胎儿炎症反应综合征与子宫内SARS-CoV-2暴露相关

M. Shinde, Anilkumar M. Khamkar, Pralhad D Pote, Pradeep Suryawanshi
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引用次数: 2

摘要

在本次covid-19大流行期间,记录了几例严重急性呼吸综合征冠状病毒-2从母亲向胎儿垂直传播的病例。抗sars CoV-2抗体介导的多系统炎症反应综合征(MIS-C)是已知的儿童现象。在本病例报告中,我们旨在证明胎儿炎症反应综合征(FIRS)与抗sars CoV-2抗体在早产新生儿中出现呼吸窘迫、癫痫发作和休克的证据。该婴儿的RTPCR检测为covid-19阴性,但抗sars CoV-2抗体阳性,炎症标志物升高,提示全身性炎症反应综合征。对其他传染性病原体的全面检查也呈阴性。婴儿接受了IvIg和类固醇治疗并完全康复。我们认为,这种全身性炎症是由于产前暴露于covid-19病毒而发生的,未来还会出现更多这样的情况。当前,由SARS-CoV-2引起的COVID-19已成为全球性的公共卫生危机。由于某些原因,新生儿和幼儿的疾病严重程度较低。1但最近报道了儿童多系统炎症综合征(MIS-C), Kathleen M et al和Shreepal J et al.2,3其具体机制尚不清楚,尽管它被认为与SARS CoV2感染引起的免疫失调有关该病表现为持续高热,累及多系统,炎症标志物升高,需要PICU管理[2]。该疾病模拟成人的川崎病和细胞因子风暴。大多数儿童抗SARS CoV2抗体阳性,少数儿童RTPCR阳性与SARS-CoV-2感染和多系统炎症发生在同一受试者中的MIS-C不同,少数病例报告表明新生儿多系统炎症继发于母体SARS-CoV-2感染。5,6在此,我们报告了一例新生儿,其SARS CoV-2抗体滴度非常高,炎症标志物升高,在生命的最初几个小时内表现为多系统炎症,也称为胎儿炎症反应综合征。在印度马哈拉施特拉邦浦那的一家私人疗养院,一名26岁的初产妇在妊娠32周时自然分娩,一名男婴(出生体重1474克)经阴道分娩。婴儿出生后立即哭泣,不需要复苏(1分钟时APGAR评分为8分,5分钟时为10分),但在30分钟内出现咕噜声和呼吸窘迫。然后,根据新生儿救护车的标准运输协议,婴儿被紧急转移到印度马哈拉施特拉邦浦那的三级护理新生儿重症监护室。婴儿最初被放置在CPAP上,PEEP为6,FiO2为30%,但由于她的呼吸工作增加,婴儿插管并给予正压通气。初始ABG显示pH为7.29,pCO2 46, pO2 97, HCO322.1, BE -4.5,乳酸1.5。由于最初的胸部x线片显示肺容量正常,未提示呼吸窘迫综合征,因此未给予表面活性剂。4小时内出现灌注不良(CRT延长5秒,低血压,心动过速,四肢冷),代谢性酸中毒。功能超声心动图显示轻度左室功能不全,左室射血分数为40%。所以在最初的液体复苏后,婴儿开始接受肌力支持。婴儿嗜睡,6小时内癫痫发作,给予苯巴比妥和左乙拉西坦治疗。出生第2天行神经超声检查,发现生发基质出血和实质斑片状出血。鉴于患儿凝血功能紊乱及血红蛋白下降,患儿接受血浆及PCV输注。发送脓毒症筛查和血培养,并按单位方案开始使用广谱静脉注射抗生素。脑脊液检查正常。脑脊液和血培养均呈阴性,因此48小时后停用抗生素。通信地址:Mahesh Shinde博士儿科和新生儿科,Noble医院和研究中心,haapsar,浦那,马哈拉施特拉邦411013,印度电子邮件:maheshh248@gmail.com©2021儿科Oncall文章历史收到2021年9月2日接受2021年12月11日
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Fetal Inflammatory Response Syndrome Associated With SARS-CoV-2 Exposure In Utero
During this covid-19 pandemic, a few cases of vertical transmission of severe acute respiratory syndrome coronavirus-2 from mothers to the fetus have been documented. Anti-SARS CoV-2 antibodies mediated multisystem inflammatory response syndrome (MIS-C) is known phenomenon in children. With this case report, we aim to demonstrate the evidence of fetal inflammatory response syndrome (FIRS) associated with anti-SARS CoV-2 antibodies in a premature neonate presenting with respiratory distress, seizures and shock in initial hours of life. The infant was RTPCR negative for covid-19, but positive for anti-SARS CoV-2 antibodies with raised inflammatory markers, suggestive of systemic inflammatory response syndrome. A comprehensive workup for other infectious pathogens also came up negative. Baby received IvIg and steroids and recovered completely. We believe that this systemic inflammation occurred due to antenatal exposure to the covid-19 virus and that more such instances will emerge in future. Introduction In current times, COVID-19, caused by SARS-CoV-2, has been a global public health crisis. The disease severity is less in neonates and young children for certain reasons .1 But recent reports of multisystem inflammatory syndrome in children, MIS-C, have been described by Kathleen M et al and Shreepal J et al.2,3 The specific mechanism is unknown, although it is thought to be related