Pathophysiology

Hypoxia → ↑ sympathetic activity → circulatory centralization to maintain perfusion of vital organs (e.g., brain, adrenal glands, heart) → reduced oxygen supply to peripheral organs → tissue damage (e.g. kidneys, costal diaphragm, skeletal muscle, liver)

Prolonged hypoxia → compromised myocardial cell function and ischemia → ↓ myocardial contractility → ↓ cardiac output → worsening of ischemia in peripheral organs

Primary energy failure: antepartum/intrapartum placental dysfunction or postpartum pulmonary gas exchange impairment → insufficient oxygen supply to organ tissue → brain tissue acidosis (due to CNS susceptibility) → osmotic dysregulation in cells → cellular edema → apoptosis

Latency period (lasting several hours): reperfusion and recovery of some brain cells

Secondary energy failure (6–48 h after initial injury): distribution of toxic neurotransmitters, oxidative stress, inflammation → widening of affected area

Brain injury (months to years after initial injury): persistent inflammation, impaired neurogenesis, reduced axonal growth → reduced neural plasticity, myelin deficits, brain cell death