Hypothermia makes cerebral resistance index a poor prognostic tool in encephalopathic newborns.

BACKGROUND: Severe neonatal encephalopathy (NE) of hypoxic-ischaemic origin may cause death or life-long disability. Acute encephalopathy may also affect cerebrovascular control. Pourcelot's cerebrovascular resistance index (RI) ≤0.55 was predictive of poor outcome in normothermic NE infants. Recent studies have questioned its predictive power during therapeutic hypothermia (HT). OBJECTIVE: To assess the predictive power of RI during HT and after rewarming. METHODS: 45 infants with NE treated with HT for 72 h had their RI calculated during early (median 11 h) and late (median 62 h) cooling and after rewarming (median 89 h). Poor outcome was defined as death or abnormalities on day 10 magnetic resonance imaging shown to predict severe neuromotor disability. RESULTS: RI ≤0.55 during cooling did not differentiate between good and poor outcome (late cooling, p = 0.08), but was powerful after rewarming (p = 0.004). RI ≤0.55 predicted true poor outcome in 43% (95% confidence interval (CI): 12, 80) during late cooling and in 100% (95% CI: 31, 100) after rewarming. RI >0.55 predicted good outcome in 86% (95% CI: 69, 95) during late cooling and in 89% (95% CI: 74, 96) after rewarming. CONCLUSIONS: Low RI is not predictive of poor outcome during HT in NE infants, but regains the predictive power seen in normothermic infants after rewarming.

Tissue Doppler imaging in very preterm infants during the first 24 h of life: an observational study.

BACKGROUND: Very preterm newborn infants often need cardiovascular support. More knowledge about myocardial function and factors that influence the immature myocardium may be helpful for optimising cardiovascular support in these infants. OBJECTIVE: Serial assessment of global myocardial function by means of colour tissue Doppler imaging (cTDI) in very and extremely preterm infants during the first 24 h of life. STUDY DESIGN: One-centre, prospective, observational longitudinal cohort study in a third level Neonatal Intensive Care Unit. Sixty-five infants with median (range) gestational age (GA) 27 (24-31) weeks and birth weight (BW) 1049 (484-1620) g underwent echocardiographic examinations including cTDI at 5, 12 and 24 h after birth. MAIN OUTCOME MEASURES: Peak systolic and peak diastolic annular velocity and peak annular displacement of the left and right ventricle. RESULTS: There was a significant reduction in systolic and diastolic velocities and displacement of both ventricles from 5 to 12 h age. From 12 to 24 h, there was a non-significant increase in myocardial velocities and displacement. At 5 h, babies with haemodynamically significant patent ductus arteriosus (PDA) had significantly higher systolic and diastolic velocities in both ventricles than those with non-significant PDA. CONCLUSIONS: Myocardial tissue velocities decrease significantly from 5 to 12 h after birth in very preterm infants. Further studies are needed to confirm these results and to determine their clinical implications.

Superior vena cava flow: feasibility and reliability of the off-line analyses.

BACKGROUND: Superior vena cava (SVC) flow has become a surrogate measure of systemic blood flow in neonates. OBJECTIVE: The aim of this study was to establish normal SVC flow values in healthy term infants the first 3 days of life and to evaluate the feasibility and reliability of the off-line analyses. DESIGN: Doppler echocardiography of SVC flow was performed in 48 healthy term infants the first 3 days of life. Off-line analyses were thereafter performed by one cardiologist to investigate the changes in SVC flow from day 1 to day 3 and to establish normal values. Intra- and inter-observer variability was analysed in a subset of 20 infants by three paediatric cardiologists. RESULTS: The authors found a decrease in mean SVC flow from 99 ml/kg/min at day 1 to 77 ml/kg/min at day 3. Reliable diameter images were obtained in 85% and velocity recordings in 81%. The mean variability of SVC flow was 17% in the intra-observer analysis and 29% in the inter-observer analysis. CONCLUSION: The main challenge of the method is the measurement of SVC diameter. The same observer should ideally perform sequential analyses. Special caution should be taken when making clinical implications from non-optimal pictures.