to immunological dysregulation caused by SARS CoV2 infection.4 The disease manifests as persistent high grade fever and multisystem involvement with raised inflammatory markers and requiring PICU management]2. The disease simulates Kawasaki disease and cytokine storm as in adults. Majority of the children are positive for anti SARS CoV2 antibodies while less number of kids are RTPCR positive.2 Unlike MIS-C, where SARSCoV-2 infection and multisystem inflammation occur in the same subject, a few case reports suggest neonatal multisystem inflammation occurs secondary to maternal SARS-CoV-2 infection.5,6 Here we report a case of a newborn with very high SARS CoV-2 antibodies titre and elevated inflammatory markers who presented as multi systemic inflammation also known as fetal inflammatory response syndrome within the first few hours of life. Case Report A 26 years old primigravida went into spontaneous labour at 32 weeks of gestation and a male neonate (birth weight 1474 grams) was delivered by vaginal delivery in a private nursing home at Pune, Maharashtra, India. Baby cried immediately at birth and did not require resuscitation (APGAR score 8 at 1 minute, 10 at 5 minutes) but within 30 minutes developed grunting and respiratory distress. Baby was then shifted urgently in a tertiary care NICU at Pune, Maharashtra, India, under standard transportation protocol in neonatal ambulance. Baby was initially placed on CPAP with a PEEP of 6 and a FiO2 of 30 percent, but due to her increasing work of breathing, baby was intubated and given positive pressure ventilation. Initial ABG was showing pH of 7.29, pCO2 46, pO2 97, HCO322.1, BE -4.5, lactate 1.5. As initial chest X-ray showed normal volume lungs and was not suggestive of respiratory distress syndrome hence surfactant was not given. Within 4 hours of life, the baby presented as poor perfusion (with prolonged CRT of 5 seconds, hypotension, tachycardia and cold extremities) and metabolic acidosis. Functional echocardiography showed mild LV dysfunction with LV ejection fraction of 40%. So baby was started on inotropic support after initial fluid resuscitation. Baby was lethargic and developed seizures within 6 hours of life, which were managed with phenobarbitone and levetiracetam. Neurosonography was done on second day of life which showed germinal matrix hemorrhage and parenchymal patchy haemorrhage. In view of deranged coagulation and drop in haemoglobin, baby received plasma and PCV transfusion. Sepsis screen and blood culture was sent and broad spectrum iv antibiotics were initiated as per unit protocol. CSF studies were normal. Both CSF and blood culture came negative so antibiotics were stopped after 48 hours of initiation. Baby’s perfusion improved gradually over 48 hours Address for Correspondance: Dr Mahesh Shinde Department of Pediatrics and Neonatology, Noble Hospital and Research Center, Hadapsar, Pune, Maharashtra 411013, India Email: maheshh248@gmail.com ©2021 Pediatric Oncall ARTICLE HISTORY Received 2 September 2021 Accepted 11 December 2021
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