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Antenatal steroids have also been shown to have definite beneficial effect in treating the condition of preterm premature rupture of membranes (PPROM). [8] Similar to its effects on preterm birth, research evidence suggests that the administration of antenatal steroids to patients with PPROM reduces risks of neonatal mortality, intraventricular hemorrhage and respiratory distress syndrome.
A Cochrane review from 2020 recommends the use of a single course of antenatal corticosteroids to accelerate fetal lung maturation in women at risk of preterm birth. Treatment with antenatal corticosteroids reduces the risk of perinatal death, neonatal death and respiratory distress syndrome and probably reduces the risk of IVH. [128]
Acute respiratory distress syndrome (ARDS) is a type of respiratory failure characterized by rapid onset of widespread inflammation in the lungs. [1] Symptoms include shortness of breath (dyspnea), rapid breathing (tachypnea), and bluish skin coloration (cyanosis). [ 1 ]
Women with PROM at any age are at high risk of infection because the membranes are open and allow bacteria to enter. Women are checked often (usually every 4 hours) for signs of infection: fever (more than 38 °C or 100.5 °F), uterine pain, maternal tachycardia, fetal tachycardia, or foul-smelling amniotic fluid. [10]
Additional steps may have to be taken to manage circulatory problems, kidney failure, and respiratory distress. Recent investigational treatment therapies include high doses of Rituxan (Rituximab) and eculizumab, which are both humanized monoclonal antibodies that target B cell malignancies and prevent C5 complement cleavage, respectively.
There are two forms of respiratory distress syndrome: ARDS , which is acute (or adult ) respiratory distress syndrome Infant respiratory distress syndrome (IRDS), which is a complication of premature birth, also known as hyaline membrane disease (HMD)
The pathophysiology of acute respiratory distress syndrome involves fluid accumulation in the lungs not explained by heart failure (noncardiogenic pulmonary edema). It is typically provoked by an acute injury to the lungs that results in flooding of the lungs' microscopic air sacs responsible for the exchange of gases such as oxygen and carbon dioxide with capillaries in the lungs. [1]
It is often impossible to distinguish TRALI from acute respiratory distress syndrome (ARDS). The typical presentation of TRALI is the sudden development of shortness of breath, severe hypoxemia (O 2 saturation <90% in room air), low blood pressure, and fever that develop within 6 hours after transfusion and usually resolve with supportive care within 48 to 96 hours.