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Management and Investigation of Neonatal Encephalopathy: 2017 Update Kathryn Martinello,1 Anthony R Hart,2 Sufin Yap,3 Subhabrata Mitra,1 Nicola J Robertson1

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Management and Investigation of Neonatal Encephalopathy: 2017 Update Kathryn Martinello,1 Anthony R Hart,2 Sufin Yap,3 Subhabrata Mitra,1 Nicola J Robertson1 Review Arch Dis Child Fetal Neonatal Ed: first published as 10.1136/archdischild-2015-309639 on 6 April 2017. Downloaded from Management and investigation of neonatal encephalopathy: 2017 update Kathryn Martinello,1 Anthony R Hart,2 Sufin Yap,3 Subhabrata Mitra,1 Nicola J Robertson1 1Department of Neonatology, ABSTRACT definite aetiological diagnosis is known, and Institute for Women’s Health, This review discusses an approach to determining the hypoxic-ischaemic encephalopathy (HIE) where University College London, UK 2 cause of neonatal encephalopathy, as well as current clear diagnosis of hypoxia-ischaemia is known to Department of Neonatal and ’ Paediatric Neurology, Sheffield evidence on resuscitation and subsequent management have led to the neonate s clinical state. Children’s Hospital NHS of hypoxic-ischaemic encephalopathy (HIE). Foundation Trust, Sheffield, UK Encephalopathy in neonates can be due to varied 3 DETERMINING THE AETIOLOGY OF NE Department of Inherited aetiologies in addition to hypoxic-ischaemia. A Metabolic Diseases, Sheffield The initial stages of managing NE will be the same Children’s Hospital NHS combination of careful history, examination and the for most babies, with good resuscitation and sup- Foundation Trust, Sheffield, UK judicious use of investigations can help determine the portive management. However, as the picture cause. Over the last 7 years, infants with moderate to evolves and investigations return, clinicians should fi Correspondence to severe HIE have bene ted from the introduction of consider the aetiology of NE as this could lead to Professor Nicola J Robertson, routine therapeutic hypothermia; the number needed to specific treatments, aid with prognosis and recur- Institute for Women’s Health, treat for an additional beneficial outcome is 7 (95% CI University College London, 74 rence risk counselling, and assist with the evalu- Huntley Street, London WC1E 5 to 10). More recent research has focused on optimal ation of medicolegal implications. 6AU, UK; n. robertson@ ucl. ac. uk resuscitation practices for babies with cardiorespiratory The other aetiologies to consider include: depression, such as delayed cord clamping after ▸ Acquired conditions, such as congenital infec- Received 9 December 2016 establishment of ventilation and resuscitation in air. Accepted 15 February 2017 tion, meningitis, haemorrhage, ischaemic or Published Online First Around a quarter of infants with asystole at 10 min after haemorrhagic stroke 6 April 2017 birth who are subsequently cooled have normal ▸ Genetic syndromes or isolated gene conditions outcomes, suggesting that individualised decision ▸ Neurometabolic disorders, particularly where making on stopping resuscitation is needed, based on the stress of delivery leads to decompensation copyright. access to intensive treatment unit and early cooling. The ▸ ‘Double trouble’ pathologies where a primary path- fi full bene t of cooling appears to have been exploited in ology leads secondarily to a hypoxic-ischaemic our current treatment protocols of 72 hours at 33.5°C; brain injury, like neuromuscular or cardiac deeper and longer cooling showed adverse outcome. The disorders – challenge over the next 5 10 years will be to assess ▸ The neonatal epilepsy syndromes and vitamin which adjunct therapies are safe and optimise responsive seizures hypothermic brain protection in phase I and phase II ▸ Non-accidental injury trials. Optimal care may require tailoring treatments Assessment should include a detailed history and according to gender, genetic risk, injury severity and neonatal examination, possibly parental examin- fl in ammatory status. ation, and the judicious use of investigations. Neonatal encephalopathy (NE) is defined as a condi- History and examination http://fn.bmj.com/ tion occurring in babies born over 35 weeks gesta- A history should be obtained from the mother or, if tional age in which there is disturbed neurological not possible, a review of the medical/antenatal function. The key feature is the disturbance in the notes or history from the extended family. Salient degree or quality of consciousness; other features, features to identify are summarised in box 1. The such as seizures, cardiorespiratory compromise or following are recommended: a three-generation abnormal tone and reflexes, may occur alongside it family tree, with focus on miscarriages, stillbirths, on September 23, 2021 by guest. Protected ‘ ’ but are not necessary to make the diagnosis.1 In child or early adult deaths, cerebral palsy , learning fi 2014, the Task Force on Neonatal Encephalopathy