ACUTE RESPIRATORY DISTRESS SYNDROME[ ARDS ]

by: Anastasia D.H.

DEFINITION: syndrome signed by: - increase of permeability alveolo capilair membrane against water, solution & plasma protein. - diffuse alveolar disturbance. - fluid accumulation inside lung parenchym consist of protein.

Based Definition by American-Europe ARDS Coference Committee 1994: 1. Respiratory failure/distress acute onset 2. Ratio of artery vessel oxygen pressure with inspiration oxygen fraction (PaO2/ Fi O2) < 200 mmHg Hipoksemia berat. 3. Chest Radiography: bilateral alveolar infiltrat represent Lung edema 4. Pulmonary capillary wedge pressure

If PaO2/Fi O2 200-300 mmHg---Acute Lung Injury, corelation of risk factor ALI with absence Chronic Lung disease.

RISK FACTORS Direct injury alveolus epithel:Aspiration of gaster contentDiffuse lung infectionLung contusioDrownningToxic inhalation

Indirect injury: 1. Septic 2. Non thoraxic trauma 3. Overload blood tranfussion 4. Pankreatitis 5. Cardiopulmonarry shunt

PATOPHYSIOLOGYBegin with alveolar epithel & microvascular dis-turbance, caused by direct/indirect injury, thenactivate cascade inflamation, divided 3 phase:

1.Initiation phase : risk factor condition cause imune & non imune cells relieves inflamatory mediators & modulators inside lung towards systemic

2.Amplification phase : efector cell/netrofil is activated,pull & persisted inside lung.

3.Injury phase : inside target organ, relieves inflamatory mediator include oxydase & protease, directly destroy the lung & stimulate next inflamatory process.Membran alveolo-capilair damage cause increase membrane permeability & flow of rich protein liquid enter alveolar space then disturb surfactan integrity cause further alveolair disturbance

3 Phase Alveolar DisturbanceExudative phase: interstitial & alveolar edema, pneumosit cell necrose & denudation basal membrane, endothel cell swelling with intercelluler junction widening, hyalin membrane formed in alveolar duct & air space, netrofil inflamation,also found pulmoner hypertension & decrease of lung compliance.Proliferative phase: fastest happened after 3 days onset, sign: pneumocyte epithel cel proliferation.Fibrotic phase: colagen increased, lung become solid caused of fibrotic

CLINICAL MANIFESTATIONSGenerally,acute onset 3 5 days since conditionas ARDS risk factor is diagnosed. First sign: tachypnea Others: hypotension, feverAuscultation: wet ronkhiDIAGNOSTIC EVALUATIONLaboratory Findings:1. Blood Gas Analyzes: hypoxemia, hypocapnea (secondary cause of hyperventilation), hypercapnea (in emphysema or further condition).

Alkalosis Respiratory in beginning process replace to Acidosis Respiratory. 2. Leucocytosis (on septic), anemia, trombosito-penia (systemic inflamatory reflection & endothelial injury), increased of amylase level (on pancreatitis)3. Renal & Liver function disturbances, dissemi-nated intravasculer coagulation (as part of MDS /multiple organ dysfunction syndrome)

Imaging:Chest X-Ray: beginning process found lung area relatively clear,then diffuse radioopaque shadow seen & no gravitation influence, without heart congestion descriptionCT scan: heterogenous pattern, infiltrat predomination on dorsal lung area (supine photo)

DIFFERENTIAL DIAGNOSTIC:Cardiogenic, Neurogenic lung edemaLung infection: (V,B,F)High Altitude Pulmonarry Edema (HAPE)Laryngospasm induce lung edemaDrug induce lung edema (heroin, salicylate, cocain)Radiation, Hypersensitivity PneumonitisFat embolic syndromeMitral stenosis with alveolar bleedingVasculitisInterstitial lung disease

MANAGEMENT1. Take over respiratory function with mechanical ventilator2. Agent therapy: - Corticosteroid on ARDS/ALI advanced phase or fibroploriferative phase.(severe persistent hypoxemia in the seventh day ARDS) - Nitric Oxide inhalation (NO) give selective vasodilatation effect on distribution lung area caused decreased pulmonarry artery,repair arterial oxyganation.Only give for refracter severe hypoxia.3. Patient position: prone position increased oxygenation but not change mortality

4. Fluid: must balance between - needs of optimal organ perfussion - fluid extravasation problem to lung & tissue: increase of intravascular hydrostatic pressure caused fluid accumulation in alveolus.Main focus: defence adequate perfussion without oxygenation victimize.Fluid restriction, best monitor by pulmonary arte-ry catheterization, defence in level: lowest intra vascular hydrostatic pressure, but adequat cardiac output

COMPLICATION: -- MODS, nosocomial pneumonia, barotrauma, pneumotorax, trakeomalasia, trakeoesofageal fistule, inominata artery errosion, death.

