Abstract
AbstractTherapeutic hypothermia (TH) either by selective head cooling or whole-body cooling decreases brain damage and provide neuroprotection and reduced mortality rate in cases of moderate-to-severe hypoxia-ischemia encephalopathy (HIE) of newborns, especially if started at first 6 hours after birth. Also, management with adjuvant therapies like magnesium sulfate (MS) provides more neuroprotection. The interventional randomized controlled research aimed to assess short-term actions of TH as sole therapy and in combination with MS as a neuroprotective agent for the treatment of HIE newborn infants. A total of 36 full-terms and near-term infants delivered at Assiut University Children's Hospital and fulfilled HIE criteria were enrolled. They were divided equally into three groups; Group 1 (n = 12) received whole body cooling during first 6 hours of life as a sole therapy; Group 2 (n = 12) received whole body cooling in addition to MS as adjuvant therapy; Group 3 (n = 12) received supportive intensive care measures as a control. TH plus MS group (group 2) had a significantly good short-term outcomes as short period of respiratory support and mechanical ventilation (p-value =0.001), less in incidence of convulsion (p-value = 0.001) and early in feeding initiation (p-value = 0.009), compared with other groups managed by TH (group 1) or by supportive treatment (group 3). In conclusion, whole body cooling in addition to MS as adjunctive therapy for the treatment of HIE neonates is safe therapy that improves short-term outcome both clinically and radiologically.
Highlights
Hypoxic-ischemic encephalopathy (HIE) is an acquired syndrome manifested by a clinical, laboratory, and radiological evidence of acute brain injury.[1]
The patients were separated into two subgroups before randomly assigning them to moderate and severe HIE, each group divided into three groups
The group that received hypothermia with magnesium sulfate (MS) had a shorter length of mechanical ventilation and respiratory support versus group that received hypothermia alone, which was likewise shorter than the control group
Summary
Hypoxic-ischemic encephalopathy (HIE) is an acquired syndrome manifested by a clinical, laboratory, and radiological evidence of acute brain injury.[1] Perinatal asphyxia affects two out of every 1,000 live births in wealthy countries, but it affects. HIE is accompanied by two phases of pathologic events, primary and secondary energy failure. Outcome of Infants with Hypoxic-Ischemic Encephalopathy Abdel-Aziz SM et al e281 blood flow and oxygen substrate, as well as significant tissue acidity, characterize primary energy failure.[3] Secondary energy failure includes several pathophysiologic actions as summation of excitatory brain neurotransmitters, oxidative stress, inflammation, apoptosis, changed growth factors, and protein formation.[4] There is a latent phase between primary and secondary energy failure, which corresponds to a therapeutic window of roughly 6 hours during which neuroprotective therapy should be started.[5]
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