Related Experiment Video
Updated: Jan 30, 2026

08:47
The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia
Published on: November 19, 2008
36.3K
Hypothermia for newborns with hypoxic-ischemic encephalopathy
1Canadian Paediatric Society, Fetus and Newborn Committee, Ottawa, Ontario.
Paediatrics & Child Health
|January 19, 2019
Summary
Therapeutic hypothermia is recommended for infants with hypoxic-ischemic encephalopathy (HIE) born at 35 weeks gestational age or later. Optimal cooling involves maintaining 33-34°C for 72 hours, followed by rewarming.
Area of Science:
- Neonatal Medicine
- Pediatric Neurology
- Critical Care
Background:
- Hypoxic-ischemic encephalopathy (HIE) is a serious condition in newborns.
- Therapeutic hypothermia is a recognized treatment for moderate-to-severe HIE.
- Evidence supports its use in infants ≥36 weeks gestational age (GA).
Purpose of the Study:
- To outline the current recommendations for therapeutic hypothermia in HIE.
- To provide guidance on its application in specific gestational age groups.
- To detail optimal cooling parameters and adjunctive treatments.
Main Methods:
- Review of existing evidence and clinical guidelines.
- Focus on gestational age criteria for hypothermia initiation.
- Emphasis on temperature monitoring and management.
Main Results:
- Therapeutic hypothermia is standard for infants ≥36 weeks GA with moderate-to-severe HIE.
- Consideration for infants at 35 weeks GA if criteria are met; not recommended for <35 weeks GA.
- Optimal core temperature is 33-34°C for 72 hours, followed by 6-12 hours rewarming.
Conclusions:
- Therapeutic hypothermia, when initiated promptly and managed optimally, is crucial for HIE.
- Adjunctive treatments include seizure management and metabolic/gas exchange control.
- Neuroimaging (MRI) and multidisciplinary follow-up are vital for assessing outcomes.
Related Concept Videos
Ischemic Heart Disease: Overview
3.4K
Ischemic heart disease occurs when the heart's blood supply dwindles, causing an ominous lack of oxygen and nutrients. This deficiency, stemming from reduced or obstructed blood flow, spells danger, leading to heart muscle damage and dysfunction.
Atherosclerosis, the primary malefactor, orchestrates this dangerous condition. It manifests as the accumulation of fatty deposits, akin to insidious plaques, within arterial walls. As time elapses, these plaques metamorphose, hardening and...
Atherosclerosis, the primary malefactor, orchestrates this dangerous condition. It manifests as the accumulation of fatty deposits, akin to insidious plaques, within arterial walls. As time elapses, these plaques metamorphose, hardening and...
3.4K
Amyloid Fibrils
11.9K
Amyloid fibrils are aggregates of misfolded proteins. Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils.
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining,...
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining,...
11.9K
Imprinting
11.1K
Behavioral imprinting is observed in some newborn animals and occurs when they develop strong and specific attachments to another animal (usually a parent) following brief, early-life exposures. Offspring imprint onto parents within a brief period after birth or hatching; this time window is called the critical period. Once imprinting occurs, the bond established between the parents and their offspring is usually long-lasting.
11.1K

