DOCSLIB.ORG

Therapeutic Hypothermia to Treat a Newborn with Perinatal Hypoxic-Ischemic Encephalopathy

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Therapeutic Hypothermia to Treat a Newborn with Perinatal Hypoxic-Ischemic Encephalopathy CASE REPORT Therapeutic Hypothermia to Treat a Newborn With Perinatal Hypoxic-Ischemic Encephalopathy Todd R. Fredricks, DO; Christopher Gibson, OMS III; Francis Essien, OMS III; Jeffrey S. Benseler, DO From the Departments of Hypoxic-ischemic encephalopathy is caused by neonatal asphyxia and can lead Family Medicine to mortality or long-term neurodevelopmental morbidity in neonates. (Dr Fredricks) and Radiology (Dr Benseler) at the Ohio Therapeutic hypothermia (TH) is one of the few effective ways to manage miti- University Heritage College of gating neurologic sequelae. The authors describe the case of a neonate who had Osteopathic Medicine a perinatal hypoxic insult and sustained no long-term sequelae after being (Student Doctors Gibson and treated with TH. It is important that osteopathic physicians who provide obstet- Essien) in Athens, Ohio. ric and gynecologic, perinatal, and emergency medical care are able to recog- Financial Disclosures: nize a perinatal hypoxic event, understand the stratification of hypoxic- None reported. ischemic encephalopathy risk factors, and implement early TH protocols. Support: None reported. J Am Osteopath Assoc. 2017;117(6):393-398 Address correspondence to doi:10.7556/jaoa.2017.078 Todd R. Fredricks, DO, Keywords: hypoxic-ischemic encephalopathy, neonate, obstetrics and gynecology, therapeutic hypothermia Grosvenor Hall 251, Department of Family Medicine, Ohio University Heritage College of Osteopathic Medicine, Athens, OH 45701-2979. ypoxic-ischemic encephalopathy (HIE) is a complication resulting from neonatal asphyxia. The incidence of HIE in full-term infants is 6 per 1000 E-mail: [email protected] births.1 If not treated, 62% of infants with perinatal hypoxic brain injury will Submitted H die or have moderate to severe disabilities by the age of 18 to 22 months; treatment July 22, 2016; 2,3 revision received reduces this rate to 41%. The incidence of long-term neurologic disabilities are as November 21, 2016; follows: 45% have cognitive and developmental delay or learning difficulties; 29%, accepted some degree of cerebral palsy; 26%, blindness or vision defects; 17%, gross motor and January 12, 2017. coordination problems; 12, epilepsy; 9%, hearing loss or deafness; and 1%, behavioral issues.4 Over the past 2 decades, several studies5-8 have attempted to elucidate the patho- physiologic and cellular mechanisms underlying HIE with the aim of expanding treat- ment options and reducing neonate mortality. We discuss the case of a patient with HIE whose symptoms were successfully managed with therapeutic hypothermia (TH). Report of Case A 28-year-old woman (gravida 3 para 2) at 39 weeks gestational age presented to the obste- trics and genecology department in active labor. On initial examination, the woman’s cervix was dilated 8 cm. Two minutes later her placental membranes ruptured, and the fetal heart rate dropped to 60 beats/min. Her obstetrician discovered an umbilical cord prolapse and unsuccessfully attempted to lift the fetus’s head to decompress the umbilical cord. Because the anesthesiologist on call was 20 minutes away and delay of delivery was not an option, the obstetrician obtained consent for an emergency cesarean delivery without anesthesia. Upon delivery, the neonate was flaccid, unresponsive, and apneic. His birth weight was 8 lb, 3 oz. A neurologic examination revealed nonreacting pupils, generalized hypotonia, The Journal of the American Osteopathic Association June 2017 | Vol 117 | No. 6 393 CASE REPORT and absent neonatal reflexes. Positive-pressure ventila- initial 72 hours of TH. After 72 hours, the neonate’s tion was initiated with a bag-valve mask. His heart rate core body temperature was increased by 0.5°C every increased to 100 beats/min within 15 seconds, but he hour until it reached a core