Characterization of the deformation behavior of intermediate porosity interconnected Ti foams using micro-computed tomography and direct finite element modeling.

Under load-bearing conditions metal-based foam scaffolds are currently the preferred choice as bone/cartilage implants. In this study X-ray micro-computed tomography was used to discretize the three-dimensional structure of a commercial titanium foam used in spinal fusion devices. Direct finite element modeling, continuum micromechanics and analytical models of the foam were employed to characterize the elasto-plastic deformation behavior. These results were validated against experimental measurements, including ultrasound and monotonic and interrupted compression testing. Interrupted compression tests demonstrated localized collapse of pores unfavorably oriented with respect to the loading direction at many isolated locations, unlike the Ashby model, in which pores collapse row by row. A principal component analysis technique was developed to quantify the pore anisotropy which was then related to the yield stress anisotropy, indicating which isolated pores will collapse first. The Gibson-Ashby model was extended to incorporate this anisotropy by considering an orthorhombic, rather than a tetragonal, unit cell. It is worth noting that the natural bone is highly anisotropic and there is a need to develop and characterize anisotropic implants that mimic bone characteristics.

[Integrated psychological parental assistance in the neonatal intensive care unit: concepts and first experiences]. / Integrative psychologische Elternbetreuung auf der neonatologischen Intensivstation: Konzept und erste Erfahrungen.

BACKGROUND AND HYPOTHESIS: Psychosocial support programs have been established in view of the burden caused to parents having their newborn admitted to the neonatal intensive care unit (NICU). Due to limited resources, preventive programs can only be offered to parents who are identified by the staff to be at risk. Based on the results of a parent questionnaire, the University Children's Hospital Vienna has developed a standardized concept of integrated psychological support. The program and first results are presented. PATIENTS AND METHODS: The psychological support is offered to parents of newborns admitted to the neonatal intensive care unit. The aim of the support is to avoid later psychosocial problems for child and parents. In an interdisciplinary collaboration, the psychologist facilitates parent-child bonding, family development and coping with the baby's illness. The standardized psychological support consists of a consultation at the beginning and end of the hospital stay. Parents are offered optional psychological support or intensive assistance. RESULTS: Parents from 152 patients received the standardized basic psychological support. The majority of the parents took advantage of the additional optional assistance. Because of external transfers (42.1 %) or infant death (18.4 %), only 39.5 % of the parents could be accompanied until discharge. CONCLUSIONS: A standardized psychological model provides parents with the psychological support as one important part of the overall concept of neonatal treatment. Additionally, the medical and nursing staff were sensitized to psychological factors. An effective psychosocial prevention requires psychological support as an essential part of intensive neonatal care.

Evaluation of a netilmicin-loading dose in very low birthweight infants.

BACKGROUND: The bactericidal efficacy of aminoglycosides is directly related to maximum serum concentrations, particularly the initial one. Therefore, several groups have recommended an aminoglycoside loading dose. Our goal was to develop a simplified dosage regimen for preterm infants which would result in therapeutic maximum serum concentrations early in the course of therapy. METHODS: Open, noncomparative study during November 2000 to April 2001. The modified netilmicin-dosing protocol included a loading dose of 5 mg/kg in the first week of life, followed by a maintenance regimen of 3.5 mg/kg every 24 h. After the first week of life the corresponding doses were 6 (loading) and 5 mg/kg (maintenance). A peak level was measured 30 min after the second dose, and a trough level immediately before the third dose. RESULTS: Thirty-five very low birthweight infants (mean birthweight 876 +/- 170, range 536-1,385 g; mean gestational age 26 +/- 1.8, range 23-30 weeks) who had 46 episodes of netilmicin treatment were included in the analysis. Mean netilmicin peak and trough values were 15.9 +/- 3.7 (range 8.9-28.9) and 3.4 +/- 1.3 (range 1.0-7.8) micromol/l, respectively. Ninety-one percent of all peak levels were within the targeted range of > or =10 micromol/l. Eleven trough values (24%) were > or =4 micromol/l: in 7 instances netilmicin was administered within the first week of life, 5 of these patients had concomitant indomethacin treatment. Only 1 of the 35 neonates had a rise in serum creatinine of > or =0.5 mg/dl during netilmicin therapy. Hearing evaluations were performed in 25 of the 29 surviving infants at discharge home, all of which gave normal results. CONCLUSIONS: The new netilmicin-dosing protocol yielded therapeutic maximum serum concentrations in 91% of cases after the second dose. However, a significant number of very low birthweight infants had elevated trough levels, particularly when netilmicin was administered in the first week of life with concomitant indomethacin treatment. We speculate that a longer interval between the loading dose and the first maintenance dose would result in fewer elevated trough levels with a similarly high number of therapeutic peak levels.

