History of neonatal encephalopathy.

History of neonatal encephalopathy. Neonatal encephalopathy is a clinical syndrome characterized by altered neurological functions in the first days of life of a newborn of 35 or more weeks of gestational age, and usually presents with one of the following:
- An altered level of consciousness.
- Epileptic seizures.
- Difficulty initiating and maintaining autonomous respiration.
- Decreased tone and reflexes.

Apgar score of less than 5 at 5 and 10 minutes of life.

A low Apgar score confers a high relative risk of cerebral palsy, and the lower the score, the higher this risk. However, most newborns with an altered Apgar score do not have cerebral palsy.

Acidosis in the umbilical cord blood sample.

Cord pH less than 7.0 or a base deficit less than 12 mmol/L, or both, increases the probability that the neonatal encephalopathy had an intrapartum hypoxia component.

Neuroimaging. Evidence of acute brain injury on MRI, consistent with hypoxic-ischemic encephalopathy.

Brain MRI is the neuroimaging technique of choice. Cranial ultrasound and computed tomography have low sensitivity.
Different neuroimaging patterns exist, and they have prognostic value to predict subsequent neurological impairment.
- A normal brain MRI after 24h of life, which does not show areas of acute injury, has a good prognosis, although all lesions may not appear until after the first week of life.
- An MRI obtained between 24 and 96 hours of life may be more sensitive to identify the timing of acute brain injury, while an MRI performed at 10 days of life (between 7 and 21) will allow identifying all lesions.
- Despite advances in neuroimaging, the ability to precisely identify the timing of the adverse event remains limited (it can estimate with a margin of error of days, not hours or minutes).

Presence of signs of multiorgan failure consistent with a diagnosis of hypoxic-ischemic encephalopathy.

Multiorgan damage can include renal or hepatic failure, hematological disorders, myocardial dysfunction, metabolic alterations, or gastrointestinal damage, or a combination of them.
Although the presence of multiorgan dysfunction increases the risk of hypoxic-ischemic encephalopathy, the severity of brain injury identifiable by MRI does not always correlate with the involvement of other organs.

Sentinel event occurring immediately before or during labor and birth.

Uterine rupture.
Severe abruptio placentae.
Umbilical cord prolapse.
Amniotic fluid embolism with maternal hypotension and severe coexisting maternal hypoxia.
Maternal cardiorespiratory arrest.
Fetal exsanguination due to vasa previa or massive fetomaternal hemorrhage.
Nuchal cord DOES NOT CONSTITUTE A SUFFICIENT SENTINEL EVENT.

Fetal heart rate monitoring patterns consistent with an acute peri- or intraparto event.

Type I and type II tracings, when associated with an Apgar score of 7 or greater at 5 minutes, normal umbilical artery pH, or both, ARE NOT CONSISTENT WITH AN ACUTE HYPOXIC-ISCHEMIC EVENT.
There is a major difference between a patient presenting initially with an abnormal CTG pattern and one developing it throughout labor.
- A type II tracing lasting more than 60 minutes, identified at initial presentation, with absent variability and absent accelerations (even in the absence of decelerations), is suggestive of a compromised or already asphyxiated fetus. If fetal well-being cannot be confirmed through scalp pH or biophysical profile, delivery must be planned immediately.
- A type I tracing that converts to type III (according to the Eunice Kennedy Shriver National Institute of Child Health and Human Development guideline) is suggestive of a hypoxic-ischemic event.
- Other tracings that can develop from type I, which may suggest the occurrence of a hypoxic-ischemic event, include tachycardia with recurrent decelerations and persistent minimal variability with recurrent decelerations.

Identifiable patterns of remote brain injury on neuroimaging that are suggestive of being caused by a peri- or intrapartum event.

Transfontanellar ultrasound lacks sensitivity for the most common forms of brain injury in encephalopathic newborns. However, since in many cases it is the only technique available in an unstable neonate, echodensity or echogenicity can be observed from 48h after the brain ischemic event. Computed tomography lacks sensitivity for neonatal brain injury and will not reveal abnormalities in the first 24-48h.
The combination of conventional brain MRI, diffusion, and spectroscopy between 24 and 96 hours of life is the technique with the best performance to determine the timing of the brain injury.
Diffusion abnormalities are most prominent between 24 and 96 hours of life. With conventional MRI, qualitative brain alterations are identifiable from day 7 after the hypoxic-ischemic event. Performing 2 MR spectroscopies, one between 24 and 96 hours (with emphasis on diffusion and spectroscopic abnormalities evaluation) and a second at day 10 of life or later, are the best strategy to define the nature and extent of brain damage.
The newborn with hypoxic-ischemic brain injury, including deep gray matter of basal ganglia and cortical watershed territories. In case a different injury pattern is observed or damage evolves on follow-up MRI, alternative diagnoses (metabolic or genetic disorders) must be assessed.
Some brain injury patterns identifiable on MRI, such as focal arterial infarction, venous infarction, isolated intraventricular or intraparenchymal hemorrhage, porencephaly, or atypical patterns of metabolic encephalopathies, suggest that peripartum hypoxia was not the primary cause of neonatal encephalopathy.
Proper interpretation of neuroimaging is important, and continuous training is necessary. If limited experience in neonatal neurorradiology is available and inconsistencies in the child's clinical profile are observed, expert opinion should be requested.
In the presence of brain damage consistent with a hypoxic-ischemic injury pattern, neuroimaging cannot determine the etiology of the hypoxic-ischemic event, such as whether it was caused by placental insufficiency or interruption of umbilical cord flow.

Absence of evidence of immediate or delayed factors that could have contributed.

In case other significant risk factors exist, such as IUGR, maternal infection, fetomaternal hemorrhage, neonatal sepsis, or chronic placental lesions, attributing the causality of neurological dysfunction to a perinatal hypoxic-ischemic event is less plausible.

Other subtypes of cerebral palsy (e.g. hemiplegic) are less associated with perinatal hypoxic-ischemic events.

Other subtypes of cerebral palsy (e.g. hemiplegic) are less associated with perinatal hypoxic-ischemic events.
Other neurodevelopmental disorders can be secondary to a hypoxic-ischemic event, but they are not specific and can be due to many other causes.