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Purpose: Electrical burn wounds are among the most devastating of burns, with wide-ranging injuries. We aimed to document the factors affecting the mortality rate of patients presenting with electrical burn wounds to our regional burn centre., Methods: This retrospective study was conducted on 101 patients from January 2009 to June 2012. Factors were classified under 11 topics and evaluated according to their relationship with the mortality rate., Results: The major causes of death in burn victims were multiple organ failure and infection. Twenty-six percent of the 101 patients died, all of whom were male. One (1.4%) of the patients who survived was female; 73 (98.6%) survivors were male. The mean age in the deceased group was statistically higher than that of the other patients (32.7 vs. 35.6 years; P < 0.05). All-cause mortality was 2.79 times higher for larger burns (> 25% total body surface area). The values for creatine kinase, creatine kinase-MB, total body surface area of burn, hospitalised period in the intensive care unit and intubation rate were significantly higher in the exitus group. Renal injury requiring haemofiltration was associated with an almost 12-fold increased risk for mortality. There was no statistically significant difference between patients regarding surgical interventions., Conclusion: Electrical injury remains a major cause of mortality and long-term disability among young people. Our data demonstrated several risk factors associated with increased mortality rate in patients with electrical burn wounds., (Copyright © 2013 Elsevier Ltd and ISBI. All rights reserved.)

Background: Congenital biliary atresia is suspected to originate from prenatal biliary duct inflammation of unknown etiology., Objective: Based on clinical grounds, we aimed to establish a hypothesis on the primary cause of inflammation, and to suggest a causal treatment modality., Case Report: History. A 28 years old Turkish woman had lost her first child aged two years from congenital biliary atresia (parents second degree cousins). After a miscarriage, in her otherwise uneventful third pregnancy sonography at 34 wks revealed echogenic material in the fetal gallbladder. Nine days later the gallbladder was completely filled with sludge. Chemical inflammation was suspected, and birth was induced at 36+3 weeks in order to allow for surgical flushing of the bile duct. Neonatal clinical chemistry was insuspicious. There was no spontaneous resolution of the sludge within the first 24 hours of life. A trial of medical treatment with intermittent i.v. secretin (0.03 CU/kg/h) and i.v. coeruletid (60 ng/kg/h) was started. Within 24 hours, sludge had resolved., Conclusions: We hypothesize that dysmaturation may lead to insufficient induction/production/activity of intrinsic gut hormones resulting in prenatally impaired bile flow, or even inspissated bile. Familial occurrence suggests a genetic defect. Exogenous hormone therapy might be an appropriate treatment modality.

Objective: To determine whether the waveform in the left portal branch is reciprocal to the waveform found in the ductus venosus and umbilical vein due to difference in pulse direction compared to flow., Methods: Ten fetuses (gestational age, 18-33 weeks), six with intrauterine growth restriction, three with non-immune hydrops and one with sacrococcygeal teratoma, were examined using ultrasound imaging and pulsed Doppler. Techniques were adjusted to record simultaneously the waveform from neighboring sections of the veins, relate wave components to each other and determine degree of pulsatility. The corresponding vessel diameters were determined. ANOVA with t-test or Wilcoxon signed rank test was used to compare paired measurements., Results: Pulsation in the left portal branch was noted in all fetuses. The pulsatility index was higher than in the umbilical vein (P = 0.005) and the diameter smaller (P = 0.001). In the left portal branch the atrial contraction wave appeared as a velocity peak while there was a nadir during ventricular systole. Simultaneous recordings showed that the waveform was reciprocal to that found in the ductus venosus and umbilical vein. In three cases an augmented pulsatility represented a pendulation of blood in the left portal branch with time-averaged velocity near zero., Conclusions: The velocity waveform recorded in the left portal vein is an inverse image of that in the ductus venosus, proving that pulse wave and blood flow run in the same direction in the left portal vein. Low compliance (i.e. small diameter) is probably a main reason for the high incidence of pulsation in this vein. Time-averaged velocity near zero recorded in three fetuses indicates that this area acts also as a watershed., (Copyright 2003 ISUOG. Published by John Wiley & Sons, Ltd.)

