scholarly journals Comparison of Uncontrolled and Device-Induced Therapeutic Hypothermia in Newborn Infants with Hypoxic Ischemic Encephalopathy

2021 ◽  
Vol 6 (1) ◽  
pp. 88-93
Author(s):  
A. A. Zarubin ◽  
E. S. Filippov ◽  
A. S. Vanyarkina ◽  
O. G. Ivanova ◽  
A. A. Shishkina
Keyword(s):  
High Risk ◽  
Body Temperature ◽  
Therapeutic Hypothermia ◽  
Neuroprotective Effect ◽  
Newborn Infants ◽  
The Body ◽  
Hypoxic Ischemic Encephalopathy ◽  
Temperature Management ◽  
Hypothermia Group ◽  
Ischemic Encephalopathy

Background. Newborn infants who have undergone severe birth asphyxia have a high risk of neurological disorders and death. The most effective method for the treatment of hypoxic ischemic encephalopathy caused by intrapartum asphyxia is therapeutic hypothermia, or targeted temperature management. Currently, there are no large studies comparing its different methods, therefore the aim of our study was to compare the effectiveness of device-induced and uncontrolled therapeutic hypothermia in newborn infants who underwent intrapartum asphyxia.Materials and methods. Study design: we conducted a retrospective, longitudinal, cohort study in 39 newborn infants born in severe asphyxia and receiving uncontrolled therapeutic hypothermia (group 1), and in 48 newborn infants born in severe asphyxia and receiving device-induced therapeutic hypothermia (group 2). Statistical data processing was carried out using standard techniques.Results. The body temperature in newborn infants of both groups was reduced to 33.5 °C within the first hour, but when using uncontrolled therapeutic hypothermia, the body temperature fluctuated from 32 to 35 °C. Device-induced therapeutic hypothermia has a more effective neuroprotective effect as compared to uncontrolled hypothermia (p< 0.05) and more rapidly stabilizes metabolism in newborns due to a decrease in lactate levels (p < 0.05). In newborns device-induced therapeutic hypothermia stabilizes hemodynamics more quickly compared to uncontrolled therapeutic hypothermia (p < 0.05). Device-induced therapeutic hypothermia reduces the period of hospitalization in the neonatal intensive care unit (p < 0.05), the risk of cerebral edema (p < 0.05) and of the repeated episodes of seizures (p < 0.05). Conclusion. Using uncontrolled therapeutic hypothermia causes a high risk of unintentional fluctuations in rectal temperature towards both hypothermia and rewarming, which can aggravate the severe condition of newborn infants. Device-induced therapeutic hypothermia has a more effective neuroprotective effect.

scholarly journals Inhaled H2 or CO2 Do Not Augment the Neuroprotective Effect of Therapeutic Hypothermia in a Severe Neonatal Hypoxic-Ischemic Encephalopathy Piglet Model

2020 ◽  
Vol 21 (18) ◽  
pp. 6801
Author(s):  
Viktória Kovács ◽  
Gábor Remzső ◽  
Valéria Tóth-Szűki ◽  
Viktória Varga ◽  
János Németh ◽  
...  
Keyword(s):  
Caudate Nucleus ◽  
Therapeutic Hypothermia ◽  
Neuroprotective Effect ◽  
Fold Increase ◽  
Hypoxic Ischemic Encephalopathy ◽  
Mrna Levels ◽  
Treatment Groups ◽  
Apoptosis Inducing Factor ◽  
Co2 Treatment ◽  
Ischemic Encephalopathy

