SYNOPSIS

Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore

“MULTIORGAN DYSFUNCTION IN NEONATES WITH PERINATAL ASPHYXIA”

Name of the candidate : Dr. Geetanjali Dambalkar

Guide : Dr. B. Sanjeev Rai

Course and Subject : M.D (Paediatrics)

Department of Paediatrics,

Father Muller Medical College and Hospital

Kankanady, Mangalore – 575002.

August - 2007

RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES

KARNATAKA, BANGALORE.

ANNEXURE-II

PROFORMA FOR REGISTRATION OF SUBJECT FOR DISSERTATION
1. / NAME OF THE CANDIDATE AND ADDRESS / DR. GEETANJALI DAMBALKAR
POST GRADUATE RESIDENT,
DEPARTMENT OF PAEDIATRICS,
FATHER MULLER MEDICAL COLLEGE,
KANKANADY,
MANGALORE- 575002
2. / NAME OF THE INSTITUTION / FATHER MULLER MEDICAL COLLEGE, KANKANADY, MANGALORE - 575002
3. / COURSE OF THE STUDY & SUBJECT / M.D. IN PAEDIATRICS
4. / DATE OF ADMISSION TO THE COURSE / 14.04. 2007
5. / TITLE OF THE TOPIC / MULTIORGAN DYSFUNCTION IN NEONATES WITH PERINATAL ASPHYXIA
6 / BRIEF RESUME OF THE INTENDED WORK
6.1 NEED FOR THE STUDY
Dysfunction of organs other than the central nervous system is often recognized after perinatal asphyxia and there is now a consensus of opinion among representative obstetric and paediatric associations that multiorgan or multisystem dysfunction is a constant feature of the neonatal post asphyxial syndrome1. However, while most studies have focused on assessing the involvement of the central nervous system2 or the renal system,3 only few have assessed multisystem involvement in asphyxiated neonates. Further, most of these studies have been conducted in developed countries and there is a lack of studies from India on the subject. This is thus a prospective study of term asphyxiated newborns to assess multiple organ dysfunction, its frequency and its effect on the immediate outcome of these infants .
6.2 REVIEW OF LITERATURE
The multiorgan system dysfunction phenomenon is mechanistically related to the diving reflex. The reflex activated by asphyxia, consists of shunting of blood from the skin and splanchnic area to the heart, adrenals and brain ostensibly to protect these vital organs form hypoxic ischaemic injury4. Thus it is likely that intrapartum asphyxia would have activated the diving reflex to protect brain and heart for long enough to cause dysfunction of one or more organs.
Martin – Ancel Ana and co-workers5 in their prospective study found that involvement of one or more organs occurred in 82% of the infants, who were asphyxiated at birth. Study by Shah and co-workers6 concluded that all infants in the study had evidence of multiorgan dysfunction while Perlman and
others7 reported that 66% of term infants after asphyxia had systemic organ injury. Study by Shankaran and others8 also demonstrated that perinatal asphyxia results in a multisystem organ involvement in term neonates with three or more organ being involved in a majority of them.
Involvement of the central nervous system in various studies varied from 26%-72%5,7-10, while renal system involvement ranged from 25%-72%5-11.Studies also documented that pulmonary dysfunction occurred in 23%-86%5-10,while involvement of cardiovascular system was seen in 29%-78%5-11 cases in various studies.
In the study by Shah and co workers6 death or adverse outcomes were seen in 76% of cases with renal, 64% of those with cardiovascular involvement, 86% of those with pulmonary involvement. Shankaran and others8 had a mortality rate of 14% of which 7% had involvement of the pulmonary system and another 7% had dysfunction of both renal and central system. Goodwin and others10 found that there were five neonatal deaths, three of them, being attributed to severe CNS involvement.
6.3AIMS AND OBJECTIVES OF THE STUDY
1.  To evaluate the frequency of organ dysfunction in perinatal asphyxia.
2.  To assess the clinical and laboratory parameters of organ dysfunction.
3.  To correlate the organ dysfunction with immediate mortality.
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MATERIALS AND METHODS
7.1 Source of data
Eighty asphyxiated neonates delivered at F.M.M.C Hospital.
Type of study: Prospective study.
Sampling procedure: Purposive sampling.
Inclusion criteria
A neonate would be included / enrolled into the study if he/she was delivered at Father Muller Medical College hospital and had features of birth asphyxia which would be defined for the purpose of study as follows.
1.  Apgar score of < 7 at 5min.
2.  Umbilical cord arterial pH of < 7.2 at birth.
3.  Requirement of more than 1minute of positive pressure ventilation before sustained respiration occurred or the need for mechanical ventilation at birth.
Exclusion criteria:
1.  Preterm neonates, i.e., those born before 37 weeks of gestation.
2.  Neonates with congenital abnormalities.
3.  Neonates with birth asphyxia, but delivered outside FMMC hospital
7.2METHOD OF COLLECTION OF DATA
Eighty consecutive newborn infants delivered at FMMC hospital and admitted to the NICU of the same hospital and found to be satisfying the aforementioned inclusion criteria would be enrolled by purposive sampling using a proforma.