PROGNOSE: mortality : 40 % affected by:--Risk factors (septic,post trauma,etc), main disease, malignancy, presence MODS ,age, alcoholism, presence gas exchange index recovery (Pa O2/FiO2) in 3 7 day.-- good response: lung function recovery in 3 months, max. 6 months post extubation.-- 50 % patient abnormality persistent, restriction disturbance & decrease difusion capacity--- decrease quality of life

MUTIPLE ORGAN FAILUREPASCA TRAUMADEFINITION MOF : found 2 / > organ / system failure1. Cardiovasculair failure: - HR 54/minute, MAP 49 mmHg, VT & orVF, pH serum 7,24 dg. PCO2 40 mmHg.2. Respiratory failure: - RR 5/min,or 49/min, PaCO2 50 mmHg, on ventilator in 4th day 3. Renal failure: diuresis 479 ml/24 h or 159 ml/8h, BUN 100 mg/dl, creatinin serum 3,5 mg/dl

4. Hepatic failure: bilirubin serum 6mg/dl, PT > 4 sec (without anticoagulant)5. Central Nervous Systemic failure: GCS 6 (without sedative)6. Hematological failure: Leuc 1000/ml, Tr 20.000/ml, Ht 20%7. Coagulation system failure: trombocytopenia, PT& APTT,BT memanjang, Hypofibrinogenemia8. ARDS : history disease, PaO2 / FIO2 < 200 mmHg, diffuse infiltrat on X-Ray, no pulmonary infection, low pulmonary compliance, Pulmonary capillary wedge pressure < 18 mmHg.

9. Acute Lung Injury: PaO2 / FIO2 < 300 mmHg, + ARDS criteria

ETIOLOGY: trauma: multiple trauma, post operation, visceral ischemia, epileptic status, heat injury, abdominal compartemen syndr

PATOGENESIS - cause of local insult or infection, pro inflamato- ry mediators released against foreign antigenes to relieve the wound. - then followed by anti inflamatory mediators released to regulate this process,homeostasis reached,patient recovered. - if there is severe pathologic insult, local defence mechanism doesnt success, inflamatory mediators will enter to systemic sirculation & new leucocyts recruit in inflamatory area. Stress respon happen in the whole body. Ones more, anti inflamatory mediators released to systemic for proinflamatory cascade recovery till homeostatic reached.

If systemic pro inflamatory respon is severe or if anti inflamatory respon as its compensa- ted isnt adequate, caused pro inflamatory respon regulation failed. In this condition, found SIRS signs,then start to threat organ dysfunction.- On the opposite, if anti inflamatory respon predo-minant, caused anergy & immunosupressi, this condition named Compensatory Antiinflamatory Respose Syndrome (CARS).- The progress of life depend on reachment of ho-meostatic.If failed, last phase patogenic process, immunological dissonance happened, imbalance pro & anti inflamatory process --- clinically find MOF signs

InsultT,B cell,NK cell, macrophagePro inflamatory response: IL-1,IL-6,TNF-Anti inflamatory response:IL-4,IL-10,IL-13 into systemic sirculationHyperinflammatory conditionHypoinflammatory conditionSIRS Systemic Inflammatory Response SyndromeCARS (Compensatory AntiinflammatoryResponse Syndrome)Cardiovascular compromised/syok,apoptosisImmunocompromisedLost of homeostaticMODS

MANAGEMENTPREVENTIONWell technical surgery is important,cause from research 40% MODS case caused of surgical error.NosocomialInfection increase twice mortality.Hand washing, isolationroom, silicon iv cathetherization can reduce MODS insidence.CAUSE CONTROLThe importance thing: remove presipitate factor & cause orinfection source.SURGERYInclude bone fracture fixation,burn debridement,ischemic/ ne-crotic bowel resection,pus removal.Source of inflamatory res-ponse not always clear,sometimes surgical exploration need, especially suspicious intra abdominal source.

ANTIBIOTICSMaximal effort to find patogen cause infection,includeblood &body liquid culture, serology examination & aspi-ration percutan. Giving appropriate antibiotic in early processof infection disease will improve prognostic, prevent se-condary infection, nosocomial disease, then reduce MODSinsidence.

SUPPORTIVE MANAGEMENTIf cant find spesific cause:Deficit must be correctedSupport system/organ which suffer dysfunctionGuard safety system/organ which still functionning

INOVATIVE THERAPYImmune ModulationBig scale research, monoclonal antibody givento manipulate immune system (magic bullets)--still notshow decrease of mortality MODS patientNO inhibitorResearch prove NOS (nitric oxide synthase) inhibitor Increase mortality.In the future, selective inhibitor toINOS (Inducible Nitric Oxide synthase) has role inmanagement MODSBLOOD FILTRATION ---still not succedHigh volume hemofiltration (2 6 filtration/h) mayfiltrate cytocines & others inflamatory mediators

CorticosteroidHigh dose CS (metilprednisolon 30 mg/kg) significantly increase mortality septic syok.Research in physiologic dose, show organ dysfunc-tion & syok recovery, suggest mechanism : 1.Anti inflamation by supression of proinflamatory cytocines transcription.2. Replacement therapy in cortex adrenal insufficiency3. Improve cathecolamine receptor sensitivity

Manipulation of coagulation cascade Research of the advantages of activated protein C & antithrombin III