Plasma thrombomodulin level in very low birthweight infants at birth

Objective: Plasma soluble thrombomodulin level reflects endothelial damage. The plasma thrombomodulin level at birth is increased in asphyxiated full-term infants. There is no report of plasma thrombomodulin level in premature infants. To determine the thrombomodulin level in premature infants and whether it might reflect endothelial damage, we examined the plasma thrombomodulin level in very low birthweight (VLBW) infants at birth. Methods: Forty-five VLBW infants, of whom 14 had perinatal asphyxia complications, were recruited. As a control, 50 full-term infants wimout complications were also studied. Plasma thrombomodulin concentration, pH, base deficit, serum creatinine and D-dimer concentration, platelet count and fibrinogen concentration were measured within 1 hour after birth. Results: There were significant differences in plasma pH, creatinine concentration, platelet count, antithrombin in activity and D-dimer concentration between VLBW infants and full-term infants. Plasma thrombomodulin concentration (39. 0 (16. 6–93. 7) vs 27. 0 (16. 6–39. 1) μg/L, p < 0. 0001) and plasma taombomodulin-to-serum creatinine ratio (0. 82 (0. 19–2. 65) vs 0. 47 (0. 24–0. 70) μg/μmol, p < 0. 0001) were significantly higher in VLBW infants than those in full-term infants. By univariate analyses for all neonates, there were significant relations between plasma thrombomodulin concentration and gestational age, birthweight, plasma pH, creatinine concentration, platelet count and antithrombin in activity. A stepwise multiple linear regression model using the above variables as dependent factors showed only birthweight contributed significantly to plasma thrombomodulin concentration (plasma thrombomodulin concentration (μg/1) = 45. 677–0. 006 (birthweight; g), r²= 0. 323, p < 0. 0001, n= 94). Plasma thrombomodulin concentration and plasma thrombomodulin-to -serum creatinine ratio in VLBW infants with asphyxia were higher than in those without asphyxia, but not significantly different (43. 2 ± 17. 7 vs 38. 3 ± 8. 5 μg/1 and 0. 92 ± 0. 60 vs 0. 83 ± 0. 37 μg/μmol). Conclusion: Plasma thrombomodulin level in VLBW infants shows a high value at birth, and we consider the main factor responsible for this elevation may be endothelial damage or low clearance rate of thrombomodulin, which may be related to early gestational age.     

Cardiac troponin I in asphyxiated neonates

BACKGROUND: Cardiac troponins T (cTnT) and I (cTnI) are well-established markers in detecting myocardial ischemic damage in adults. Perinatal asphyxia is associated with cardiac dysfunction. OBJECTIVES: To evaluate serum concentrations of cTnI in asphyxiated neonates and to investigate whether cTnI is correlated with the traditional markers of asphyxia. METHODS: Blood samples were collected from 13 asphyxiated neonates (umbilical artery pH<7.18 and either a 1-min Apgar score<4 or a 5-min Apgar score<7) and 39 controls. Data on gestation, birth weight, sex, Apgar scores, mode of delivery, umbilical pH, creatinine, serum activity of aspartate and alanine aminotransferase, and QTc interval were investigated. RESULTS: Median (range) cTnI concentrations were significantly higher in asphyxiated neonates with respect to healthy infants: 0.36 microg/l (0.05-11) versus 0.04 microg/l (0.04-0.06); p<0.01. In asphyxiated babies, no statistically significant correlations were found between concentrations of cTnI and the other markers of asphyxia. CONCLUSIONS: In asphyxiated neonates, cTnI concentrations are higher with respect to healthy infants, suggesting the presence of myocardial damage in this group of high-risk patients. cTnI does not correlate with the traditional markers of asphyxia.     

Is serum troponin T a useful marker of myocardial damage in newborn infants with perinatal asphyxia?

