of Antimicrobial Chemotherapy (2008) 62, 5–34

HAP clinical diagnostic - 2

HAP radiological diagnostic

• CT scanning may assist in the differential

Journal of Antimicrobial Chemotherapy (2008) 62, 5–34

HAP microbiological diagnostic

• not all organisms isolated from respiratory

Journal of Antimicrobial Chemotherapy (2008) 62, 5–34

HAP microbiological diagnostic

• when probable (universally accepted)

• the significance of blood isolates should be

Journal of Antimicrobial Chemotherapy (2008) 62, 5–34

Journal of Antimicrobial Chemotherapy (2008) 62, 5–34

• For patients with early-onset infections who have

Journal of Antimicrobial Chemotherapy (2008) 62, 5–34

Journal of Antimicrobial Chemotherapy (2008) 62, 5–34

• no firm conclusion can be reached on the use of