temperature of 37°C. No remained apneic and was intubated. Apgar scores were aberrations were noted during the cooling or rewarming 1, 4, 4, and 7 at 1, 5, 10, and 20 minutes, respectively. period. Transient renal dysfunction, which responded to Laboratory tests conducted 25 minutes after birth fluid boluses and bumetanide, was noted during the first yielded the following results: arterial blood pH, 7.09; 24 hours of TH. base excess, 18 mmol/L; lactate, 10.9 mmol/L; lactate A cranial sonograph of the neonate was taken the day dehydrogenase, 741 U/L; creatine kinase, 1594 U/L; after birth and no hemorrhage due to perinatal stress glucose, 126 mg/dL; and troponin I, 0.06 ng/mL. was identified (Figure 1). A magnetic resonance image Neonatal neurointensivist consultation was of the brain was taken 10 days after birth (Figure 2). requested, and the neonate was given the diagnosis of Periventricular white matter signal characteristics were stage II HIE. Whole-body therapeutic hypothermia unremarkable, with no focal parenchymal cystic (TH), also referred to as targeted temperature manage- changes or cystic encephalomalacia identified. ment, was recommended. Two hours after birth, TH Because the sucking reflex was absent at birth, paren- was initiated, and the neonate’s core body temperature teral feeding was initiated the day after birth and was was maintained at 33.5°C for 72 hours. Sedation was complemented by the initiation of breast milk nasogas- achieved using a weight-based (0.05-0.2 mg/kg) bolus tric tube feedings once cooling stabilized at the end of dose of morphine sulfate over 5 minutes followed by a continuous intravenous infusion of 10 to 20 mg/kg per hour. Remote monitoring with amplitude-integrated electroencephalography was conducted during the Figure 1. Figure 2. Sagittal cranial ultrasound image demonstrating normal, Diffusion magnetic resonance image showing no evidence slitlike lateral ventricles in a neonate 1 day after birth while of anoxic injury in a neonate 10 days after undergoing undergoing therapeutic hypothermia for hypoxic-ischemic therapeutic hypothermia for hypoxic-ischemic encephalopathy. encephalopathy. 394 The Journal of the American Osteopathic Association June 2017 | Vol 117 | No. 6 CASE REPORT the day. Mild truncal hypotonia persisted until 7 days secondary energy failure phase. This period is a critical after birth. Tube feeding ceased 8 days after birth, and time during which much of the damage created during bottle and breastfeeding were introduced the next day. the PEF phase can be mitigated with proper interven- A speech pathologist was consulted to help the tion.10 If prompt restoration of cerebral oxygen and neonate learn the sucking reflex. The newborn was dis- glucose levels does not occur, the secondary energy charged 13 days after birth, after unremarkable neuro- failure phase will be initiated.5 The exact mechanisms logic examination findings. The neonate was able to of this phase are not fully understood. The phase drink 70 mL of breast milk from a bottle for 15 begins 6 to 24 hours after the initial insult and is hall- minutes before tiring. By age 14 days, the neonate was marked by continued apoptosis and overproduction of exclusively breastfed. Follow-up appointments were free radicals, which cause further damage to the scheduled every 2 to 3 months until the patient was 1 neonatal brain.6 The inflammatory cascade generated year old, at which time the appointments were sched- by neonatal cerebral hypoxia leads to the accumulation uled for every 6 months until he was 2 years old. of neutrophils that further exacerbate cerebral edema.6 Then, the follow-up appointments were annual. At the Excitotoxicity of sensory, learning, and memory neuro- patient’s 3-year appointment, no sequelae from HIE pathways caused by elevated glutamate levels is also were identified. thought to have a negative effect on neonates with HIE.7 The tertiary phase of brain injury includes the events that follow the primary and secondary phases, and this Discussion phase can last from weeks to