AIM: To assess the correlation of echocardiographic signs of myocardial damage to serum cardiac troponin T (cTnT) concentrations in newborn infants with perinatal asphyxia. METHODS: Electocardiograms (ECG) and echocardiograms (Echo) were obtained during the first 24 h of life from 29 asphyxiated and 30 control infants and correlated with cTnT concentrations. The echocardiographic parameters included systolic ventricular performance, preload, afterload, diastolic function, stroke volume (SV), left ventricular output (LVO), hyperechogenity of the papillary muscles and insufficiency of the atrioventricular valves. RESULTS: LVO and SV were lower but CTnT were significantly higher in asphyxiated than in control infants: 0.15 (010-0.23) vs. 0.05 (0.02-0.13), p < 0.001). Asphyxiated infants with signs of myocardial damage were associated with significantly higher cTnT than those without, 0.20 (0.11-0.28) and 0.11 (0.05-0.14 ug/L), p = 0.04. CONCLUSION: Cardiac troponin may prove to be valuable in evaluating myocardial damage in birth asphyxia. However, the degree of prematurity may complicate the assessment.     

Thrombomodulin serum levels in ventilated preterm babies with respiratory distress syndrome

A soluble form of thrombomodulin (TM), an anticoagulant proteoglycan of the endothelial cell membrane, considered a marker of vascular endothelial damage, was measured in plasma of preterm infants with respiratory distress syndrome (RDS). In these patients, lung immaturity leads to endothelial leak of plasma proteins and to surfactant inhibition. In 18 babies with RDS, plasma TM concentration was significantly elevated compared with values of a matched group of babies without pulmonary disease (276.1 ng/ml vs 141.3 ng/ml) (P<0.05). Furthermore, TM levels of mechanical ventilated babies (IPPV) with severe RDS were higher than those of babies with moderate RDS and treated with nasal CPAP (340.9 ng/ml vs 174.2 ng/ml) (P<0.05). Conclusion These data show that TM can be used as marker of pulmonary endothelial damage in preterm babies treated with mechanical ventilation for RDS and suggest early intervention with exogenous surfactant to limit alveolar protein leakage and surfactant inactivation. Received: 20 February 1997 and in revised form: 7 July 1997 / Accepted: 8 July 1997     

Elevation of Plasma Concentrations of Arginine Vasopressin Following Perinatal Asphyxia

Hypoxic ischemic encephalopathy is a major cause of mortality in neonates. Studies in experimental subjects have shown differing responses of plasma arginine vasopressin to hypoxia. Plasma arginine vasopressin levels, serum osmolality, urine osmolality and fluid intakes were measured in thirteen asphyxiated and nineteen control newborn infants during the first seventy-two hours of life. In the asphyxiated infants plasma arginine vasopressin was found to be elevated as compared to control infants on days one ( p < 0.001) and two ( p < 0.007) but not on day three of life. Urine osmolality was also elevated in the study patients on days one ( p < 0.01) and two ( p < 0.001) but not on day three, in spite of equal intakes of fluid on day one in both groups and significantly diminished fluid intake on days two and three in the study patients. Serum osmolality was not different between the two groups on any day studied, and was felt to be on the basis of diminished intake in the study infants. The data presented in this study support the concept that arginine vasopressin release occurs following perinatal asphyxia in term newborn infants     

Pathogenesis of early neonatal hypocalcemia: studies of serum calcitonin, gastrin, and plasma glucagon

In 64 maternal-infant pairs, we tested the hypotheses that serum calcitonin, serum gastrin, and plasma glucagon concentrations are elevated in infants at risk for early neonatal hypocalcemia, and that elevated serum gastrin and plasma glucagon result in elevated serum calcitonin and low serum calcium values in neonates. Serum Ca declined significantly in neonates at 24 hours of age, and was inversely correlated with serum calcitonin. Cord serum calcitonin, gastrin, and plasma glucagon concentrations rose significantly at 24 hours of age. Cord calcitonin was significantly higher in preterm compared with term infants, and there was no significant difference between asphyxiated and nonasphyxiated preterm neonates; in term neonates cord calcitonin concentration was inversely correlated with Apgar scores at 1 and 5 minutes. Cord calcitonin was not correlated with cord gastrin or glucagon. Cord and 24-hour gastrin and glucagon values were not related to prematurity; cord glucagon, but not gastrin, was related to birth asphyxia. We conclude that (1) serum calcitonin, gastrin, and plasma glucagon values rise postnatally; cord calcitonin is elevated in preterm and in asphyxiated term infants; serum calcitonin concentration does not correlate with the elevated serum gastrin and plasma glucagon values; and at 24 hours of age, decreased serum Ca is correlated with serum calcitonin, and hence calcitonin might play a role in the pathogenesis of early neonatal hypocalcemia.     