Hypoxic-ischemic encephalopathy (HIE) is still a major cause of neonatal death and disability as therapeutic hypothermia (TH) alone cannot afford sufficient neuroprotection. The present study investigated whether ventilation with molecular hydrogen (2.1% H2) or graded restoration of normocapnia with CO2 for 4 h after asphyxia would augment the neuroprotective effect of TH in a subacute (48 h) HIE piglet model. Piglets were randomized to untreated naïve, control-normothermia, asphyxia-normothermia (20-min 4%O2–20%CO2 ventilation; Tcore = 38.5 °C), asphyxia-hypothermia (A-HT, Tcore = 33.5 °C, 2–36 h post-asphyxia), A-HT + H2, or A-HT + CO2 treatment groups. Asphyxia elicited severe hypoxia (pO2 = 19 ± 5 mmHg) and mixed acidosis (pH = 6.79 ± 0.10). HIE development was confirmed by altered cerebral electrical activity and neuropathology. TH was significantly neuroprotective in the caudate nucleus but demonstrated virtually no such effect in the hippocampus. The mRNA levels of apoptosis-inducing factor and caspase-3 showed a ~10-fold increase in the A-HT group compared to naïve animals in the hippocampus but not in the caudate nucleus coinciding with the region-specific neuroprotective effect of TH. H2 or CO2 did not augment TH-induced neuroprotection in any brain areas; rather, CO2 even abolished the neuroprotective effect of TH in the caudate nucleus. In conclusion, the present findings do not support the use of these medical gases to supplement TH in HIE management.

scholarly journals Efficiency Evaluation of Neuroprotection for Therapeutic Hypothermia to Neonatal Hypoxic-Ischemic Encephalopathy

2021 ◽  
Vol 15 ◽  
Author(s):  
Bowen Weng ◽  
Chongbing Yan ◽  
Yihuan Chen ◽  
Xiaohui Gong ◽  
Cheng Cai
Keyword(s):  
Therapeutic Hypothermia ◽  
Conventional Therapy ◽  
Infant Development ◽  
Therapy Group ◽  
Hypoxic Ischemic Encephalopathy ◽  
Neuron Development ◽  
Significant Difference ◽  
Hypothermia Group ◽  
Conventional Therapy Group ◽  
Ischemic Encephalopathy

Background: To evaluate the safety and neurological outcomes of therapeutic hypothermia to neonatal hypoxic-ischemic encephalopathy (HIE).Materials and Methods: Medical records of 61 neonates with moderate to severe HIE were retrospectively enrolled and divided into a therapeutic hypothermia group (n = 36) and conventional therapy group (n = 25).Results: No significant difference in the incidence of severe adverse events was found between the two groups. Minimum and maximum voltages of amplitude-integrated electroencephalography (aEEG) recording results showed statistically significant differences in therapeutic hypothermia group after 72 h. The neonatal behavioral neurological assessment (NBNA) on the 28th day after birth and Bayley Scales of Infant Development, second edition (BSID II) scores at 18 months old were significant higher in the therapeutic hypothermia group than the conventional therapy group.Conclusion: Therapeutic hypothermia for neonates with moderate to severe HIE improved the development of the nervous system in 0–18-month-old infants and showed a predominant role in reducing death and major neuron development-associated disabilities.

P0250COLD DIURESIS DURING TARGETED TEMPERATURE MANAGEMENT AFTER CARDIAC ARREST, MYTH OR FACT?

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Min-Jeong Lee ◽  
Minjung Kathy Chae
Keyword(s):  
Cardiac Arrest ◽  
Body Temperature ◽  
Therapeutic Hypothermia ◽  
Urine Output ◽  
The Body ◽  
Targeted Temperature Management ◽  
Neurologic Outcome ◽  
Temperature Management ◽  
Induction Phase ◽  
Target Temperature

