ARDS

MSMSICU ד"ר אלחנן פריד

)ישנה...()ישנה...(הגדרה הגדרה : :

First described in 1967 as Adult Respiratory Distress Syndrome

יקר, הורג! שנות אדם(,100/100,000)~שכיח

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

ARDSARDS

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

First Berlin definitionFirst Berlin definition

Second Berlin fefinitionSecond Berlin fefinition

:הפרוגנוזה קשורה לקבוצהMILD ~27%, MOD ~35%, SEVERE ~45%

ARDS: CausesARDS: Causes

ARDS:EpidemiologyARDS: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

ARDS:PathogenesisARDS: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

ARDS:PathogenesisARDS: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

ARDS: Exudative PhaseARDS: 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

ARDS:PathogenesisARDS:Pathogenesis

ARDS: Exudative PhaseARDS: Exudative Phase CT Scan During Acute Phase

ARDS: Fibroproliferative phaseARDS: 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

ARDS:PathogenesisARDS:Pathogenesis

ARDS: Fibroproliferative phaseARDS: Fibroproliferative phaseCT Scan during fibroproliferative phase.

– Diffuse interstitial opacities and bullae

DDDD

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

DDDDNon 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(

ARDS:TreatmentARDS:Treatment

Recent decrease of mortality – Treatment of underlying cause– Better supportive ICU Care

Prevention of infections Appropriate nutrition GI prophylaxis Thromboembolism prophylaxis

ARDS: TreatmentARDS: Treatment

Protective ventilation– Smaller tidal volumes

• Avoid overdistention• Tolerate “permissive hypercarbia”

– “Open lung” ventilation• Avoid alveolar collapse and reopening

Ventilation with Lower Tidal Volumes Ventilation with Lower Tidal Volumes as Compared with Traditional Tidal as Compared with Traditional Tidal

Volumes for Acute Lung Injury and the Volumes for Acute Lung Injury and the Acute Respiratory Distress SyndromeAcute Respiratory Distress Syndrome

The Acute Respiratory Distress Syndrome Network The Acute Respiratory Distress Syndrome Network N Engl J Med 2000;342:1301-8N Engl J Med 2000;342:1301-8

Study stopped after 2nd interim analysis

Reduction of mortality by 22%

NIH/ARDS NetworkNIH/ARDS Network VARIABLES

– 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

ARDS:Permissive HypercapniaARDS: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?

Optimal “PEEP”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 12-15 cm H2O(

– Allows maximal alveolar recruitment

– Decreases injury by repeated opening and closing of small airways

ARDS: TreatmentARDS: 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

APRVAPRV

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

ARDS:TreatmentARDS:Treatment Inhaled nitric oxide and other vasodilators

– 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

Recruitment maneuversRecruitment maneuvers

Lung recruitment in patients with ARDS Gattinoni NEJM 2006;354:1175-86

– 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(

RecruitmentRecruitment

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

ARDS TreatmentARDS 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

ARDS TreatmentARDS 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

ARDS: TreatmentARDS: Treatment Glucocorticoids

– No benefits in acute phase– Some evidence of improvement during

proliferative phase (Meduri et al JAMA 1998;280:159-165)

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

ARDS: TreatmentARDS: TreatmentOmega-3 )immunonutrition(

Prostacyclines Surfactant NMA Ketoconazole Pentoxifylline Antioxidants, NAC

Swan and ARDSSwan and ARDS

PAC versus CVP to guide treatment of ALI NEJM 2006; 354: 2213-2224

– 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

ARDS- Survival & Follow-upARDS- 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