//Background//---
Hypoxic ischemic encephalopathy emerges due to
not enough oxygen or blood flow, which may develop during pregnancy, delivery
or in the postnatal period. In only mild or moderate case, some children will
experience no health issues, but in severe case, some children have permanent
disability including developmental delay, cerebral palsy, epilepsy or cognitive
impairment. However, mild hypoxic ischemic encephalopathy may be associated
with adverse cognitive and motor outcome(2). Furthermore, negative health
effect is also induced in the other organ including the heart, liver, kidneys
and bowels by oxygen deficient. The cause of hypoxic ischemic encephalopathy is
following(*).
*Problems with blood flow to the placenta
*Preeclampsia
*Maternal diabetes with vascular disease
*Congenital fatal infection
*Drug or alcohol abuse
*Severe fetal anemia
*Heart disease
*Lung malformations
*Umbilical cord problems
*Abruption of the placenta or rupture of
the uterus
*Excessive bleeding from the placenta
*Abnormal fetal position, such as the
breech position
*Prolonged late stages of labor
*Very low blood pressure in the mother
The
standard care for hypoxic ischemic encephalopathy in high-income countries is
therapeutic hypothermia(3-6). However, long-term health impairment after
treatment still remain open issue(7). Combination therapy of therapeutic hypothermia
and (non) pharmacological intervention is under progression. Current cooling
protocols for 72h are reasonably optimal(8).
Mark
Adams, Barbara Brotschi, André Birkenmaier, Katharina Schwendener, Verena
Rathke, Michael Kleber, Cornelia Hagmann & Swiss National Asphyxia and
Cooling Register Group present a Swiss unit-to-unit comparison of theraputic
hypothermia outcome for the children with hypoxia ischemia encephalopathy based
on internationally agreed standardized procedures(1). I hope to share a part of
these contents and general explanation with the global important readers.
//Therapeutic hypothermia//---
Hypothermia decreases spontaneous repolarization of cardiac myocytes
and prolongs duration of action potential and impulse conduction. The
polarization between neurons (cell) is related to cell communication.
Therefore, heart function could improve by therapeutic hypothermia. Actually, J
waves, which is most classic electrocardiographic abnormality, are rarely seen
in mild (32-34℃) hypothermia(9,10). Therefore, hypoxia
could be alleviated through improved heart function by therapeutic hypothermia.
In addition, hypothermia decrease cell metabolic rate, so demand of oxygen is
modified, and has tissue-specific effect such as decreasing excitotoxicity,
limiting inflammation, preventing ATP deletion, reducing free radical
production, and intracellular calcium overload to avoid apoptosis(11). Hence,
neuron and glia cell in the brain of the neonate could be protected by
therapeutic hypothermia.
//Condition(1)//---
Participants: 570 neonates with
hypoxic-ischemic encephalopathy (HIE)
Periode: 2011 to 2018
Place: 10 Swiss units
Based on the standardized Swiss protocol
(SSP) for treatment of HIE with TH
//Short term outcome(1)//---
*Unit 1~10 Total
Time to reach target temperature: 4.1h
Temperature on admission: 34.9℃
Over or undercooling: 29%
Passive cooling: 30%
Hypotension: 67%
Seizures: 36%
Coagulopathy: 40%
Infection: 7%
Persistent pulmonary hypertension of the
newborn: 18%
Died during primary hospitalization: 16%
(84% discharged)
-
//Conclusion(1)//---
The therapeutic
hypothermia for the children with hypoxia ischemia encephalopathy is effective
in short-term, but we have room to improve.
//Special note//---
Timing of hypothermia treatment for the child
with hypoxia ischemic encephalopathy is important. It is shown that this
treatment before 3h of age is better outcome than that after 3h of age(12).
Therefore, we need to implement therapeutic hypothermia immediately after the
birth, so time to reach target temperature may be important. In Mark Adams et
al study, reaching time is about 4.1h. The set cooling temperature was
effective at 33.5℃ in some clinical studies(8,13).
Therefore, the temperature trajectory including over- or under cooling needs to
be refined.
