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Maternal holding during therapeutic hypothermia for infants with neonatal encephalopathy is feasible.

ABSTRACT: AIM:Concerns for infant destabilisation often prohibit parental holding of infants during therapeutic hypothermia (TH). We assessed the feasibility of maternal holding during TH, as the inability to hold can impede bonding. METHODS:Vital signs were assessed in stable infants before, at two-minute intervals during and 30 minutes after a single 30-minute holding session. The infant remained on the blanket throughout holding, and both infant and blanket were placed into the mother's arms on top of a thin foam insulating barrier. Mothers and nurses were surveyed about their experience. RESULTS:Ten infants undergoing TH for neonatal encephalopathy had no equipment malfunctions or dislodgement. The mean temperature was 33.4°C prior to and 33.5°C (p = 0.18) after holding. There was no significant bradycardia (heart rate <80 beats per minute), hypotension (mean arterial pressure <40 mm Hg) or oxygen desaturation (<93%). Nurses either strongly agreed (75%) or agreed (25%) with the statement 'After assisting with the holding protocol, I feel that holding during cooling is safe'. Mothers (100%) strongly agreed that other parents would benefit from holding. CONCLUSION:In a small sample of ten stable infants treated with TH for neonatal encephalopathy, holding resulted in no adverse events and positive feedback from mothers and nurses.

SUBMITTER: Craig A

PROVIDER: S-EPMC6682469 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature

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Clonidine for sedation in infants during therapeutic hypothermia with neonatal encephalopathy: pilot study.

Project description:ObjectiveTo determine a safe dose of clonidine (CLON) to be used in infants with hypoxic ischemic encephalopathy (HIE) undergoing therapeutic hypothermia (TH).Study designA pilot prospective study was performed to determine the effect of CLON on autonomic parameters, the pharmacokinetics (PK) of CLON, and the amount of morphine (MOR) given "as needed" for shivering and agitation in a cohort of infants (n = 12) with HIE undergoing TH compared to a historical control group (n = 28).ResultsThe CLON group received less "as needed" MOR than the MOR-only group for agitation/shivering (p < 0.001), and the CLON vs. MOR-only group spent 92% vs. 79% of cooling time at the target core body temperature (CBT; p = 0.03, CLON vs. MOR).ConclusionsIntravenous CLON (1 mcg/kg Q8h) is well tolerated in infants treated with TH for HIE. CLON stabilizes CBT in the ideal range during cooling, which may be optimal for neuroprotection.

| S-EPMC8917970 | biostudies-literature

Therapeutic hypothermia for neonatal encephalopathy.

Project description:Opinion statementNeonatal Hypoxic-ischemic encephalopathy in full term infants has been associated with a high risk for morbidity and mortality. The patho-physiology of brain injury following hypoxia-ischemia, noted in preclinical models, is a cascade of events resulting from excitotoxic and oxidative injury culminating in cell death. Hypothermia has been noted to be protective by inhibiting various events in the cascade of injury. Major randomized clinical trials in neonatal HIE have demonstrated reduction in death and disability and continued safety and efficacy of neuroprotection in childhood. There is now clinical and imaging evidence for hypothermia as neuroprotection. Hypothermia should be offered to term infants with either severe acidosis at birth or resuscitation needing continued ventilation and evidence of either moderate or severe encephalopathy within 6 hours of birth. The target temperature should be 33° to 34 °C and duration of cooling should be 72 hours, as per the published trials. Rewarming should be slow, at 0.5 °C per hour. Infants should have serial neurological examinations during and at the end of cooling and at discharge. Multiorgan function should be supported and hypocarbia should be avoided during ventilator therapy. If available, the amplitude integrated EEG should be obtained prior to cooling and following rewarming. All infants should have magnetic resonance brain imaging studies within 1 to 2 weeks of age. Information from the neurological examination, aEEG and MRI studies will be helpful in discussing prognosis with parents. All infants should be followed for a minimum of 18 months to evaluate growth parameters and neurodevelopment al outcome.

| S-EPMC3519960 | biostudies-literature

Dysregulated Monocyte and Neutrophil Functional Phenotype in Infants With Neonatal Encephalopathy Requiring Therapeutic Hypothermia.