The outcome in newborns with congenital diaphragmatic hernia in a Norwegian region.

AIM: To evaluate the therapeutic strategies used in neonates with congenital diaphragmatic hernia (CDH) during the last 15 years in our department. METHOD: A retrospective study of 27 neonates with CDH treated at the Neonatal Intensive Care Unit at Ullevaal University Hospital between 1992 and 2006. Since 1992 we have used delayed operative repair and high-frequency ventilation (HFV). Because surfactant replacement and inhaled nitric oxide (iNO) therapy have been used since 1997, we divided the patients into two groups; group 1 from 1992 to 1996 (9 patients) and group 2 from 1997 to 2006 (18 patients). RESULTS: The overall survival was 70%. Group 1 had an exceptionally good outcome, 100% survival versus 56% in the last group. CONCLUSION: Pulmonary hypoplasia and pulmonary hypertension are still the most challenging factors in treatment of neonates with CDH, despite novel therapeutic modalities, such as HFV, surfactant and iNO. Delayed surgery in CDH allows pre-operative stabilization. Extracorporeal membrane oxygenation must be considered in the most severe cases.

Restoration of cardiopulmonary function with 21% versus 100% oxygen after hypoxaemia in newborn pigs.

OBJECTIVE: To assess the consequences of hypoxaemia and resuscitation with room air versus 100% O(2) on cardiac troponin I (cTnI), cardiac output (CO), and pulmonary artery pressure (PAP) in newborn pigs. DESIGN: Twenty anaesthetised pigs (12-36 hours; 1.7-2.7 kg) were subjected to hypoxaemia by ventilation with 8% O(2). When mean arterial blood pressure fell to 15 mm Hg, or arterial base excess was < or = -20 mmol/l, resuscitation was performed with 21% (n = 10) or 100% (n = 10) O(2) for 30 minutes, then ventilation with 21% O(2) for 120 minutes. Blood was analysed for cTnI. Ultrasound examinations of CO and PAP (estimated from tricuspid regurgitation velocity (TR-Vmax)) were performed at baseline, during hypoxia, and at the start of and during reoxygenation. RESULTS: cTnI increased from baseline to the end point (p<0.001), confirming a serious myocardial injury, with no differences between the 21% and 100% O(2) group (p = 0.12). TR-Vmax increased during the insult and returned towards baseline values during reoxygenation, with no differences between the groups (p = 0.11) or between cTnI concentrations (p = 0.31). An inverse relation was found between increasing age and TR-Vmax during hypoxaemia (p = 0.034). CO per kg body weight increased during the early phase of hypoxaemia (p<0.001), then decreased. Changes in CO per kg were mainly due to changes in heart rate, with no differences between the groups during reoxygenation (p = 0.298). CONCLUSION: Hypoxaemia affects the myocardium and PAP. During this limited period of observation, reoxygenation with 100% O(2) showed no benefits compared with 21% O(2) in normalising myocardial function and PAP. The important issue may be resuscitation and reoxygenation without hyperoxygenation.

Cardiac output, pulmonary artery pressure, and patent ductus arteriosus during therapeutic cooling after global hypoxia-ischaemia.