Abstract Background and Aims Therapeutic hypothermia or targeted temperature management (TTM) has been standard treatment for cardiac arrest survivors with suspected hypoxic ischemic brain injury for improvement in both survival and neurological outcomes. TTM is consisted of an induction phase of quickly lowering the temperature to target temperature (ranging from 32°C -36°C) as soon as possible, a hypothermia maintenance phase of keeping the body temperature at target temperature for at least 24 hours, a rewarming phase of slowly rewarming the temperature to normothermia, and a normothermia phase of keeping the body temperature at normothermia. During the dynamic changes in body temperature, cold-diuresis is a commonly described phenomenon. However, limited studies have characterized cold-induced diuresis during TTM. In this study, we sought to determine urine output changes during post cardiac arrest therapeutic hypothermia. Method This retrospective cohort study included adult patients who underwent TTM after out-of-hospital cardiac arrest and were admitted to the intensive care unit for post cardiac arrest care between January 2012 and August 2018. The exclusion criteria of this study were as follows: 1) deceased status before the completion of all phase of TTM; 2) previous end stage kidney disease patients, 3) undergoing renal replacement therapy due to AKI within 48 hours of TTM termination; 4) terminal cancer less than 6 months of life expectancy or previously cerebral performance category (CPC) 3 or more. The neurologic outcome was assessed using the CPC score after 1 month. Good neurologic outcome was defined as a CPC score of 1, 2 and poor neurologic outcome as a CPC score of 3 to 5. The post cardiac arrest protocol recommends a target temperature of 33°C unless the patient is hemodynamically unstable or has a bleeding tendency or severe infection. Rewarming rate was 0.15°C/hr or 0.25°C/hr. TTM was conducted with the use of temperature managing devices with a feedback loop system (Artic Sun Energy Transfer Pads, Medivance Corp., Louisville, CO, USA; Cool Guard Alsius Icy Heat Exchange Catheter, Alsius Corporation, Irvine, CA, USA). We calculated the hourly IV fluid input and urine output rates for each TTM phase. To compare the mean of urine volume between each TTM phase, we used repeated measure analysis of variance (ANOVA). Results 178 Patients included in the analysis. We observed a increase in urine output rates during hypothermia induction. This effect persisted even after adjustment for variable clinical confounders, including intravenous fluid input rate, mean arterial pressure (MAP), initial shockable rhythm, SOFA score, body mass index, and IV furosemide use. However, we did not detect any evidence of urine output increases or decreases during the hypothermia maintenance or rewarming phases. By repeating measures ANOVA and a linear mixed model, it was confirmed that there is a difference in urine output for each TTM phase. Even after the post hoc analysis was calibrated with several variables, only the hypotheria induction phase differed significantly from the urine output of the phase. Conclusion Although our results are some limitations, the findings support the potential presence of cold-induced dieresis, but not rewarm anti-diuresis during TTM. Our study may not fully capture the extent of renal impairment in post cardiac arrest undergoing TTM. However, our objective was to characterize urine output during TTM in post cardiac arrest patients. This has important implications for fluid management in patients undergoing TTM.

scholarly journals Treating Seizures after Hypoxic-Ischemic Encephalopathy—Current Controversies and Future Directions

2021 ◽  
Vol 22 (13) ◽  
pp. 7121
Author(s):  
Kelly Q. Zhou ◽  
Alice McDouall ◽  
Paul P. Drury ◽  
Christopher A. Lear ◽  
Kenta H. T. Cho ◽  
...  
Keyword(s):  
Therapeutic Hypothermia ◽  
Newborn Infants ◽  
Developing Brain ◽  
Hypoxic Ischemic Encephalopathy ◽  
Neurodevelopmental Outcomes ◽  
High Quality ◽  
Future Directions ◽  
Phenobarbital Administration ◽  
The Impact ◽  
Ischemic Encephalopathy

Seizures are common in newborn infants with hypoxic-ischemic encephalopathy and are highly associated with adverse neurodevelopmental outcomes. The impact of seizure activity on the developing brain and the most effective way to manage these seizures remain surprisingly poorly understood, particularly in the era of therapeutic hypothermia. Critically, the extent to which seizures exacerbate brain injury or merely reflect the underlying evolution of injury is unclear. Current anticonvulsants, such as phenobarbital and phenytoin have poor efficacy and preclinical studies suggest that most anticonvulsants are associated with adverse effects on the developing brain. Levetiracetam seems to have less potential neurotoxic effects than other anticonvulsants but may not be more effective. Given that therapeutic hypothermia itself has significant anticonvulsant effects, randomized controlled trials of anticonvulsants combined with therapeutic hypothermia, are required to properly determine the safety and efficacy of these drugs. Small clinical studies suggest that prophylactic phenobarbital administration may improve neurodevelopmental outcomes compared to delayed administration; however, larger high-quality studies are required to confirm this. In conclusion, there is a distinct lack of high-quality evidence for whether and to what extent neonatal seizures exacerbate brain damage after hypoxia-ischemia and how best to manage them in the era of therapeutic hypothermia.

scholarly journals The feasibility of Telemedicine in Implementation of Therapeutic Hypothermia for Management of Neonatal Hypoxic-Ischemic Encephalopathy in Resource-Limited Areas.

