toic pediatric acute respiratory distress syndrome

1. PEDIATRIC- ACUTE
RESPIRATORY DISTRESS
SYNDROME
Presented By:
Dr. Afaq Ahmad Khan
PG 1(DcH)

2.  Acute respiratory distress
syndrome(ARDS) is a non
cardiogenic pulmonary
edema with arterial
hypoxemia refractory to
oxygen therapy, due to
intrapulmonary shunt.
 Pediatric ARDS is a
complex inflammatory
disorder of the lungs
characterized by
hypoxemia and respiratory
failure.

3. OXYGENATION INDEX:[(FiO2 * mean airway pressure* 100)/PaO2]
OXYGEN SATURATION INDEX: [(FiO2 *mean airway pressure * 100/ SpO2}

5. CLINICAL
FEATURES
 Characterized by an acute severe progressive hypoxemia
after an inciting event or clinical condition
 There is dyspnea and increased work of breathing due to
poor compliance and increased dead space
 The auscultation could reveal diminished breath sounds and
crackles, although these are not necessarily present.
 The chest radiographs often will reveal bilateral patchy
radio densities/infiltrates
 The CT scan reveals patchy distribution of the disease with
areas of atelectasis and other areas of relatively preserved
lungs

8. PATHOGENESIS AND
PATHOPHYSIOLOGY
During the early phases of ARDS, there is intense inflammatory
response that leads to endothelial injury and increased
permeability of the alveolar-capillary interface
↓
Exudation of protein-rich edema fluid in the alveolar air space
↓
Presence of fluid in the air space leads to activation of cytokines
and other proinflammatory mediators, neutrophil and
macrophage activation causing further inflammatory response
↓
Due to the alveolar air space fluid exudation and increased lung
water, the pulmonary compliance is significantly reduced and it
leads to poor gas exchange, mismatch between ventilation-
perfusion ratio (V/Q) and hypoxemia.
Accompanying
alveolar epithelial
injury
↓
Dysfunction and loss
of type I cells as well
as the cuboid type II
alveolar epithelial
cells.
↓
Alveolar epithelial
disruption, alveolar
flooding, loss of gas
exchange capability,
loss of surfactant,
potential for secondary
bacterial infection and
ultimately fibrosis

9.  There are many areas of the lung that have nonexistent gas exchange leading to
significant intrapulmonary shunt and severe pulmonary venous desaturation
 The desaturated pulmonary venous admixture leads to severe arterial hypoxemia, a
hallmark of ARDS.
 The lung is not uniformly affected, and has areas of relatively preserved alveolar units
interspersed with severely atelectatic lung segments
 Along with the severe arterial hypoxemia, hypercapnea is often present in ARDS due
to decreased effective area for alveolar ventilation secondary to the alveolar injury
and increased physiological dead space.
 Secondary pulmonary hypertension is often seen in cases of ARDS. This is a result of
parenchymal destruction, microvascular thrombosis, vascular spasm and compression
and hypoxic pulmonary vasoconstriction.
 The initial exudative phase of ARDS is often followed by a proliferative phase when
new type II alveolar cells proliferate, along with fibroblasts, myofibroblasts and new
matrix is deposited as there is a slow resolution of the pulmonary edema.
 This proliferative phase can start as early as 72 hours after the onset of ARDS and can
last for 7–10 days. This phase could resolve and lead to reconstitution and repair or
sometimes it could lead to progressive fibrosis phase that often leads to progressive
hypoxemia, increased dead space and hypercapnea, and inability to wean from
respirator and can lead to mortality

11. RESPIRATORY SUPPORT
 Respiratory support in ARDS ranges from NIV to
invasive ventilation. However it is complicated by
ventilator induced lung injury resulting from alveolar
over distension(volutrauma) due to low lung compliance
and high ventilatory pressures combined with repeated
alveolar collapse or reexpansion and oxygen toxicity.
 The goal of ventilating children with ARDS is to maintain
adequate gas exchange with minimal ventilator induced
lung injury
 NIV such as BiPAP in patients with ARDS reduces the
intrapulmonary shunt and decreases the work of
breathing. Because of the high risk of failure ,NIV should
be reserved for mild ARDS who are hemodynamically
stable.

12. VENTILATORY SUPPORT
 ENDOTRACHEAL
INTUBATION: cuffed ET tube
are recommended with cuff
pressure <20 cm h2o
 OXYGENATION: strategy of
permissive hypoxemia is
followed to minimize the adverse
effect of high ventilatory support
 mild PARDS with
PEEP<10mmof Hg target SpO2
92-97%
 PARDS with PEEP>10mm of Hg
target SpO2 88-92%
 When SpO2 <92% monitoring of
central venous saturation and
marker of oxygen delivery is
recommended.
 Target PaO2 55-80 mm
Hg(SpO2 target 88%-95%)
 High FiO2 should be avoided to
minimize the risk of direct cellular
toxicity.

13.  VENTILATION: permissive
hypercapnia maintaining a pH of
atleast 7.15-7.30.
 Pressure regulated ventilation: peak
pressure is used
 Volume controlled ventilator mode :
plateau pressure is used
 CO2 MONITORING: end tidal CO2
monitoring is recommended
inpatients on invasive ventilation as
it provides dead space to tidal
volume ratio, end tidal alveolar
dead space fraction and ventilation
index. These indices are useful
markers of severity of lung injury ,
recruitment vs over distension.
Proportion of delivered tidal
volume not participating gas
exchange constitutes VD/VT

14.  TIDAL VOLOUME: Physiological tidal volume :6-8
ml/kg of predicted body weight. Patients with lung
injury should receive tidal volume below
physiological values:3-6 ml/kg.
 PEEP: PEEP improves oxygenation by recruitment
of small airways and collapsed alveoli and an
increase in functional residual capacity. In severe
PARDS , PEEP level are usually >10 cm H2O
which is titrated to achieve adequate oxygenation
and hemodynamic response.
 INSPIRATORY PRESSURE: 28 cm of water.
 DRIVING PRESSURE: respiratory system
compliance depends upon the functional lung size
available for ventilation

16. COMPLICATIONS
 Can be related to the underlying clinical disorder that led to
ARDS or due to the progressive hypoxemia and impaired
lung mechanics.
 Very high incidence of MOSF associated with ARDS. Acute
kidney injury and renal failure are common in children with
ARDS.
 There could be ventilator-induced lung injury secondary to
high settings of the ventilator required
 Secondary infections are often a risk due to presence of
endotracheal tube, invasive vascular lines and urinary
catheter.
 Prolonged mechanical ventilation, need for tracheostomy
and chronic ventilation, muscular weakness due to disuse,
critical illness myopathy or malnutrition.

17. THANK
YOU