Mortalite Gelişen Perinatal Asfiksi Olguların Retrospektif İncelenmesi

Year 2020, , 247 - 250, 20.08.2020

Abit Demir , Halil Dolap , Nurgül Ataş , Yasin Özcan Müslüm Toptan

https://doi.org/10.35440/hutfd.752095

Abstract

Bu çalışmada perinatal asfiksi (PA) tanısı alan ve mortalite gelişen olguların pH, baz eksikliği (BD), retina değişiklikleri ve amplitüd-entegre elektroensefalografi (aEEG) bulgularını araştırmayı amaçladık. Materyal ve metod: Çalışmaya perinatal asfiksi nedeniyle mortalite gelişen yedi hasta dahil edildi. Olguların kan gazı analizi, 72 saatlik aEEG bulguları kaydedildi. Tüm bebekler aynı göz doktoru tarafından muayene edildi. Veri analizleri SPSS Statistics yazılımı kullanılarak yapıldı. Bulgular: Takip sırasında mortalite gelişen yedi perinatal asfiksi olgusu çalışmaya dahil edildi. Olguların pH değeri 6.30-6.98 (6.84) ve BD 18-40 (23) mmol / L arasındaydı. İki hastada masif retinal kanama saptandı. Bir hastada, spot kanama odakları sağ göz retinasında daha belirgindi. Olguların postnatal 24. saatteki aEEG bulguları değerlendirildiğinde, altı hastada düşük voltaj (LV), bir hastada patlama bastırma (BS) paterni saptandı. İki olgumuz 24. ve 48. saatler arasında öldü ve her iki olgu da LV modelindeydi. Dört olgunun takibinde mortalitenin 72 saat sonra geliştiği gözlendi. Bu dört vakadan biri LV paterni ve ikisi BS paterniydi. Son vakanın 24-48 ve 72. saatteki paternleri sırasıyla BS-LV ve DNV idi.
Sonuçlar: Çalışmamızda mortalite gelişen olgularda ciddi anormal aEEG bulguları olduğu bulundu. 24-48 saat devam eden LV ve BS paterninin mortalite gelişimi ile ilişkili olduğu ve bu sonuçların literatürle uyumlu olduğu belirlendi.

Keywords

mortalite, baz defisiti, aEEG, retinal kanama, Perinatal asfiksi

Supporting Institution

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Project Number

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Retrospective Study of the Perinatal Asphyctic Cases That Developed Mortality

Abstract

In this study, we aimed to investigate the pH, base deficit (BD), retinal changes, and amplitude-integrated electroencephalography (aEEG) findings of cases diagnosed with perinatal asphyxia (PA) and developing mortality.
Material – Methods
Seven patients with mortality due to perinatal asphyxia were included in this study. Blood gas analysis of cases, 72-hour aEEG findings were recorded. All babies were examined by the same ophthalmologist. Data analyses were performed using SPSS Statistics software
Results
Seven cases with perinatal asphyxia who developed mortality during follow-up were included in this study. The pH value of the cases was between 6.30-6.98 (6.84) and the BD was between 18-40 (23) mmol / L. Massive retinal hemorrhage was detected in 2 patients. In one patient, spot bleeding foci were more prominent in the right eye retina. When the aEEG findings of the postnatal 24th hour of the cases were evaluated, it was found that six patients had low voltage (LV) and one patient had burst suppression (BS) pattern. Our two cases died between the 24th and 48th hours and both cases were in the LV pattern. In the follow-up of four cases, it was observed that mortality developed after 72 hours. One of these four cases was the LV pattern and two were BS patterns. The patterns of the last case at 24-48 and 72 hours were BS-LV and DNV, respectively.
Conclusions
In our study, it was found that cases with developed mortality had severe abnormal aEEG findings. It was determined that the LV and BS pattern, which continued for 24-48 hours, were associated with the development of mortality and these results were consistent with the literature.