Critical fetal organs are preferentially supplied with oxygenated blood from the umbilical vein (UV) by way of the ductus venosus (DV). Under normal conditions a significant part of UV-blood flows steadily forward through the left portal vein (LPV). Blood flow through the LPV could reverse, however, in cases of absent or reversed endodiastolic flow in the umbilical arteries. We tested when fetal blood flow reversal occurs by studying 28 cases with pathological flow in the umbilical artery. In the LPV we observed normal nonpulsatile forward flow in 9 cases, pulsatile forward flow in 10 cases, and reversed flow in 9 cases. Reverse flow in the LPV correlated significantly with an elevated resistance index of the umbilical arteries. This reversal could have major physiological implications: Deoxygenated blood may be added via the LPV to the blood shifted through the DV and ultimately reach critical fetal organs. In extremis there could be a waterhose effect, whereby more blood flows through the DV than the UV that supplies it. The LPV is thus the watershed of the venous circulation of the fetus.

Objective: To determine maternal parameters with the strongest influence on fetal growth in different periods of pregnancies complicated by an abnormal glucose tolerance test (GTT)., Research Design and Methods: Retrospective study of 368 women with gestational diabetes mellitus (GDM; > or = 2 abnormal GTT values, n = 280) and impaired glucose tolerance (IGT; one abnormal value, n = 88) with 869 ultrasound examinations at entry to and during diabetic care. Both groups were managed comparably. Abdominal circumference (AC) > or = 90th percentile defined fetal macrosomia. Maternal historical and clinical parameters, and diagnostic and glycemic values of glucose profiles divided into five categories of 4 weeks of gestational age (GA; <24 weeks, 24 weeks/0 days to 27 weeks/6 days, 28/0-31/6, 32/0-35/6, and 36/0-40/0 [referred to as <24 GA, 24 GA, 28 GA, 32 GA, and 36 GA categories, respectively]) were tested by univariate and multiple logistic regression analysis for their ability to predict an AC > or = 90th percentile at each GA group and large-for-gestational-age (LGA) newborn. Data obtained at entry were also analyzed separately irrespective of the GA., Results: Maternal weight, glycemia after therapy, rates of fetal macrosomia, and LGA were not significantly different between GDM and IGT; thus, both groups were analyzed together. LGA in a previous pregnancy, (odds ratio [OR] 3.6; 95% CI 1.8-7.3) and prepregnancy obesity (BMI > or = 30 kg/m(2); 2.1; 1.2-3.7) independently predicted AC > or = 90th percentile at entry. When data for each GA category were analyzed, no predictors were found for <24 GA. Independent predictors for each subsequent GA category were as follows: at 24 GA, LGA history (OR 9.8); at 28 GA, LGA history (OR 4.2), and obesity (OR 3.3); at 32 GA, fasting glucose of 32 GA (OR 1.6 per 5-mg/dl increase); at 36 GA, fasting glucose of 32 GA (OR 1.6); and for LGA at birth, LGA history (OR 2.7), and obesity (OR 2.4)., Conclusions: In the late second and early third trimester, maternal BMI and LGA in a previous pregnancy appear to have the strongest influence on fetal growth, while later in the third trimester coincident with the period of maximum growth described in diabetic pregnancies, maternal glycemia predominates.