OBJECTIVE: To assess by Doppler echocardiography the effects of 24 hours of whole body mild hypothermia compared with normothermia on cardiac output (CO), pulmonary artery pressure (PAP), and the presence of a persistent ductus arteriosus (PDA) after a global hypoxic-ischaemic insult in unsedated newborn animals. DESIGN: Thirty five pigs (mean (SD) age 26.6 (12.1) hours and weight 1.6 (0.3) kg) were anaesthetised with halothane, mechanically ventilated, and subjected to a 45 minute global hypoxic-ischaemic insult. At the end of hypoxia, halothane was stopped; the pigs were randomised to either normathermia (39 degrees C) or hypothermia (35 degrees C) for 24 hours. Rewarming was carried out for 24-30 hours followed by 42 hours of normothermia. Unanaesthetised pigs were examined with a VingMed CFM 750 ultrasound scanner before and 3, 24, 30, and 48 hours after the hypoxic-ischaemic insult. Aortic valve diameter, forward peak flow velocities across the four valves, and the occurrence of a PDA were measured. Tricuspid regurgitation (TR) velocity was used to estimate the PAP. Stroke volume was calculated from the aortic flow. RESULTS: Twelve animals (seven normothermic, five hypothermic) had a PDA on one or more examinations, which showed no association with cooling or severity of insult. There were no differences in stroke volume or TR velocity between the hypothermic and normothermic animals at any time point after the insult. CO was, however, 45% lower at the end of cooling in the subgroup of hypothermic pigs that had received a severe insult compared with the pigs with mild and moderate insults. CO and TR velocity were transiently increased three hours after the insult: 0.38 (0.08) v 0.42 (0.08) litres/min/kg (p = 0.007) for CO; 3.0 (0.42) v 3.4 (0.43) m/s (p < 0.0001) for TR velocity (values are mean (SD)). CONCLUSIONS: The introduction of mild hypothermia while the pigs were unsedated did not affect the incidence of PDA nor did it lead to any changes in MABP or PAP. Stroke volume was also unaffected by temperature, but hypothermic piglets subjected to a severe hypoxic-ischaemic insult had reduced CO because the heart rate was lower. Global hypoxia-ischaemia leads to similar transient increases in CO and estimated PAP in unsedated normothermic and hypothermic pigs. There were no signs of metabolic compromise in any subgroup, suggesting that 24 hours of mild hypothermia had no adverse cardiovascular effect.

Perfluorochemical liquids do not stimulate endothelin-1 or nitric oxide production in human blood leukocytes.

The purpose of these studies was to examine if perfluorochemical (PFC) liquids stimulate blood leukocytes to secrete nitric oxide (NO) and/or endothelin-1 (ET-1). As such, NO and ET-1 may modulate broncho- and vascular dilatation and constriction, respectively, and thereby influence the clinical condition of a patient in respiratory distress with persistent pulmonary hypertension. Blood leukocytes in their natural habitat (whole blood) were incubated in the presence of two different perfluorochemicals (perflubron and perfluorodecalin). The overall response in ET-1 or NO (indirectly measured as nitrite/nitrate) production was examined at increasing PFC percentages (wt/vol) of PFC/whole blood. The lowest proportion used, 0.001% (wt/vol), was relevant to serum concentrations of PFC observed in liquid-ventilated individuals, whereas the highest proportion PFC, 50% (wt/vol), would mimic a situation where leukocytes are presented to PFC-filled airways. Plasma levels of freshly drawn blood, similar to levels of incubated (6 h) non-PFC-supplemented cultures, were ET-1 0.59 +/- 0.07 pg/ml (6 h, mean +/- SEM) and NO(-2)/NO(-3) 50 +/- 9 microM (6 h). Perflubron or perfluorodecalin did not induce significant differences in ET-1 or NO(-2)/NO(-3) levels as function of PFC type or dose. In conclusion, PFC liquids do not stimulate production in leukocytes in vitro of substances that may modulate constriction or dilatation in the vascular and respiratory tract systems.

Perfluorochemical liquids modulate cell-mediated inflammatory responses.

