Acute Respiratory Distress Syndrome(ARDS)

Acute Respiratory Distress Syndrome(ARDS)

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what is ARDS?

ARDS or acute respiratory distress syndrome is nothing but a very common respiratory problem now. Although the reason behind this disease is something else, the people are still suffering from it.

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Somehow ARDS is also known as hyaline membrane disease. Lack of surfactant and the fluid fills lungs are mainly responsible for its occurrence. Premature infants are most sufferers of ARDS.


Who are the going under risk groups?

The person having some acute and chronic diseases like:

1.maternal diabetes



4.metabolic acidosis




There are some pulmonary risk factors like:



3.smoke inhalation

4.oxygen toxicity


6.congenital malformation 



Extrapulmonary risk factors like:




Pathophysiology of ARDS

Investigation       Antenatal period      Examination of the amniotic fluid Lecithin sphingomyelin ratio ; -         > ...

  • In adults, the fluid fills the lungs and in preemies having immature lungs with underdeveloped alveoli are considered as etiological factors. 


  •  They can lead to decreased surfactant in the alveolar surface. now, the surface tension becomes increases and causes atelectasis.


  • After atelectasis, carbon dioxide retention along with hypoxemia takes place in the lungs.


  • These types of conditions always cause pulmonary vasoconstriction and hypoperfusion of the parenchyma cells.


  • Due to the excess vasoconstriction, the capillary becomes damaged. Plasma comes out from the cells. At last, the protein called fibrinogen ( responsible for blood clot) leads to ARDS.


Clinical manifestation of ARDS 

The hallmark sign of ARDS is the grunting sound. It is produced when the patient uses his accessory muscle during respiration.

Other clinical features are:



3.intercostal and subcostal retraction

4.crackles sound expiratory grunt







What are the diagnostic tests?

The diagnostic tests are like:

1.history taking

2.physical examination, main auscultation to here the abnormal breath sounds

3.chest x-ray ARDSSevere.png

4.Allen test

5.pulse oximetry

6.shake test

7.down’s score

8.Sputum culture test and analysis


Other tests are like;

Chest ct scan and echocardiogram


How can we manage ARDS?


Medical management

  • Monitor the vitals of the patient.
  • Maintain the oxygen saturation ( minimum 93-95%)
  • Continuously give positive pressure ventilation.
  • Provide nebulization therapy.
  • Administer exogenous surfactant in the ET tube.
  • ARDS patients need help to open closed airspaces, get oxygen into the blood, and make it easier to breathe. A ventilator and extra oxygen are used for these reasons and maintained until the injury .


Pharmacological management

Characteristics of trials to date

Study title and abbreviation Design (all placebo-controlled) The population of ALI/ARDS A) Timing from ALI onset B) P/F ratio Number recruited Intervention Primary outcome Result (intervention vs control) Mortality (intervention vs control)
Neuromuscular Blockade in Early ARDS []

Phase 2 RCT

A) 48 hours B) <150


Cisatracuriumbesylate: 15 mg initially, then 37.5 mg per hour for 48 hours

90-day survival

31.6% vs 40.7% (P= 0.08)

28-day: 23.7% vs 33.3% (P= 0.05)

The β-Agonist Lung Injury Trial (BALTI) []

Phase 1 RCT

A) 48 hours B) <300


Intravenous (IV) salbutamol for seven days (15 μg kg-1 h-1)

Extravascular lung water (EVLW) at Day 7

9.2 ± 6 vs 13.2 ±3 ml kg-1 (P= 0.04)

28-day: 58% vs 66% (P= 0.4)

Randomized, Placebo-Controlled Clinical Trial of an Aerosolized β2-Agonist for Treatment of Acute Lung Injury (ALTA) []

Phase 2 RCT

A) 48 hours B) < 300


Inhaled salbutamol (5 mg) every 4 hours for 10 days/24 hours after extubation

Ventilator-free days (VFD)

Stopped early 14.4 ± 0.9 vs 16.6 ± 0.9 (P= 0.087)

Death before discharge: 24.3 ± 3.5 vs 18.5 ± 3.4 (P= 0.261)

Effect of Intravenous β-2 Agonist Treatment on Clinical Outcomes in Acute Respiratory Distress Syndrome (BALTI-2) []

Phase 2 RCT

A) 72 hours B) <200


IV salbutamol for seven days (15 μg kg-1 (ideal body weight) h-1)

28-day mortality

Stopped early 34% vs 23% (P= 0.03)

Neutrophil Elastase Inhibition in Acute Lung Injury (STRIVE) []

Phase 3 RCT

A) 48 hours B) <300


Sivelestat infusion

1. 28-day mortality2. VFD

Stopped early 1 26.6% vs 26% (P= 0.847)2. 11.4 ±10.27 vs 11.9 ± 10.1 (P= 0.536)

Efficacy and Safety of Corticosteroids for Persistent ARDS (LaSRS) []

Phase 2 RCT

A) 7 to 28 days B) P/F <200


Moderate-dose IV methylprednisolone, for up to 25 days

60-day mortality

29.2% vs 28.6% (P= 1.0)

Methylprednisolone Infusion in Early Severe ARDS []

Phase 1 RCT

A) 72 hours B) <300


Low-dose IV methylprednisolone, for up to 28 days

Improvement in Lung Injury Score by Day 7

69.8% vs 35.7% (P= 0.002)

Hospital survival 76.2% vs 57.1% (P= 0.07)

A Randomized Clinical Trial of Hydroxymethylglutaryl–Coenzyme A Reductase Inhibition for Acute Lung Injury (HARP) []

Phase 2 RCT

A) 48 hours B) <300


Simvastatin 80 mg daily, up to 14 days

Reduction in EVLW indexed to actual body weight

13.7 vs 13.4 (P= 0.90) Improvements in secondary outcomes

Hospital survival: 19 vs 19 (P= 1.0)

Nebulized Heparin is Associated with Fewer Days of Mechanical Ventilation in Critically Ill Patients: a Randomized Controlled Trial [] Phase 2 RCT Patients expected to require ventilation for >48 hours, and within 24 hours of ventilation 50 Heparin 25,000 units every 4 to 6 hours, for up to 14 days Average daily P/F ratio 194.2 ± 62.8 vs 187 ± 38.6 mmHg (P= 0.6) Improvements in secondary outcomes 28-day: 20% vs 16% (P= 0.7)






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