years.8,11 This period is In neonates, HIE can cause death or severe disabilities, marked by the long-term sensitization to the inflamma- especially if it is not properly managed. Brain injury in tion found in the first 2 phases. It is during this phase patients with HIE is the result of pathologic events that patients have increased seizure susceptibility, divided into 3 phases: the primary energy failure, impaired oligodendrocyte function, persistent inflam- secondary energy failure, and tertiary phases. The mation, and gliosis. These phenomena pose serious primary energy failure phase begins with the initial long-term disability implications for patients.8,11 hypoxic insult and lasts approximately 6 hours. Although there are no specific diagnostic tests for Reduced cerebral blood flow results in lowered oxygen patients with possible HIE, some general diagnostic and glucose delivery to the brain. This reduction leads criteria include suspected perinatal insult, gestation to lowered adenosine triphosphate and a switch to anaer- greater than 36 weeks, a 10-minute Apgar score lower obic metabolism and elevated serum lactate levels. The than 5, the need for continued resuscitation, a pH score reduced accessibility to adenosine triphosphate leads to of less than 7.0 or base deficit greater than 16 mmol/L, failure of the sodium-potassium pumps and the accumu- signs of neonatal neurologic dysfunction (eg, lethargy, lation of intracellular ions such as calcium and sodium, irritability, seizures), and evidence of multisystem organ which cause neuron depolarization. Additional mem- dysfunction.12 The diagnosis of HIE is primarily clinical brane depolarization yields the release of excitatory neu- in nature. Thus, attending physicians should maintain a rotransmitters such as glutamate. This release leads to a high index of suspicion for HIE during any delivery in cascade of events that include cerebral edema, cellular which there is evidence of potential perinatal hypoxia. necrosis, and apoptosis.9 Disruption of cell membranes When HIE is suspected, TH is initiated on the basis leads to the release of intracellular inflammatory media- of a combination of clinical signs, laboratory test tors, which causes further damage to the brain.
Load more

Recommended publications
  • MRI Changes of Brain in Newborns with Hypoxic Ischemic Encephalopathy Clinical Stage Ii Or Stage Iii- a Descriptive Study
    Original Research Article DOI: 10.18231/2455-6793.2017.0009 MRI changes of brain in newborns with hypoxic ischemic encephalopathy clinical stage ii or stage iii- a descriptive study Jose O1,*, Sheena V2 1Assistant Professor, 2Junior Resident, Dept. of Pediatrics, Govt. TD Medical College, Alappuzha *Corresponding Author: Email: [email protected] Abstract Objectives: The aim of the study was to estimate the proportion of MRI changes in newborns with HIE, to compare the findings of term and preterm babies and to identify if there is any clinical stage specific MRI findings Methods: After obtaining clearance from ethical committee, 30 newborns with either stage II or stage III HIE are included in the study. MRI brain was taken between one to two weeks of age once the vitals of the babies are stable & after ensuring euthermia. Results: Out of the 30 babies, 19 were male babies and 11 female babies. 16 of them were term and 14 of them preterm babies.27 of the total 30 patients had MRI changes of HIE, which accounts for 90%. 17of the 30 mothers were primi mothers which accounts for 56.7%. Most important antenatal factors associated with HIE are gestational hypertension and UTI. Gestational diabetes mellitus and placental/cord factors are also found to be important contributing factors. 33.4% had a history of UTI, 30% gestational hypertension, 23.4% gestational diabetes mellitus in the antenatal period. Conclusion: Basal ganglia and/or thalamus were affected in 50% of term babies. 87.5% of babies with periventricular leucomalacia are preterms. Intracranial hemorrhage was seen in 7.4% of the babies and all of them were preterms.