dif culties, seizures, encephalopathy, metabolic published new guidelines on criteria for retrospect- conditions and early onset ischaemic strokes. ive definition of an intrapartum event sufficient to A detailed examination of the baby is needed, cause cerebral palsy (CP).1 The title of the report including a neurological assessment, and repeated was changed from Neonatal Encephalopathy and neurological examination may be required, as signs Cerebral Palsy to Neonatal Encephalopathy and can change quickly. Where a neuromuscular dis- Neurological Outcome to emphasise that there are order is possible, the parents should be examined. many causes of encephalopathy in a newborn baby Important features to identify in the examination and that an array of developmental outcomes may are summarised in box 1, and neonatal features 2 arise in addition to CP. Knowledge gaps preclude a suggestive of a metabolic disorder in box 2. fi To cite: Martinello K, de nitive test or set of markers that accurately iden- Hart AR, Yap S, et al. Arch tifies, with high sensitivity and specificity, an infant First line investigations Dis Child Fetal Neonatal Ed in whom NE is attributable to an acute intrapartum Routine first line bloods are shown in table 1. 2017;102:F346–F358. event. The term NE should be used where no These basic tests will also allow calculation of the F346 Martinello K, et al. Arch Dis Child Fetal Neonatal Ed 2017;102:F346–F358. doi:10.1136/archdischild-2015-309639 Review Arch Dis Child Fetal Neonatal Ed: first published as 10.1136/archdischild-2015-309639 on 6 April 2017. Downloaded from Box 1 Features to look out for in history and examination Pregnancy/labour history: ▸ Was there an acute event occurring around the time of birth, such as non-reassuring or abnormal trace on cardiotocograph,99 antepartum haemorrhage, placenta previa, cord prolapse? ▸ Fetal growth on antenatal scans ▸ Fetal abnormalities on ultrasound scan or antenatal MRI ▸ Was this a multiple pregnancy (twins, triplets, etc)? ▸ Maternal infections or carriage of group B Streptococcus ▸ Maternal hypertension ▸ Pre-eclampsia ▸ HELLP syndrome, particularly if associated with acute fatty liver infiltration, may indicate long chain 3 hydroxyacyl-coenzyme A dehydrogenase (LCHAD) deficiency2 ▸ Maternal hypotension ▸ Maternal prescribed drug use ▸ Maternal illicit drug use, particularly cocaine ▸ Illness during pregnancy, such as may occur in viral infections that may affect the fetus ▸ Gestational diabetes ▸ Trauma, such as accidental falls or road traffic accident, and inflicted (assault) ▸ Evidence of maternal haemorrhage ▸ Any predisposing features to a non-accidental injury of baby, if presenting following normal period of consciousness? Maternal past medical history: ▸ Multiple miscarriages, stillbirths or neonatal deaths—consider genetic, thrombophilia and metabolic causes ▸ Diabetes: associated with brain injuries, such as fetal thrombotic vasculopathy and postnatal hypoglycaemia ▸ Deep vein thrombosis or other clotting disorders: suggestive of thrombophilia or clotting disorder and classical homocystinuria ▸ Arterial ischaemic stroke: suggestive of thrombophilia or vascular abnormalities, such as COL4A1 gene mutations ▸ Learning difficulties: suggestive of genetic/metabolic disorder, including myotonic dystrophy which may lead to secondary hypoxic brain injury copyright. ▸ ‘Family history of cerebral palsy’: suggestive of vascular abnormalities, such as COL4A1 gene mutations, or thrombophilia ▸ Cataracts: may indicate inborn error of metabolism, myotonic dystrophy, COL4A1 mutations ▸ Stiffness or startling: consider myotonic disorders or hyperekplexia ▸ Weakness or muscle fatigue: consider neuromuscular problem like myasthenia gravis or congenital myaesthenic syndrome, especially if ophthalmoplegia or unexplained squint present. If muscle aches, pains and tetany exist, consider maternal hyperparathyroidism ▸ Features of autoimmune disorder: involvement of several endocrine abnormalities, rash or other skin abnormalities like Raynaud’s syndrome, eye and kidney abnormalities, muscle aches and pains, heart block ▸ Distal weakness of hands or feet, or abnormally shaped toes: consider peripheral neuropathy Examination of the parents This is important where a neuromuscular disorder is suspected. ▸ Neuropathies—reduced strength distally, suppressed or absent reflexes, abnormally shaped feet/toes, possible loss of sensation in either parent http://fn.bmj.com/ ▸ Myopathies—proximal weakness, reduced reflexes and normal sensation in either parent ▸ Neuromuscular junction defects like maternal myasthenia gravis or myaesthenic syndromes—fatigue/weakness on repeated or prolonged testing of grip strength, upward eye gaze or ptosis ▸ Maternal myotonia in congenital myotonic dystrophy. Neonatal examination on September 23, 2021 by guest. Protected ▸ Head circumference abnormalities ▸ Dysmorphic features ▸ Abnormal fontanelle shape or size ▸ Features suggestive
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