At the time of enrollment, a written informed consent would be obtained from the parents. A detailed history would be elicited and examination performed at the time of admission. The neonatal clinical course would be followed up prospectively upto 7 days of birth with special emphasis on the systems under study i.e., the central nervous system, renal system, respiratory system and cardiovascular system. The data so obtained would be recorded on the proforma.
For the assessment of the central nervous system, a detailed neurologic examination would be performed daily upto 7 days of life and any features of
CNS injury e.g., seizures, abnormal tone would be noted. Sarnath and Sarnath staging (without EEG) would be used to classify the neurologic status clinically. In order to provide objective evidence of central nervous system injury a neurosonogram would be carried out within 2 days of life in all asphyxiated newborns.
For the evaluation of renal system, urine output would be monitored daily upto 7 days of life by urobag collection, oliguria would be defined as a urine flow of <1ml/kg/hour for >24 hours. Urine analysis for protein and haematuria would be carried out on day 2, proteinuria >2+ would be considered as evidence of renal dysfunction. Serum creatinine estimation would be done on day 3 and value found greater than 1.0mg/dl would be considered as evidence of renal injury.
Respiratory system will be clinically assessed on the basis of presence of respiratory distress, need for oxygen supplementation, need for mechanical ventilation and the presence of meconium aspiration syndrome. A chest X-ray would be done in all infants on day 1 and serial arterial blood gas analyses would be done for all infants who require mechanical ventilation.
For cardiac assessment, the cardiovascular system would be examined daily to look for heart murmurs, dysrhythmias, features of congestive cardiac failure and shock. An electrocardiogram would be taken on day 1 of life and Creatinine kinase-MB isoenzyme levels would be estimated on day 1 in all neonates. In cases with persistent murmurs and other abnormal findings, an echocardiogram would be carried out.
Results would be analysed for statistical significance using chi-square test for frequency of organ dysfunction and logistic regression to correlate organ dysfunction with mortality.
7.3 Does this study require any investigations to be conducted on patients or other humans or animals? If so, please describe briefly.
No
7.4 Has ethical clearance been obtained from your institution in case of 7.3?
Yes
LIST OF REFERENCES
1.  American college of Obstetrics and Gynaecology Committee opinion. Inappropriate uses of the terms fetal distress and birth asphyxia Int J. Gynaecol Obstet 1998:61:309-10.
2.  Brown JK, Purvis RJ, Forfar JO et al. Neurological aspects of perinatal asphyxia. Dev. Med. Child. Neurol 1996; 16: 777-781.
3.  Perlman JM, Tack ED. Renal injury in the asphyxiated newborn infant. Relationship to neurologic outcome. The Journal of Pediatrics. 1988; Vol 113; No.5.
4.  Bocking AD, Gagnon R, White SE, et al. Circulatory responses to prolonged hypoxaemia in fetal sheep. Am J. Obstet Gynaecol 1988; 159: 1418-24.
5.  Martin–Ancel Ana, Garcia Alix Alfredo, Gaya Francisco, Catanas Fernando, Buergeros Margarita and Quero Fort. Multiple organ involvement in perinatal asphyxia : The Journal of Pediatrics. 1995; 127: 786 – 93.
6.  Shah P., Riphagen S., Beyene J., Perlman M. Multiorgan dysfunction in infants with post asphyxial hypoxic ischaemic encephalopathy. Archives of Diseases of childhood. Fetal and neonatal edition 2004; 89: F152 – F155.
7.  Perlman JM, TackE.D., Martin T., Shackelford G., Amin E. Acute systemic organ injury in term infants after asphyxia. American Journal Diseases in Children: 1988; 43: 617 – 620.
8.  Shankaran Seetha, Woldt Eunice, Koepke Thomas, Bedard Mary P. and Nandyal Raja. Acute neonatal morbidity and long term central nervous system sequalae of perinatal asphyxia in term infants: Early Human Development, 1991; 25: 135 – 148.
9.  Low James A; Panagiotopuls, Constadina, Derrick, E. Jane – American Journal of Obstetrics and Gynaecology: 1994; 170: 1081-1087.
10.  Goodwin Thomas Murphy, Belai Issac, Hernandez Patricia, Durand Manual, Paul Richard H. Aspyxial complications in term newborn with severe umbilical acidaemia. American Journal of Obstetrics and Gynaecology 1992; 162: 1506 – 12.
11.  Hankins Gary D.V., Koen Sophia, Gei Alfredo F., Lopez Suzanne M., Van Hook James W., Anderson Garland D. Neonatal organ system injury in acute birth asphyxia sufficient to result in neonatal encephalopathy. Obstetrics and Gynaecology 2002; 99: 688-91.
9. / Signature of the candidate
10. / Remarks of the guide
11. / Name and Designation of
(in block letters)
11.1 Guide / DR. B. SANJEEV RAI, M.D, D.C.H,
DEAN & PROFESSOR
DEPARTMENT OF PAEDIATRICS
FR. MULLER MEDICAL COLLEGE,
KANKANADY, MANGALORE.
11.2 Signature
11.3 Head of the department / DR. K. VARADARAJ SHENOY M.D, D.C.H
PROFESSOR AND HEAD
DEPARTMENT OF PAEDIATRICS
FATHER MULLER MEDICAL COLLEGE
KANKANADY, MANGALORE
11.6  Signature
12. / 12. 1 Remarks of the Chairman and Principal
12.2 Signature

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