Severe liver haemorrhage during laparotomy in very low birthweight infants.

UNLABELLED: A review is presented of severe liver haemorrhage as a serious complication in surgery on very low birthweight (VLBW) infants. Clinical data and pathological findings, as well as the outcome of the treatment, of five VLBW infants (<1000 g) who experienced liver haemorrhage during surgical exploration for necrotizing enterocolitis or spontaneous intestinal perforation were reviewed retrospectively. At the time of surgery, all infants had signs and symptoms of impending sepsis. The bleeding was predominantly "spontaneous" without obvious iatrogenic liver damage. In three infants, severe liver haemorrhage could be stabilized by early liver tamponade using absorbable thrombostatic sponges and polyglactin mesh. CONCLUSION: Intraoperative liver haemorrhage potentially life-threatening complication of surgery in preterm infants, which is not frequently investigated. Immediate perihepatic liver packing may be used to achieve adequate bleeding control.

Comparison between hypothermia and glutamate antagonism treatments on the immediate outcome of perinatal asphyxia.

This study investigated the influence of temperature or glutamate antagonism on the immediate outcome of perinatal asphyxia. Perinatal asphyxia was produced by water immersion of fetus-containing uterus horns removed by cesarean section from ready to deliver rats. The uterus horns were kept in a water bath for different time periods, before the pups were delivered and stimulated to breathe. After delivery, the pups were assessed for behavior and for systemic glutamate, aspartate, lactate and pyruvate levels measured with in vivo microdialysis, or ex vivo for energy-rich phosphates, including adenosine triphosphate (ATP), in brain, heart and kidney. In a series of experiments, asphyxia was initiated in a water bath at 37 degrees C, before the pup-containing uterus horns were moved for different time intervals to a 15 degrees C bath. In another series of experiments, the mothers were treated with N-methyl-D-aspartate (NMDA) antagonist, dizocilpine (MK-801), or alpha-amino-3-hydroxy-methylisoxazole-4-propionic acid (AMPA) antagonist,2,3-dihydroxy-6-nitro-7-sulfamoyl benzo(f) quinoxalin NBQX) 1 h before hysterectomy and asphyxia at 37 degrees C. The rate of survival rapidly decreased following exposure to more than 16 min of asphyxia, and no survival could be observed after 22 min of asphyxia. An LD50 was estimated to occur at approximately 19 min of asphyxia. The outcome was paralleled by a decrease in ATP in kidney, followed by a decrease in heart and brain. A maximal decrease in ATP was observed after 20 min of asphyxia in all tissues. Systemic microdialysis revealed that glutamate, aspartate and pyruvate levels were increased with a peak after 5 min of asphyxia. In contrast, lactate levels increased along with the length of the insult. Survival was increased when the pup-containing uterus horns were moved from a 37 degrees C to a 15 degrees C bath, at 15 min of asphyxia (the LD50 was thus increased to 30 min). If the shift occurred at 10 or 5 min of asphyxia, the LD50 increased to 80 or 110 min, respectively. The effect of glutamate antagonism was minor compared to hypothermia; the best effect (an increase in the LD50 to approximately 22 min) was observed after combining AMPA and NMDA antagonists.

Sleep-wake cycles in preterm infants below 30 weeks of gestational age. Preliminary results of a prospective amplitude-integrated EEG study.