2022 ◽  
Author(s):  
Adnan Hadid ◽  
Taher AL-Shantout ◽  
Rayan Terkawi ◽  
Baraa Aldbes ◽  
Manal Zahran ◽  
...  
Keyword(s):  
Therapeutic Hypothermia ◽  
Newborn Infants ◽  
Developed Countries ◽  
Mobile App ◽  
Hypoxic Ischemic Encephalopathy ◽  
Target Range ◽  
North West ◽  
The North ◽  
Resource Limited ◽  
Ischemic Encephalopathy

Abstract Background: Telemedicine is widely used in neonatal services in developed countries. Lack of expertise and/or facilities, however, limited its use in developing countries and around areas of military conflicts. To our knowledge, no reports are demonstrating the feasibility of administering therapeutic hypothermia (TH) through telemedicine to neonates with hypoxic-ischemic encephalopathy (HIE) in resource-limited areas.Methodology: This is a retrospective study, evaluating 22 patients who received TH, guided by telemedicine, through a mobile app (Telegram®). We assessed the feasibility of utilizing Telemedicine in guiding the application of TH to infants affected with HIE in the North-West of Syria between July 2020 and July 2021.Results: Out of 5,545 newborn infants delivered during the study period, 22 patients were eligible for TH guided by Telemedicine. Patients were referred for consultation at a median (IQR) of 137 (35-165) minutes of life. A median (IQR) of 12 (3-18) minutes elapsed between the call for a consultation and the consultant response, and a median (IQR) of 30 (0-42) minutes elapsed between seeking the consultation and the initiation of cooling therapy. Eighteen patients completed cooling for 72 hours. The patients' temperatures were within the target range (33-34°C) most of the time (84.1%).Conclusion: Telemedicine is a feasible method to guide the implementation TH for HIE in resource-limited areas. The short-term success rate is relatively high; however, further studies with a larger population are needed to confirm these findings.

Therapeutic Hypothermia for Management of Neonatal Asphyxia: What Nurses Need to Know

2011 ◽  
Vol 31 (3) ◽  
pp. e1-e12 ◽  
Author(s):  
Nevart Chirinian ◽  
Nancy Mann
Keyword(s):  
Body Temperature ◽  
Therapeutic Hypothermia ◽  
Birth Asphyxia ◽  
Mount Sinai Hospital ◽  
Cerebral Injury ◽  
Hypoxic Ischemic Encephalopathy ◽  
Normal Body Temperature ◽  
Normal Body ◽  
Wide Range ◽  
Ischemic Encephalopathy

Birth asphyxia can induce a cascade of reactions that result in altered brain function known as hypoxic-ischemic encephalopathy. Possible outcomes for survivors of birth asphyxia vary widely, from a normal outcome to death, with a wide range of disabilities in between, including long-term neurodevelopmental disability, cerebral palsy, neuromotor delay, and developmental delay. Treatment of hypoxic-ischemic encephalopathy has centered on dampening or blocking the biochemical pathways that lead to death of neuronal cells. The reduction of body temperature by 3ºC to 5ºC less than normal body temperature can reduce cerebral injury. At Mount Sinai Hospital in Toronto, Ontario, the goal of therapeutic hypothermia is to achieve a rectal temperature of 33ºC to 34ºC, and the protocol is started within 6 hours after birth. The hypothermia is maintained for 72 hours, and then the infant is gradually warmed to normal body temperature (36.8ºC–37ºC). The protocol and nursing implications are presented.

Visual outcomes in children with neonatal hypoxic ischemic encephalopathy treated with therapeutic hypothermia

2021 ◽  
Author(s):  
Jerry Hsu ◽  
Noreen Shaikh ◽  
Hantamalala Ralay Ranaivo ◽  
Andrea C. Pardo ◽  
Rebecca B. Mets-Halgrimson
Keyword(s):  
Therapeutic Hypothermia ◽  
Hypoxic Ischemic Encephalopathy ◽  
Visual Outcomes ◽  
Ischemic Encephalopathy
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