1. ARDS
ד"ר אלחנן פריד MSMSICU

2. ARDS
First described in 1967 as Adult Respiratory Distress Syndrome
שכיח (~100/100,000 שנות אדם), יקר, הורג!
American-European Consensus Conference Committee (AECC 1994) criteria
Acute onset
Bilateral infiltrates in chest radiography
Pulmonary-artery wedge pressure<18 mmHg
Acute lung injury PaO2/FiO2<300
Acute respiratory distress syndrome PaO2/FiO2<200
הגדרה (ישנה...) :

5. Piantadosi, Annals Int Med 2004; 141:460-470

8. First Berlin definition

9. Second Berlin fefinition
הפרוגנוזה קשורה לקבוצה: MILD ~27%, MOD ~35%, SEVERE ~45%

13. ARDS: Causes

15. ARDS:Epidemiology Incidence: 80 per 100,000 Outcomes:
Traditionally 40-60% mortality
Majority of deaths due to MSOF
Low tidal volume ventilation decreases mortality
Other critical care improvements may be involved
Predictive factors for death: CLD, non pulmonary organ dysfunction, sepsis and advance age
Survivors: Most of them will have normal pulmonary function within a year

16. ARDS:Pathogenesis ARDS is the manifestation of SIRS in the lungs
Influx of protein rich edema into the air spaces due to increased permeability of the alveolar-capillary barrier
Endothelial damage pathophysiology is similar to that of SIRS/SEPSIS

17. ARDS:Pathogenesis Insult! Cytokines!!
PMN infiltration – predominate in BAL profile Pathology: Exudative Fibroproliferative Fibrotic
Type II Pneumocyte damage – decreased surfactant – atelectasis
Loss of compliance
Shunt, VQ mismatch, Diffusion abnormality: HYPOXEMIA

19. ARDS: Exudative Phase
The definition applies for the acute “exudative” phase
Rapid onset
Hypoxemia refractory to supplemental oxygen
CXR similar to pulmonary edema
CT Scan: Alveolar filling, consolidation and atelectasis in the dependent lung zones
Pathologic findings:
diffuse alveolar damage with capillary injury and disruption of the alveolar epithelium
hyaline membranes
protein rich fluid edema with neutrophils and macrophages

20. ARDS:Pathogenesis

21. ARDS: Exudative Phase
CT Scan During Acute Phase

22. ARDS: Fibroproliferative phase
Some patients progress to fibrosing alveolitis with persistent hypoxemia, increase alveolar dead space and further decrease in pulmonary compliance
The process may start as early as 5-7 days
The alveolar space becomes filled with mesenchymal cells and their products as well as new blood vessels

23. ARDS:Pathogenesis

24. ARDS: Fibroproliferative phase
CT Scan during fibroproliferative phase.
Diffuse interstitial opacities and bullae

26. DD
Infectious causes
Bacteria - Gm neg & pos , mycobacteriae, mycoplasma, rickettsia, chlamydia
Viruses- CMV, RSV, hanta virus, adeno virus, influenza virus
Fungi- H.capsulatum, C.immitis
parasites- pneumocytis carinii, toxoplasma gondii

27. DD Non infectious causes CCF
Drugs & toxins (paraquat, aspirin, heroin, narcotics, toxic gas, tricyclic anti depressants, acute radiation pneumonitis)
Idiopathic (esinophilic pneumonia, Acute interstitial pneumonitis, BOOP, sarcoidosis, rapidly involving idiopathic pulmonary fibrosis)
Immunologic (acute lupus pneumonitis, Good Pastures syndrome, hypersensitivity pneumonitis)
Metabolic (alveolar proteinosis)
Miscellaneous (fat embolism, neuro/high altitude pulmonary oedema)
Neoplastic (leukemic infiltration, lymphoma)

28. ARDS:Treatment Recent decrease of mortality
Treatment of underlying cause
Better supportive ICU Care
Prevention of infections
Appropriate nutrition
GI prophylaxis
Thromboembolism prophylaxis

31. ARDS: Treatment Protective ventilation Smaller tidal volumes
Avoid overdistention
Tolerate “permissive hypercarbia”
“Open lung” ventilation
Avoid alveolar collapse and reopening

33. Ventilation with Lower Tidal Volumes as Compared with Traditional Tidal Volumes for Acute Lung Injury and the Acute Respiratory Distress Syndrome The Acute Respiratory Distress Syndrome Network N Engl J Med 2000;342:1301-8
Study stopped after 2nd interim analysis
Reduction of mortality by 22%