In the newborn, presence of sleep-wake cycles indicates integrity and maturity of the central nervous system. By spectral EEG analysis and polygraphic recordings subtle variations of EEG background activity and behavioural patterns corresponding to early sleep-wake cycles have been found in preterm infants as young as 27 weeks of gestation. The emergence of sleep-wake cycles at early gestational ages may have a positive predictive value for long-term neurological outcome. Sleep-wake cycles and their significance for later outcome have not been studied in very preterm infants so far. Accordingly, we prospectively investigated maturational changes of EEG activity and sleep-wake cycles in preterm infants below 30 weeks of gestational age using the Cerebral Function Monitor, an amplitude-integrated EEG. We present preliminary data on the emergence of sleep-wake cycles in preterm infants from this ongoing study. Of 100 infants enrolled during a 1-year period, 38 infants without neurological complications were included in the reference group. In this group (mean gestational age 27 weeks), we observed cyclical variations of EEG background activity resembling early sleep-wake cycles at a mean gestational age of 28 weeks and a median postnatal age of 6 days. It is hypothesised that these cyclical variations of EEG background activity may represent switches between thalamo-cortical and neo-cortical pattern generators and indicate integrity of central nervous system function. Amplitude-integrated EEG may thus serve as a useful noninvasive test for brain function in preterm infants.

Microdissection and reverse painting reveals a microdeletion 6(q26qter) in a de novo r(6) chromosome.

Ring chromosomes 6 are rare constitutional abnormalities with inconsistent phenotypic and clinical features. One of the reasons for this variability is the cytogenetically undetectable loss of chromosomal material from the telomeric segments at 6p or 6q. We have therefore used fluorescence in situ hybridization (FISH) to analyse a ring chromosome 6 that was detected in a newborn boy with dysmorphic features. Reverse painting of the microdissected ring chromosome onto normal metaphase spreads revealed a small deletion of the terminal region of the long arm, 6(q26qter). Moreover, the simple all-telomeric sequence (TTAGG)n was lost, whereas the p-specific subtelomeric sequence was still present. Our findings confirm that microdeletions occur during the formation of r(6) chromosomes and, therefore, are an important determinator of the associated phenotype.

Myelination deficits in brain of rats following perinatal asphyxia.

Perinatal asphyxia remains a major cause of acute mortality and of permanent neurodevelopmental disability in infants and children. However, the pathophysiologic features of hypoxic-ischemic encephalopathy are still incompletely understood. Animal studies have been focussing on grey matter pathology but information on white matter lesions is limited. The aim of the study was to investigate white matter lesions after three months following graded perinatal asphyxia in the rat using a well-documented, reproducible, clinically relevant and simple animal model of perinatal asphyxia. Brains of rat pups (n=10 per group) exposed to asphyctic periods of 10 and 20 minutes were examined histologically and compared to normoxic brain using Kluever-Barrera myelin staining, immunohistochemically with antibodies against myelin basic protein, 2',3'-cyclic-nucleotide'-phosphodiesterase as markers for myelination, antibodies against neurofilaments for the evaluation of axonal density and antibodies against glial fibrillary acidic protein as a marker for astrocytic gliosis. Morphometry three months after perinatal asphyxia showed significant reduction of corpus callosum in asphyctic brains. Patchy myelination deficits were found in hippocampal fimbriae and cerebellum, lobulus L 8, accompanied by reduced axonal density. Hypothalamus and striatum did not show any myelination deficit. Up to now only short term effects of perinatal asphyxia on myelination have been reported and this communication reveals long-term myelination deficit in three brain regions after three months following perinatal asphyxia. As myelination deficit was regularly accompanied by reduction of neurofilament immunoreactivity, we suggest that white matter lesions are paralleling grey matter damage, a subject still controversial in pathophysiology of brain damage in perinatal asphyxia.

Excitatory amino acids, monoamine, and nitric oxide synthase systems in organotypic cultures: biochemical and immunohistochemical analysis.

