Diagnostics

• Should be performed within the first 6 hours of life, in all newborns showing clinical signs of neonatal encephalopathy (e.g., difficulty initiating and/or maintaining breathing, seizures, abnormal level of consciousness) as neuroprotective treatment is time-sensitive

• Allows estimation of the likelihood that perinatal asphyxia contributed to the development of neonatal encephalopathy

• Neurological damage is the major concern after a hypoxic-ischemic event.

a hypoxic-ischemic etiology of neonatal encephalopathy is most likely if one or more of these signs are present

• APGAR score at 5 min and 10 min: < 5

• Fetal umbilical artery pH: < 7.0

• Arterial base deficit ≥ 12 mmol/L

• Neuroimaging evidence of acute brain injury

• Presence of multisystemic organ failure consistent with HIE (e.g., renal failure, hepatic injury, hematological changes)

• Birth-related events that might have lead to hypoxic-ischemic complications:

  • Uterine rupture

  • Severe abruptio placentae

  • Umbilical cord prolapse

  • Severe and prolonged maternal hypoxia and hypotension

  • Maternal cardiovascular collapse

  • Fetal exsanguination

  • Abnormal fetal heart rate monitoring during labor

• Neuroimaging patterns consistent with neonatal hypoxic-ischemic brain injury (e.g., watershed cortical injury in MRI)

• No evidence of other causes for neonatal encephalopathy (e.g., inborn errors of metabolism, genetic disorders)

• Umbilical arterial blood gas analysis: arterial pH, venous pH, base deficit

• CBC: may show signs of infection, hemorrhage, or thrombocytopenia

• Electrolytes: monitoring and treatment guidance

• Liver function tests: evaluation of possible damage

• Kidney function tests: evaluation of possible damage

• Cardiac enzymes: if myocardial injury is clinically suspected

• Coagulation tests: in case of bleeding, to exclude disseminated intravascular coagulation

• Bacterial blood culture: to exclude neonatal sepsis

• Lumbar puncture: if there is clinical suspicion of meningitis/encephalitis

• EEG

  • Conducted on the first day of life, continued monitoring for at least 24 hours

  • Evaluation of seizure activity and background electrical activity

• Biomarkers: Recent studies indicate that VEGF is significantly increased in neonates that subsequently develop encephalopathy.

• Cranial MRI

  • Most sensitive tool for detecting hypoxic-ischemic injury in the brain to exclude other causes of neonatal encephalopathy

  • Patterns consistent with HIE include deep nuclear gray matter injury, parasagittal injury of the cerebral cortex, and watershed cortical injury

  • Magnetic resonance spectroscopy can be performed additionally.

• CNS ultrasound

  • Alternative if MRI is unavailable (e.g., condition of the newborn, missing resources), but less sensitive for hypoxic-ischemic injury

  • Perfusion measurement and evaluation of morphological changes (e.g., hemorrhages, ventricular size, cerebral edema, severe white-matter damage)

• Echocardiography

  • If myocardial injury is suspected

  • May show decreased ventricular contractility, valve dysfunction, or enlargement of the heart