One of the most important antenatal therapies that can improve neonatal outcomes in the event of an imminent preterm birth is the administration of antenatal corticosteroids. We either use betamethasone or dexamethasone, depending on the national clinical guidelines. Administration of corticosteroids to women who are at increased risk of a preterm delivery significantly reduces neonatal morbidity and mortality. They lower the severity or frequency of;
-respiratory distress syndrome,
-necrotizing enterocolitis, and
-death when compared to those women who do not receive such therapy.
There’s no superiority of betamethasone over dexamethasone according to the available evidence. Either of these drugs fastens organ maturation of the fetus like the lungs. Both drugs cross the placenta. They lack a mineralocorticoid activity.
Their biologic activity is identical. The drugs also have a relatively weak immunosuppressive effect when used in the short-term. Betamethasone, however, has a longer half-life. We administer betamethasone as 12mg for two doses given intramuscularly 24 hours apart. On the other hand, dexamethasone is given in 6mg for four doses 12 hours between each dose. However, you can check your national clinical guidelines for any changes.
There are several recommendations regarding the use of antenatal corticosteroids for fetal maturation as postulated by the American College of Obstetricians and Gynecologists. These include;
- A single course of corticosteroid is recommended for pregnant women between 24 weeks, 0 days and 33 weeks, six days of gestation who are at risk of preterm delivery within seven days, including for those with ruptured membranes and multiple pregnancies. You may also consider it for pregnant women starting at 23 weeks, 0 days of gestation who are at risk of preterm delivery within seven days, based on a family’s decision regarding resuscitation, irrespective of membrane rupture status and regardless of fetal number.
- Administration of corticosteroids for pregnant women during the periviable period who are at risk of preterm delivery within seven days- links to a family’s decision regarding resuscitation. Consider it in that context.
- We recommend a single course of betamethasone for pregnant women 34 weeks, 0 days and 36 weeks, six days of gestation at risk of preterm birth within seven days, and who have not received a previous course of antenatal corticosteroids.
- We currently do not recommend regularly scheduled repeat courses or serial courses (more than two).
- Consider single repeat course of antenatal corticosteroids in women who are less than 34 weeks, 0 days of gestation who are at risk of preterm delivery within seven days, and whose prior course of antenatal corticosteroids occurred than 14 days previously. You can provide a rescue course corticosteroids as early as seven days from the before dose if indicated by the clinical scenario.
- Whether to administer a repeat or rescue course of corticosteroids with preterm pre-labour rupture of membranes is controversial, and there’s insufficient evidence to make a recommendation whatsoever.
- Continued surveillance of long-term outcomes after in utero corticosteroid exposure should be supported.
- Quality improvement strategies to optimize appropriate and timely antenatal corticosteroid administration are productive and should be encouraged.
Antenatal corticosteroids, in particular, accelerate lung maturity and enhance the production of surfactant a fluid that lines the alveoli of the lungs to reduce surface tension, which prevents lung collapse and partly leads to neonatal respiratory distress syndrome. If you still don’t understand this, let’s get to the basics of surface tension of the alveoli and surfactant in a few statements below.
Surface tension in the alveoli results from the forces between molecules of liquid lining the alveoli. And because of this, alveoli tend to collapse. To expound on this, we illustrate this observation using Laplace’s law which states that “the pressure tending to collapse alveoli is directly proportional to surface tension and inversely proportional to the alveolar radius.” We derive the following equation,
The bigger the radius, the lower the collapsing pressures and the more serene keeping the alveoli open. Small alveoli have higher collapsing pressures and do not easily remain patent. The absence of surfactant, these small alveoli will have a higher tendency to collapse. The diagrams below illustrate this principle.
Surfactant is the liquid that lines the alveoli and reduces surface tension. The type II alveolar cells (pneumocytes) produce it. It comprises mainly dipalmitoyl phosphatidylcholine – a lipid. The presence of surfactant in the alveoli reduces surface tension, preventing the alveoli from collapsing at the end of expiration, thus increasing lung compliance. In the fetus, surfactant synthesis is variable. It may occur as early as week 24 and is almost always present by week 35 of gestation.
Premature babies may develop neonatal respiratory distress syndrome due to a lack of surfactant. They exhibit atelectasis during expiration.
They have difficulty re-inflating the lungs (due to decreased lung compliance), and hypoxaemia from the ventilation-perfusion (V/Q) mismatch.
In a nutshell, whether you use dexamethasone or betamethasone, you should use it correctly. We welcome your comments in the comment section below.