The nigrostriatal and mesolimbic systems of the rat have been re-constructed using the organotypic culture model, whereby neonatal brain tissue is grown in vitro for approximately one month. The nigrostriatal cultures consisted of tissue from the substantia nigra, dorsal striatum and frontoparietal cortex; while the mesolimbic cultures included the ventral tegmental area, ventral striatum and cingulate cortex. The cultures were grown at 35 degrees C in normal atmosphere, using a tuberoller device placed in a cell incubator and changing the medium every 3-4 days. The in vitro development was evaluated with an inverted microscope equipped with a variable relief contrast function. Samples were taken directly from the medium in the culture tube and analysed for several amino acids with HPLC. After a month the cultures were fixed and processed for immunohistochemistry. High levels of glutamate and aspartate were observed every time the medium was changed, but the levels rapidly decreased reaching a steady state after approximately 24h. A decrease in the levels was also observed along development, reaching stable values (approximately 2 microM and approximately 0.12 microM for glutamate and aspartate, respectively) at approximately two weeks, but only when the cultures showed an apparently healthy development. The levels were approximately 10 times higher in deteriorating or apparently damaged cultures. Glutamine levels were in the mM range and remained stable along the entire experiment. No differences were observed among nigrostriatal and mesolimbic cultures. Immunohistochemistry confirmed the impressions obtained from microscopic and biochemical analysis along the in vitro development, revealing apparently healthy neuronal systems with characteristics similar to those observed in vivo, when tyrosine hydroxylase and nitric oxide synthase, markers for dopamine and nitric oxide containing neurons, respectively, were analysed. In the substantia nigra, nitric oxide synthase-positive networks surrounded tyrosine hydroxylase-positive neurons, while in the striatum nitric oxide synthase dendrites were surrounded by tyrosine hydroxylase-positive nerve terminals, suggesting a reciprocal interaction among dopamine and nitric oxide containing neurons. Thus, the organotypic model appears to capture many of the neurochemical and morphological features seen in vivo, providing a valuable model for studying in detail the neurocircuitries of the brain.

Energy metabolism in graded perinatal asphyxia of the rat.

Although information on energy metabolism during hypoxemic-ischemic states is abundant, data on perinatal asphyxia (PA) are limited. As results from hypoxia-ischemia cannot be directly extrapolated to PA, a clinical entity characterized by acidosis, hypoxemia and hypercapnia, we decided to use a rat model of graded PA during delivery. Cesarean section was performed at the 21st day of gestation and the pups, still in the uterus horns, were asphyxiated from 0 to 20 minutes. In this model survival decreases with the length of asphyxia. Early changes of energy-rich phosphates in brain, heart and kidney were determined by HPLC. ATP and phosphocreatine gradually decreased with the length of asphyxia, with highest ATP depletion rate occurring in the kidney. ATP: brain 1.39 +/- 0.71 (0 min) to 0.06 microM/g wwt (20 min); heart 4.73 +/- 0.34 (0 min) to 1.08 +/- 0.47 (20 min); kidney 1.62 +/- 0.11 (0 min) to 0.02 +/- 0.02 (20 min). Phosphocreatine: brain 1.65 +/- 0.68 (0 min) to 0.51 +/- 0.45 microM/g (20 min); heart 6.98 +/- 0.38 (0 min) to 6.17 +/- 1.07 (20 min); kidney 8.23 +/- 0.86 (0 min) to 3.76 +/- 0.54 (20 min). We present data on energy derangement in a rat model of PA, closely resembling the clinical situation, showing that energy depletion precedes cell damage and death.

Outcome of very-low-birth-weight infants at 1 and 2 years of age. The importance of early identification of neurodevelopmental deficits.

The developmental and neurologic outcome of very-low-birth-weight infants (n=76) at 1 and 2 years, corrected for postconceptional age, and variables predicting outcome were assessed. At 1 year 24% of tile children were neurologically normal and at 2 years 61%. Developmental status was evaluated by use of the Griffiths Developmental Scales. The rate of cognitively normal children remained constant (58% at 1 year and 59% at 2 years) indicating that developmental status at 1 year was predictive for the second year. This early period is important, therefore, for the identification of developmental deficits and for establishing early, adequate interventions.

