ACUTE RESPIRATORY DISTRESS SYNDROME Dr Tasaduk Khan. MD. FRCP(UK). FCCP(USA) Consultant Internist & Pulmonologist. Security Forces Hospital Riyadh.

History In 1960s military clinicians in Vietnam called it shock lung. Civilian clinicians called it Adult respiratory distress. Subsequent finding in all age groups labeled it as Acute respiratory distress syndrome (ARDS).

ACUTE RESPIRATORY DISTRESS SYNDROME Synonyms: Non-Cardiogenic pulmonary edema Adult hyaline membrane disease Capillary leak syndrome Stiff lung syndrome Shock lung

ARDS: Definitions First described in 1967 as Adult Respiratory Distress Syndrome American-European Consensus Conference Committee (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

Diagnostic criteria Berlin definition of ARDS. Respiratory symptoms must have begun within 1 week of clinical insult or new or worsening symptoms during past week. Bilateral edema consistent with pulmonary edema on CXR/ CT. Pts resp failure must not e fully explained by CCF or volume overload. A moderate to severe impairment of oxygenation must be present as defined by PaO2/ FIO2 ratio. Severity of hypoxia defines severity of ARDS. Mild ARDS: PaO2/FIO2> 200 but <300 on vent settings with PEEP>5cm H2O. Mod: PaO2/ FIO2 >100 but< 200 with PEEP >5 cm H2O Severe: PaO2/ FIO2 < 100 on PEEP >5cm H2O.

DEFINITION ACUTE LUNG INJURY (ALI): ARDS: Severe form of ALI. A syndrome of inflammation and increased permeability that is associated with a constellation of clinical, radiologic, and physiologic abnormalities that cannot be explained by, but may co-exist with, left atrial or pulmonary hypertension. ARDS: Severe form of ALI.

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

CRITERIA FOR ALI & ARDS PARAMETER ALI ARDS ONSET ACUTE HYPOXEMIA Pao2/ Fio2 < 300 mm Hg Pao2/ Fio2 < 200 mm Hg CHEST XRAY B/L DIFFUSE INFILTRATES NONCARDIAC CAUSE PULMONARY ARTERY WEDGE PRESSURE < 18 mm of Hg. No clinical evidence of left atrial hypertension

ARDS causes Direct Lung Injury: Aspiration of gastric contents Diffuse pulmonary infections (bacterial, viral, fungal) Pulmonary contusion Near drowning Inhalation injury Reperfusion pulmonary edema after lung transplant Radiation

ARDS causes Indirect lung injury: Sepsis Severe trauma w/ shock hypoperfusion Acute pancreatitis Severe burns TRALI (Transfusion related acute lung injury) Cardiopulmonary bypass Anaphylaxis Lymph reticular malignancy

ARDS - PATHOGENESIS Insult (direct or indirect) Activation of inflammatory cells & mediators Damage to alveolar capillary membrane Increased permeability of alveolar capillary membrane Influx of protein rich edema fluid and inflammatory cells into air spaces Dysfunction of surfactant

PATHOLOGICAL STAGES OF ARDS Exudative (acute) phase (0- 4 days) Proliferative phase (4- 8 days) Fibrotic phase ( >8 days) Recovery

ARDS: Exudative Phase CT Scan During Acute Phase

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

PHYSIOLOGICAL ABNORMALITIES Decreased ventilation Impaired diffusion Reduced perfusion

CLINICAL FEATURES – symptoms Precipitating insult is usually evident Early (24 – 48hrs) - cough, breathlessness, fatigue Late (after 48hrs) - due to worsening hypoxemia - agitation, anxiety, confusion

CLINICAL FEATURES – signs Dyspnoea Tachypnoea Tachycardia Restlessness Cyanosis even with supplemental oxygen ( refractory hypoxemia)

Differential diagnosis Cardiogenic pulmonary edema Diffuse alveolar hemorrhage Acute pulmonary embolism Acute eosinophilic pneumonia Hypersensitivity pneumonitis Pulmonary alveolar protienosis Sarcoidosis Leukemic infiltration Drug induced pulmonary edema Acute exacerbation of IPF/ chronic ILD. Cryptogenic Organizing Pneumonia( COP).

Investigations Chest x-ray & CT thorax: Bilateral diffuse alveolar infiltrates more on the peripheral lung fields. R/O Cardiogenic edema if there is * cardiomegaly * pulmonary artery dilatation * bat’s wing perihilar distribution * responding to diuretics

Ards

Cardiogenic pulmonary edema

NEONATAL RESPIRATORY DISTRESS SYNDROME

INVESTIGATIONS Arterial blood gas analysis: PaO2 range 55 – 60 mm of Hg Initially respiratory alkalosis later mixed acidosis Routine CBC, urea, creatinine, Na, K Echocardiogram to R/O Cardiogenic cause. PAWP < 18mm of Hg  ALI / ARDS Bronchoscopy ( DAH, AEP, PAP)

ASSESSMENT OF SEVERITY Murray lung injury score: - Chest x-ray - Hypoxemia - PEEP - Compliance Score 0  no lung injury 0.1 – 2.5  mild to moderate lung injury > 2.5  severe lung injury

Complications (ACUTE) Acute respiratory failure. Delirium. Ventilator associated pneumonia(VAP) Ventilator associated lung injury. Barotrauma ( pneumothorax). DVT and Pulmonary embolism. Gastrointestinal bleeding. Catheter related infections.

Complications (CHRONIC) Reduced exercise capacity due to abnormal lung functions. Post trauma stress disorder (PTSD) (depression, anxiety, decreased memory & concentration) Bed sores. Critical illness polymyoneuropathy. Pulmonary fibrosis. Rarely acquired cystic lung disease.

Treatment of ALI/ARDS 1 TREATMENT OF CAUSE e.g. antibiotics for pneumonia 2 Supportive therapy (5P’s) Perfusion, position, protective lung ventilation, protocol weaning, preventing complications 3 Pharmacological treatment Steroids, vasodilators, surfactant, anti inflammatory , DVT Px, Reflux Px & sedation.

Long term management. Quit smoking. Quit alcohol. Vaccinations. Pulmonary rehabilitation. Join a support group. Seek professional help/ treat depression.

POOR PROGNOSIS FACTORS Advanced age Male sex Extra pulmonary organ dysfunction Sepsis HIV Alcoholism Active malignancy Organ transplantation

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