Evaluation of portal venous gas detected by ultrasound examination for diagnosis of necrotising enterocolitis.

BACKGROUND: Early diagnosis of necrotising enterocolitis (NEC) is difficult but essential for timely therapy. The diagnostic hallmarks and specific radiological signs for NEC are pneumatosis intestinalis (PI) and portal venous gas (PVG), but PVG in abdominal ultrasound (PVG-US) has been proposed as an effective tool in the diagnosis of NEC as well. OBJECTIVE: To prospectively assess the value of PVG-US for the diagnosis of NEC. METHODS: The study screened 352 neonates for PVG-US (n = 796 routine examinations) and performed 48 additional screenings in 34/352 neonates with suspected (stage I, n = 28) or definite NEC (stage > or =II, n = 20). Sensitivity and specificity of PVG-US for detection of NEC were computed by using NEC stage > or =II as the reference standard. RESULTS: PVG-US was only present in cases of suspected or definite NEC. The study observed PVG-US in 4/28 NEC stage I and in 9/20 NEC stage > or =II episodes corresponding to a 86% specificity and a 45% sensitivity for diagnosis of NEC stage > or =II. However, 7/20 patients with NEC stage > or =II showed intraoperative findings other than NEC and another 3/20 infants presented with radiologically unspecific intestinal dilatation. None of these 10 infants had detectable PVG-US. Thus, with application of specific radiological signs the sensitivity of PVG-US for diagnosis of NEC stage > or =II increased to 90%. CONCLUSION: Screening for PVG-US is a useful, easy and quick bedside test with a high specificity for NEC. Moreover, these results question the value of the Walsh criteria in the diagnosis of NEC.

Antenatal ultrasonographic appearance of isolated fetal ascites. A case report of sinus urogenitalis.

BACKGROUND: Isolated fetal ascites can be caused by many heterogeneous disorders and is associated with a variety of conditions. Cloacal anomalies are rare abnormalities with a highly variable array of sonographic symptoms, which make them difficult to diagnose antenatally. We present a case with isolated fetal ascites without hydronephrosis caused by a cloacal malformation. CASE: A 28-year-old woman, gravida 2, para 1, was referred to our unit at 18 weeks gestation with a hyperdense structure in the fetal liver. Cordocentesis revealed a normal karyotype and negative viral titers. Isolated fetal ascites occurred for the first time at 23 weeks gestation. Serial ultrasounds showed progressive fetal ascites with no hydronephrosis at any time and no other malformations apart from the previously diagnosed hyperechogenic liver structure. After the insertion of an abdomino-amniotic shunt, a temporary reduction of the sonographically detectable ascites could be achieved. Cesarean delivery was necessary due to a pathological CTG at 33 weeks of gestation. The baby was born with a markedly distended abdomen. Postnatal radiologic examination showed two fistulae between the cloaca and the notedly dilated vagina and the rectum respectively. At the age of 3 months a vaginoplasty was performed, which involved creating a correctly positioned vaginal opening, reconstruction of the urethra and rectum as well as occlusion of the two fistulae. CONCLUSION: In view of the examinations, performed before and after delivery, it has to be assumed that fetal urine drained via the cloaca through the fallopian tubes into the abdomen. In contrast to usual appearance of cloacal malformations no hydronephrosis was detected and the kidney function was normal at all times. To our knowledge, this is the first published case of isolated fetal ascites without hydronephrosis caused by a cloacal malformation.

Phosphatidylcholine molecular species in lung surfactant: composition in relation to respiratory rate and lung development.

Surfactant reduces surface tension at the air-liquid interface of lung alveoli. While dipalmitoylphosphatidylcholine (PC16:0/ 16:0) is its main component, proteins and other phospholipids contribute to the dynamic properties and homeostasis of alveolar surfactant. Among these components are significant amounts of palmitoylmyristoylphosphatidylcholine (PC16:0/ 14:0) and palmitoylpalmitoleoylphosphatidylcholine (PC16:0/ 16:1), whereas in surfactant from the rigid tubular bird lung, PC16:0/14:0 is absent and PC16:0/16:1 strongly diminished. We therefore hypothesized that the concentrations of PC16:0/14:0 and PC16:0/16:1 in surfactants correlate with differences in the respiratory physiology of mammalian species. In surfactants from newborn and adult mice, rats, and pigs, molar fractions of PC16:0/14:0 and PC16:0/16:1 correlated with respiratory rate. Labeling experiments with [methyl-(3)H]choline in mice and perfused rat lungs demonstrated identical alveolar proportions of total and newly synthesized PC16:0/14:0, PC16:0/16:1, and PC16:0/16:0, which were much higher than those of other phosphatidylcholine species. In surfactant from human term and preterm neonates, fractional concentrations not only of PC16:0/16:0 but also of PC16:0/14:0 and PC16:0/ 16:1 increased with maturation. Our data emphasize that PC16:0/14:0 and PC16:0/16:1 may be important surfactant components in alveolar lungs, and that their concentrations are adapted to respiratory physiology.

