ards

1. ARDS
DR. PANKAJ KATARIYA
PDCC Senior resident,CCU,
Trauma Centre KGMU,Lucknow(UP)

2. ARDS OBJECTIVES
Updated Definition /Diagnostic Criterion Of ARDS
Etiology/Risk Factors
Briefly Review Pathophysiology And Pathogenesis
Ventilatory Management
Non Ventilatory Management
Management For Refractory Hypoxemia.

3. • Definitions of acute lung injury (ALI) and
acute respiratory distress syndrome (ARDS)
have varied over time
• ARDS was first described by Ashbaugh and
Petty in 1967 in a case series of 12 ICU
patients who shared the common features of
unusually persistent tachypnea and hypoxemia
accompanied by opacification on chest
radiographs and poor lung compliance,
despite different underlying causes
• For more than 20 years, there was no common
definition of ARDS.

4. AECC1994 BERLIN 2012

5. • Note that the Berlin definition requires a minimum positive
end expiratory pressure (PEEP)of 5 cmH2O for consideration
of the PaO2/FiO2 ratio. This degree of PEEP may be delivered
noninvasively with CPAP to diagnose mild ARDS.

6. MEDICAL IMAGING
Original definitions of ARDS specified that
correlative chest X-ray findings were required for
diagnosis, the diagnostic criteria have been expanded
over time to accept CT and ultrasound findings as
equally contributory. Generally, radiographic findings
of fluid accumulation (pulmonary edema) affecting
both lungs and unrelated to increased cardiopulmonary
vascular pressure (such as in heart failure) may be
suggestive of ARDS.

7. Ultrasound findings suggestive of ARDS include the
following:
• Anterior subpleural consolidations
• Absence or reduction of lung sliding
• “Spared areas” of normal parenchyma
• Pleural line abnormalities (irregular thickened fragmented
pleural line)
• Nonhomogeneous distribution of B-lines (a characteristic
ultrasound finding suggestive of fluid accumulation in the
lungs)

10. BAL in ARDS diagnosis
• In normal subjects, neutrophils make less than 5% of
cells recovered in lung lavage fluid, in ARDS as many as
80% of the recovered cells are neutrophils.
• Inflammatory exudates are rich in proteinaceous
material, lung lavage fluid that is rich in protein is used
as evidence of ARDS.
• Lavage fluid protein/ plasma protein < 0.5( hydrostatic
edema)
• Lavage fluid protein/plasma protein >0.7 (ARDS)

12. PATHOPHYSIOLOGY
The natural history of ARDS is marked by three phases
• exudative
• Proliferative
• fibrotic

13. EXUDATIVE PHASE
• In this phase alveolar capillary endothelial cells and
type 1 pneumocytes (alveolar epithelial cells) are
injured with consequent loss of the normally tight
alveolar barrier to tluid and macromolecules. Edema
tluid that is rich in protein accumulates in the
interstitial and alveolar spaces.
• The exudative phase encompasses the first 7 days of
illness after exposure to a precipitating ARDS risk
factor, with the patient experiencing the onset of
respiratory symptoms.

15. PROLIFERATIVE PHASE
• This phase of ARDS usually lasts from day 7-day 21.
• Most patients recover rapidly and are liberated from
mechanical ventilation during this phase.
• Histologically, the first signs of resolution are often evident in
this phase, with the initiation of lung repair, the organization of
alveolar exudates, and a shift from a neutrophil- to a
lymphocyte-predominant pulmonary infiltratrate.
• As part of the reparative process, typeII pneumocytes
proliferate along alveolar basement membranes. These
specialized epithelial cells synthesize new pulmonary
surfactant and differentiate into typeI pneumocytes.

16. FIBROTIC PHASE
• 3-4 weeks after the initial pulmonary injury, some enter a
fibrotic phase that may require long-term support on
mechanical ventilators and/or supplemental oxygen.
• Histologically,the alveolar edema and inflammatory exudates
of earlier phases are now converted to extensive alveolar-duct
and interstitial fibrosis. Marked disruption of acinar
architecture leads to emphysema-like changes, with large
bullae. Intimal fibroproliferation in the pulmonary
microcirculation causes progressive vascular occlusion and
pulmonary hypertension.

17. MANAGEMENT
• There is no definitve therapy for ARDS treatment, only
supportive therapy.
• Identify the precipitating factors and managed
accordingly.
• Ventilatory management( lung protective ventilation)
• Non ventilatory management ( fluid management,
corticosteroid therapy, general icu care)

19. Benefits over conventional ventilation
• Protection against VILI( ventilator induced lung injury),
atelectrauma, biotrauma.

21. CORTICOSTEROID IN ARDS
• Meduri 2007 methylprednisolone protocol(early ARDS)
doses given as iv infusions once daily. Once able to take
PO, doses were given as single oral doses. Protocol:
1mg/kg LD then 1mg/kg/day(0-14),then
0.5mg/kg/day(15-21),then 0.25mg/kg/day(22-25),then
0.125mg/kg/day(26-28)
• MPS was associated with fewer days of mechanical
ventilation, reduction in icu stay and greater icu survival

22. • Meduri 1998 MPS protocol (un resolving ARDS not
improving after 7 days)
• doses given as iv infusions and divided into Q6h.once
able to take PO doses given as single oral doses.
Protocol 2mg/kg LD, then 2mg/kg/day(0-14), then
1mg/kg/day(15-21),then 0.5mg/kg/day(22-28), then
0.25mg/kg/day(29-30), then 0.125mg/kg/day(31-32)
• MPS improved icu mortality (0% vs 63%), improvement
in lung injury score after 10 days.

23. REFRACTORY HYPOXEMIA
• Prone ventilation( proseva 2013: early and severe within 36 hrs of
ARDS, P/F ratio <150 mmhg) 28 days mortality was significantly
lower with prone positioning(16% vs 32.8%), 90 days mortality was
also reduced with proning (23.6% vs 41%).
• On avg prone patient received 4+/- prone sessions lasting for 17+/-
3 hrs, these patients were proned for 73% of time spent on a
ventilator.
• HFOV ( oscar 2013 and oscillate2013) no benefit in mortality ,
require likely more vasopressor therapy and neuromuscular
blockers.
• IRV ( Inverse Ratio Ventilaton)
• APRV ( airway pressure release ventilation )
• ECMO ( extra corporeal membrane oxygenation)
• Inhaled nitric oxide