34. NIH/ARDS Network PROTOCOL VARIABLES Volume assist control
Ventilator mode
Tidal Volume
Plateau Pressure
Ventilation rate/pH goal
Inspiration flow, I:E
Oxygenation goal
FIO2/PEEP
Weaning
PROTOCOL
Volume assist control
< 6mL/Kg body weight
<30 cm H2O
6-35/min adjusted for pH of 7.30 if possible
Adjust to 1:1-1:3
PaO2>55 and or SpO2>88%
Combinations
PS wean when FiO2/PEEP<.40/8

35. ARDS:Permissive Hypercapnia
Hypercarbic acidosis
Hypoxemia
Respiratory failure and arrest
Decrease myocardial contractility
Cerebral vasodilatation
Decrease seizure threshold
Hyperkalemia
Permissive hypercapnia
Supplemental oxygen overcomes CO2 induced hypoxia
No evolution to respiratory arrest
Lack of significant deleterious effects
Is hypercarbia beneficial?

36. Optimal “PEEP”
Positive end-expiratory pressure should be high enough to shift the end-expiratory pressure above the lower inflection point by 2-3 cm H2O (usually cm H2O)
Allows maximal alveolar recruitment
Decreases injury by repeated opening and closing of small airways

37. ARDS: Treatment Recruiting maneuvers NO Prone positioning Steroids
APRV
ECMO
Volume cycle vs. pressure cycle
Inverse-Ratio Ventilation
Non invasive Positive Pressure Ventilation
High-Frequency Ventilation
Tracheal Gas Insufflation
Extracorporeal gas exchange
Fluorocarbon Liquid Gas Exchange

38. APRV
It uses a release of airway pressure from an elevated baseline to simulate expiration.
The elevated baseline facilitates oxygenation avoids collapsing of alveoli and the timed releases aid in carbon dioxide removal.
Potential advantages of APRV include lower airway pressures, lower minute ventilation, minimal adverse effects on cardio-circulatory function.
Airway pressure release ventilation is consistent with lung protection strategies that strive to limit lung injury associated with mechanical ventilation, particularly recruitment/derecruitment
More (larger) studies are needed to define its role in ALI/ARDS

40. ARDS:Treatment Inhaled nitric oxide and other vasodilators Surfactant
Most ARDS/ALI patient may have mild to moderate pulmonary HTN
Improvement in oxygenation was small and not sustained
No change on mortality or duration of mechanical ventilation
May be used as “rescue” therapy
Surfactant
Successful in neonatal respiratory distress syndrome

41. Recruitment maneuvers
Lung recruitment in patients with ARDS Gattinoni NEJM 2006;354:
Sixty eight patients with ALI/ARDS underwent whole lung CT Scan during breath holding session at airway pressures of 5, 15 and 45 cm of water
The percentage of potentially recruitable lung was defined as the proportion of lung tissue in which aeration was restored (Recruited)

42. Recruitment
Knowing the % of recruitable lung might be the key to the effects of PEEP
PEEP in patients with limited recruitable areas might be of little benefit or harmful
Overdistention
Worsening of Shunt
Authors suggest PEEP of 15 for those recruitables and 10 for those who are not

43. ARDS Treatment Gattinoni et al, NEJM 2001;345:568-573
304 patients with ARDS
Prone group: at least six hours/day for ten days
Better oxygenation in the prone patients
Similar incidence of complications
No improvement in survival
However patient only prone for 7 hours a day and up to 10 days

44. ARDS Treatment Fluid and hemodynamic management
Optimal fluid management is controversial
There is data supporting fluid restriction as a mean to minimize lung edema
However maintenance and preservation of oxygen delivery may require fluid administration
Euvolemia, judicious use of vasopressors
Effects of ventilation in circulation
To Swan or not to Swan

45. ARDS: Treatment Glucocorticoids No benefits in acute phase
Some evidence of improvement during proliferative phase (Meduri et al JAMA 1998;280: )
Methylprednisolone 2mg/kg initially for 32 days
Improvement in Lung injury scores, MOSD scores and mortality
Benefits may be noticed by day 3
High risk of infection
? May consider a short course of high dose as rescue therapy

46. ARDS: Treatment Omega-3 (immunonutrition) Prostacyclines Surfactant
NMA
Ketoconazole
Pentoxifylline
Antioxidants, NAC

47. Swan and ARDS
PAC versus CVP to guide treatment of ALI NEJM 2006; 354:
1000 patients
Mortality at 60 days was similar between groups, as well as the ventilator free days and days not spent in the ICU
Fluid balances were similar among the groups
PAC had double complications mainly arrhythmias

48. ARDS- Survival & Follow-up
One year post discharge, 49% of survivors had returned to work, most to prior positions
Those not returning: - persistent weakness & fatigue - job stress - poor mobility - poor functional status Herridge et al NEJM 2003; 348(8)683-93