Continuity of care for children with anorexia nervosa in the Netherlands: a modular perspective.

Care provision for children with anorexia nervosa is provided by outpatient care teams in hospitals, but the way these teams are organized differs per hospital and hampers the continuity of care. The aim of this study is to explore the organization and continuity of care for children with anorexia nervosa in the Netherlands by using a modular perspective.We conducted a qualitative, exploratory case study and took the healthcare provision for children with anorexia nervosa, provided by outpatient care teams, as our case. We conducted nine interviews with healthcare professionals involved in outpatient care teams from six hospitals. A thematic analysis was used to analyze the data.The modular perspective offered insights into the work practices and working methods of outpatient care teams. We were able to identify modules (i.e. the separate consultations with the various professionals), and components (i.e. elements of these consultations). In addition, communication mechanisms (interfaces) were identified to facilitate information flow and coordination among healthcare professionals. Our modular perspective revealed gaps and overlap in outpatient care provision, consequently providing opportunities to deal with unnecessary duplications and blind spots.   Conclusion: A modular perspective can be applied to explore the organization of outpatient care provision for children with anorexia nervosa. We specifically highlight gaps and overlap in healthcare provision, which in turn leads to recommendations on how to support the three essential parts of continuity of care: informational continuity, relational continuity, and management continuity. What is Known: • Care provision for children with anorexia nervosa requires a network of health care professionals from different organizations, as a result the organization and provision of care faces challenges. What is New: • Modular care provision sheds light on the complexity and organization of outpatient care provision and supports the three dimensions of continuity of care as experienced by children with anorexia nervosa and their parents/caregivers.

Treatment with exogenous surfactant stimulates endogenous surfactant synthesis in premature infants with respiratory distress syndrome.

OBJECTIVE: Treatment of preterm infants with respiratory distress syndrome (RDS) with exogenous surfactant has greatly improved clinical outcome. Some infants require multiple doses, and it has not been studied whether these large amounts of exogenous surfactant disturb endogenous surfactant metabolism in humans. We studied endogenous surfactant metabolism in relation to different amounts of exogenous surfactant, administered as rescue therapy for RDS. DESIGN: Prospective clinical study. SETTING: Neonatal intensive care unit in a university hospital. PATIENTS: A total of 27 preterm infants intubated and mechanically ventilated for respiratory insufficiency. INTERVENTIONS: Infants received a 24-hr infusion with the stable isotope [U-13C]glucose starting 5.3 +/- 0.5 hrs after birth. The 13C-incorporation into palmitic acid in surfactant phosphatidylcholine (PC) isolated from serial tracheal aspirates was measured. Infants received either zero (n = 5), one (n = 4), two (n = 15), or three (n = 3) doses of Survanta (100 mg/kg) when clinically indicated. MEASUREMENTS AND MAIN RESULTS: Using multiple regression analysis, the absolute synthesis rate (ASR) of surfactant PC from plasma glucose increased with 1.3 +/- 0.4 mg/kg/day per dose of Survanta (p = .007) (mean +/- SEM). The ASR of surfactant PC from glucose was increased by prenatal corticosteroid treatment with 1.3 +/- 0.4 mg/kg/day per dose corticosteroid (p = .004), and by the presence of a patent ductus arteriosus with 2.1 +/- 0.7 mg/ kg/day (p = .01). CONCLUSION: These data are reassuring and show for the first time in preterm infants that multiple doses of exogenous surfactant for RDS are tolerated well by the developing lung and stimulate endogenous surfactant synthesis.

The effect in premature infants of prenatal corticosteroids on endogenous surfactant synthesis as measured with stable isotopes.