OBJECTIVE: To examine whether chemically different perfluorochemical liquids (PFC) (perfluorodecalin [PFD]; perflubron [PFB]) induce inflammatory responses in blood leukocytes. SETTING: University research laboratory. DESIGN: Whole blood from 12 healthy adults was incubated with increasing PFC concentrations and/or bacterial lipopolysaccharide. MEASUREMENTS AND MAIN RESULTS: Adhesion molecules (CD62L, CD11b), reactive oxygen species, and cytokine responses in resting and activated leukocyte subtypes were studied. Scanning and transmission electron microscopies were performed. At the highest concentrations, PFB stimulated a significant increase in resting monocytic reactive oxygen species production; all types of blood leukocytes were unresponsive to PFD. Neither PFB nor PFD changed CD62L expression; PFB increased CD11b expression in monocytes and granulocytes. PFD induced a small though significant increase in interleukin-8 secretion. When simulating a condition in which patients with severe lung disease or sepsis would be ventilated with PFC, neither PFB nor PFD plus lipopolysaccharide stimulated tumor necrosis-alpha or interleukin-8 production above levels induced by lipopolysaccharide alone, but rather demonstrated a trend for decreased tumor necrosis factor-alpha production. Expression of CD11b and CD62L and the production of reactive oxygen species were not changed beyond the levels induced by lipopolysaccharide alone. As a morphologic correlate to the above proinflammatory changes, surface-bound blebs and intracellular vacuoles were seen by electron microscopy. CONCLUSIONS: At PFC concentrations comparable with those in blood during liquid ventilation, PFC liquids did not induce variables associated with inflammation. In the presence of high PFC concentrations, simulating the condition in which bronchoalveolar cells are exposed to PFC, monocytes may be induced by PFB to produce reactive oxygen species, and blood leukocytes induced by PFB to express CD11b and by PFD to secrete interleukin-8; the presence of either PFC attenuated tumor necrosis factor-alpha production after lipopolysaccharide stimulation.

[Neonatal hypoglycemia]. / Neonatal hypoglykemi.

BACKGROUND: The definition, significance, and management of neonatal hypoglycaemia and the establishment of a safe, lower limit for blood glucose concentration in the newborn is still a matter of controversy. METHODS: A review of the literature on neonatal hypoglycaemia is presented and guidelines for prevention and treatment discussed. RESULTS: Healthy, full-term, appropriate for gestational age infants are thought to have a better tolerance for low blood glucose values during the first days of life than later in life. The infant's brain is capable of utilizing alternative energy substrates, such as ketone bodies and lactate. Intracerebral glycogen stores in the astrocytes and increased cerebral blood flow in response to hypoglycaemia maintain a sufficient substrate delivery. Infants at risk of developing neurological impairment following hypoglycaemia have a reduced capacity for mobilizing glucose from the glycogenolysis or gluconeogenesis and for utilizing alternative substrates for energy. INTERPRETATION: There are no established lower limits defining neonatal hypoglycaemia of the healthy infant, but operational guidelines exist for prevention and intervention in infants at risk, for whom the blood glucose concentration should be maintained > or = 2.6 mmol/l. Very few healthy, breastfed, term infants have blood glucose levels < 2 mmol/l. It is suggested that values down to 1.7 mmol/l should be accepted as normal during the first day of life. Parenteral glucose should be administered to all infants with blood glucose levels < 1.4 mmol/l. The main goal is to prevent neonatal hypoglycaemia. Early and exclusive breastfeeding and the maintenance of normal body temperature are usually sufficient preventive measures in healthy infants.

Patent ductus venosus does not lead to alimentary galactosaemia in preterm infants.

UNLABELLED: The aim of this study was to investigate if an open ductus venosus representing a portal-caval shunt can lead to transient "alimentary galactosaemia" in preterm infants fed human breast milk. Twenty-six preterm infants (28-34 wk of gestational age) with open ductus venosus were included. Capillary blood samples for measurement of galactose and glucose were collected before, 30 and 50 min after a meal with breast milk (range 12-23 mL/kg). Ultrasound studies of the blood flow in the ductus venosus, truncus coeliacus, superior mesenteric artery and left hepatic vein were performed before and 30 min after the meal. There was a significant rise in blood glucose after 30 and 50 min, indicating a sufficient lactose load. Galactose, however, was either not detectable or was just above the detectable limit (0.1-0.4 mmol/L), with no changes after the meal. An increased flow velocity was found in the ductus venosus and superior mesenteric artery after 30 min (p < or = 0.001) indicating increased entero-hepatic and portal-caval shunting. CONCLUSION: A patent ductus venosus does not lead to a significant hypergalactosaemia in preterm infants fed human breast milk. Thus, in respect to breast-milk feeding, this is regarded safe in healthy preterm infants even with an open ductus venosus. The increased portal-caval shunting may, however, influence the hepatic metabolism of other enterally absorbed substances.