    [Show full text]
  • Prognostication in Neonatal Hypoxic Ischemic Encephalopathy: a Qualitative Research Study
    Prognostication in Neonatal Hypoxic Ischemic Encephalopathy: A Qualitative Research Study Lisa Anne Rasmussen Department of Medicine, Division of Experimental Medicine and Biomedical Ethics Unit McGill University Montreal, Quebec, Canada November 2017 A thesis submitted to McGill University in partial fulfillment of the requirements of the degree of Master of Science in Experimental Medicine, Specialization in Biomedical Ethics ©Lisa Anne Rasmussen, 2017 Abstract Background Hypoxic ischemic encephalopathy is the most frequent cause of neonatal encephalopathy, and results in significant morbidity and mortality. From an ethical and clinical standpoint, neurological prognosis is fundamental in the care of neonates with hypoxic ischemic encephalopathy. However, accurately predicting neurodevelopmental outcomes for neonatal hypoxic ischemic encephalopathy is particular difficult, and fraught with challenges. At present, focused research in this area is limited. Objectives This thesis aims to present a review of the current literature on prognosis and the practice of prognostication in neonatal hypoxic ischemic encephalopathy, focusing on the integral challenges posed by this vulnerable group of neonates. Furthermore, this thesis incorporates an original qualitative study that explores physician perspectives about prognostication in neonatal hypoxic ischemic encephalopathy. The main objective of this thesis is to advance the current understanding of the practice of prognostication in neonatal hypoxic ischemic encephalopathy, in hopes of opening
    [Show full text]
  • 235 © Springer Nature Switzerland AG 2019 G. I. Martin, W. Rosenfeld
    Index A hemolytic disease, 90 Abdominal distension, 161, 166 hereditary elliptocytosis, 97 Aberrant ventricular conduction, 153, 154, 156 hereditary spherocytosis, 97 Absent uvula, 31 initial laboratory assessment, 94 Adenoviral conjunctivitis, 221 packed red blood cell transfusion, 94 Adenovirus, 77 peripheral smear, 96 Alopecia, 18 red cell indices, reference range, 90 Ambiguous genitalia reticulocyte count, 96 androgen insensitivity syndrome, 211 Rh incompatibility, 90 CAH (see Congenital adrenal hyperplasia (CAH)) rhinovirus, 97 causes of, 206, 211 signs and symptoms, 89, 94 chromosomal analysis, 205, 209 sources of blood loss, 94 DSD, 205 subgaleal hemorrhages, 92 evaluation of, 210 transfusion guidelines, 95 genetic factors for, 204 vascular access, 94 21-hydroxylase deficiency, 207 vital signs per nursery protocol, 92 incidence of, 203 Ankyloglossia, 31 pelvic sonogram, 209 Antacids, 166 sex assignment, 211 Antiarrhythmic medications, 150 sex determination and differentiation, 204 Anti-Ro and anti-La maternal antibodies, 152 46 XY karyotype and, 206 Apgar score, 183, 184 Amblyopia, 218 Aplasia cutis congenita (ACC), 44, 45 American Congress of Obstetricians and Gynecologists Arrhythmia (ACOG), 2, 55, 57 antiarrhythmic medications, 150 Amplitude electroencephalograph (aEEG), 6, 9 benign arrhythmias, 149 Androgen insensitivity syndrome (AIS), 209, 211 bradyarrhythmia Anemia atrioventricular block, 152, 153 ABO incompatibility, 90 EKG rhythm, 151 acute blood loss, 93 initial therapy, 151 blood transfusion therapy, 95, 96 management,
    [Show full text]
  • Perinatal Asphyxia in the Term Newborn
    www.jpnim.com Open Access eISSN: 2281-0692 Journal of Pediatric and Neonatal Individualized Medicine 2014;3(2):e030269 doi: 10.7363/030269 Received: 2014 Oct 01; accepted: 2014 Oct 14; published online: 2014 Oct 21 Review Perinatal asphyxia in the term newborn Roberto Antonucci1, Annalisa Porcella1, Maria Dolores Pilloni2 1Division of Neonatology and Pediatrics, “Nostra Signora di Bonaria” Hospital, San Gavino Monreale, Italy 2Family Planning Clinic, San Gavino Monreale, ASL 6 Sanluri (VS), Italy Proceedings Proceedings of the International Course on Perinatal Pathology (part of the 10th International Workshop on Neonatology · October 22nd-25th, 2014) Cagliari (Italy) · October 25th, 2014 The role of the clinical pathological dialogue in problem solving Guest Editors: Gavino Faa, Vassilios Fanos, Peter Van Eyken Abstract Despite the important advances in perinatal care in the past decades, asphyxia remains a severe condition leading to significant mortality and morbidity. Perinatal asphyxia has an incidence of 1 to 6 per 1,000 live full-term births, and represents the third most common cause of neonatal death (23%) after preterm birth (28%) and severe infections (26%). Many preconceptional, antepartum and intrapartum risk factors have been shown to be associated with perinatal asphyxia. The standard for defining an intrapartum hypoxic-ischemic event as sufficient to produce moderate to severe neonatal encephalopathy which subsequently leads to cerebral palsy has been established in 3 Consensus statements. The cornerstone of all three statements is the presence of severe metabolic acidosis (pH < 7 and base deficit ≥ 12 mmol/L) at birth in a newborn exhibiting early signs of moderate or severe encephalopathy. Perinatal asphyxia may affect virtually any organ, but hypoxic-ischemic encephalopathy (HIE) is the most studied clinical condition and that is burdened with the most severe sequelae.
