Acute respiratory distress syndrome (ARDS)

Acute respiratory distress syndrome(ARDS)

Overview
Etiology
Risk Factors
Pathophysiology
Clinical Manifestations
Diagnostic Examination
Therapeutic Management
Complication
Medical Management

Acute respiratory distress syndrome (ARDS) or also known as Respiratory Distress Syndrome (RDS) is an immature development of the respiratory system or an inadequate amount of surfactant in the lung. RDS is said to be hyaline membrane disease (HMD).
Respiratory Distress Syndrome (RDS) is the immature development of the respiratory system or an inadequate amount of surfactant in the lung. RDS is said to be hyaline membrane disease (HMD).

ARDS formerly most commonly signified adult respiratory distress syndrome to differentiate it from infant respiratory distress syndrome in premature infants. However, as this type of pulmonary edema also occurs in children, ARDS has gradually shifted to mean acute rather than adult. The differences with the typical infant syndrome remain(Wikipedia)



Etiology
Associated with gestational age, the younger the infant, the higher the risk of RDS so that makes the immature development of the respiratory system or an inadequate amount of surfactant in the lung.
RDS there are two times more in males than females, incidence increased in infants with certain factors, such as: maternal diabetes who gave birth to a baby less than 38 weeks, perinatal hypoxia, was delivered by cesarean section.
ARDS develops as a result of dangerous conditions or the occurrence of lung tissue injury either directly or indirectly.

Risk Factors
1. Direct trauma to the lung

• Viral Pneumonia, Bacterial Pneumonia, Fungal Pneumonia
• Contusio lung
• Aspiration of gastric fluid
• Inhalation of excessive smoke
• Inhalation of toxin
• Inhaling high concentrations of O2 in a long time

2. Indirect Trauma

• Sepsis
• Shock
• DIC (Dissemineted intravascular coagulation)
• Pancreatitis
• Uremia
• Drug Overdose
• Idiophatic (unknown)
• Surgery of the old Cardiobaypass
• Blood transfusions are a lot of
• PIH (Pregnand Induced Hipertension)
• Improved ICT
• Radiation therapy

Pathophysiology
Various theories have been found as the cause of this disorder. Formation surtaktan lung substance is not perfect in the lungs, is one theory that many embraced. Surfactant is a substance that plays a role in lung development and is a complex consisting of proteins, carbohydrates and fats. The main compound substance is lecithin. This substance began to be formed at 22-24 weeks of pregnancy and reached a maximum at 35 week. The role of surfactant is to lower alveolar surface tension so it does not happen to collapse and be able to withstand the functional residual air at the end of expiration. Deficiency of surfactant substance found in hyaline membrane disease causes the lung to maintain stability wherever disturbed. Alveoli would come back every end-expiratory collapse, so for the next breath it takes a negative intrathoracic pressure accompanied yanglebih great inspiration stronger effort. Lung collapse will cause disruption of ventilation to hypoxia, CO2 retention and acidosis. Hypoxia will lead to:
1. decreased tissue oxygenation, anaerobic metabolism that would occur with the accumulation of lactic acid and other organic acids that cause metabolic acidosis in infants.
2. apitel capillary endothelial damage and alveolar ducts and that will lead to transudation into the alveoli and the subsequent formation of fibrin and fibrin together with the necrotic epithelial tissues form a layer called the hyaline membrane. Acidosis and atelectasis also cause disruption of blood circulation to and from the heart. Similarly, pulmonary blood flow will decrease and this will result in reduced formation of surfactant substance.

Clinical Manifestations
1. Rapid breathing (takipneu)
2. Nostril breathing
3. Clients complain of difficulty breathing, retractions and cyanosis
4. Cyanosis in line with hypoxemia
5. An increasing number of respiratory
6. On auscultation of breath sounds there may be additional
7. Systemic hypotension (peripheral pallor, edema, delayed capillary refill longer than 3 to 4 seconds)
8. Decrease in urine output
9. Decreased breath sounds with ronkhi
10. Takhikardi at the time of the occurrence of acidosis and hypoxemia

Diagnostic Examination
1. Chest X-ray

• Retikulogranular diffuse pattern with air bronkhogram overlapping each other.
• Signs of central lung, heart border is difficult to see, inflation is a bad lung.
• Chances are kardoimegali when other systems are also exposed (infants of diabetic mothers, hypoxia, congestive heart failure)
• Shadow of a large thymus
• Bergranul bronkhogram evenly on the air, which indicates severe disease if present in the first few hours.

2. Arterial blood gas showed respiratory and metabolic acidosis is a decrease in pH, PaO2 decreased and PaCO2 increased, decreased HCO3.
3. Complete blood count
4. Perubahabn electrolytes, tends to decrease levels: calcium, sodium, potassium and serum glucose.


Complication

1. Pneumothorax
2. Pneumomediastinum
3. Hypotension
4. The decline of urine
5. Acidosis
6. Hyponatremia
7. Hipernatremi
8. Hypokalemia
9. Disseminated intravascular coagulation (DIC)
10. Convulsions
11. Intraventricular hemorhagi
12. Secondary infections
13. Murmur

Therapeutic Management

• Administration of oxygen
• Maintain adequate nurtrisi
• Maintain a neutral ambient temperature
• Diet 60 kcal / kg per day (adjust with the existing protocols) with amino acids sufficient to prevent endogenous protein catabolism and ketoacidosis.
• Keep the pO2 within normal limits
• Intubation if necessary with positive pressure ventilation

Medical Management

Tags : ARDS, RDS, Acute Respiratory Distress, Adult Respiratory Distress Syndrome, respiratory failure, acute respiratory failure, What Is Respiratory Distress,