新生儿HIE脐血IL-6、IL-8与TNF-α变化及临床意义探讨

为探讨新生儿缺氧缺血性脑病 ( HIE)脐血 IL - 6、IL - 8与 TNF-α的变化及临床意义 ,应用放射免疫法检测了 4 0例 HIE患儿 IL- 6、IL- 8与 TNF- α水平 ,并与 4 0例正常新生儿比较。结果显示与正常新生儿比较 ,HIE患儿与正常对照儿相比脐血IL - 6水平分别为 ( 61.0 4± 2 3 .0 6)对 ( 91.83± 3 7.5 4 ) ng/L ( P<0 .0 1) ,IL - 8分别为( 0 .3 4± 0 .0 9)对 ( 0 .2 6± 0 .0 7) μg/L( P<0 .0 1) ,TNF- α分别为 ( 1.0 3± 0 .3 0 )对 ( 0 .83± 0 .3 1) μg/L( P<0 .0 1) ;而且病情越重改变越明显。因此 ,我们认为 ,围产期窒息与HIE患儿脐血 IL - 6水平减低、IL - 8与 TNF-α水平升高有关 ;它们可能参与了新生儿缺氧缺血性脑损伤的某些发病过程     

The Scottish perinatal neuropathology study: clinicopathological correlation in early neonatal deaths

BACKGROUND: A proportion of neonatal deaths from asphyxia have been shown to be associated with pre-existing brain injury. OBJECTIVES: (a) To compare the epidemiology of infants displaying signs of birth asphyxia with those not showing signs; (b) to examine the neuropathology and determine if possible the timing of brain insult comparing asphyxiated with non-asphyxiated infants; (c) to compare the clinical features of those born with birth asphyxia with and without pre-labour damage. METHODS: Over a two year period, all 22 Scottish delivery units collected clinical details on early neonatal deaths. Requests for post mortem included separate requests for detailed neuropathological examination of the brain. Infants were classified into two groups: birth asphyxia and non-birth asphyxia. Clinicopathological correlation was used to attempt to define the time of brain insult. RESULTS: Detailed clinical data were available on 137 of 174 early neonatal deaths that met the inclusion criteria. Seventy of 88 parents who had agreed to post mortem examination consented to a detailed examination of additional samples from the brain; in 53 of these cases the infant was born in an asphyxiated condition. All asphyxiated and encephalopathic infants, 38% of mature and 52% of preterm infants with features of birth asphyxia but without encephalopathy, and only one of 12 infants without any signs of birth asphyxia showed damage consistent with onset before the start of labour. CONCLUSIONS: In a large proportion of neonatal deaths, brain injury predates the onset of labour. This is more common in infants born in an asphyxiated condition.     

Estimation of Digoxin Dosage in VLBW Infants Using Serum Creatinine Concentrations

ABSTRACT. Digoxin steady state plasma concentrations (C_ss) and the corresponding serum creatinine concentrations were studied in 17 VLBW infants. Birth weight was in the range of 760-1500 g (mean 1068 g), gestational age ranged from 26 to 32 weeks (mean 28.7 weeks). Digoxin steady state plasma concentrations were found in the range of 0.5-6.5 μg/ml (mean 1.88 μg/ ml) during maintenance therapy with 1.6-8.4 μg/kg BW/24 h (mean 4.4 μg/kg BW724 h) given in two divided doses intravenously. No digoxin-like immunoreactive substance could be detected in the plasma of 18 infants (10 patients with a birth weight <1500 g, 8 patients with a birth weight of 2100-4 730 g) that were not treated with digoxin. The calculated digoxin clearance ranged from 0.38-4.03 ml/min/kg BW. Serum creatinine concentrations were found in the range of 35-274 μmol/l (0.4-3.1 mg/100 ml). A hyperbolic correlation may be derived from the digoxin clearance and the corresponding serum creatinine concentration. A linear relationship was observed between the dose normalized digoxin concentrations (y=C_ss/dose in 24 h) and the respective creatinine concentrations x (v=0.52x-0.05; n=17; 5=0.24; r=0.86; p<0.01). According to this equation we suggest a dosing schedule for digoxin in VLBW infants with impaired renal function. Digoxin maintenance dose is derived from the digoxin target and the creatinine serum concentration. This dose recommendation proved reliable on four VLBW infants (birth weight 770-1260 g) with decreased renal function.     

