ARDS
ABDULLAH M. AL-OLAYAN
MBBS, SBP, ABP.
ASSISTANT PROFESSOR OF PEDIATRICS.
PEDIATRIC PULMONOLOGIST.
OUTLINES
 Definition AND Diagnosis.
 Pathophysiology.
 Pulmonary (Direct) Versus Non-pulmonary
(Indirect) ALI/ARDS.
 Differences Between Children and Adult.
 Treatment.
Definition AND Diagnosis
 (ARDS) is a diffuse, progressive inflammatory
lung disease.
Bilateral pulmonary infiltrate on CXR.
2. Pulmonary capillary wedge pressure of 18 mmHg
(for pediatric purpose excluding heart failure due
to congenital heart disease or cardiomyopathy).
3. PaO2 / FIO2 ratio , >200 or >300 for ARDS and
ALI respectively.
1.
Pathophysiology
 ALI/ARDS arises as a consequence of an
inflammatory process at the alveolar-capillary
interface in the lung.
 The resultant endothelial and epithelial disruption
leads to increased alveolar-capillary permeability
and flooding of alveoli with protein rich edema fluid.
 Alveolar gas exchange is impaired and surfactant
function is disrupted.
Pathophysiology
 Acute Exudative Phase characterized by the
production of pulmonary edema, cytokine release,
and activated neutrophils.
 The acute exudative stage is associated with
increased intrapulmonary shunting, reduced
functional residual capacity (FRC), and a decrease in
lung and chest wall compliance.
Pathophysiology
 The acute exudative phase may resolve within hours
or days, and not all patients progress to the
subsequent fibroproliferative—early repair—phase.
 “Repair” may not result in disease resolution in all
patients but may presage the development of
fibrosing alveolitis.
Pathophysiology
 The recovery stage, occurs within 10 to 14 days,
with gradual improvement in lung compliance and
oxygenation.
 The mechanism of resolution of the acute
inflammatory process and fibrosis is not well
established.
Etiology
 Direct Injury :
 Common Causes :
 Pneumonia 28%.
 Aspiration 14%.
 Less Common Causes :
 Pulmonary contusion.
 Fat emboli.
 Near drowning.
 Inhalational injury.
Davis et al., J Peds1993;123:35
Etiology
 Indirect Injury :
 Common Causes :
 Sepsis 32%.
 Shock after severe trauma 5%.
 Less Common Causes :
 Cardiopulm. Bypass.
 Drug overdose.
 Acute pancreatitis.
 Massive blood transfusions.
Davis et al., J Peds1993;123:35
Pulmonary Versus Non-pulmonary
ALI/ARDS
 In 1994, the NAECC made a distinction between :
 (ARDSp) such as aspiration pneumonia.
 (ARDSexp) such as sepsis.
 Data provided by Flori and colleagues suggest that
ARDSp constitutes 60% of pediatric ARDS.
 The same authors also reported sepsis as the major
cause (13% to 21%) of ARDSexp in children.
Pulmonary Versus Non-pulmonary
ALI/ARDS
 Differences between ARDSp and ARDSexp may be
most apparent in the acute exudative phase of the
disease.
 These differences may impact the response to
treatment and outcome.
 Recent study in children reported that ARDSexp had
a greater mortality than ARDSp.
Pulmonary Versus Non-pulmonary
ALI/ARDS
 ARDSp is characterized by a primary injury to the
alveolar epithelium resulting in intra-alveolar
edema, and reduced lung compliance with
preservation of the chest wall compliance.
 In ARDSexp, the primary insult is systemic and the
major injury is to the capillary endothelium;here the
edema is predominantly interstitial, and the greater
reduction of compliance occurs in the chest wall.
Pulmonary Versus Non-pulmonary
ALI/ARDS
 Gross pathology of the lung in ARDSp suggests
predominant consolidation, and in ARDSexp the
striking finding is atelectasis.
Pulmonary Versus Non-pulmonary
ALI/ARDS
Epidemiology and Outcome
 The incidence of ALI in children is 3 to 5/100,000/Y.
 5 to 10 times less than that in adults.
 2% to 10% of all PICU admissions.
 80% of children with ALI will progress to ARDS and
2/3 require early mechanical ventilation.
