Perinatal asphyxia results from compromised placental or pulmonary gas exchange. This disorder can lead to hypoxia (lack of oxygen) and hypercarbia (increased carbon dioxide levels) in the blood. Severe hypoxia results in anaerobic glycolysis and lactic acid production first in the peripheral tissues (muscle and heart) and then in the brain. Ischemia (lack of sufficient blood flow to all or part of an organ) is both a cause and a result of hypoxia. Hypoxia and acidosis can depress myocardial function, leading to hypotension and ischemia. Ischemia can impair oxygen delivery, causing further compromise, as well as disrupt delivery of substrate and removal of metabolic and respiratory by-products (eg, lactic acid, carbon dioxide).
The systemic complications of perinatal asphyxia are reviewed here. Hypoxic-ischemic encephalopathy (HIE), including pathogenesis, pathology, diagnosis, prognosis, and treatment, is discussed elsewhere. (See "Etiology and pathogenesis of neonatal encephalopathy" and "Clinical features, diagnosis, and treatment of neonatal encephalopathy".)
TIMING OF INJURY
Asphyxia can occur before, during, or after birth. Based on a review of multiple studies that have examined the temporal relationship between obstetric events and neonatal outcomes, predominantly hypoxic-ischemic encephalopathy (HIE) in term infants, the proportion of conditions that occurs in each time period can be estimated .
Antepartum events, such as maternal hypotension or trauma, account for 4 to 20 percent of cases. Intrapartum events, such as placental abruption or umbilical cord prolapse, are seen in 56 to 80 percent. Evidence of intrapartum disturbance (eg, meconium-stained amniotic fluid or severe fetal heart rate abnormalities) occurs in 10 to 35 percent, usually in association with an antenatal risk factor, such as diabetes mellitus, preeclampsia, or intrauterine growth restriction (IUGR). In approximately 10 percent of cases, a postnatal insult occurs, usually caused by severe cardiopulmonary abnormalities or associated with prematurity.
However, the timing of injury often is difficult to establish for an individual infant, in part because antepartum and intrapartum events may not lead to signs that are detectable in the fetus. In addition, a fetus who has suffered an antepartum insult may be at increased risk of incurring further intrapartum injury.