[Persistent pulmonary hypertension in newborn infants]. / Persisterende pulmonal hypertensjon hos nyfødte.

BACKGROUND: Persistent pulmonary hypertension of the newborn is a clinical syndrome caused by failure in the transition from fetal to neonatal circulation either to achieve or to maintain low pulmonary vascular resistance after birth. The syndrome is a complex condition associated with different cardiopulmonary disorders. METHODS: This article presents a review of the literature and the author's own experience regarding the fetal circulation, the transition to the newborn circulation, and the mechanical and molecular regulatory factors, including a discussion of the pathophysiology, aetiology, diagnostics and main goal of treatment for persistent pulmonary hypertension of the newborn. RESULTS: The pathophysiology of persistent pulmonary hypertension is characterised by high pulmonary vascular resistance and high pulmonary artery pressure. The blood is shunted from the right to the left circuit through the foramen ovale, ductus arteriosus and also by intrapulmonal shunts. The aetiologies can be classified as underdevelopment, maldevelopment and maladaptation of the pulmonary vasculature. The clinical signs are hypoxaemia, higher oxygenation tension and saturation in the upper rather than the lower limbs, respiratory failure, systemic hypotension and systolic cardiac murmur. The differential diagnoses are primarily serious lung disorders without persistent pulmonary hypertension, and congenital cyanotic heart defects. The diagnostic investigations are blood gas analysis, X-ray of the lung, and Doppler echocardiographic examination of the heart. INTERPRETATION: The main treatment goal is good oxygenation, pH in upper normal and pCO2 in lower normal levels. Positive pressure ventilation, sedation, NO gas inhalation and supporting treatment of the systemic blood pressure are usually necessary. Extracorporeal membrane oxygenation is considered as a last option.

Ductus venosus flow velocity in newborn lambs during increased pulmonary artery pressure.

The aim of the present study was to assess with ultrasound the ductus venosus flow velocity in newborn lambs with increasing pulmonary artery pressures and to evaluate whether this is a useful method to detect elevated pulmonary artery pressure. The ductus venosus flow velocity was studied with pulsed-wave Doppler echocardiography in nine newborn lambs < or = 30 h old. The lambs were anesthetized, mechanically ventilated, and instrumented to measure mean airway pressure and pulmonary artery and arterial blood pressures. A vascular occluder was placed around the main pulmonary artery. With mean pressures ranging from 20 to 50 mm Hg in the pulmonary artery, the ductus venosus flow velocity was examined. In seven lambs, the mean portal pressure and central venous pressure were also measured. With a stepwise increase in the pulmonary artery pressure, the minimum ductus venosus flow velocity during atrial systole decreased to a reversed flow, and the duration of this reversed flow component increased. The systolic forward peak flow velocity signal also gradually decreased. No changes were detected in the mean central venous or in the portal pressure with increasing pulmonary artery pressure or changes in ductus venosus flow. The flow velocity in the ductus venosus, which is higher than in other precordial veins, shows a reduction and even reversal of the nadir and an increase of the duration of reversed flow during atrial systole as a response to increased pulmonary artery pressure. Thus, Doppler ultrasound of the ductus venosus flow velocity may be a useful noninvasive diagnostic supplement to detect pulmonary hypertension of the newborn.

Ductus venosus blood velocity in persistent pulmonary hypertension of the newborn.

