1454 a Pathologic Reappraisal of Kernicterus

Abstract

Continuous monitoring of v i t a l s i g n s , e . g . temperature, blood pressure, heart and r e s p i r a t i o n r a t e s , and E C G , f o r the care of c r i t i c a l l y s i c k infants has become an established hospital routine. W e have compared various non-invasive and invasive continuous Pa02 monitors with a r t e r i a l blood Pa02 levels and find t h a t there i s a considerable c o r r e l a t i o n between the values obtained by d i f f e r e n t procedures. Continuous monitoring procedures permit b e t t e r evaluation of the p a t i e n t than skin c o l o r , ECG monitoring o r c l i n i c a l observation.I t s immediate a v a i l a b i l i t y a t bedside and the capacity t o detect i r r e g u l a r i t y in oxygen supply i s of major c l i n i c a l advantage. These devices help in preventing t h e e f f e c t s of hyperoxemia and hypoxemia. S t a b i l i z a t i o n of s i c k infants can be achieved rapidly without repeated a r t e r i a l blood sampling f o r Pa02 determinations. The r e s u l t s suggest t h a t these continuous Pa02 monitors (invasive o r non-invasive) may be a b l e t o eliminate or minimize conditions l i k e bronchopulmonary dysplasia, r e t r o l e n t a l f i b r o p l a s i a and brain damage due t o lack of oxygen during neonatal development. INTRAUTERINE FETAL RESUSCITATION WITH TERBUTALINENer esh A. Te a n i , Uma L. Verma, S amali Chatter ee.1451 Spo:. by P l a t i n J. Collipp. NassavlCty Med C t r , i l t h S c i C t r , SUNY a t Stony Brook, Dept. of Ob/Gyn, East Meadow, NY Cases of i n t r a p a r t a l f e t a l d i s t r e s s from any cause s u s t a i n f u r t h e r hypoxia during u t e r i n e contractions due t o t h e concomit a n t reduction i n u t e r i n e blood flow during u t e r i n e a c t i v i t y . Therapeutic reduction of u t e r i n e a c t i v i t y should, t h e r e f o r e , res u l t i n recovery of f e t a l h e a r t r a t e (FHR) and f e t a l a c i d o s i s , and t h e b i r t h of a neonate i n a b e t t e r s t a t e of owgenation and acid-base balance. Towards t h i s , t e r b u t a l i n e 250 Ug subcutaneously was i n j e c t e d i n p a t i e n t s with evidence of f e t a l d i s t r e s s . A l l 1 1 p a t i e n t s showed ominous FHR changes. I n 2 of t h e s e , f e t a l s c a l p blood pH (FSB-pH) was not t e c h n i c a l l y possible. I n 2 , t h e FSB-pH was b 7.25. The remaining 7 p a t i e n t s showed FSB-pH 4 7.25.Results: Where adequate FHR t r a c e was a v a i l a b l e , 9/10 pat i e n t s showed marked reduction t o cessation of u t e r i n e a c t i v i t y , and complete o r p a r t i a l recovery of ominous FHR changes. FSB-pH was compared t o t h e mid-point of t h e umbilical vein and a r t e r y pH's. I n t h e 2 cases where t h e o r i g i n a l FSB-pH was b 7.25, no change was seen. However, i n cases with FSB-pH 5 7.25, a s i gn i f i c a n t improvement from a mean of 7.180 + .038 t o 7.270 2 .066 (P = 4 .005) was seen. No major s i d e e f f e d s were noted. ST of AP l i p . e x t . meas...

Experimental Bilirubin Encephalopathy: Importance of Total Bilirubin, Protein Binding, and Blood-Brain Barrier

“…This experimental model supports the proposal that yellow staining cannot be equated with bilirubin toxicity and provides a possible explanation for the neuropathological observations of Turkel et al (26). In many sick premature infants with yellow staining, they found spongy changes in brain consistent with interstitial edema (or interstitial bilirubin-albumin), but few changes in neurons that could be attributed to bilirubin.…”

Bilirubin Binding in the Plasma of Newborns: Critical Evaluation of a Fluorescence Quenching Method and Comparison to the Peroxidase Method

“…But, in reviewing this data, Wennberg and Ahlfors (46) found that the combination of unbound bilirubin levels and serum pH resulted in a much better correlation with risk for kernicterus. Furthermore, Levine et al (26) presented evidence which implicates opening of the bloodbrain barrier in the pathogenesis of gross staining of the brain by bilirubin, and Turkel et al (43) pointed out that gross bilirubin staining of the neonatal brain is often not associated with histopathologic changes indicative of bilirubin toxicity. These studies indicate the need for further studies to carefully delineate the relationships between serum unbound bilirubin levels, brain bilirubin levels, physiologic and pathologic signs of bilirubininduced neurocytotoxicity, and grossly visible staining of the brain.…”

Changes in Globus Pallidus With (Pre)Term Kernicterus

“…Postmortem cohort studies introduced controversy about the role of acidosis. 3,11 Some did correlate free serum unconjugated bilirubin with autopsy-confirmed preterm kernicterus. 36 Focusing on sensorineural deafness without cerebral palsy in preterms of gestational age Ͻ34 weeks and TSB peak level Ͼ240 mol/L (14 mg/dL), de Vries et al in 1985 37 correlated bilirubin toxicity with spells of respiratory acidosis and with duration of hyperbilirubinemia (5 of 12 deaf children with at least 48 hours of TSB Ͼ240 mol/L, versus 1 of 12 matched control subjects).…”

“…11 Macroscopic staining of brain areas occurs in the absence of neuronal cell loss, troubling the histopathologic diagnosis. Regional exudation of bilirubin should not be equated with kernicterus.…”