Project description:Neonatal encephalopathy (NE) is a significant cause of morbidity and mortality. Persistent inflammation and activation of leukocytes mediate brain injury in NE. The standard of care for NE, therapeutic hypothermia (TH), does not improve outcomes in nearly half of moderate to severe cases, resulting in the need for new adjuvant therapies, and immunomodulation holds promise. Our objective was to explore systemic leukocyte phenotype in infants with NE and healthy controls in response to lipopolysaccharide (LPS). Twenty-four infants with NE (NE II-20; NE III = 4) requiring TH and 17 term neonatal controls were enrolled, and blood samples were analyzed between days 1 and 4 of life at a mean (SD) timepoint of 2.1 (± 0.81) days of postnatal life at the time of the routine phlebotomy. Leukocyte cell surface expression levels of Toll-like receptor 4, NADPH oxidase (NOX2), CD11b, mitochondrial mass, and mitochondrial superoxide production were measured by flow cytometry. Gene expression of TRIF (TIR domain-containing adapter-inducing interferon-β), MyD88 and IRAK4 was measured by reverse transcription-polymerase chain reaction. Infants with NE had significantly lower expression of neutrophil CD11b and NOX2 with LPS stimulation compared to healthy term controls. Mitochondrial mass in neutrophils and monocytes was significantly increased in NE infants with LPS compared to controls, potentially indicating a dysregulated metabolism. Infants with NE had significantly lower IRAK4 at baseline than controls. NE infants display a dysregulated inflammatory response compared to healthy infants, with LPS hyporesponsiveness to CD11b and NOX2 and decreased IRAK4 gene expression. This dysregulated immune profile may indicate an adaptable response to limit hyperinflammation.

| S-EPMC7917189 | biostudies-literature

Pharmacokinetics during therapeutic hypothermia for neonatal hypoxic ischaemic encephalopathy: a literature review.

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| S-EPMC7299043 | biostudies-literature

Serial plasma biomarkers of brain injury in infants with neonatal encephalopathy treated with therapeutic hypothermia.

Project description:BackgroundNeonatal encephalopathy (NE) is a major cause of long-term neurodevelopmental disability in neonates. We evaluated the ability of serially measured biomarkers of brain injury to predict adverse neurological outcomes in this population.MethodsCirculating brain injury biomarkers including BDNF, IL-6, IL-8, IL-10, VEGF, Tau, GFAP, and NRGN were measured at 0, 12, 24, 48, 72, and 96 h of cooling from 103 infants with NE undergoing TH. The biomarkers' individual and combinative ability to predict death or severe brain injury and adverse neurodevelopmental outcomes beyond 1 year of age was assessed.ResultsEarly measurements of inflammatory cytokines IL-6, 8, and 10 within 24 HOL (AUC = 0.826) and late measurements of Tau from 72 to 96 HOL (AUC = 0.883, OR 4.37) were accurate in predicting severe brain injury seen on MRI. Late measurements of Tau were predictive of adverse neurodevelopmental outcomes (AUC = 0.81, OR 2.59).ConclusionsTau was consistently a predictive marker for brain injury in neonates with NE. However, in the first 24 HOL, IL-6, 8, and 10 in combination were most predictive of death or severe brain injury. The results of this study support the use of a serial biomarker panel to assess brain injury over the time course of disease in NE.ImpactWhile recent studies have evaluated candidate brain injury biomarkers, no biomarker is in current clinical use. This study supports the use of a serial biomarker panel for ongoing assessment of brain injury neonates with NE. In combination, IL6, IL8, and IL10 in the first 24 h of cooling were more predictive of brain injury by MRI than each cytokine alone. Individually, Tau was overall most consistently predictive of adverse neurological outcomes, particularly when measured at or after rewarming.

| S-EPMC8483583 | biostudies-literature

Cerebral oxygen metabolism in neonatal hypoxic ischemic encephalopathy during and after therapeutic hypothermia.

Project description:Pathophysiologic mechanisms involved in neonatal hypoxic ischemic encephalopathy (HIE) are associated with complex changes of blood flow and metabolism. Therapeutic hypothermia (TH) is effective in reducing the extent of brain injury, but it remains uncertain how TH affects cerebral blood flow (CBF) and metabolism. Ten neonates undergoing TH for HIE and seventeen healthy controls were recruited from the NICU and the well baby nursery, respectively. A combination of frequency domain near infrared spectroscopy (FDNIRS) and diffuse correlation spectroscopy (DCS) systems was used to non-invasively measure cerebral hemodynamic and metabolic variables at the bedside. Results showed that cerebral oxygen metabolism (CMRO2i) and CBF indices (CBFi) in neonates with HIE during TH were significantly lower than post-TH and age-matched control values. Also, cerebral blood volume (CBV) and hemoglobin oxygen saturation (SO2) were significantly higher in neonates with HIE during TH compared with age-matched control neonates. Post-TH CBV was significantly decreased compared with values during TH whereas SO2 remained unchanged after the therapy. Thus, FDNIRS-DCS can provide information complimentary to SO2 and can assess individual cerebral metabolic responses to TH. Combined FDNIRS-DCS parameters improve the understanding of the underlying physiology and have the potential to serve as bedside biomarkers of treatment response and optimization.

| S-EPMC3887346 | biostudies-literature

Neonatal Encephalopathy: Update on Therapeutic Hypothermia and Other Novel Therapeutics.