AIMS: To investigate the ductus venosus flow velocity (DVFV) in infants with persistent pulmonary hypertension of the newborn (PPHN); to evaluate the DVFV pattern as a possible diagnostic supplement in neonates with PPHN and other conditions with increased right atrial pressure. METHODS: DVFV was studied in 16 neonates with PPHN on days 1-4 of postnatal life using Doppler echocardiography. DVFV was compared with that in mechanically ventilated neonates with increased intrathoracic pressure, but without signs of PPHN (n=11); with neonates with congenital heart defects resulting in right atrial pressure (n=6); and with preterm neonates without PPHN (n=46); and healthy term neonates (n=50). RESULTS: Infants with PPHN and congenital heart defects with increased right atrial pressure were regularly associated with an increased pulsatile pattern and a reversed flow velocity in ductus venosus during atrial contraction. A few short instances of reversed velocity were also noted in normal neonates before the circulation had settled during the first day after birth. CONCLUSIONS: A reversed velocity in the ductus venosus during atrial contraction at this time signifies that central venous pressure exceeds portal pressure. This negative velocity deflection is easily recognised during Doppler examination and can be recommended for diagnosing increased right atrial pressure and PPHN.

Cardiac function and morphology studied by two-dimensional Doppler echocardiography in unsedated newborn pigs.

The newborn pig is currently the most used species in animal neonatal research. Valid non-invasive monitoring is important in particular for long-term survival of unsedated animals. In the unsedated newborn pig (n = 35, median age 24 h, range 7-48 h) we standardized two-dimensional Doppler echocardiography and determined the normal ranges for cardiac function. Probe positioning had to be adjusted to the V-shaped thorax and the mid-line position of the heart. Six out of the sixteen animals < 20 h had a patent ductus arteriosus compared with one of the twenty animals > 20 h old. One atrial septal defect (5 mm) and one small ventricular septal defect were diagnosed. The average heart size was 0.7-0.9% of body weight which is similar to human infants of the same size. The mean aortic diameter was 6.0 +/- 0.5 mm (mean +/- S.D.) and cardiac output was 0.38 +/- 0.08 l min-1; both correlate with body weight (r = 0.80 and 0.73, respectively). Tricuspid regurgitation velocity was 3.0 +/- 0.4 m s-1 (mean +/- S.D.), giving an estimated pressure gradient across the tricuspid valve of 37 +/- 9.7 mmHg. The aortic diameter and the heart weight per kg body weight are comparable to those reported for preterm neonates. The cardiac output and velocities across the four valves are more comparable with term neonates.

Nicotine concentration in the hair of nonsmoking mothers and size of offspring.

OBJECTIVES: The purpose of this study was to estimate the risk of small-for-gestational-age birth by levels of nicotine in the hair of mothers and offspring. METHODS: In a sample of 58 case subjects and 105 control subjects, hair nicotine concentrations were measured by gas chromatography and mass spectrometry. RESULTS: With women whose hair nicotine concentrations were in the lowest quartile as the reference group, the odds ratio (OR) for small-for-gestational-age birth was increased among women with concentrations in the upper and two middle quartiles (OR=4.2, 95% confidence interval [CI]=1.5, 11.5, and OR = 3.2, 95% CI=1.3, 8.0). When smoking mothers were excluded from the analysis, the corresponding odds ratios were 2.1 (95% CI=0.4, 10.1) and 3.4 (95 % CI= 1.3, 8.6). CONCLUSIONS: The results suggest that passive maternal smoking increases the risk of small-for-gestational-age births.

Sibs with Ritscher-Schinzel (3C) syndrome and anal malformations.

Ritscher-Schinzel syndrome (cranio-cerebello-cardiac syndrome, 3C syndrome) is a recently delineated disorder with Dandy-Walker malformation, congenital heart defects, and characteristic face. Various other defects, including eye and kidney malformations, have been described in the few patients reported. Here we describe 3 sibs born to consanguineous Pakistani parents with 3C syndrome. All 3 children had atrial septal defects II and ventricular septal defects and died within 3 months. Two of them had a Dandy-Walker malformation, whereas 1 had only slightly dilated ventricles. One sib had anal atresia, and another a ventrally displaced anus. The findings in the 3 sibs demonstrate the intrafamilial variation in the Ritscher-Schinzel syndrome, because the second sib did not have a Dandy-Walker malformation. Anal anomalies have not been previously reported as a component manifestation of the disorder. The occurrence of 3 affected sibs in a consanguineous family confirms autosomal recessive inheritance.