Cranial ultrasound immediately after birth in
the case of brain dysfunction can differentiate several abnormalities including
other cause of neonatal encephalopathy such as hypoplastic corpus callosum,
germinolytic cysts. MRI can provide a reliable guide to progonosis of
neurodevelopmental outcome up to childhood(14-16).
//Contributions(1)//---
All authors were involved in data
collection and study design. MA performed all statistical analyses. MA and CH
analyzed the data, interpreted the results, and wrote the first draft of the
paper and revised the subsequent drafts. All authors critically reviewed the
drafts, read, and approved the final paper.
//Ethics declarations(1)//---
Competing interests
MA receives a salary as network coordinator
for SwissNeoNet, the host of the National Asphyxia and Cooling Register. The
remaining authors have no potential conflicts of interest relevant to this
article to disclose.
//Ethics approval and consent to
participate//---
Data collection, evaluation, and
publication for this study was approved by the Swiss Ethical Committee and the
Swiss Federal Commission for Privacy Protection in Medical Research
(KEK-ZH-Nr2014-0551 and KEK-ZH-Nr2014-0552).
(Reference)
(1)
Mark Adams, Barbara Brotschi, André
Birkenmaier, Katharina Schwendener, Verena Rathke, Michael Kleber, Cornelia
Hagmann & Swiss National Asphyxia and Cooling Register Group
Process variations between Swiss units
treating neonates with hypoxic-ischemic encephalopathy and their effect on
short-term outcome
Journal of Perinatology (2021)
---
Author information
Affiliations
Newborn Research, Department of
Neonatology, University and University Hospital Zurich, Zurich, Switzerland
Mark Adams, Dirk Bassler, Giancarlo
Natalucci & Susanne Böttger
Division of Neonatology and Pediatric
Intensive Care, Children’s University Hospital Zurich, Zurich, Switzerland
Barbara Brotschi, Verena Rathke, Cornelia
Hagmann, Bernhard Frey, Vera Bernet & Beate Grass
Department of Neonatology and Pediatric
Intensive Care, Children’s Hospital St. Gallen, Neonatal and Pediatric
Intensive Care Unit, St. Gallen, Switzerland
André Birkenmaier, Bjarte Rogdo & Irene
Hoigné
Department of Neonatology and Pediatric
Intensive Care, Children’s Hospital, Spitalstrasse, Lucerne, Switzerland
Katharina Schwendener, Martin Stocker,
Thomas M. Berger & Matteo Fontana
Clinic of Neonatology, Cantonal Hospital
Winterthur, Winterthur, Switzerland
Michael Kleber & Lukas Hegi
Department of Neonatology, Children’s
Clinic, Cantonal Hospital Aarau, Aarau, Switzerland
Philipp Meyer & Gabriel Konetzny
Department of Neonatology, University
Children’s Hospital Basel (UKBB), Basel, Switzerland
Sven M. Schulzke, Sven Wellmann & Maya
Hug
Department of Pediatric Intensive Care,
University Hospital Berne, Berne, Switzerland
Tilman Humpl, Bendicht Wagner & Karin
Daetwyler
Department of Neonatology, Children’s
Hospital Chur, Chur, Switzerland
Thomas Riedel, Brigitte Scharrer &
Nicolas Binz
Department of Neonatology, University
Hospital (CHUV), Lausanne, Switzerland
Anita Truttmann & Juliane Schneider
Consortia
Swiss National Asphyxia and Cooling
Register Group
Dirk Bassler, Giancarlo Natalucci, Susanne
Böttger, Bernhard Frey, Vera Bernet, Beate Grass, Bjarte Rogdo, Irene Hoigné,
André Birkenmaier, Martin Stocker, Thomas M. Berger, Matteo Fontana, Katharina
Schwendener, Lukas Hegi, Michael Kleber, Philipp Meyer, Gabriel Konetzny, Sven
M. Schulzke, Sven Wellmann, Maya Hug, Tilman Humpl, Bendicht Wagner, Karin
Daetwyler, Thomas Riedel, Brigitte Scharrer, Nicolas Binz, Anita Truttmann
& Juliane Schneider
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