Placental Transfusion for Asphyxiated Infants

Abstract

The current recommendation for umbilical cord management of non-vigorous infants (limp, pale, and not breathing) who need resuscitation at birth is to immediately clamp the umbilical cord. This recommendation is due in part to insufficient evidence for delayed cord clamping (DCC) or umbilical cord milking (UCM). These methods may provide a neuroprotective mechanism that also facilitates cardiovascular transition for non-vigorous infants at birth.

Keywords: asphyxia; cord milking; delayed cord clamping; newborn; placental transfusion.

Figure 1

Cord compression and hypovolemia: (A) normal fetus with thin walled umbilical vein (UV) transferring blood from the placenta to the fetus and two thick walled umbilical arteries (UA) bringing blood from the fetus to the placenta. (B) Cord compression initially occludes the thin-walled UV limiting umbilical venous flow to the fetus. The thick-walled UAs continue to maintain blood flow from the fetus to the placenta (blue arrow). This process leads to increased placental blood volume and reduced fetal blood volume. (C) Graph from a full-term fetus showing umbilical arterial flow (persists during cord compression), umbilical venous flow (abolished after cord compression), systemic blood pressure, and right atrial pressure. Selective loss of umbilical venous flow causes hypovolemia. Copyright Satyan Lakshminrusimha, MD.

Figure 2

Mode of delivery, anesthesia, and neonatal vigor influence placental transfusion: (A) following a spontaneous vaginal delivery without general anesthesia, uterine contractions generate high intrauterine pressure (~100 mm Hg). A baby held below the introitus may benefit from gravity to enhance placental transfusion although gravity is not an absolute requirement for transfer of blood to the newly born infant. Negative intrathoracic pressure induced by active crying in a vigorous neonate can assist placental transfusion. (B) Following stat cesarean section under general anesthesia for fetal distress or asphyxia, uterus is atonic, infant is depressed and may not be active and baby is held at the level of the abdomen. These factors can potentially reduce the volume of placental transfusion. Copyright Satyan Lakshminrusimha, MD.

Figure 3

Negative consequences of early cord clamping in asphyxia: asphyxia increases the need for resuscitation and is associated with hypoxic-ischemic encephalopathy (HIE) and persistent pulmonary hypertension of the newborn (PPHN). Early cord clamping reduces blood and RBC volume in the neonate and increases fetal blood left in the placenta. Hypovolemia and hypoxia contribute to cerebral hypoperfusion and HIE and exacerbate pulmonary hypoperfusion and PPHN. Studies have shown increased oxidative stress with early cord clamping compared to delayed cord clamping and umbilical cord milking. Oxidative stress contributes to HIE and PPHN. Copyright Satyan Lakshminrusimha, MD.

Figure 4

Benefits of ventilation of the lungs with an intact umbilical cord: optimal performance of the left ventricle (LV) is important for hemodynamic transition at birth. Umbilical venous return from the placenta and pulmonary venous return both contribute to LV preload. Ventilation of the lung leads to pulmonary vasodilation and increases pulmonary venous return. Umbilical arteries perfusing the placenta maintain low LV afterload. High diastolic pressure due to higher RBC volume following placental transfusion leads to better coronary perfusion. Copyright Satyan Lakshminrusimha, MD.

Figure 5

Role of delayed cord clamping in congenital diaphragmatic hernia (CDH): oxidative stress plays an important role in the pathogenesis of pulmonary hypertension and injury to hypoplastic lungs in CDH. Delayed cord clamping, limiting barotrauma (with low ventilator pressures), restricting FiO₂ to target preductal SpO₂ in the mid-80s to low 90s are important strategies to limit oxidative stress in CDH. Copyright Satyan Lakshminrusimha, MD.

Figure 6

Umbilical cord milking and carotid and pulmonary hemodynamics in preterm lambs: a graph showing carotid arterial pressure, left carotid blood flow, left pulmonary arterial flow, ductus arteriosus flow, umbilical arterial, and venous flow and end-tidal CO₂ in preterm lambs undergoing umbilical cord milking (pink vertical bar) without or with simultaneous ventilation of the lungs. Units are shown to the left and right of the figure. Interestingly, umbilical arteries went into spasm after initiation of PPV and did not demonstrate pulsatile flow. Courtesy/Copyright Praveen Chandrasekharan MD (with permission).