 60% with ALI are less than 4 years of age and have
an underlying chronic disease.
Epidemiology and Outcome
 Mortality among children with ARDS decreased from
between 65%-80% in the 1980s, to less than 20% now.
 In clinical trials, the reported mortality among children
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with ALI ranges from :
7% to 20% (degree of hypoxemia)
Country (28% to 44% in developed countries, 61% in a
developing country).
Etiology (up to 40% to 60% in immunocompromised
children, minimal in bronchiolitis).
Comorbidities (e.g., nonpulmonary organ dysfunction,
CNS dysfunction).
Severity Score
 Blood gas analysis, specifically oxygenation, is
regarded as the standard for assessment of severity
of ARDS.
 (A − a) O2 difference can express the degree of
hypoxemia.
 (OI) = [(MAP × Fio2)×100]/PaO2.
Severity Score
 In contrast to oxygenation ,

VI [Paco2 × peak airway pressure × respiratory
rate]/1,000 has been employed to reflect the
difficulty involved in clearing CO2.
Severity Score
Genetic Modifiers of ALI/ARDS
 In 2002, Marshall and colleagues were the first
investigators to describe a preliminary association
between a gene variant and ALI mortality.
 This group described the increased incidence of a
high producer polymorphism of the ACE gene in
patients with ARDS.
 Pulmonary surfactant- associated protein B (SFTPB),
interleukin-6 (IL-6), and coagulation factor V (F5).
Differences Between Children and Adult
 The mechanical properties of the lungs of children
and infants are different from those of adults.
 Chest wall compliance is inversely related to age, and
with pressure preset ventilation, higher chest wall
compliance may increase delivered tidal volume and
thereby increase the risk for ventilator-associated
lung injury (VALI) in young children.
Differences Between Children and Adult
 The infant lung has low inherent elastic recoil, which
may protect against lung collapse, so lower PEEP
levels may be required to maintain lung recruitment.
 Finally, there are important outcome differences:
Mortality for children with ARDS is less than in
adults and high Fio2 is associated with worse
outcome in children but not in adults.
Treatment
 Conventional Mechanical Ventilation :
 28% of patients with ALI do not require mechanical
ventilation at the onset of the lung injury and almost all
children with ARDS require mechanical ventilation.
 The ventilation parameters associated with this
iatrogenic lung injury are high levels of end-inspiratory
airway pressure, large tidal volumes, low levels of endexpiratory airway pressure, and possibly high Fio2.
Treatment
 Conventional Mechanical Ventilation :
 lower VT, up to 10 mL/kg; lower inflation pressure
(<30 cm H2O); higher PEEP (~5 to 12 cm H2O); and
lower Fio2.
 If the achievement of normal pH, Paco2, and Pao2
levels require respiratory support strategies that may
injure the lungs, then lower pH, Pao2, and higher
Paco2 (permissive hypercapnia) are tolerated.
Treatment
 Conventional Mechanical Ventilation :
 Because the likelihood of lung injury is greater if the
airway pressure, VT, and concentration of inspired
oxygen are elevated, many clinicians will reduce the
target SaO2 (85% to 88%) if necessary.
 Permissive hypercapnia (Paco2 60 to 80 mm Hg)
with a pH > 7.2 .
Treatment
 Conventional Mechanical Ventilation :
 Few studies regarding mechanical ventilation have
been performed in children, and as a result, no
specific approaches have been proved superior to
others.
 Currently there are no data to support the
superiority of one mode of ventilation over another
(e.g., pressure control versus volume control).
Treatment
 Noninvasive Ventilation :
 A trial of NIPPV may be attempted in any child with
early respiratory failure; however, one should
not persist with its use if there is no clinical benefit
within 2 to 3 hours.
Treatment
 High Frequency Oscillatory Ventilation :
 HFOV achieves effective gas exchange while avoiding
high peak airway pressures and the inflationdeflation cycles.
 Lung volume is maintained by the application of a
high continuous mean airway pressure.
 CO2 removal is achieved despite small tidal volumes
(2 to 4 mL/kg) by imposing a breath frequency of
300 to 900 (5 to 15 Hz) per minute, resulting in large
minute volumes.