Most in vitro studies show that prenatal administration of corticosteroids stimulates the synthesis of surfactant phosphatidylcholine (PC), but studies in animals are controversial. Whether prenatal corticosteroids stimulate surfactant PC synthesis in humans has not been studied. We studied endogenous surfactant PC synthesis in relation to prenatal corticosteroid treatment in 27 preterm infants with respiratory distress syndrome. Infants received a 24-h infusion of the stable isotope [U-(13)C]glucose, starting approximately 5 h after birth. We measured (13)C-incorporation into palmitic acid in surfactant PC from serial tracheal aspirates and in plasma triglycerides and phospholipids by isotope-ratio mass spectrometry. Premature infants had received either zero (n = 11), one (n = 4), or two doses (n = 12) of prenatal betamethasone (12 mg intramuscularly). The fractional synthesis rate (FSR) of surfactant PC from glucose was 1.7 +/- 0.3%/d without corticosteroid treatment, 2.9 +/- 1.4%/d with one dose of prenatal corticosteroid, and 5.8 +/- 1.3%/d after two doses of prenatal corticosteroid. Using multiple regression analysis, we found that the FSR of surfactant PC increased by 40% (confidence interval: 7 to 82%/d, p < 0.02) per dose of corticosteroid and doubled after two doses of corticosteroid. The (13)C-enrichment of plasma triglycerides and phospholipids was not increased by corticosteroid. These data show for the first time that prenatal corticosteroid treatment stimulates surfactant synthesis in the preterm infant.

Metabolism of endogenous surfactant in premature baboons and effect of prenatal corticosteroids.

We studied the synthesis of surfactant and the effect of prenatal betamethasone treatment in vivo in very preterm baboons. Ten pregnant baboons were randomized to receive either betamethasone (beta) or saline (control) 48 and 24 h before preterm delivery. The newborn baboons were intubated, treated with surfactant, and ventilated for 6 d. They received a 24-h infusion with the stable isotope [U-(13)C]glucose as precursor for the synthesis of palmitic acid in surfactant phosphatidylcholine (PC). Palmitic acid in surfactant PC became enriched 27 +/- 2 h after the start of the isotope infusion and was maximally enriched at 100 +/- 4 h. The fractional synthesis rate of PC palmitate in the beta group (1.5 +/- 0.2%/d) was increased by 129% above control (0.7 +/- 0.1%/d) (p < 0.02, Mann- Whitney U test). The absolute synthesis rate of PC in the beta group [1.6 +/- 0.3 micromol/kg/d] was increased by 128% above controls [0.7 +/- 0.2 micromol/kg/d] (p < 0.02). These data show that the synthesis of endogenous surfactant from plasma glucose as precursor is a slow process. It is shown, for the first time in vivo, that prenatal glucocorticosteroids stimulate the synthesis of surfactant PC in the very premature baboon.

Endogenous surfactant metabolism in critically ill infants measured with stable isotope labeled fatty acids.

Little is known about endogenous surfactant metabolism in infants, because radioactive isotopes used for this purpose in animals cannot be used in humans. We developed a novel and safe method to measure the endogenous surfactant kinetics in vivo in humans by using stable isotope labeled fatty acids. We infused albumin-bound [U-13C]palmitic acid (PA) and [U-13C]linoleic acid (LLA) for 24 h in eight critically ill infants (mean+/-SD: weight: 3.7+/-1.3 kg: age: 51.3+/-61.6 d) who required mechanical ventilation. The 13C enrichment of PA and LLA in surfactant phosphatidylcholine (PC), obtained from tracheal aspirates, was measured by gas chromatography combustion interface-isotope ratio mass spectrometry. We measured a significant incorporation of both 13C-PA and 13C-LLA into surfactant PC. PC-PA and PC-LLA became enriched after 8.7+/-4.9 h (range: 3.4-17.3) and 10.0+/-7.2 h (range: 3.0-22.4), respectively; the times at maximum enrichment were 49.2+/-8.9 and 45.6+/-19.3 h, respectively. The fractional synthesis rate of surfactant PC-PA ranged from 0.4 to 3.4% per h, whereas the fractional synthesis rate of PC-LLA ranged from 0.5 to 3.8% per h. The surfactant PC-PA and PC-LLA half-lives ranged from 16.8 to 177.7 and 23.8 to 144.4 h, respectively. This method provides new data on surfactant metabolism in infants requiring mechanical ventilation. We found that synthesis of surfactant from plasma PA and LLA is a slow process and that there were marked differences in PC kinetics among infants. This variability could be related to differences in lung disease and could affect the clinical course of the respiratory failure.

Prospective evaluation of surfactant composition in bronchoalveolar lavage fluid of infants with congenital diaphragmatic hernia and of age-matched controls.