Project description:Neonatal encephalopathy (NE) is a major cause of neonatal mortality and morbidity. Therapeutic hypothermia (TH) is standard treatment for newborns at 36 weeks of gestation or greater with intrapartum hypoxia-related NE. Term and late preterm infants with moderate to severe encephalopathy show improved survival and neurodevelopmental outcomes at 18 months of age after TH. TH can increase survival without increasing major disability, rates of an IQ less than 70, or cerebral palsy. Neonates with severe NE remain at risk of death or severe neurodevelopmental impairment. This review discusses the evidence supporting TH for term or near term neonates with NE.

| S-EPMC4987711 | biostudies-literature

Evolution of encephalopathy during whole body hypothermia for neonatal hypoxic-ischemic encephalopathy.

Project description:To examine the predictive ability of stage of hypoxic-ischemic encephalopathy (HIE) for death or moderate/severe disability at 18 months among neonates undergoing hypothermia.Stage of encephalopathy was evaluated at <6 hours of age, during study intervention, and at discharge among 204 participants in the National Institute of Child Health and Human Development Neonatal Research Network Trial of whole body hypothermia for HIE. HIE was examined as a predictor of outcome by regression models.Moderate and severe HIE occurred at <6 hours of age among 68% and 32% of 101 hypothermia group infants and 60% and 40% of 103 control group infants, respectively. At 24 and 48 hours of study intervention, infants in the hypothermia group had less severe HIE than infants in the control group. Persistence of severe HIE at 72 hours increased the risk of death or disability after controlling for treatment group. The discharge exam improved the predictive value of stage of HIE at <6 hours for death/disability.On serial neurologic examinations, improvement in stage of HIE was associated with cooling. Persistence of severe HIE at 72 hours and an abnormal neurologic exam at discharge were associated with a greater risk of death or disability.

| S-EPMC3299861 | biostudies-other

Therapeutic Hypothermia for Neonatal Hypoxic-Ischemic Encephalopathy?-?Where to from Here?

Project description:Hypoxia-ischemia before or around the time of birth occurs in approximately 2/1000 live births and is associated with a high risk of death or lifelong disability. Therapeutic hypothermia is now well established as standard treatment for infants with moderate to severe hypoxic-ischemic encephalopathy but is only partially effective. There is compelling preclinical and clinical evidence that hypothermia is most protective when it is started as early as possible after hypoxia-ischemia. Further improvements in outcome from therapeutic hypothermia are very likely to arise from strategies to reduce the delay before starting treatment of affected infants. In this review, we examine evidence that current protocols are reasonably close to the optimal depth and duration of cooling, but that the optimal rate of rewarming after hypothermia is unclear. The potential for combination treatments to augment hypothermic neuroprotection has considerable promise, particularly with endogenous targets such as melatonin and erythropoietin, and noble gases such as xenon. We dissect the critical importance of preclinical studies using realistic delays in treatment and clinically relevant cooling protocols when examining combination treatment, and that for many strategies overlapping mechanisms of action can substantially attenuate any effects.

| S-EPMC4568393 | biostudies-literature

Therapeutic hypothermia for neonatal encephalopathy with sepsis: a retrospective cohort study.

Project description:ObjectiveNeonatal encephalopathy remains a major cause of infant mortality and neurodevelopmental impairment. Infection may exacerbate brain injury and mitigate the effect of therapeutic hypothermia (TH). Additionally, infants with sepsis treated with TH may be at increased risk of adverse effects. This study aimed to review the clinical characteristics and outcomes for infants with sepsis treated with TH.Design and settingRetrospective cohort study of infants treated with TH within Australia and New Zealand.Patients1522 infants treated with TH, including 38 with culture-positive sepsis from 2014 to 2018.InterventionAnonymised retrospective review of data from Australian and New Zealand Neonatal Network. Infants with culture-positive sepsis within 48 hours were compared with those without sepsis.Main outcome measuresKey outcomes include in-hospital mortality, intensive care support requirements and length of stay.ResultsOverall the rate of mortality was similar between the groups (13% vs 13%). Infants with sepsis received a higher rate of mechanical ventilation (89% vs 70%, p=0.01), high-frequency oscillatory ventilation (32% vs 13%, p=0.003) and inhaled nitric oxide for persistent pulmonary hypertension (38% vs 16%, p<0.001). Additionally, the sepsis group had a longer length of stay (20 vs 11 days, p<0.001).ConclusionInfants with sepsis treated with TH required significantly more respiratory support and had a longer length of stay. Although this may suggest a more severe illness the rate of mortality was similar. Further research is warranted to review the neurodevelopmental outcomes for these infants.

| S-EPMC8943717 | biostudies-literature

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