    [Show full text]
  • Role of Thompson Score in Predicting Neurodevelopmental Outcome
    ROLE OF THOMPSON SCORE IN PREDICTING NEURODEVELOPMENTAL OUTCOME Dissertation submitted to THE TAMILNADU DR.M.G.R.MEDICAL UNIVERSITY In partial fulfilment of the regulations for the award of degree of M.D DEGREE (PEDIATRICS) BRANCH VII INSTITUTE OF SOCIAL PEDIATRICS STANLEY MEDICAL COLLEGE CHENNAI – 600 001 APRIL 2016 DECLARATION I, Dr.B.RUPA , solemnly declare that the dissertation titled “ROLE OF THOMPSON SCORE IN PREDICTING NEURODEVELOPMENTAL OUTCOME”was doneby me at Government Stanley MedicalCollege during 2013- 2016 under the guidance and supervision of my chief Prof. SHANTHI M.D, D.C.H. The dissertation is submitted to The Tamil Nadu Dr.M.G.R Medical University towards the partial fulfilment of the rules and regulations for the M.D. Degree Examination - BRANCH VII - in Pediatrics . Signature of the candidate Dr.B.RUPA Place : Chennai Date: CERTIFICATE BY THE GUIDE This is to certify that the dissertation titled “ROLE OF THOMPSON SCORE IN PREDICTING NEURO DEVELOPMENTAL OUTCOME” is a bonafide research work done under my guidance by Dr.B.RUPA, Postgraduate student, Department of Pediatrics, Government Stanley medical college, The Tamil Nadu Dr.M.G.R Medical University, Chennai, in partial fulfilment of the requirement of the award for the degree of M.D PEDIATRICS - BRANCH VII. Place : Chennai Signature of the guide Date : Dr.Aravind MD, DCH Professor of NICU RSRM hospital Institute of Social Pediatrics Stanley medical college, Chennai – 600001 CERTIFICATE BY THE INSTITUTION This is to certify that the dissertation titled “ROLE OF THOMPSON SCORE IN PREDICTING NEURO DEVLOPMENTAL OUTCOME”is submitted by Dr.B.RUPA to The Tamilnadu Dr.M.G.R Medical University, Chennai in partial fulfilment of the requirement of the award for the degree of M.D BRANCH VII (PEDIATRICS) and is a bonafide work done by her under our direct supervision and guidance, during the academic year 2014 -2015 Place: Chennai DR.Aravind MD, DCH Date: Professor of NICU RSRM Hospital Institute of Social Pediatrics Stanley Medical College Chennai –600001.