Pulmonary surfactant in birds: coping with surface tension in a tubular lung.

As birds have tubular lungs that do not contain alveoli, avian surfactant predominantly functions to maintain airflow in tubes rather than to prevent alveolar collapse. Consequently, we have evaluated structural, biochemical, and functional parameters of avian surfactant as a model for airway surfactant in the mammalian lung. Surfactant was isolated from duck, chicken, and pig lung lavage fluid by differential centrifugation. Electron microscopy revealed a uniform surfactant layer within the air capillaries of the bird lungs, and there was no tubular myelin in purified avian surfactants. Phosphatidylcholine molecular species of the various surfactants were measured by HPLC. Compared with pig surfactant, both bird surfactants were enriched in dipalmitoylphosphatidylcholine, the principle surface tension-lowering agent in surfactant, and depleted in palmitoylmyristoylphosphatidylcholine, the other disaturated phosphatidylcholine of mammalian surfactant. Surfactant protein (SP)-A was determined by immunoblot analysis, and SP-B and SP-C were determined by gel-filtration HPLC. Neither SP-A nor SP-C was detectable in either bird surfactant, but both preparations of surfactant contained SP-B. Surface tension function was determined using both the pulsating bubble surfactometer (PBS) and capillary surfactometer (CS). Under dynamic cycling conditions, where pig surfactant readily reached minimal surface tension values below 5 mN/m, neither avian surfactant reached values below 15 mN/m within 10 pulsations. However, maximal surface tension of avian surfactant was lower than that of porcine surfactant, and all surfactants were equally efficient in the CS. We conclude that a surfactant composed primarily of dipalmitoylphosphatidylcholine and SP-B is adequate to maintain patency of the air capillaries of the bird lung.

Pulmonary and gastric surfactants. A comparison of the effect of surface requirements on function and phospholipid composition.

Surfactant is present in the alveoli and conductive airways of mammalian lungs. The presence of surface active agents was, moreover, demonstrated for avian tubular lungs and for the stomach and intestine. As the surface characteristics of these organs differ from each other, their surfactants possess distinct biochemical and functional characteristics. In the stomach so-called 'gastric surfactant' forms a hydrophobic barrier to protect the mucosa against acid back-diffusion. For this purpose gastric mucosal cells secrete unsaturated phosphatidylcholines (PC), but no dipalmitoyl-PC (PC16:0/16:0). By contrast, surfactant from conductive airways, lung alveoli and tubular avian lungs contain PC16:0/16:0 as their main component in similar concentrations. Hence, there is no biochemical relation between gastric and pulmonary surfactant. Alveolar surfactant, being designed for preventing alveolar collapse under the highly dynamic conditions of an oscillating alveolus, easily reaches values of <5 mN/m upon cyclic compression. Surfactants from tubular air-exposed structures, however, like the conductive airways of mammalian lungs and the exclusively tubular avian lung, display inferior compressibility as they only reach minimal surface tension values of approximately 20 mN/m. Hence, the highly dynamic properties of alveolar surfactant do not apply for surfactants designed for air-liquid interfaces of tubular lung structures.

Commercial versus native surfactants. Surface activity, molecular components, and the effect of calcium.