Effects of endotracheal suctioning in high-frequency oscillatory and conventionally ventilated low birth weight neonates on cerebral hemodynamics observed by near infrared spectroscopy (NIRS).

Adverse changes in cerebral hemodynamics during endotracheal suctioning have been reported in conventionally ventilated newborns, whereas observations on the effect of endotracheal suctioning during high-frequency ventilation have not been reported to date. The present study was designed to investigate the effect of endotracheal suctioning on cerebral hemodynamics in high-frequency and conventionally ventilated infants. Changes in cerebral concentration of oxygenated (cO(2)Hb) and deoxygenated hemoglobin (cHHb) and oxidized cytochrome aa3 (cCyt.aa3) were measured by noninvasive near-infrared spectroscopy. In an open prospective study, 26 suctioning periods in 9 high-frequency and in 6 conventionally ventilated newborn infants were investigated. Heart rate, arterial oxygen saturation (SaO(2)), mean blood pressure (MABP), and transcutaneous carbon dioxide tension (TcpCO(2)) were monitored continuously. In both groups, a marked decrease in heart rate, SaO(2) and in cO(2)Hb, an increase in cHHb, and a variable pattern in the concentration of total hemoglobin were noted during endotracheal suctioning. During suctioning, no statistically significant differences between the two methods of mechanical ventilation could be observed. We conclude that the mode of ventilation had no significant effect on changes in cerebral hemodynamics during endotracheal suctioning.

Long-term experience with subcutaneously tunneled external ventricular drainage in preterm infants.

We previously reported on a series of 27 newborn infants treated for posthemorrhagic hydrocephalus with external ventricular drainage during 1984 to 1989. In the present study we continued to evaluate this technique during the subsequent 8 years (37 patients; mean birthweight 1251+/-478 g; mean gestational age 29+/-2.9 weeks; 51 drains), and we now report on the long-term experience with this method, complications, and neurodevelopmental outcome of the survivors. The mean age at drain insertion was 21 days, and the mean duration of drainage 23 days. Eight infants died of causes unrelated to external ventricular drainage. Eleven of the survivors did not require a permanent shunt. Two patients experienced ventriculitis, resulting in an infection rate of 5.4% per patient and 3.9% per drain. The neurodevelopmental outcome was mainly dependent on the extent of the pre-existing parenchymal injury. We conclude that external ventricular drainage is a safe and effective technique for the management of preterm infants with posthemorrhagic hydrocephalus.

Cholinergic, monoaminergic and glutamatergic changes following perinatal asphyxia in the rat.

Perinatal asphyxia (PA) is considered to lead to a variety of brain disorders including spasticity, epilepsy, mental retardation, and minimal brain disorder syndromes and may form the basis for psychiatric and neurodegenerative diseases later in life. We examined markers for neuronal transmission involved in the pathomechanisms of PA and candidates as mediators for long-term sequelae. We tested tyrosine hydroxylase (TH) and the vesicular monoamine transporter (VMAT) representing the monoaminergic system, the vesicular acetylcholine transporter (VAChT), and the excitatory amino acid carrier 1 (EAAC1), a neuronal subtype of the glutamate transporter, using immunohistochemistry on brain sections of rats subjected to graded PA. Three months following the asphyxiant insult immunoreactive (IR)-TH was decreased in striatum, hippocampus, thalamus, frontal cortex, and cerebellum; IR-VMAT was increased, and IR-VAChT was decreased in striatum. IR-EAAC1 glutamate transporter was increased in frontal cortex. The cholinergic, monoaminergic, and glutamatergic changes, still observed 3 months after the asphyxiant insult, may reflect their involvement in the pathomechanisms of PA and indicate mechanisms leading to long-term complications of PA. The variable consequences on the individual markers in several brain regions may be explained by specific susceptibility of cholinergic, monoaminergic, and glutamatergic neurons to the asphyxiant insult.

Histological changes and neurotransmitter levels three months following perinatal asphyxia in the rat.