    [Show full text]
  • Adolescent Medicine and General Pediatrics III Concurrent Session 8
    Abstracts J Investig Med: first published as 10.1136/jim-d-15-00013.378 on 11 January 2016. Downloaded from prevalent in pediatric patients hospitalized with espiratory syncytial virus (RSV). However, published literature on their use is limited. The objective of our study is review the use of hypertonic saline and high flow oxygen in infants hospitalized with RSV. Methods Used We performed a retrospective chart review of pediatric patients less <1 year of age who were hospita- lized at Children’s Hospital of Orange County during the 2013–14 RSV season with a diagnosis of RSV. We docu- mented the management regimen, with a particular look at the use of HS and HFNC. 165 patients less <1 year of age fulfilled our inclusion criteria. 6 patients were omitted from data analysis due to incomplete outside records. Summary of Results For patients <2 months of age, 9 (53%) of 17 with underlying conditions vs. 39 (66%) of 59 patients without underlying conditions required HS (P=0.3956). Although it didn’t meet statistical significance, it seems that the use of HFNC tended to be more frequent in patients <2 months of age with underlying conditions (29% vs. 10%, P=0.062). Use of HFNC or HS was not different for those >2 months of age with or without underlying conditions. The mean length of stay (LOS) for different types of treatment is summarized in the table below. Conclusions Our study shows that the use of HFNC tended to be more frequent in young infants with an underlying condition. The use of HFNC or HS was asso- ciated with longer LOS.
    [Show full text]
  • PAEDIATRIC PROTOCOLS for Malaysian Hospitals 3Rd Edition
    PAEDIATRIC PROTOCOLS For Malaysian Hospitals 3rd Edition Hussain Imam Hj Muhammad Ismail Ng Hoong Phak Terrence Thomas Kementerian Kesihatan Malaysia PAEDIATRIC PROTOCOLS For Malaysian Hospitals 3rd Edition Hussain Imam Hj Muhammad Ismail Ng Hoong Phak Terrence Thomas Scan this QR code to download the electronic Paediatric Protocol 3rd Edition Kementerian Kesihatan Malaysia i ii FOREWORD BY THE DIRECTOR GENERAL OF HEALTH Malaysia like the rest of the world has 3 more years to achieve the Millennium Developmental Goals (MDG). MDG 4 is concerned with under 5 mortality. Although we have done very well since lndependence to reduce our infant and toddler mortality rates, we are now faced with some last lap issues in achieving this goal. Despite urbanization there are still many children in the rural areas. This constitutes a vulnerable group in many ways. Among the factors contributing to this vulner- ability is the distance from specialist care. There is a need to ensure that doctors in the frontline are well equipped to handle common paediatric emergencies so that proper care can be instituted from the very beginning. Although all doctors are now required to do 4 months of pre-registration training in Paediatrics, this is insufficient to prepare them for all the conditions they are likely to meet as Medical Officers in district hospitals and health clinics. Hence the effort made by the paediatricians to prepare a protocol book covering all the common paediatric problems is laudable. I would also like to congratulate them for bringing out a third edition within 4 years of the previous edition. l am confident that this third edition will contribute to improving the care of children attending the Ministry’s facilities throughout the country.
    [Show full text]
  • Blood-Based Neurology Biomarkers: a New Approach for HIE Diagnosis and Prognosis
    Blood-based Neurology biomarkers: a new approach for HIE diagnosis and prognosis Zhihui (Sunny) Yang, PhD University of Florida [email protected] July 2019 Hypoxic Ischemic Encephalopathy (HIE) ● full-term infants------HIE occurs in approximately 3-20 per 1000 live births ● preterm infants------HIE occurs in up to 60% of live births Criteria for cooling ? Hypothermia Therapy Lack of a standardized definition for mild HIE; ● Clinical Evaluation: How to accurately identify APGAR Score the hypothermia ● Physical exam responder versus the non- ● EEG responder? ● Laboratory Evaluation: Birth blood Umbilical cord ● Radiological Evaluation: Ultrasound, CT scans, MRI How dose therapeutic hypothermia work? Primary energy failure (minutes) O2 O2 Hypoxia ---a shortage of oxygen in the blood O2 Ischemia --- a shortage of blood flow to the brain cooling Secondary energy failure (hours to days) Restoration of blood flow Mitochondrial dysfunction Delated apoptotic cell death Caspases activation Chronic brain injury (days to months) Astrogliosis, tissue repair remolding, inflammation Encephalopathy Cell loss, Cerebral atrophy The current standard tools to predict outcome in perinatal asphyxia Predictors of outcome Pros Cons Acid-base balance Widely available test, can be measured Cannot differentiate degree of severity of injury, early by scalp and cord sampling invasive testing pH Responds early to HI Low PPV for abnormal outcome Lactate Better reflects metabolic mechanism No advantage over pH Apgar score Quick assessment of neonatal condition High
    [Show full text]
  • To Observe the Clinical Presentation of Seizure Disorder in 0-1 Month Age Group
    IP International Journal of Medical Paediatrics and Oncology 2020;6(3):110–113 Content available at: https://www.ipinnovative.com/open-access-journals IP International Journal of Medical Paediatrics and Oncology Journal homepage: www.ipinnovative.com Original Research Article To observe the clinical presentation of seizure disorder in 0-1 month age group Prachi Goyal1, Prashant Kumar Choudhary1,*, Ali Mehdi Johar2 1Dept. of Pediatrics, MGM Medical College, Indore, Madhya Pradesh, India 2Red Cross Hospital, Mhow, Indore, Madhya Pradesh, India ARTICLEINFO ABSTRACT Article history: Background: This prospective study was conducted over the period of one year at M.Y. Hospital & Chacha Received 21-08-2020 Nehru Bal Chikitsalaya, Indore, in the Department of Pediatrics, M.G.M. Medical College, Indore. Accepted 22-08-2020 Materials and Methods: Detailed history of present illness with duration of convulsion were enquired. A Available online 29-09-2020 detailed history of mother during antenatal, natal and post natal period was taken. Type of delivery (vaginal/ LSCS ; full term / preterm), enquired about the indication of LSCS. History of labour with particular ref to birth injury, asphyxia (delayed cry), neonatal history regarding jaundice & feeding history, detailed family Keywords: history in relation to epilepsy convulsion and mental diseases were recorded. Incidence Results: Out of 100 cases 64% were males and 36% were females. Male female ratio was 1.77:1. Male Seizure & Neonates cases were predominantly present in all 3 age groups. Majority of seizures occurred within 24 hrs. P value is not significant. Out of 100 cases 43 had tonic convulsions, 38 had subtle, and 19 had focal convulsions.43 neonates had seizures in 1st 24 hrs.
    [Show full text]
  • Fas-Ligand and Interleukin-6 in the Cerebrospinal Fluid Are Early
    Leifsdottir et al. Journal of Neuroinflammation (2018) 15:223 https://doi.org/10.1186/s12974-018-1253-y RESEARCH Open Access Fas-ligand and interleukin-6 in the cerebrospinal fluid are early predictors of hypoxic-ischemic encephalopathy and long-term outcomes after birth asphyxia in term infants Kristin Leifsdottir1,3, Huseyin Mehmet2,4, Staffan Eksborg1 and Eric Herlenius1* Abstract Background: Cerebral ischemia generates neuroinflammation that can induce neural cell death. This cohort study assessed whether Fas-ligand (FasL) and interleukin (IL)-6 levels in the cerebrospinal fluid (CSF) after hypoxic-ischemic encephalopathy (HIE) can serve as biomarkersofhypoxicbraininjuryinneonates. Methods: Term infants (> 37-week gestational age) who were admitted to the neonatal intensive care unit of Karolinska University Hospital in years 2002 to 2004 with perinatal asphyxia were enrolled prospectively. Control infants without brain pathology underwent lumbar puncture for suspected infection. FasL and IL-6 levels were measured in the CSF, by enzyme-linked immunosorbent assays. All patients underwent neurological assessment at 18 months. HIE was classified as mild, moderate, or severe (HIE I–III). Adverse neurological outcome at 18 months was defined as a mental developmental index < 85, deafness, blindness, cerebral palsy, or seizure disorder. Results: Of the 44 HIE patients, 14, 16, and 14 had HIE-I, HIE-II, and HIE-III, respectively. HIE-II and HIE-III patients had higher FasL and IL-6 levels than HIE-I patients and the 20 controls (all p < 0.0001). Patients with adverse outcomes had higher FasL and IL-6 levels than patients with normal outcomes and controls (both p < 0.0001).