Despite their broad clinical use, there is no standardized comparative study on the functional, biochemical, and morphologic differences of the various commercial surfactants in relation to native surfactant. We investigated these parameters in Alveofact, Curosurf, Exosurf, and Survanta, and compared them with native bovine (NBS) and porcine (NPS) surfactant. For Curosurf and Alveofact the concentrations necessary for minimal surface tensions < 5 mN/m were six to 12 times higher (1.5 and 3 mg/ml, respectively) than with NPS and NBS. Exosurf and Survanta only reached 22 and 8 mN/m, respectively. Increasing calcium to nonphysiologic concentrations artificially improved the function of Alveofact and Curosurf, but it had little effect on Exosurf and Survanta. Impaired surface activity of commercial versus native surfactants corresponded with their lack in surfactant protein SP-A and decreased SP-B/C. The higher surface activity of Curosurf compared with Alveofact corresponded with its higher concentration of dipalmitoylphosphatidylcholine (DPPC). Despite their enrichment in DPPC Survanta and Exosurf exhibited poor surface activity because of low or absent SP-B/C. Ultrastructurally, Curosurf and Alveofact consisted mainly of lamellar and vesicular structures, which were also present in NPS and NBS. Exosurf contained crystalline structures only, whereas the DPPC-enriched Survanta contained separate lamellar/vesicular and crystalline structures. We conclude that in vitro surface activity of commercial surfactants is impaired compared with native surfactants at physiologic calcium concentrations. In the presence of SP-B/C, surface activity corresponds to the concentration of DPPC. Our data underscore the importance of a standardized protocol at physiologic calcium concentrations for the in vitro assessment of commercial surfactants.

Determinants of lung volume in spontaneously breathing preterm infants.

To study the effects of apneic pauses, sighs, and breathing patterns on functional residual capacity (FRC), we measured FRC repeatedly in 48 healthy preterm infants (weight at study 2,042 +/- 316 g [mean +/- SD], postconceptional age 36.6 +/- 2.0 wk), during unsedated sleep using a modified heliox/nitrogen washout technique. Breathing movements and pulse oximeter saturation (SpO2) were recorded throughout and recordings analyzed for the presence of regular and nonregular breathing pattern, apneic pauses, sighs, and desaturations (SpO2 < 90%) during the last 2 min prior to each FRC measurement. FRC was lower during nonregular than during regular breathing pattern (23.3 +/- 7.2 ml/kg versus 26.9 +/- 7.8 ml/kg, p < 0.02); however, this apparent effect of breathing pattern disappeared after controlling the data for apneic pauses. Apneic pauses resulted in a significant decrease in FRC: mean FRC was 20.0 +/- 6.8 ml/kg if measured within 2 min of an apneic pause, 26.0 +/- 6.9 ml/kg if measured after a sigh (p < 0.001), and 24.0 +/- 7.7 ml/kg if there had been neither a sigh nor an apneic pause (p < 0.05). The interval between the apneic pause and the FRC measurement had no effect on FRC. There was an inverse correlation between FRC and the speed with which SpO2 fell during desaturation (r = -O.5, p < 0.03). Apneic pauses resulted in a persistent reduction in FRC in these preterm infants. Sighs appeared to restore FRC. The significant relationship between FRC and the speed of desaturation found in this study underscores the importance of endogenous or exogenous strategies that help to increase FRC, such as sighs or the application of continuous positive airway pressure, for the stability of oxygenation in preterm infants who have difficulty maintaining their oxygenation.

Comparison of heliox and oxygen as washing gases for the nitrogen washout technique in preterm infants.

The nitrogen washout technique usually involves exposure of the patient to 100% oxygen for several minutes. This may be dangerous in preterm infants who are at risk of retinopathy of prematurity (ROP). We wanted to know whether heliox (79% He, 21% O2) can be used instead of oxygen when determining functional residual capacity (FRC). FRC measurements were made in 14 preterm infants [median (range) gestational age at birth 34 wk (27-37 wk), and at time of study 36 wk (33-40 wk)] who were breathing room air. FRC was measured using a computerized infant pulmonary function system, beginning in random order with either 100% O2 followed by heliox or vice versa. There was no systematic difference between the two methods with regard to lung volume measurements: mean (SD) FRC values, corrected for body weight, were 22.9 (7.1) mL/kg for O2 and 23.4 (7.0) mL/kg for heliox. We did not observe a systematic influence of the type of washing gas used (heliox or oxygen) on FRC in these infants. Our results suggest that the use of heliox instead of pure oxygen may be a suitable and safer alternative for FRC measurements with the nitrogen washout technique in preterm infants who are breathing low concentrations of inspired oxygen and are still at risk of ROP.