血清S100B蛋白在新生儿窒息后脑损伤中的临床意义

目的：S100B蛋白是一种脑特异性蛋白,可反映脑损伤的程度。该研究旨在探讨窒息新生儿脐血及生后血清S100B蛋白的变化及对新生儿窒息诊断和窒息后脑损伤判断的价值。方法：对窒息新生儿的脐血及生后1,3,7d血清S100B蛋白变化进行分析。结果：①窒息新生儿脐血S100B蛋白水平高于正常对照组,差异有显著性(P<0.05),轻度窒息与重度窒息患儿脐血S100B蛋白含量差异无显著性;②出生后1～7d内轻度窒息患儿血清S100B蛋白无明显变化,重度窒息脑损伤患儿血清S100B蛋白呈逐渐增高趋势,生后第7天时重度窒息脑损伤患儿血清S100B蛋白明显高于轻度窒息患儿(P<0.01);③死亡的窒息患儿生后第7天的血清S100B蛋白含量高于存活儿,但差异无显著性(P>0.05);④发生颅内出血和/或脑水肿的患儿生后第3天血清S100B蛋白含量增高,差异有显著性(P<0.05)。结论：血清S100B蛋白检测有助于新生儿窒息的诊断及窒息后脑损伤的判断。     

Effect of birth asphyxia on serum calcium levels in neonates

Serum calcium and phosphorus levels were measured at birth, 6 hours, 24 hours, and on 5th day of life in 35 neonates with birth asphyxia (one-minute Apgar score of 6 or less), and in 37 neonates without asphyxia (one-minute Apgar score of 7 or more). Infants were divided into three groups: FT-AGA (n=30, asphyxia=15), FT-IUGR (n=20, asphyxia=10) and PT-AGA (n=22, asphyxia=10). Asphyxiated infants-FT-AGA as well as FT-IUGR-had significantly lower serum calcium levels than control infants during each of the time period studied. In PT-AGA infants with asphyxia, the serum calcium was significantly low only on 5th day of life. Lack of calcium intake, and hyperphosphatemia were identified as possible risk factors for low serum calcium in asphyxiated infants. No change in serum calcium levels was found in bicarbonatetreated asphyxiated infants in comparison to those who did not receive sodium bicarbonate. In view of the high incidence of low serum calcium in asphyxiated infants, serial monitoring of serum calcium levels is recommended in these infants.     

Troponin-T levels in perinatally asphyxiated infants during the first 15 days of life

Aim: To measure serial cardiac troponin‐T, creatine kinase, creatine kinase‐MB, aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase levels in asphyxiated newborn infants during the first 15 d of life. Methods: Troponin‐T, creatine kinase, creatine kinase‐MB, aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase (LDH) concentrations were measured prospectively in blood samples obtained from 45 asphyxiated and 15 healthy term neonates within the first 2–4 h, third, seventh and 15th days. Results: Infants with severe asphyxia had significantly higher cardiac troponin‐T levels than grade I and II asphyxiated and healthy neonates within the first 2–4 h of life (0.34 ± 0.21 ag/ml vs 0.07 ± 0.03 ag/ml, 0.12 ± 0.07 ag/ml, 0.04 ± 0.02 ag/ml, respectively). Troponin‐T levels remained high on days 3 and 7 in severely asphyxiated neonates. The creatinine kinase‐MB levels were significantly higher in grade II and III asphyxiated neonates than grade I asphyxiated and healthy neonates within the first 2–4 h. No difference was found in creatinine kinase‐MB on day 3. There was cardiac involvement in 12 (80%) newborns of group III on B mode echocardiographic images on day 1. However, no echocardigraphic pathology was found in the seventh‐ and 15th‐day echocardiographic analysis in any groups. Conclusion: Our results suggest that asphyxia‐related cardiac changes were significant but reversible in severely asphyxiated neonates, and troponin T is a good determinant of the degree of injury to the heart within the first week of life. Cardiac troponin T also has a wider diagnostic frame than other diagnostic markers of myocardial damage.     