    [Show full text]
  • SOUTHERN REGIONAL MEETING ABSTRACTS Cardiovascular Club I
    Abstracts SOUTHERN REGIONAL MEETING 2 ATTENUATION OF RENAL FIBROSIS AND ABSTRACTS INFLAMMATION IN NATRIURETIC PEPTIDE RECEPTOR A GENE-TARGETED MICE BY EPIGENETIC Cardiovascular Club I MECHANISMS OF SODIUM BUTYRATE- AND 11:00 AM RETINOIC ACID Thursday, February 18, 2016 P Kumar, R Periyasamy, K Pandey. Tulane University Health Sciences Center, New Orleans, LA 1 ROLE OF CYCLIN DEPENDENT KINASE INHIBITOR 10.1136/jim-2015-000035.2 P27 IN CARDIOMYOCYTE REGENERATION Purpose of Study Mice lacking functional guanylyl SK Sen, H Sadek. UT Southwestern Medical Center, Dallas, TX cyclase/natriuretic peptide receptor-A (GC-A/NPRA) gene 10.1136/jim-2015-000035.1 (Npr1) exhibit hypertension, kidney disease, and heart failure. The objective of the present study was to determine Purpose of Study Neonatal mammalian hearts have the the combined effect of sodium butyrate (NaBu), a histone ability to undergo cardiomyocyte regeneration for a short deacetylase (HDAC) inhibitor and all-trans retinoic acid period of time after birth through proliferation of pre- (ATRA) on attenuation of renal fibrosis and inflammation existing cardiomyocytes. This regenerative window is lost in Npr1 gene-disrupted mutant mice. by the first week of life coinciding with cell cycle arrest. Methods Used Adult (18–20 week old) male Npr1 gene- − The exact mechanism of how postnatal cardiomyocytes disrupted heterozygous (1-copy; Npr1+/ )wild-type regulate proliferation remains unclear. We hypothesize a (2-copy; Npr1+/+), and gene-duplicated (3-copy; Npr1++/+) Kip1 specific cyclin-dependent kinase inhibitor p27 (p27) mice were treated by injecting ATRA-NaBu hybrid drug plays a prominent role in cardiomyocyte proliferation both (1.0 mg/kg/day) intraperitoneally for 2-weeks.
    [Show full text]
  • Neonatal Encephalopathy Management in NICU JHCH NICU 14.02
    Neonatal Encephalopathy Management in NICU JHCH_NICU_14.02 Local Guideline Neonatal Encephalopathy management in NICU Sites where Local Guideline applies Neonatal Intensive care Unit, JHCH This Local Guideline applies to: 1. Adults No 2. Children up to 16 years No 3. Neonates – less than 29 days Yes Target audience NICU clinical staff who provide care to neonatal patients with Neonatal Encephalopathy Description Guideline for the description of neonatal encephalopathy and treatment Hyperlink to Guideline Keywords Asphyxia, Cooling, Electroencephalogram (EEG), Hypoxic Ischaemic Encephalopathy (HIE), Sarnet, Seizures Document registration number JHCH_NICU_14.02 Replaces existing document? Yes Registration number and dates of Moderate systemic hypothermia for the treatment of neonatal superseded documents hypoxic ischaemic encephalopathy (HIE) 5.8.9 2008 Related Legislation, Australian Standard, NSW Ministry of Health Policy Directive or Guideline, National Safety and Quality Health Service Standard (NSQHSS) and/or other, HNE Health Document, Professional Guideline, Code of Practice or Ethics: NSW Health Policy Directive 2014_036 Clinical Procedure Safety http://www0.health.nsw.gov.au/policies/pd/2014/pdf/PD2014_036.pdf NSW Health Policy Directive 2010_006 Whole Body Cooling - Neonates Suspected Moderate or Severe Hypoxic Ischaemic Encephalopathy(HIE) http://www0.health.nsw.gov.au/policies/pd/2010/PD2010_006.html Prerequisites (if required) Nil Local Guideline note This document reflects what is currently regarded as safe and appropriate practice. The guideline section does not replace the need for the application of clinical judgment in respect to each individual patient but the procedure/s require mandatory compliance. If staff believe that the procedure/s should not apply in a particular clinical situation they must seek advice from their unit manager/delegate and document the variance in the patients health record.
    [Show full text]