Aim: The current therapeutic strategies to reduce macrosomia rates in gestational diabetes (GDM) have focused on the normalizing of maternal glucose levels. The aim of our study was 1.) to compare maternal glycemic values with the presence of fetal macrosomia at different gestational ages (GA) and with LGA at birth in a cohort of women with glucose intolerance and standard diabetic therapy., Methods: 306 women with GDM and 97 with impaired glucose tolerance underwent ultrasound examinations at entry and, after initiation of therapy, monthly in addition to standard diabetic therapy. Measurements from the entry diagnostic oGTT, glucose profile and HbA1c and from subsequent glucose profiles obtained within 3 days of the ultrasound at 5 categories of GA age (20-23, 24-27 etc) were retrospectively compared between pregnancies with and without fetal macrosomia, defined as an abdominal circumference (AC) > or = 90th percentile. Maternal prepregnancy BMI was adjusted for and BMI > or = 30 kg/m2 was defined as obesity., Results: At entry, neither the hourly oGTT values, HbA1c, nor the entry glucose profile differed significantly between pregnancies with and without fetal macrosomia. In a total of 919 pairs of ultrasound/glucose profiles there was no significant difference in glucose levels at every GA category neither in lean nor in obese woman except for the fasting glucose of 32-35 GA. The fetal macrosomia rate in each GA category and the rate of LGA were significantly higher in obese women: e.g. 14.5 vs 28% at diagnosis, 15.7 vs 26.7% at 32-35 weeks, 15.5 vs 25.0% at birth (p < 0.05 for each comparison)., Conclusion: The association of maternal glucose values and fetal macrosomia was limited to the fasting glucose values between 32-35 weeks while maternal obesity appeared to be a strong risk factor for macrosomia throughout pregnancies with GDM. In obese women the high fetal macrosomia rate did not appear be normalized by therapy based on maternal euglycemia.

In this study we compared the distribution of blood flow to the liver in growth-retarded fetuses whose estimated weight was < 5th centile with normal-weight fetuses. As expected, the relative venous blood flow to the liver was reduced, with blood flowing preferentially through the ductus venosus. However, the total blood supply seemed to be maintained by a concomitant, significant increase in arterial blood flow through the hepatic artery. Absolute flow velocities such as the peak, minimum diastolic and temporal average velocities were changed, as was the flow waveform. Effectively, the deficiency in venous supply was made up for by an increase in arterial blood flow. This compensatory effect may be crucial for maintaining liver function in times of low portal venous blood supply. It thus makes sense to regard the liver as the fourth preferential organ for arterial blood supply in the compromised fetus, besides heart, brain, and adrenals.

In this study, the effect of the umbilical ring on blood flow velocities in the umbilical vein was examined using Doppler sonography. The maximum blood flow velocity in the umbilical vein was measured just before and behind the umbilical ring in eleven normal singleton pregnancies at 24-34 gestational weeks. The maximum velocity increased in each single case (p < 0.0001), the mean increase was from 16 cm/sec to 31 cm/sec. Thus, the narrowing of the umbilical ring serves as the first rapid in venous fetoplacental circulation. The physiological role of the acceleration of venous blood flow remains to be elucidated. Possible functions include stabilizing venous blood flow or preferential streaming.

The aim of the study was to evaluate the effect of the introduction of fetal heart rate monitoring on perinatal mortality rates in high-risk pregnancies. Results were compared with the perinatal mortality rates published previously from our clinics. The study group consisted of 2165 high-risk pregnant patients. The perinatal mortality rate in the study group was 28.6%, and the corrected rate 15.9%. The rates were significantly lower in comparison with the total perinatal mortality rates in former years. We are convinced that fetal heart-rate monitoring resulted in a significant decrease in the perinatal mortality rate. Although the increased use of fetal monitoring cannot reduce perinatal mortality resulting from problems such as genetic disorders, this study shows improved outcomes for many high-risk conditions, in particular postmature pregnancies.

The predictive value of fetal heart-rate monitoring on fetal well-being was studied in 2165 high-risk pregnancies. 1883 reactive nonstress test (NST) patterns and 278 nonreactive NST patterns and 4 cases of sinusoidal pattern were obtained. Oxytocin challenge test (OCT) was applied to 263 nonreactive cases. OCT was not applied to 15 cases out of 278 nonreactive NST cases, because of placenta previa, abruptio placenta and previous cesarean section. There were 155 cases with negative OCT, 84 cases with positive OCT and 24 cases with equivocal, prolonged or severe variable decelerations. Sensitivity and specificity were for NST 50 and 88% and for OCT 60 and 67%. The positive and negative predictive values were 11 and 98% for NST and 18 and 93% for OCT. It is concluded that the reactive nonstress test is a reliable test for good outcome but a positive oxytocin challenge test is not a reliable test for poor outcome. Additional procedures are necessary such as assessment of fetal growth, doppler velocity waveforms and fetal biophysical profile to avoid unnecessary obstetric interventions and to reach good fetal outcome.