Treatment
 Airway Pressure Release Ventilation (APRV):
 APRV is a ventilator modality characterized by cyclical
alternation between two levels (high and low) of positive
airway pressure, while permitting spontaneous breathing
activity at both levels of pressure support.
 APRV, facilitates an open lung ventilatory approach,
avoids cyclical recruitment and derecruitment of alveolar
units, permits homogenous gas distribution during
inspiration, minimizes (volutrauma), and reduces the
risk of (atelectrauma).
Treatment
 Neurally Adjusted Ventilatory Assist (NAVA):
 The NAVA system utilizes the electrical activity of
diaphragmatic muscle to signal the initiation of
patient inspiratory effort.
 Although there are few reports of NAVA use in either
adults or children, it has been demonstrated that
NAVA prevents excessive lung distension, efficiently
unloads respiratory muscles, and improves but does
not abolish patient-ventilator dyssynchrony
Adjuvants to Mechanical Ventilation :
 Prone Positioning :
 Prone positioning is safe and has been reported to
produce a rapid and sustained improvement in
oxygenation in 90% of children with ALI/ARDS.
 NO reduction in days of ventilation or mortality.
 Prone positioning is best reserved for patients with
persistent refractory hypoxemia.
 If it is not improve oxygenation, it should be
discontinued.
Adjuvants to Mechanical Ventilation :
 Inhaled Nitric Oxide (iNO):
 It has been shown to result in short-term
improvements in oxygenation in some patients with
ARDS/ALI, but it has no substantial impact on
the duration of ventilator support or mortality when
used as a routine part of care.
 Inhaled NO is best reserved for patients with
refractory hypoxemia,with Fio2 > 0.6.
Adjuvants to Mechanical Ventilation :
 Surfactant:
 Despite several studies in adults and children with ALI/ARDS
the role of surfactant administration has not been
established.
 Walmrath and colleagues reported improvement in
oxygenation when a high dose of bovine surfactant was
administered to patients with ARDS and sepsis.
 In children, a relatively small randomized controlled trial
(RCT) reported a reduction in mortality following
administration of natural calf surfactant,however, no effect
on ventilator-free days or length of hospitalization
was reported.
Adjuvants to Mechanical Ventilation :
 Corticosteroids:
 The anti-inflammatory properties of corticosteroids
and the potential inhibition of both fibroblast
proliferation and collagen deposition make
corticosteroids an attractive option.
 High doses (≥30 mg/kg/day) of corticosteroids for a
short period of time (≤24 hours) either had no
impact on mortality or, in one case, increased
mortality.
Adjuvants to Mechanical Ventilation :
 Corticosteroids:
 A more recent study of early low-dose corticosteroids
(1 mg/kg/day) for 25 days demonstrated a treatment
benefit with improvements in lung injury score, days
of ventilation, and mortality.
 In summary, current evidence from clinical trials
does not support the use of corticosteroids in any
phase of ARDS in adults. In children, no data are
available.
Adjuvants to Mechanical Ventilation :
 Neuromuscular Blocking Agents:
 No data are available regarding the use of
neuromuscular blocking agents (NMBA) among
ventilated children.
 A recent RCT in adults has suggested that
continuous neuromuscular blockade (with
cisatracurium besylate) in the first 48 hours of
ventilation in ARDS significantly reduced mortality.
 Optimization of patient/ventilator synchronization.
Adjuvants to Mechanical Ventilation :
 Beta-Adrenergic Agonists:
 The alveolar edema in ALI/ARDS is mainly due to increased
permeability and increased capillary hydrostatic pressure.
 Alveolar fluid clearance is enhanced through upregulation of
Na+ transport in the alveolar epithelial cells. In addition,
pulmonary vasodilatation and resulting reduction of
pulmonary vascular pressure results in lowered capillary
hydrostatic pressures, and β agonism may independently
decrease endothelial permeability.
 An observational review of children with ARDS suggested that
inhaled bronchodilators were associated with a lower
mortality.
Adjuvants to Mechanical Ventilation :
 Tracheostomy:
 There is no literature describing the preemptive use
of tracheostomy in children in whom prolonged
ventilation is anticipated, nor is it frequently
employed in the pediatric population.
 A recently published study revealed that among
ventilated children in Canada, the prevalence of
tracheostomy was less than 1.5%.
Reference
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