Effect of thyroxine administration on renal functions in newborn infants with perinatal asphyxia.

The study was undertaken to assess the influence of thyroxine given to improve respiratory adaptation in asphyxiated neonates on the recovery of compromised renal functions. Two groups of infants with perinatal asphyxia were selected for the study. Group I consisted of 8 infants treated conventionally, while Group II included 7 infants who in addition to standard therapy were administered 50 micrograms thyroxine at admission and repeated 24 hours later. Their respective mean gestational ages were 38.7 weeks (range: 34-42 weeks) and 37.4 weeks (range: 34-41 weeks). The studies were performed on days 1, 7 and 14 and the results compared to those obtained in 13 healthy neonates with the gestational age of 39.2 weeks (range: 38-41 weeks) (Group III). Asphyxiated neonates had significantly higher plasma uric acid, xanthine, hypoxanthine and creatinine levels (p < 0.05), while their GFR proved to be markedly reduced (p < 0.01) when compared to the values of healthy controls. Moreover, there was a significant elevation of urinary excretion of NAGA (p < 0.001), urine osmolality (p < 0.05), PENa, FECa, RFI (p < 0.05) in infants presenting with perinatal asphyxia. Renal tubular responsiveness to aldosterone measured as TTKG was also found to be depressed (p < 0.025). In response to thyroxine therapy renal functional recovery appeared to be accelerated as indicated by the lower plasma creatinine level, lower rate of fractional electrolyte and urinary NAGA excretion and improved reactivity to aldosterone on days 7 and/or 14 as compared to those obtained in neonates presenting with asphyxia but without thyroxine therapy. The results seem to suggest that thyroid hormones may have an important role in the recovery of renal functions in newborn infants suffering from perinatal asphyxia.     

窒息新生儿脑干听觉诱发电位与血清神经元特异性烯醇化酶的相关性分析

目的：通过研究窒息患儿脑干听觉诱发电位（BAEP）异常与神经元特异性烯醇化酶（NSE）的相关性,探讨NSE对早期了解窒息患儿听神经损害的临床意义和应用前景。方法：选择该院窒息足月新生儿52例作为研究组,根据Apgar评分以及是否合并缺氧缺血性脑病(HIE)分为单纯轻度窒息组23例、单纯重度窒息组15例和窒息合并HIE组14例。采用双盲试验在生后7 d同一时间检测BAEP和NSE,初次BAEP检测异常者在生后3个月同一时间进行第2次BAEP和NSE检测。正常足月新生儿30例作为对照组。结果：窒息患儿两次听力损伤检出率分别为50.0%,21.2%。BAEP两次检出异常率,重度窒息组(63.3%,26.3%)与轻度窒息组(36.9%,5.9%)比较,差异均有显著性意义(P<0.05),HIE组(57.1%,31.3%)与重度窒息组比较差异无显著性意义。各研究组NSE水平均明显高于对照组(P<0.01),重度窒息组为26.70±2.34 μg/L明显高于轻度窒息组的17.18±3.16 μg/L,差异有显著性意义(P<0.01),HIE组为27.00±2.01 μg/L,与重度窒息组比较差异无显著性意义。BAEP异常组NSE水平为25.69±4.12 μg/L高于BAEP正常组的17.15±3.09 μg/L(P<0.01),NSE水平随着V波反应阈值的增高而增高(P<0.05)。结论：血清NSE水平与BAEP密切相关,可作为早期评估窒息患儿听神经损害和判断预后的指标之一。     

