hypoxiaischemia

Hypoxia-ischemia, or hypoxic-ischemic injury, is tissue damage caused by a combination of reduced oxygen delivery (hypoxia) and diminished blood flow (ischemia). The dual insult disrupts cellular energy production and homeostasis and can affect multiple organs, with the brain being particularly vulnerable.

Pathophysiology involves rapid ATP depletion due to impaired oxidative phosphorylation. Loss of Na+/K+ ATPase activity leads to cellular swelling and depolarization. Excess neurotransmitter release, especially glutamate, triggers excitotoxicity and calcium influx. Mitochondrial dysfunction and oxidative stress promote inflammation, apoptosis, and necrosis, and reperfusion can exacerbate injury.

In neonates, perinatal hypoxic-ischemic encephalopathy presents with altered consciousness, abnormal tone, seizures, and autonomic instability. In adults, the syndrome typically follows acute ischemic events such as stroke. Imaging shows early cytotoxic edema on diffusion-weighted MRI; later scans reveal regional patterns that reflect vulnerable brain areas.

Management focuses on stabilization and prevention of secondary injury. Therapeutic hypothermia is standard for eligible neonates when started within about 6 hours. Supportive care includes seizure control, maintaining oxygenation and perfusion, glucose management, and rehabilitation planning. Prognosis depends on severity and treatment timing; early intervention improves outcomes, but long-term neurodevelopmental deficits may occur.

Prevention emphasizes high-quality obstetric and neonatal care, intrapartum fetal monitoring, and rapid response to fetal distress. The term hypoxia-ischemia differentiates the two underlying deficits, though they commonly co-occur in conditions such as birth asphyxia and cerebral stroke.