Keywords

perinatal asphyxia, aEEG, mortality, base deficit, retinal hemorrhage

Project Number

yok

References

• 1. Eken P, Toet MC, Groenendaal F, Devries LS. Predictive value of early neuroimaging, pulsed doppler and neurophysiology in full-term infants with hypoxic-ischemic encephalopathy. Arch Dis Child 1995; 73: 75–80.
• 2. Gümüş H, Kazanasmaz H, Solmaz A, Aslan H. An ınvestigation of the relationship between base deficit and CRP in asphytic ınfants. Annals of Medical Research,2020,27.1:92-6
• 3. Papile LA, Baley JE, Benitz W , Cummings J , Carlo WA , Eichenwald E , Kumar P , Polin RA , Tan RC , Wang KS Hypothermia and neonatal encephalopathy. Committee on Fetus and Newborn, Pediatrics 2014;133:1146
• 4. Chandrasekaran M, Chaban B, Montaldo P, Thayyil S. Predictive value of amplitude-integrated EEG (aEEG) after rescue hypothermic neuroprotection for hypoxic ischemic encephalopathy: a meta-analysis. J Perinatol. 2017 ;37(6):684-9.
• 5. Giampietri M, Biver P , Ghirri Paolo , Bartalena Laura , Scaramuzzo R.T, Guzzetta A at al. Recovery of aEEG Patterns at 24 Hours of Hypothermia Predicts Good Neurodevelopmental Outcome. J Neonatal Biol, 2016, 5.230: 2167-0897.1000230.
• 6. Levene MI, Fenton AC, Evans DH, Archer LN, Shortland DB, Gibson NA. Severe birth asphyxia and abnormal cerebral blood-flow velocity. Dev Med Child Neurol. 1989;31(4):4. 27-34.
• 7. Eken P, Toet MC, Groenendaal F, de Vries LS. Predictive value of early neuroimaging pulsed Doppler and neurophysiology in full term infants with hypoxic-ischemic encephalopathy. Arch Dis Child Fetal Neonatal Ed. 1995;73(2):75-80.
• 8. Toet MC, Hellström-Westas L, Groenendaal F, Eken P, de Vries LS. Amplitude integrated EEG 3 and 6 hours after birth in full term neonates with hypoxic-ischemic encephalopathy. Arch Dis Child Fetal Neonatal Ed. 1999;81(1):19-23.
• 9. Aluvaala J, Collins GS, Maina M, Berkley JA, English M. A systematic review of neonatal treatment intensity scores and their potential application in low-resource setting hospitals for predicting mortality, morbidity and estimating resource use. Systematic reviews, 2017, 6.1: 248. 10. Hellstrom-Westas L, Bell AH, Skov L, Greisen G, Svenningsen NW. Cerebroelectrical depression following surfactant treatment in preterm neonates. Pediatrics 1992; 89: 643–7.
• 11. Spitzmiller RE, Phillips T, Meinzen-Derr J, Hoath SB. Amplitude-integrated EEG is useful in predicting neurodevelopmental outcome in full-term infants with hypoxic-ischemic encephalopathy: a meta-analysis. J Child Neurol 2007; 22: 1069–78.
• 12. Skov L, Hellstrom-Westas L, Jacobsen T, Greisen G, Svenningsen NW. Acute changes in cerebral oxygenation and cerebral blood volume in preterm infants during surfactant treatment. Neuropediatrics 1992; 23: 126–30.
• 13. Evans E, Koh S, Lerner J, Sankar R, Garg M. Accuracy of amplitude-integrated EEG in a neonatal cohort. Arch Dis Child Fetal Neonatal Ed 2010; 95: 169-73.
• 14. Rosen I. The physiological basis for continuous electroencephalogram monitoring in the neonate. Clin Perinatol 2006; 33: 593-611.
• 15. Gümüş H. Perinatal asfikside amplitüd-entegre elektroensefalografi’nin önemi, Tıp Bilimlerinde Farklı Bakışlar, Iksad Publications, Ankara 2019:273-284
• 16. Kliegman, Robert M. Hypoxic ischemic encephalopathy. Nelson Textbook Of Pediatrics (20th ed) Vol 1 IN: Nervous System Disorders. philadelphia: Elsevier, 2016;99.5:834-42.
• 17. Baum JD, Bulpitt CJ. Retinal and conjunctival haemorrhage in the newborn. Arch Dis Child 1970;45:344-9.
• 18. Schoenfeld A, Buckman G, Nissenkorn I, Cohen S, Ben-Sira I, Ovadia J. Retinal hemorrhages in the newborn following labour induced by oxytocin or dinoprostone. Arch Ophthalmol 1985;103:932-4.
• 19. Critchley ER. Observations on retinal haemorrhages in the newborn.J Neurol NeuroswurgPsychiatry 1968;31:259-62.
• 20. Callaway NF, Ludwig CA, Blumenkranz MS, Jones JM, Fredrick DR, Moshfeghi DM. Retinal and optic nerve hemorrhages in the newborn infant: one-year results of the newborn eye screen test study. Ophthalmology, 2016, 123.5: 1043-1052