Asphyxia at birth, also known as perinatal asphyxia, occurs when a newborn infant is deprived of adequate oxygen supply during the birth process. This oxygen deprivation can lead to a cascade of physiological disturbances affecting multiple organ systems, including the brain, heart, lungs, kidneys, and blood. One important question is whether asphyxia at birth damages white blood cells (WBCs), which are crucial components of the immune system responsible for fighting infections and maintaining overall health.
White blood cells are part of the hematologic system, and their function and numbers can be influenced by systemic stress and injury. Severe asphyxia causes systemic hypoxia (lack of oxygen) and ischemia (lack of blood flow), which triggers a redistribution of blood flow to prioritize vital organs like the brain, heart, and adrenal glands. This compensatory mechanism can lead to inadequate perfusion and injury in other organs and tissues, including the hematologic system. In cases of severe neonatal asphyxia, abnormalities in blood components have been observed, such as anemia (low red blood cell count), thrombocytopenia (low platelet count), and coagulation dysfunction, including disseminated intravascular coagulation (DIC), a serious condition involving widespread clotting and bleeding. These changes indicate that the blood system is significantly affected by asphyxia[1].
Regarding white blood cells specifically, the stress and injury caused by asphyxia can alter their levels and function. For example, inflammatory responses triggered by hypoxia and tissue damage can lead to elevated white blood cell counts as the body attempts to fight potential infections or repair damage. Conversely, severe systemic injury and shock may impair bone marrow function or cause consumption of white blood cells, potentially leading to leukopenia (low white blood cell count). Additionally, inflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), which are elevated in response to hypoxic injury and infection risk, can influence white blood cell behavior and survival[2].
It is important to note that the damage to white blood cells from asphyxia is not usually direct destruction of the cells themselves but rather a consequence of the systemic inflammatory and ischemic environment. The hypoxic-ischemic injury primarily targets organs with high oxygen demand, but the hematologic system is indirectly affected through mechanisms such as oxidative stress, inflammation, and coagulation abnormalities. These systemic effects can impair the immune response by altering white blood cell counts and function, potentially increasing vulnerability to infections and complicating recovery[1][2].
In neonates who suffer from hypoxic-ischemic encephalopathy (HIE), a brain injury caused by oxygen deprivation, the immune system’s response is complex. The brain injury itself can trigger systemic inflammatory responses that affect white blood cells. Moreover, therapeutic interventions such as cooling therapy (therapeutic hypothermia) used to protect the brain may also influence immune function, including white blood cell activity, although the primary goal is neuroprotection[3][5].
In summary, asphyxia at birth does not typically cause direct, isolated damage to white blood cells but leads to significant systemic effects that impact the hematologic system, including white blood cells. These effects include changes in white blood cell counts, activation of inflammatory pathways, and coagulation disturbances. The overall immune function may be compromised due to these systemic changes, which can influence the newborn’s ability to respond to infections and recover from injury. The severity of these effects depends on the duration and intensity of the oxygen deprivation and the newborn’s overall condition.