The involvement of excitatory amino acids (EAA) in the pathogenesis of hypoxic-ischemic states is well-documented. Information on the role of overexcitation by EAA in perinatalasphyxia (PA), however, is limited and data from adult models cannot be directly extrapolated to immature systems. Moreover, most adult models of ischemia are representing stroke rather than PA. We decided to study long term effects in a non-invasive rat model of PA resembling the clinical situation three months following the asphyctic insult. Morphometry on Nissl - stained sections was used to determine neuronal death in frontal cortex, striatum, hippocampus CA1, hypothalamus and cerebellum L1, and the amino acids glutamate, glutamine, aspartate, GABA, taurine, arginine as well as histamine, serotonin and 5-hydroxy-indoleacetic acid were determined in several brain regions and areas. Morphometry revealed that neuronal loss was present in the hippocampal area CA1 in all groups with PA and that morphological alterations were significantly higher in the cerebellar granular layer. The prominent light microscopical finding in all areas of asphyctic rats studied was decreased Nissl-staining, suggesting decreased cellular RNA levels. Glutamate, aspartate and glutamine were significantly elevated in the hypothalamus of asphyctic rats probably indicating overstimulation by EAA. Excitotoxicity in this area would be compatible with findings of emotional / behavioral deficits observed in a parallel study in our model of PA. Our observations point to and may help to explain behavioral and emotional deficits in Man with a history of perinatal asphyxia.

Treatment of peripubertal children after renal transplantation (RTX) with recombinant human growth hormone: auxological data and effects on insulin-like growth factor-I (IGF-I) and IGF-binding protein-3 (IGFBP-3) during 24 months.

OBJECTIVE: To evaluate growth and endocrine parameters in RTX children with GH treatment during 24 months. SUBJECTS: 18 children (13 boys), age 13.1 yr (8.0-16.6), bone age 10.1 yr (5.4-15.3). Patients were 2.8 yr (0.5-7.5) after RTX and had immunosuppressive therapy, prednisone 0.16 mg/kg/d (0.08-0.68). METHODS: GH (4 IU/m2/day s.c.) was given and patients were seen every 3 months for evaluation of height, height velocity, bone age, and hormone parameters. Serum IGF-I was determined by RIA, IGFBP-3 by RIA and Western ligand blotting (WLB). Renal function and adverse effects (GFR, glucose tolerance, rejection episodes) were monitored. RESULTS: Height (+1 SDS) and height velocity (+2.2 SDS) increased significantly during 24 months GH treatment, but delta BA/delta CA was 1.7 and 1.5 during the first and second treatment year, respectively, and all patients entered puberty during the treatment period. GFR decreased slightly during 2 yr (p = 0.048), two patients had chronic rejection and GH therapy was terminated in one patient because of glucose intolerance. The ratio IGF-I/IGFBP-3 rose during the first year (p = 0.002) indicating more bioavailable IGF-I. IGFBP-3 determined by WLB was decreased, but IGFBP-1, -2 and -4 were elevated as compared to a standard. CONCLUSIONS: GH treatment increased height and growth rate in children after RTX. This may be due to significant changes in IGF-I and IGFBP-3 relationship. However, bone maturation was also accelerated thus diminishing height potential. From month 12 to 24 a continuous decrease of IGF-I was observed. There was a slight but significant deterioration of graft function. Adverse events that led to termination of GH therapy were observed in 3 of 18 patients.

Neonatal cholestasis and focal medullary dysplasia of the kidneys in a case of microcephalic osteodysplastic primordial dwarfism.

We report on a male infant who presented with intrauterine growth retardation, severe postnatal failure to thrive, microcephaly, facial dysmorphism, and skeletal dysplasia. The clinical and radiological findings are consistent with former descriptions of microcephalic osteodysplastic primordial dwarfism (MOPD) type I/III. In addition to previously published features, multiple fractures of the long bones, severe neonatal cholestasis, and histological dysplasia of the kidneys were found. The boy died at the age of 8 months. The new finding of focal renal medullary dysplasia further supports the hypothesis of a basic defect in tissue differentiation in the pathogenesis of this rare condition.

