SEARCH RESULTS FOR: Hypoxic-Ischemic-Encephalopathy

Hypoxic Ischemic Encephalopathy

Authors: Isabella Reis, Alam Randhawa Reviewers: Annie Pham, Taylor Krawec, Emily J. Doucette, Danielle Nelson* *MD at the time of publication **See corresponding Calgary Guide slide Legend: Pathophysiology Mechanism Hypoxic Ischemic Encephalopathy: Pathogenesis and clinical findings Intrauterine growth restriction** (most important) ↑ Maternal age Gestational hypertension** Chorioamnionitis** Oligohydramnios Antepartum risk factors Intrapartum risk factors Antenatal trauma Maternal illness Maternal thyroid disease Gestational age > 41 weeks Preeclampsia** Hypoxic Ischemic Encephalopathy (HIE) Brain injury resulting from disrupted cerebral oxygen (hypoxia) & blood flow (ischemia) before, during or shortly after birth 1. Primary Energy Failure (within minutes to hours) Insufficient cerebral perfusion triggers anaerobic metabolism 2. Latent Phase (within hours) 3. Secondary Energy Failure (within days) ↑ Lactic acid ↓ ATP production High anion gap metabolic acidosis** ATP-dependent pumps fail (i.e., Na+/K+ -ATPase, Ca2+ -ATPase) in areas with ↑ demand Return of O2 supply allows transient recovery of oxidative metabolism Prolonged reaction to primary insult Intracellular acidosis ↓ enzyme, mitochondria & membrane function ↑ Na+ & Ca2+ influx & K+ efflux Reperfusion Ion imbalance Widespread of surviving ↓ Umbilical drives H2O influx depolarization brain cells cord blood gas (pH ≤7.0 mEq/L, base excess ≥-16 Cellular swelling & edema Glutamate release mEq/L) Cell lysis ↑↑ Ca2+ influx Early necrotic injury Transient improvement after initial event Delayed necrosis Need for prolonged resuscitation Diffuse brain injury Diffuse neurological deficits (e.g., coma, generalized seizure) Focal brain injury Focal neurological deficits (e.g., focal seizure, hemiparesis) Complications Reperfusion generates reactive O2 species Apoptotic cascade is activated Shoulder dystocia** Operative vaginal delivery Uterine rupture Placental abruption** Prolonged ruptured membranes &/or active labour Cord prolapse** Prematurity Nuchal cord DNA, cell & mitochondria damage 4. Tertiary Energy Failure (within weeks to months) Persistent glial cell activation Gliosis & glial scar formation Chronic inflammation Impaired oligodendrocyte maturation ↓ Neuronal myelination by oligodendrocytes Impaired synaptogenesis & abnormal pruning Motor & sensory deficits Ongoing synaptic dysfunction Ongoing white matter loss Sign/Symptom/Lab Finding Global deficits persist Focal deficits persist Global/systemic complications (e.g., global developmental delay, quadriplegic cerebral palsy) Focal complications (e.g., focal epilepsy, visual impairment, hemiplegic cerebral palsy) Published Dec 7, 2025 on www.thecalgaryguide.com