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.
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
2.preeclampsia
3.hypoglycemia
4.metabolic acidosis
5.pancreatitis
6.sepsis
There are some pulmonary risk factors like:
1.aspiration
2.contusion
3.smoke inhalation
4.oxygen toxicity
5.embolism
6.congenital malformation
7.pneumothorax
Extrapulmonary risk factors like:
1.sepsis
2.trauma
3.anaphylaxis
Pathophysiology of ARDS
- 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:
1.tachypnea
2.dyspnea
3.intercostal and subcostal retraction
4.crackles sound
5.audible expiratory grunt
6.apnea
7.Flaccidity
8.mottling
9.shock
10.cyanosis
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 
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 [5]
|
Phase 2 RCT
|
A) 48 hours B) <150
|
340
|
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) [6]
|
Phase 1 RCT
|
A) 48 hours B) <300
|
40
|
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) [7]
|
Phase 2 RCT
|
A) 48 hours B) < 300
|
282
|
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) [8]
|
Phase 2 RCT
|
A) 72 hours B) <200
|
326
|
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) [9]
|
Phase 3 RCT
|
A) 48 hours B) <300
|
492
|
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) [14]
|
Phase 2 RCT
|
A) 7 to 28 days B) P/F <200
|
180
|
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 [15]
|
Phase 1 RCT
|
A) 72 hours B) <300
|
91
|
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) [19]
|
Phase 2 RCT
|
A) 48 hours B) <300
|
60
|
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 [21] | 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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