Medico-legal considerations in the context of neonatal encephalopathy and therapeutic hypothermia

Neonatal encephalopathy (NE) is a significant complication of the peripartum period. It can lead to lifelong neurologic disabilities, including cerebral palsy, cognitive impairments, developmental delays, and epilepsy. Induced hypothermia is the first therapy, which has shown promise in improving the outcomes for neonates with moderate to severe NE following a presumed intrapartum insult.NE is also a frequent source of medical malpractice litigation. In this paper, we will review salient features of the American Tort System as it pertains to medical malpractice. We will discuss the obstetric medico-legal implications of therapeutic hypothermia and suggest a five-step approach to analyzing neonatal cases for causation, etiology, timing of occurrence, responsibility, and liability. We will close with three illustrative clinical cases.     

Supporting families in their child's journey with neonatal encephalopathy and therapeutic hypothermia

Neonates and families face challenges in hypothermic therapy, including trauma to parents, extreme emotions, and unfamiliarity with the medical system. Communication is an essential element to supporting parents while their children are in the NICU, and beyond, building the foundation for the ongoing relationship the family has with the medical system. Significant consideration needs to be given to the critical element of integrating the family into the care of a baby being treated with therapeutic hypothermia. Clinicians can promote healing of accumulated traumas of parents through ensuring parent's emotional safety, facilitating a trusting relationship, and promoting parent empowerment. Connecting parents with resources, especially peer support, is an essential part of a hospital stay. In this chapter, we explore best practices to support families during and after hypothermic therapy.     

Cuidados enfermeros a neonatos con encefalopatía hipóxico-isquémica en hipotermia terapéutica. Revisión bibliográfica

IntroductionHypoxic-ischaemic encephalopathy is one of the main causes of neurological damage in the new-born. Therapeutic hypothermia is the current treatment to reduce mortality and disability in new-borns with this condition.ObjectiveTo identify nursing care in new-borns with severe to moderate hypoxic-ischaemic encephalopathy, treated with active therapeutic hypothermia.Materials and methodsA review of the scientific literature was carried out in different databases (PubMed, Lilacs, IBECS, Cinhal, OvidSP, Cuiden, Embase and Cochrane Plus) over the last five years. The documentary assessment was carried out by peers and the quality was evaluated using the CEBM and GRADE scales.ResultsOf the 22 articles selected and reviewed, it is evident that therapeutic hypothermia is effective in reducing the mobility and mortality of neo-nates with hypoxic-ischaemic encephalopathy. Nursing care during hypothermia treatment focuses on four basic pillars: general care for stabilisation of the new-born, preparation of the material, administration of medical treatment in all its phases and emotional support of the family.ConclusionsTherapeutic hypothermia is effective in reducing the sequelae and mortality of neonates with hypoxic-ischaemic encephalopathy. Nursing care is essential throughout the treatment, in the early detection of complications in the infant and psychological support for parents. It is essential for nurses to receive training in this care.     

亚低温联合神经营养因子治疗新生儿缺氧缺血性脑病的效果及预后分析

目的:分析亚低温(Mild hypothermia,MH)联合神经营养因子治疗新生儿缺氧缺血性脑病(Neonatal hypoxic-ischemic encephalopathy,HIE)的效果及预后。方法:将2017年12月至2019年3月在我院出生的64例HIE患儿按随机数字表法分为观察组与对照组,每组各32例。其中对照组患儿接受亚低温治疗,观察组患儿联合神经营养因子治疗,对比两组患儿临床症状恢复时间,之前前后血清生化指标、氧化应激水平情况。两组患儿治疗28天后,分别采用新生儿神经行为测定(Neonatal behavioral assessment scale,NBNA)评分、婴幼儿发育贝利量表(Bayley scales of infant development,BSID)对新生儿及18月龄的患儿发育情况进行评定。结果:观察组患儿意识、反射及肌张力恢复时间明显短于对照组(P<0.05);治疗后两组患儿神经营养因子(Neurotrophin,NTF)、神经生长因子(Nerve growth factor,NGF)、超氧化物歧化酶(Oxide dismutase,SOD)水平上升,血清髓鞘碱性蛋白(Serum myelin basic protein,MBP)、神经元特异性烯醇化酶(Neuron specific enolase,NSE)及丙二醛(Malondialdehyde,MDA)水平下降,但观察组更显著;且治疗28d后观察组患儿新生儿神经行为测定(Neonatal behavioral assessment scale,NBNA)评分、18月龄时婴幼儿发育贝利量表(Bayley scales of infant development,BSID)各项目评分均显著优于对照组(P<0.05)。结论:亚低温联合神经营养因子治疗新生儿缺氧缺血性脑病疗效显著,于预后有益。     

Cerebrovascular events during pregnancy and puerperium

Though cerebrovascular complications of pregnancy remain relatively rare, they represent a potentially devastating event that necessitates prompt identification and treatment. Eighteen percent of strokes occurring in young women are linked to pregnancy. They occur mostly in the third trimester or during the post-partum period. Their biggest risk factors are hypertension, preeclampsia/eclampsia and migraine. Cerebrovascular events occurring during this period may involve specific pathophysiological processes that include embolic phenomena or endothelial dysfunction, but can also have common etiologies that are simply favored by the context of pregnancy. Thus, posterior encephalopathy and vasoconstriction cerebral syndrome are relatively frequently involved in cerebrovascular complications of pregnancy. Other very specific causes like amniotic fluid embolism or postpartum cardiomyopathy can also be responsible for such events. The management of stroke during pregnancy must be multidisciplinary and include a neurovascular expertise. Some conditions can lead to a long-life follow-up and modify the management of a future pregnancy.     

Infiltrated regulatory T cells and Th2 cells in the brain contribute to attenuation of sepsis-associated encephalopathy and alleviation of mental impairments in mice with polymicrobial sepsis

Sepsis-associated encephalopathy (SAE) increases not only morbidity and mortality but has been associated with long-lasting mental impairment after hospital discharge in septic patients. Recently, studies have shown that these mental impairments are caused by infection-induced neuroinflammation. However, the role of T cells in the pathogenesis of SAE and mental impairments remains unclear. Thus, in this study, we aimed to clarify how immune cells, especially T cells, influence the development and recovery of these disorders. In the cecal slurry (CS)-induced septic mouse model, we performed three different kinds of behavioral tests, open-field test, marble burying test, and forced swimming test, and observed anxiety-like behavior in septic mice. Additionally, increased interleukin (IL)-1β and IL-6 expression levels, and infiltration of neutrophils and T cells were examined in the brain of septic mice, 10 days after sepsis onset. Twenty days after sepsis onset, the septic mice could recover the number of astrocytes. At day 30, expression levels of IL-1β and tumor necrosis factor (TNF)-α returned to normal levels in the cerebral cortex of septic mice. Interestingly, resolution of neuroinflammation and alleviation of depression were delayed in septic mice treated with FTY720, which inhibits sphingosine-1-phosphate (S1P)-dependent lymphocyte egress from lymph nodes. On analyzing the brain T cells with or without FTY720 in septic mice, the FTY720 untreated mice presented increased regulatory T cells (Treg) and Th2 cells in the brain, whereas the FTY720 treated mice demonstrated increased Th17 in the brain at day 30. Furthermore, in FTY720 treated septic mice, the number of astrocytes in the cerebral cortex remained reduced at day 30. These results suggest that infiltrated Treg and Th2 cells contribute to the attenuation SAE and alleviate SAE-induce mental disorder by resolving neuroinflammation in the chronic phase of sepsis.