ACUTE RESPIRATORY DISTRESS SYNDROME

By

Dr Tahir JavedAssistant Professor of Pediatrics,King Edward Medical University

LAHORE

HISTORY• Ashbaugh: 1967, “adult respiratory distress

syndrome” • American-European Consensus Conference

(AECC) : 1994 “ Acute substituted for ADULT”• B/L Lung infiltrates & severe hypoxemia

without cardiogenic pulmonary edema• The Berlin Definition: 2012-The PaO2/FiO2

• mild ARDS: 201 - 300 mmHg (≤ 39.9 kPa)• moderate ARDS: 101 - 200 mmHg (≤ 26.6 kPa)• severe ARDS: ≤ 100 mmHg (≤ 13.3 kPa)

The Respiratory System: Gross Anatomy

• The Airway– Extra thoracic

» Supraglottic» Glottic Conduction of Air» Infraglottic

– Intrathoracic• The Lungs– Lobes Conduction of Air + gas Exchange

– Segments• The Pleura• Blood Supply

The extrathoracic airway is1-Pleura2-Supraglottic3-Lobe of the lung4-Chest wall muscle

The Trachea

• Extent• The length• The AP diameter• The layers: Mucosa, Submucosa, Cartilage/ Muscle, Adventitia• The Bronchi• The blood supply

• Inferior Thyroid• Intercostal• Bronchial

Question

Length of trachea at birth isa-7cmb-3cmc-10cmd-14cm

Answer

• B

The Trachea: Histology

The Bronchial Epithelium

The Lungs

The Lungs

Functional unit of the lung is called1-Lobe2-Segment3-Alveoli4-Bronchus

The Pleura

The Pulmonary Vasculature

The Respiratory Zone

Mechanics of Breathing

• Inspiration• Expiration• Compliance• Resistance

The Gas Exchange

Lung Volumes

The Protective Mechanisms

• The Nose

• The Cough

• The Mucociliary Escalator

• The Alveolar Macrophages

A C U T E R E S P I R A T O R Y

D I S T R E S S S Y N D R O M E

ARDS

• Disease of Alveoli: ↓ Gas Exchange– Diffuse Alveolar damage– Lung capillary endothelial Injury

• Early Phase: Exudative• Late Phase: Fibro-proliferative

Pathophysiology

• ↑capillary permeability: fluid accumulation• Type 1 cell damage: ↓clearance from alveolar spaces• Type 2 cell damage: ↓Surfactant→ ↓Compliance ALVEOLAR COLLAPSE• Role of Neutrophils: Reactive rather than causative• Role of cytokines

Question

Type-II cell damage is caused by1-Surfactant deficiency2-Oxygen inhalation3-Sepsis4-Barotrauma

Answer

• 1

Pathophysiology

• Barotrauma: Pneumothorax & Interstitial leaks• Volutrauma: Further damage• Intra pulmonary shunting• High FiO2: DAD (diffuse alveolar damage) Hyaline membrane formation and fibrosis • Pulmonary Hypertension• Pulmonary fibrosis: ↑PCP-III: High mortality

Causes

• No risk factors in 20% cases• Advanced age, female gender, alcoholism and

smoking increase the risk of ARDS• Sepsis is the most common cause• Other causes include Pneumonia, fractures,

trauma, burns, drug overdose, Aspiration, near drowning, post perfusion injury, pancreatitis and fat embolism

Epidemiology

• Incidence: 75/100,000 population in USA• Incidence increases with age– 15-19 Yrs-16 cases /100,000 person Yrs– 75-84 Yrs-306 cases/100,000 person Yrs

• Gender: Incidence slightly more in females when cause is Trauma

• 190,600 new cases every year with 74,500 deaths

Prognosis• MORTALITY• 40-70% mortality in 1990• 30-40 % recently• Better understanding of Sepsis• Use of mechanical ventilation• MORBIDITY• long hospital Stays• High risk of Nosocomial infections• Muscle wasting• Functional impairment

History

• Dyspnea 1st at exertion and soon at rest• Anxiety & agitation• Increasing need for higher O2 concentrations• Onset: 12-48 Hrs but may take several days• Patients are critically ill, may be already

admitted with multi-organ failure & may not furnish Hx

Examination

• Tachypnea• Dyspnea• Cyanosis• Hypotension: ↑CRT, cold extremities, weak

thready pulses• Rales in the chest• Absent breath sounds if pneumothorax• Agitation, Somnolence

Investigations

• Hematologic: TLC, Platelet count esp. with DIC B:N• Renal: deranged function tests when ATN• Hepatic: Disturbed functions• ABGs: Respiratory alkalosis later metabolic acidosis

as CO2 rises• PaO2/FiO2<200• High IL-1, IL-6, IL-8• Normal Echocardiogram. May help diagnose

Pulmonary Hypertension

What is pneumothorax?

Question

Pneumothorax is suggested by1-Absent breath sound2-Stony dull percussion3-Bronchial breathing4-Vesicular breathing

Radiology

Radiology

Radiology

CT Chest

• More sensitive to detect – Pulmonary interstitial Emphysema– Pneumothorax– pneumomediastinum– Pleural effusion– Cavitation– Mediastinal lymphadenopathy

SEQ

• A 6 hours old neonate born at 28 weeks of gestation, to Para5 mother via emergency C-section, weighing 0.9 kg. He has developed respiratory distress at 2 hours of birth. There is nasal flaring and intercostal and subcostal recessions. Baby is cyanosed & grunting. Chest X-ray shows ground glass appearance with air bronchogram throughout the lungs. His condition is worsening.

• 1-What is diagnosis?• 2-What further investigations you will do?• 3-What is treatment option?

Answer

• Hyaline membrane disease• ABGs• Mechanical ventilation

Complications• Barotrauma: high PEEP, CPAP & mean AWP leading to leak pathologies• Accidental extubation & right mainstem intubation• Prolonged ventilation requiring tracheostomy will eventually lead to sub-glottic stenosis• Nosocomial infections: VAP, Line sepsis, UTI, Sinusitis,

Clostridium difficile colitis, MRSA,VRE.• Renal failure esp. When cause of ARDS is sepsis, • Stress gastritis, Anemia• PCM and difficult rehabilitation