Follow-up of infants with congenital toxoplasmosis detected by polymerase chain reaction analysis of amniotic fluid.

This study was conducted to assess the validity of performing the polymerase chain reaction (PCR) on amniotic fluid for detecting fetal Toxoplasma infection. The primary endpoint was the outcome of the infant at 1 year of age. A prospective, consecutive study was performed in 49 infants born to mothers with primary Toxoplasma infection during pregnancy. PCR determinations of Toxoplasma gondii DNA in amniotic fluid were carried out as part of their prenatal management. Infants were examined at birth, and at 1, 3, 6, 9, and 12 months of age. Nine of 11 infants from pregnancies with positive PCR results proved to be infected based on follow-up serological investigations conducted during the first year of life. Two fetal deaths occurred. All 38 infants with negative PCR results remained uninfected at 1 year of age, irrespective of whether their mothers had received treatment with sulfadiazine/pyrimethamine or spiramycin alone. Psychomotor development was normal in all infants. This follow-up study confirms that PCR performed on amniotic fluid is a useful method for identification or exclusion of fetal Toxoplasma infection. Treatment of infected pregnant women and - in the event of a positive PCR result subsequent treatment of their infants is associated with a favorable outcome.

Echocardiographic evidence of aortopulmonary collaterals in premature infants after closure of ductus arteriosus.

Aortopulmonary collaterals occur in a variety of congenital heart diseases, in chronic pulmonary infection and abscesses, in association with lung tumors, and after multiple pulmonary emboli. In patients with congenital cyanotic heart disease aortopulmonary collaterals mainly occur in conditions with reduced pulmonary blood flow. We investigated 12 preterm low-birth-weight infants, gestational age 29.3+/-3.3 weeks, with respiratory failure who suffered from moderate to severe chronic lung disease after a period of mechanical ventilation. All patients developed aortopulmonary collaterals after closure of a patent ductus arteriosus. Aortopulmonary collaterals could be displayed clearly by color Doppler echocardiography and originated mainly from the descending aorta or the aortic arch. Hypoxic and hypercapnic episodes favored the development of aortopulmonary collaterals, which disappeared after pulmonary hemodynamics and respiratory function had improved. In only one patient coiling of a large col lateral vessel had to be performed. Systemic-to-pulmonary collateral vessels potentially aggravate chronic lung disease by increasing collateral pulmonary blood flow and reducing lung compliance. We conclude that aortopulmonary collaterals occur in bronchopulmonary dysplasia and can cause major problems in ventilated premature infants. Echocardiographic evaluation is important to prevent aggravation of chronic lung disease of infants at risk.

Effects of umbilical arterial catheterization on mesenteric hemodynamics.

Impairment of mesenteric blood flow due to the use of umbilical artery catheters (UAC) may increase the risk of necrotizing enterocolitis (NEC) in newborn infants. We used Duplex Doppler sonography to investigate the degree of vessel obstruction due to UAC and their effect on visceral hemodynamics in 12 newborn infants. Ultrasonography was performed before and immediately after removal of the UAC, which was positioned above the ostia of the celiac and superior mesenteric arteries (SMA). Vessel diameter, peak systolic blood flow velocity (PSFV), end diastolic blood flow velocity (EDFV), and Pourcelot's resistance index (RI) were measured in the celiac trunk and the SMA within 1 cm of their origins. Removal of the UAC led to a significant increase in mean PSFV (celiac trunk: 50 cm/s +/- 15 vs 62 cm/s +/- 0.22, P < 0.05; SMA: 52 cm/s +/- 0.17 vs 72 cm/s +/- 0.21, P < 0.05). RI increased from 0.7 +/- 0.14 to 0.74 +/- 0.13 and from 0.73 +/- 0.1 to 0.76 +/- 0.13 for the celiac trunk and SMA, respectively. The EDFV and vessel diameters did not change significantly after UAC removal. Our results suggest that UAC cause a decrease in mesenteric blood flow. Therefore, their use in hemodynamically unstable neonates or in those with gastrointestinal disease should be very carefully considered.