Renal injury in sick newborn infants: a prospective evaluation using urinary beta 2-microglobulin concentrations

Urinary concentrations of beta 2-microglobulin and creatinine were measured serially in 140 sick infants, of whom 109 were asphyxiated, and in 35 healthy preterm and term infants. First voided urines and samples from days 3 and 7 postpartum were studied. Urinary beta 2-microglobulin concentrations in healthy infants averaged 1.34 +/- 1.34 mg/L (mean +/- SD) in first voided specimens and 1.32 +/- 0.98 mg/L in day 3 samples; the calculated upper limit of normal (95% confidence limit) was 4.00 mg/L. Elevated values (those exceeding the 95% confidence limit) occurred most often in the sick asphyxiated patients (56%); the first voided sample value in these patients was 10.0 +/- 10.4 mg/L. The equivalent value in the sick nonasphyxiated infants was 8.32 +/- 7.27 mg/L. Values were significantly and persistently elevated in the sick infants on days 3 and 7. Factoring beta 2-microglobulin levels by urinary creatinine concentration did not affect the significance of the findings. The increased urinary beta 2-microglobulin levels were not (1) related to gestational age; low beta 2-microglobulin values occurred at all gestational ages for both healthy and sick infants; (2) a consequence of urine flow rate; urinary beta 2-microglobulin did not correlate with urinary creatinine concentration or with urine to plasma creatinine ratio; and (3) a consequence of increased production of beta 2-microglobulin; urinary and serum beta 2-microglobulin values did not correlate (r = .03). Thus, we propose that the elevated levels of urinary beta 2-microglobulin in the sick infants were the consequence of tubular injury. This was associated with hematuria but not with a high incidence of azotemia or oliguria.(ABSTRACT TRUNCATED AT 250 WORDS)     

THE CONCENTRATIONS OF TOTAL CORTISOL AND CORTICOSTERONE IN MIXED CORD PLASMA

ABSTRACT: Homoki, J., Teller, W. M., Tschürtz, D., and Fazekas, A. T. A. (Department of Paediatrics, Division of Endocrinology and Metabolism, University of Ulm/Donau, BRD). The concentrations of total Cortisol and corticosterone in mixed cord plasma. Acta Paediatr Scand, 64:587, 1975.–Cortisol and corticosterone were determined in mixed umbilical cord plasma of 43 healthy full-term newborns. The method consisted of a combined thin-layer chromatographic-ftuorimetric procedure which proved to be specific and reliable. The mean concentration in cord plasma of Cortisol was 10.6±4.9 μ.g/100 ml, of corticosterone 1.8±0.8 μg/100 ml. The mean ratio cortisol/corticosterone F/B was 6.3±2.5. Neither the duration nor the time of day of delivery appeared to influence the concentration of Cortisol or corticosterone in umbilical cord plasma. Also, there was no significant difference between male and female infants. In 18 instances of a pathological course of gestation and/or delivery the mean Cortisol level was 9.1±4.7 μg/ml, the mean corticosterone level 2.2±9 μg/100 ml. The mean F/B ratio was slightly but not significantly decreased (4.2±1.4 μg/100 ml; p >0.05). It is speculated that the high corticosterone concentration in umbilical cord plasma reflects a defect in Cortisol biosynthesis (17α-hydroxylase deficiency) in the newborn, compared with later life.     

Interleukin-6 and tumor necrosis factor-alpha levels in plasma and cerebrospinal fluid of term newborn infants with hypoxic-ischemic encephalopathy

