ACUTE RESPIRATORY DISTRESS SYNDROME

(ARDS)

Dewa Artika

DEVISI PARU / LAB.IP.DALAM

FK UNUD – RSUP Sanglah

INTRODUCTION

• Acute Respiratory Distress Syndrome (ARDS) is an acute and severe breathing failure syndrome, indicated by acute breathing distress, with oxygenation disorder caused by non cardiogenic lung oedem.

• Distinguished by Acute Lung Injury (ALI) which is a series of pathologic process, while ARDS is an end of this process which has more severe characteristics.

• Asbough, 1967 introduced it for the first time

• Murray, 1988 defined it using scoring system

• In year 1994, AECC (American European Consensus Conference) on ARDS recommended a new definition → ARDS spectrum

DEFINITION

• ALI or ARDS is a kind of inflammation syndrome causing increase of permeability with lung oedem clinical, radiological and physiological defect was occured that is not due to left side heart failure.

• ALI distinguished from ARDS

On ALI PaO2/FiO2 < 300

while ARDS PaO2/FiO2 < 200

EPIDEMIOLOGY

• In the US in 1972 : 150.000 cases/year or 75 cases / 100.000 population

• In Scandinavia, 17.9/100.000/year for ALI and 13.5/ 1000.000/year for ARDS

• Survey by Intensive Care Unit in AS : 9% from Intensive Care Unit filled by ARDS patients

RISK FACTOR

• Direct lung injury

Digestive aspiration, thorax trauma, severe lung infection, toxic gas inhalation, drown.

• Indirect lung injury

Severe sepsis, non thorax trauma, transfusion, acute pancreatic, medication overdose.

• Generally, sepsis very much related to ARDS creation, where incidence ± 40 %.

PATHOPHYSIOLOGY

• The principal of ARDS occurrence, liquid overflowing from capillary to alveoli, therefore lung oedema occurred.

• Normal, liquid in alveoli is regulated by– Hydrostatics pressure & osmotic capillary– Interstitial lymphatic– Tight junction between alveolar epithelium cell

• On ARDS, / permeability barrier alv capillary occurred, due to cell endothelia capillary or epithelium alveoli injury

Disintegrity of epithelium causing :– Oedema alveoli– Disturbing transportation of epithelium liquid– Reducing the production of surfactant– In pneumonia septic shock can happen

There are 4 stages of ARDS pathophysiology :1. Degradation of alv-cap membrane → interstitial

fluid accumulation. 1. Lung become stiff → ventilation disorder and V/Q

mismatch heavy hypoxemia2. Liquid entered into alveoli area → no ventilation,

proportion of V/Q become 0 → shunt3. Closing of terminal airway occurred → atelectasis,

so los of lung volume which causing decreasing of artery oxygen pressure.

Picture 1

PATHOLOGY

• Exudative phase (day 1 – 7)– Edema interstitial and intra alveolar– Bleeding– Leuco-aglutination– Necrosis (pneumocite 1 and endothelium cell)– Hyalin membrane– Trombus fibrin platelet

• Proliferative phase (day 7 – 21)– Interstitial myofibroblast reaction– Organization of fibrosis lumenal– Chronic inflammation– Parenchyma necrotic– Hyperplasia pneumocite II– Endarteritis obliterative– Macro thrombi

• Fibrotic phase ( > day 21)– Fibrosis collagen– Microcystic honeycombing– Bronchiektasis traction– Artery pulls

• Fibrosis mural• Hypertrophy medial

CLINICAL MANIFESTATION

• During acute phase or exudative– Complaint: high fever, abdominal pain, shock,

pulmonary dysfunction such as dispnea, hypoxemia, coughing, chest pain, uncomfortable feeling.

– Physic: cyanosis, tachicardia, tachipnea, ronchi– Lab: blood gas analysis, alkalosis respiratoric,

increase of PaO2/PAO2 ratio, severe hypoxemia.– Hematologis dis; anemia, leucositosis, leucopenia,

trombositopenia, while DIC rarely found.

• On BAL examination, it biochemistry and cellular abnormality were observed

• On thorax photo, early stage may still be normal. After 12 – 24 hours there will be cloudy bilateral opacities. After 24 hours, opacities become more compacted.

• Abnormality of kidney and liver occured.

THORAX PHOTO

• On chronic phase, severity tending to fibrosis alveolitic occurred with persistent hypoxemia. Pulmonal hypertension occurred → failure of right side ventricle. In this phase, there is a complication of nosokomial infection and multi organ failure.

- On thorax photo it appear as steady opacity - CT scan examination on thorax showing opacities reticuler, difuse ground glass to both lung areas and bula picture.

MANAGEMENT

• General carea. Identification and handling of the basic

cause such as infection, sepsis with correct antimicrobial

b. Profilaxis / nosokomial infection therapy

c. Adequate nutrition

d. Profilaxis for GI organ bleeding with H2 blocker, antacid or sukralfat

e. Profilaxis tromboemboli

• Medication for hypoxemiaa. Need high FiO2 to overcome severe

hypoxemia. For that, we need intubations using Ventilator

b. Reduce consumption and improve oxygen transportation

c. Mechanical ventilation• Exhalation technique (using PEEP)• Inhalation technique

• Procedure for liquid and haemodynamic– Limitation of liquid to reduce lung oedema– Intravascular volume will be maintain, which is able to

support systemic perfusion– If perfusion do not achieved, can be given vasopresor

such as shock septic

• Surfactant therapy– The main function is to regulate surface retention of

alveoli, so atelectasis will not be occurred.– Using exogenous surfactant → results is not good

enough, therefore aerosol therapy will be preferred

• Nitric-Oxide (NO) inhalation– A potential vasodilator– Able to improve artery oxygenation– Has an anti inflammation function

• Glucokortikoid– Has an anti inflammation characteristics– Can be given at the end phase of ARDS– High dose prescription in a short time period

→ as a rescuer for patient with severe disease who do not shows any improvement

• Resolution acceleration– Can be achieved with oedema alveoli liquid

transfer using catecholamine or non catecholamine

– non catecholamine group (beta agonist) has been extensively applied can also increase surfactant and anti

inflammation effect– Recently Keratinocyte growth factor has been

attempted, where it can help epithelium alveoli II cell proliferation → shield for lung injury

Learning task A patient was brought to Emergency Unit by their family with complaint of sudden breathing difficulties and decrease in consciousness. Five days before the patient suffered from high temperature until shivering together with purulent cough and breathing difficulties. Vital sign it was found BP:100/70, N. 120/m, RR. 30 times/m temp. 39oC. On physical examination it was found ronchi diffuse, wheezing. On the thorax photo it was found opacity covering on the two lung areas and consolidation in the center-right side part. Examination of blood gas analyses it was found PaO2, 45 mmHg while PaCO2 65 mmHg, PH 7,25.

Self Assessment - Discuss about that case assessment - Other recommended examination - What is the diagnostic procedure - How is the pathophysiology of ARDS - How is the management of ARDS

THANK - YOU

Learning Task