Postnatal closure of ductus venosus in preterm infants < or = 32 weeks. An ultrasonographic study.

AIM: To assess ultrasonographically the flow pattern and the time of postnatal closure of ductus venosus in preterm infants < or = 32 weeks. METHODS: Thirty-three preterm infants < or = 32 weeks were studied within the first 1 to 5 days of life and followed every second day with ultrasound until no flow was detected either through the ductus venosus or the ductus arteriosus. RESULTS: The ductus venosus was closed in only 9% by day 3, in 40% by day 8 and 88% by day 18. All were closed by day 37. This is significantly later than in healthy term neonates. Closure of the ductus venosus was not significantly correlated with closure of ductus arteriosus. CONCLUSION: The ductus venosus shows a delayed closure in preterm infants, with no significant correlation to the closure of the ductus arteriosus or the condition of the infant. We speculate that immaturity of the ductus venosus and possibly increased levels of dilating prostaglandins leads to a delayed obliteration of the vessel. An open ductus venosus represents a portocaval shunt and may have metabolical and pharmacological consequences.

Ultrasonographic study of ductus venosus in healthy neonates.

AIM: To assess ultrasonographically the flow pattern and the time of postnatal closure of ductus venosus related to the other fetal shunts. METHODS: Fifty healthy, term neonates were studied from day 1 up to day 18 using a VingMed CFM 800A ultrasound scanner. RESULTS: Ductus arteriosus was closed in 94% of the infants before day 3. Ductus venosus, however, was closed in only 12% at the same time, in 76% before day 7, and in all infants before day 18. A closed ductus venosus or ductus arteriosus did not show signs of reopening. Pulsed and colour Doppler flow could be detected across the foramen ovale in all infants during the sequential investigation. At day 1, when the pulmonary vascular resistance was still high, a reversed Doppler flow velocity signal was seen in ductus venosus in 10 infants (20%) and a bidirectional flow in ductus arteriosus in 26 (52%). Closure of the ductus venosus was not significantly correlated with closure of the ductus arteriosus nor related to sex nor weight loss. CONCLUSIONS: The time of closure of the ductus venosus evaluated by ultrasonography is much later than that of the ductus arteriosus. The flow pattern in ductus venosus reflects the portocaval pressure gradient and the pressure on the right side of the heart and in the pulmonary arteries. Both the flow pattern in the ductus venosus as well as that in the ductus arteriosus may be an indication of compromised neonatal haemodynamics.

[Bacterial endocarditis in premature children. A complication caused by central venous catheters]. / Bakteriell endokarditt hos premature barn. En komplikasjon til sentralt venekateter.

During the last ten years, the literature has included an increasing number of reports of bacterial endocarditis in prematurely born neonates. We describe the cases of two prematurely born infants with structurally normal hearts who, when examined by echo cardiography, were shown to have intercardial vegetations. They were diagnosed as having infective endocarditis caused by coagulase negative staphylococci. Both infants had central venous lines and received total parenteral nutrition. Both infants were treated successfully with antibiotics. One of them died later of sudden infant death syndrome.

[Maternal blood group 0 as a risk factor of neonatal hyperbilirubinemia requiring treatment]. / Blodtype O hos mor som risikofaktor for behandlingstrengende hyperbilirubinemi hos nyfødte.

The present prospective study indicates that children of mothers with blood group O run a double risk of hyperbilirubinemia requiring treatment as compared to children of mothers of blood group A, and 5-10 times increased risk of needing exchange transfusion. The most frequent cause of need for exchange transfusion was ABO-incompatibility between mother and child. A positive direct antiglobulin reaction in an ABO-incompatible child in need of treatment doubles the risk of exchange transfusion being required. Blood group O in the mother should be considered to be an independent risk factor for the child, and O-pregnant women should be ABO-grouped for this reason.