Pulmonary surfactant is a complex, fatty substance produced within the lungs, composed mainly of phospholipids (fats) and specialized proteins. It acts as a coating on the inner surface of the tiny air sacs in the lungs, enabling them to function correctly. The presence of surfactant largely determines the survival prospects of infants born prematurely.
How Surfactant Supports Breathing
The lungs contain millions of microscopic air sacs called alveoli, where oxygen enters the blood and carbon dioxide is removed. These sacs are lined with fluid, which creates surface tension that constantly pulls the walls inward, causing them to collapse upon exhalation.
Surfactant’s primary function is to counteract this collapsing force. It works by inserting itself between water molecules, effectively reducing surface tension to near zero. This allows the alveoli to remain slightly inflated, even after the breath is expelled, reducing the physical effort required for the next breath and preventing lung exhaustion.
The Timeline of Fetal Lung Development
Surfactant production is a developmental process carried out by specialized cells within the lungs, known as Type II alveolar cells. These cells begin producing small amounts of surfactant as early as 20 to 24 weeks of pregnancy.
However, this initial quantity is insufficient for independent breathing. Production accelerates significantly during the late second and third trimesters. Lung maturity, defined by having enough surfactant to prevent collapse, is typically achieved between 32 and 36 weeks of gestation. Premature birth before this window means the lungs are biologically immature and lack the necessary coating for breathing air.
Understanding Respiratory Distress Syndrome
A deficiency of pulmonary surfactant in a newborn leads to Respiratory Distress Syndrome (RDS). Without the stabilizing effect of surfactant, the infant’s alveoli repeatedly collapse upon exhalation. The baby must use significant effort to re-inflate the lungs with every breath, quickly leading to fatigue.
This struggle is visible as rapid, shallow breathing, often accompanied by an audible grunting sound. Since the lungs are not fully expanding, gas exchange is compromised, resulting in low oxygen levels. A severe lack of oxygen causes a bluish discoloration of the skin and mucous membranes, known as cyanosis.
Treating Surfactant Deficiency
Two main strategies manage surfactant deficiency in premature infants. The first is antenatal treatment, where corticosteroids (typically betamethasone) are administered to the mother when premature delivery is anticipated between 24 and 34 weeks gestation. These injections cross the placenta, accelerating the maturation of the Type II alveolar cells. Corticosteroids stimulate the production and release of natural surfactant, significantly reducing the severity of RDS at birth.
The second strategy is postnatal treatment, which involves administering exogenous surfactant replacement therapy directly to the newborn’s lungs. This liquid suspension, often derived from animal sources or made synthetically, is delivered through a tube placed in the baby’s windpipe. Administering this replacement surfactant immediately coats the alveolar surfaces, restoring the necessary surface-tension-lowering properties. Early administration, often within the first two hours of life, can reduce mortality and the risk of complications associated with the syndrome.