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I. Intensive care

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Asphyxia and hypoxic ischemic encephalopathy

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  1. Definitions

    1. Perinatal asphyxia: Historically, the term perinatal asphyxia has been used to describe a clinical condition in the newborn associated with hypoxia and acidemia of sufficient magnitude to cause harm. In clinical practice, this term is nonspecific and should be avoided.

    2. Hypoxic ischemic encephalopathy: Hypoxic ischemic encephalopathy (HIE) is a form of neonatal encephalopathy that occurs in term neonates who have

      1. Evidence of severe acidosis or need for resuscitation at birth

      2. Direct evidence of an abnormal neurobehavioral state characterized by seizures and/or abnormalities in consciousness, tone, posture, and reflexes

      3. Evidence of an acute perinatal or sentinel event

      4. Characteristic neuroimaging findings

      5. Exclusion of other etiologies of neonatal encephalopathy Fulfillment of all five criteria is not always possible, particularly in the immediate postnatal period. Neonates with the majority of these findings often are treated as having presumptive HIE as early recognition is paramount to the initiation of neuroprotective therapies within the therapeutic window.

    3. The terminology associated with this condition is controversial.

  2. Incidence or prevalence

    1. The prevalence of HIE is 0.5 to 1 per 1000 live births in the United States and developed nations and significantly higher in low and midresource settings where precise figures are unavailable.

    2. Limited data on the true incidence exist.

  3. Pathophysiology

    1. The pathophysiology of HIE is extrapolated from human neuropathological studies and preclinical models with clearly defined hypoxic-ischemic insults (systemic hypoxemia, cerebral hypoperfusion or both) and is characterized at the cellular level by a biphasic process of primary and secondary energy failure.

    2. The initial phase consists of the triggering hypoxic-ischemic interval that leads to primary energy failure (a reduction in high-energy phosphorylated metabolites and intracellular pH). This phase may be so severe that it results in permanent brain injury or if subacute may be responsive to resuscitation.

    3. Approximately 6 to 24 hours later, secondary energy failure ensues characterized by activation of proteases and endonucleases, neuronal apoptosis, microglial activation, reduction of growth factors and protein synthesis, and further accumulation of excitatory neurotransmitters.

    4. Neuronal cell death may be immediate or delayed and result from neuronal apoptosis or necrosis.

    5. In human neonates, the pathway to brain injury is not always clear. Many factors such as etiology, brain maturation, extent and timing of hypoxia-ischemia, cerebral blood flow patterns, and the general health of the fetus prior to injury can affect the outcome.

  4. Risk factors: Risk factors include any condition in which resuscitation at birth may be required and may be divided into

    1. Maternal factors: Hypertension, cardiopulmonary abnormalities, cardiac arrest, hypovolemic shock, severe anaphylactoid reactions, status epilepticus, etc.

    2. Uteroplacental factors: Uterine rupture, placental abruption, infarction, fibrosis, underperfusion, placenta previa, etc.

    3. Umbilical cord factors: Umbilical cord prolapse, cord entanglement or compression, abnormalities of umbilical vessels, tight nuchal cord, true knot, etc.

    4. Intrapartum factors: Abnormal presentation, nonreassuring fetal status, thick meconium, prolonged labor, precipitous delivery, difficult delivery requiring instrumentation (forceps, vacuum), prolonged pregnancy, etc.

    5. Fetal factors: Fetomaternal hemorrhage, severe isoimmune hemolytic disease, arrhythmias, twin-to-twin transfusion syndrome, etc.

    Perinatal ...

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