OBJECTIVES: To determine plasma and cerebrospinal fluid (CSF) levels of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) in hypoxic-ischemic encephalopathy (HIE). STUDY DESIGN: A controlled, prospective study of 20 control neonates, 19 term newborn infants presenting with sepsis and no meningitis, and 19 asphyxiated term newborn infants. Blood and CSF samples were collected within 48 hours of birth for IL-6 and TNF-alpha determinations. RESULTS: Median plasma IL-6 was similar in sepsis and asphyxia but significantly higher than in control neonates. Median plasma TNF-alpha was similar in asphyxia and control neonates but significantly lower than in sepsis. In asphyxiated newborn infants, median CSF IL-6 and TNF-alpha were significantly higher than in sepsis and control neonates. Median CSF IL-6 was significantly higher in sepsis than in control neonates. Median CSF TNF-alpha was similar in newborn infants with sepsis and control neonates. IL-6 and TNF-alpha CSF/plasma ratios were similar in newborn infants with sepsis and control neonates but lower than in asphyxiated newborn infants. CONCLUSIONS: Term newborn infants with HIE have elevated CSF IL-6 and TNF-alpha levels. Plasma IL-6 is increased in asphyxia and sepsis. Plasma TNF-alpha is increased only in sepsis. High IL-6 and TNF-alpha CSF/plasma ratios in asphyxia suggest that these cytokines are produced in the brain of term newborn infants with HIE.     

Postnatal changes in serum immunoreactive erythropoietin in relation to hypoxia before and after birth

To assess the immediate postnatal changes of serum immunoreactive erythropoietin (EP) in infants born after acute or chronic fetal hypoxia, and to estimate the rate of EP disappearance, we studied EP concentration, measured by double-antibody radioimmunoassay, in cord venous plasma and in serum at a mean age of 8 hours in a control group (n = 9) and in three patient groups: (1) infants with polycythemia (n = 10), (2) infants born to mothers with preeclampsia of pregnancy, without (n = 22) or with (n = 11) acidosis at birth, and (3) infants with acute birth asphyxia (n = 19), seven of whom had postnatal hypoxia. In all patient groups, cord venous EP was elevated in comparison with values in control infants. No change was found in EP level between birth and 8 hours in control infants (geometric mean in cord and 8-hour sample: 20 and 16 mU/ml, not significant) or in acutely asphyxiated infants with postnatal hypoxia (122 and 72 mU/ml, not significant), whereas the EP level decreased in all other groups: infants with polycythemia (123 to 24 mU/ml, p less than 0.001), nonacidotic infants (78 to 26 mU/ml, p less than 0.001) and acidotic infants (176 to 38 mU/ml, p less than 0.001) of the preeclampsia group, and acutely asphyxiated infants without postnatal hypoxia (58 to 30 mU/ml, p less than 0.001). The mean (+/- SD) half-time of EP disappearance was 2.6 +/- 0.5 hours in infants with polycythemia and 3.7 +/- 0.9 hours in infants of the preeclampsia group.     

窒息新生儿凝血功能状态的研究

目的探讨窒息足月、早产新生儿凝血功能的变化。方法检测10例正常儿、44例窒息足月儿、32例窒息早产儿凝血指标。结果与对照组比较,窒息足月儿PT、APTT、FIB、PLT无显著差异,D-D明显升高,且与窒息程度正相关。窒息早产儿与窒息足月儿比较PT、APTT延长,FIB、PLT降低,D-D无明显差异。结论窒息足月儿大都存有高凝为特征的前DIC或DIC早期;窒息早产儿更易发生DIC,且有向低凝期发展的趋势。     

Fetal and Neonatal Cortical Adrenal Function in Birth Asphyxia

ABSTRACT. Eighteen newborn infants, gestational age between 36 and 42 weeks with birth asphyxia were compared with 23 normal newborn infants to determine serum cortisol and dehydroepiandrosterone sulfate levels in cord blood and in venous blood samples collected 12–18 hours after birth. Both groups were similar in gestational age, birthweight, proportion of small for gestational age and large for gestational age infants, proportion of infants delivered by cesarean section with and without labor, and proportion of mothers with pre-eclampsia. There was no antenatal exposure to corticosteroid. The asphyxiated newborn infants had a significantly higher mean cord serum level of cortisol, and a significantly lower mean cord serum level of dehydroepiandrosterone sulfate than the control group. Mean serum cortisol and dehydroepiandrosterone sulfate levels collected 12–18 hours after birth were similar between both groups. It is suggested that elevated cord serum level of cortisol is related to birth asphyxia stress stimulating the adrenal definitive zone, and the low cord serum level of dehydroepiandrosterone sulfate is secondary to a transient hypoxemic-ischemic insult to the adrenal fetal zone.