Perinatal asphyxia is a common pathology of the neonatal period. It is one of the most frequent causes of neonatal death in the perinatal period and the most important cause of neurodevelopmental disorders later in life. It arises as a result of hypoxemia, i.e., reduced oxygen tension in the blood, or ischemia, i.e., impaired blood flow to brain tissue. In newborns delivered after 35 weeks of gestation, brain hypoxia leads to the development of hypoxic-ischemic encephalopathy (HIE).
Depending on the degree of hypoxia, hypoxic-ischemic encephalopathy may have a mild, moderate, or severe course. Symptoms of mild HIE include hyperexcitability, sympathetic predominance, tachycardia, and a normal EEG. The moderate form is characterized by drowsiness, muscle hypotonia, parasympathetic predominance, bradycardia, intermittent seizures, and an EEG with epileptiform activity. The severe form includes coma, flaccidity, disturbances of both the sympathetic and parasympathetic systems, and an isoelectric EEG. As a consequence, hypoxia may lead to death, cerebral palsy, intellectual disability, cognitive impairment, and epilepsy.
Hypothermia is a method of neuroprotection for the central nervous system. In 2010 it was recognized as a therapeutic method in European guidelines on neonatal resuscitation. Currently, two methods of therapeutic cooling exist—head (selective) hypothermia and whole-body hypothermia. Whole-body cooling together with selective brain cooling (using the Olympic Cool-Cap System) have been accepted as effective treatments for hypoxic-ischemic encephalopathy in newborns by the U.S. Food and Drug Administration (FDA) and the European Medicines Agency (EMEA) and approved for use in Poland [5].
The neuroprotective effect of hypothermia is associated with slowing brain tissue metabolism, leading to reduced glucose and oxygen demand. Brain tissue metabolism decreases by 6–10% for each 1˚C drop in body temperature, which reduces the release of excitatory amino acids and free radicals. When the temperature drops to 32˚C, metabolism as well as oxygen demand and CO₂ production fall to 50–65% of normal. This requires adjusting ventilation parameters in newborns with HIE to avoid hyperventilation.
The protective effect of hypothermia is probably related to inhibition of proteases and calpains. Other metabolic changes during cooling include increased glycerol, free fatty acids, ketones, and lactate—leading to mild metabolic acidosis. Hypothermia also reduces insulin secretion, which may cause hyperglycemia. Hypothermia delays apoptosis.
Therapeutic hypothermia after perinatal asphyxia is offered to newborns born at or after 36 weeks of gestation who meet at least one of the following criteria:
Patients are also assessed for neurological criteria such as:
In every newborn considered for therapeutic hypothermia, anorectal malformation, head injury or skull fracture—which may cause severe intracranial hemorrhage—and a birth weight below 1800 g should be excluded. In cases of extremely severe encephalopathy, for example when aEEG/EEG shows an isoelectric line at 12–24 hours of life, hypothermia treatment is considered inappropriate.
If the newborn meets the above criteria and fewer than 6 hours have passed since birth, the infant is qualified for hypothermia therapy. If possible, the newborn is monitored with aEEG.