|Year : 2016 | Volume
| Issue : 1 | Page : 1-2
Neonatal hypoxic ischemic encephalopathy: From bench to bedside
Sajjad ur Rahman1, Kivilcim Gucuyener2, Mohamed Tagin3
1 Professor of Pediatrics and Neonatology, Peshawar Medical College, Peshawar, Pakistan
2 Professor of Pediatric Neurology, Gazi University, Ankara, Turkey
3 Consultant Neonatologist Women's Hospital, 735 Notre Dame Ave, Winnipeg, MB, Canada
|Date of Web Publication||6-Jan-2016|
Sajjad ur Rahman
Department of Pediatrics, Peshawar Medical College, Warsak Road, Peshawar
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Rahman S, Gucuyener K, Tagin M. Neonatal hypoxic ischemic encephalopathy: From bench to bedside. J Clin Neonatol 2016;5:1-2
Hypoxia ischemic encephalopathy (HIE), secondary to perinatal asphyxia continues to be a major global cause of neonatal mortality and morbidity. Therapeutic hypothermia (TH), started within first 6 h of birth, has become a well-established standard treatment for newborn infants with moderate to severe HIE. The current standard treatment includes induction of hypothermia (33.5°C) for 72 h (using total body cooling or selective head cooling) followed by slow rewarming. Despite the effectiveness of TH, about 50% of affected newborns will die or suffer long-term neurodevelopmental delay. A recent clinical trial by Shankaran et al. failed to show any superiority of longer and/or deeper cooling as compared to the current standard use of TH. Clinical trials using adjuvant treatments to TH using pharmacologic and nonpharmacologic neuroprotective agents (e. g., Xenon, Erythropoietin, Melatonin, MgSO4, and other neuroprotective agents) are underway. Stem cell research has been fascinating with a promising mechanism of action that may extend to the tertiary phase of brain injury including axonal restoration, migration, maturation, and trophic support.
The current issue of JCN includes three reviews addressing three different important aspects related to the current management of newborns with HIE. The first review “delayed neuroprotection in the era of hypothermia what can we add?” by Alistair J. Gunn and Floris Groenendaal (JCN_57_15), not only reviewed the pathophysiologic mechanisms of injury during HIE, it also identifies hypothermia plus therapy as the future research target. The authors suggested that clinical trials of neuroprotection should extend to cases of mild HIE, especially borderline cases that do not completely fulfill the current criteria of TH. The authors also recommended erythropoietin as the most promising preclinical neuroprotective candidate. The authors have suggested that erythropoietin could be used as a co-treatment to TH to support neuroregeneration after the therapeutic window for acute neuroprotection. They have also proposed using erythropoietin in mild HIE cases that do not fulfill the current TH criteria during the first 6 h of life and who may become symptomatic and require treatment later on.
The second review by Ebru Ergenekon (JCN_148_15) provides a practical hands-on bedside guideline on managing cases with HIE and the potential complications in clinical settings from 1st h of therapy until the end of re-warming after 3 days of treatment. Neonatal staff worldwide is currently going through a learning curve of TH as a new modality of treatment for infants with moderate to severe HIE. TH has significant multisystem effects (cardiopulmonary, renal, hematological, and metabolic effects) on both physiologic and pathologic processes. It is crucial that clinicians are well-versed in the understanding and management of these pathophysiologic effects of TH while clinically managing infants with neonatal HIE. Optimal patient care including adequate sedation, antibiotic treatment, fluid and nutritional management, renal perfusion, management of seizures, etc., are extremely important during the course of TH.
The third review by Kivilcim Gucuyener (JCN_149_15) provides a comprehensive understanding of amplitude-integrated electroencephalography (aEEG) which is a very useful bedside diagnostic and management tool for the neonatologists. The aEEG trace in term infants with HIE is a sensitive and specific test for early prediction of later adverse neurodevelopmental outcomes. aEEG reflects the degree of encephalopathy and cerebral abnormality on MRI. Digital aEEG monitors provide one or two channels of raw EEG. The aEEG trace has been shown to detect 80% of all electrographic seizures in the newborn. Since seizures after HIE are an important marker of severity of neuronal injury, monitoring by aEEG is crucial in the management of newborns with HIE.
We are grateful to the authors of these three review articles for sharing their knowledge, expertise and time by creating an excellent sequential update for neonatal clinicians, nurses and researchers worldwide.
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