OBJECTIVES: Infants with congenital diaphragmatic hernia may have biochemically immature lungs. However, normal lecithin/sphingomyelin ratios and phosphatidylglycerol concentrations have been reported in the amniotic fluid of congenital diaphragmatic hernia patients. We hypothesized that if the lungs of congenital diaphragmatic hernia patients are surfactant deficient, that this condition would be reflected in an altered surfactant composition in the bronchoalveolar lavage fluid compared with that composition in age-matched controls. DESIGN: Prospective, controlled study. SETTING: Surgical intensive care unit in a Level III pediatric university hospital. PATIENTS: Four groups were studied: two groups of congenital diaphragmatic hernia patients (conventionally ventilated, n = 13; treated with extracorporeal membrane oxygenation, n = 5); and two control groups (conventionally ventilated, n = 13; extracorporeal membrane oxygenation, n = 6). INTERVENTIONS: Bronchoalveolar lavage, using a blind, standardized technique, was performed in conventionally ventilated congenital diaphragmatic hernia patients, extracorporeal membrane oxygenation-treated congenital diaphragmatic hernia patients, age-matched conventionally ventilated controls without pulmonary abnormalities, and extracorporeal membrane oxygenation-treated infants without congenital diaphragmatic hernia. MEASUREMENTS AND MAIN RESULTS: The concentrations of different surfactant phospholipids and the fatty acid composition of phosphatidylcholine in bronchoalveolar lavage fluid were measured. No significant differences between the concentrations of phosphatidylcholine and phosphatidylglycerol, and the lecithin/sphingomyelin ratios, were found between the four groups. The fatty acid composition of phosphatidylcholine in conventionally ventilated patients showed a median percentage of palmitic acid within the normal range for age in both groups: 68% in congenital diaphragmatic hernia patients and 73% in controls (p < .001). CONCLUSIONS: Our findings indicate that the concentrations of different phospholipids are similar in congenital diaphragmatic hernia patients and controls without congenital diaphragmatic hernia. A primary surfactant deficiency is unlikely in infants with congenital diaphragmatic hernia. However, secondary surfactant deficiency after respiratory failure may be involved.

Endogenous surfactant turnover in preterm infants measured with stable isotopes.

We studied surfactant synthesis and turnover in vivo in preterm infants using the stable isotope [U-13C]glucose, as a precursor for the synthesis of palmitic acid in surfactant phosphatidylcholine (PC). Six preterm infants (birth weight, 916 +/- 244 g; gestational age, 27.7 +/- 1.7 wk) received a 24-h [U-13C]glucose infusion on the first day of life. The 13C-enrichment of palmitic acid in surfactant PC, obtained from tracheal aspirates, was measured by gas chromatography-combustion interface-isotope ratio mass spectrometry. We observed a significant incorporation of carbon-13 from glucose into surfactant PC palmitate. PC palmitate became enriched after 19.4 +/- 2.3 (16.5 to 22.3) h and reached maximum enrichment at 70 +/- 18 (48 to 96) h after the start of the label infusion. The fractional synthesis rate (FSR) of surfactant PC palmitate from glucose was 2.7 +/- 1.3%/d. We calculated the absolute production rate of surfactant PC to be 4.2 mg/kg/d, and the half-life to be 113 +/- 25 (87 to 144) h. Data on endogenous surfactant production and turnover were obtained for the first time in human infants with the use of stable isotopes. This novel and safe method could be applied to address many important issues concerning surfactant metabolism in preterm infants, children, and adults.

The influence of acute hypoxemia and hypovolemic hypotension of neuronal brain activity measured by the cerebral function monitor in newborn piglets.

Little is known about the cerebral electrical response to short periods of hypoxemia, hypotension and their combination. These conditions occur frequently in critically ill newborn infants; their cerebral electrical activity can be registrated easily with the Cerebral Function Monitor (CFM). Therefore we recorded on-line cortical electrical activity during hypoxemia and hypotension in 11 newborn piglets aged 13-18 days. Hypoxemia was induced by reducing inspired oxygen fraction. Hypotension was induced by withdrawal of blood. The experimental groups were: Group I: arterial oxygen saturation (SaO2) 45-85%, group II: SaO2 < 45%, group III: mean arterial pressure (MAP) 50-75 mmHg, group IV: MAP < 50 mmHG, group V: SAO2 < 85% and MAP 50-75 mmHg and group VI: SaO2 < 85% and MAP < 50 mmHg. CFM registrated normal cortical electrical activity during periods of moderate or severe hypoxemia (group I and II) and during isolated moderate hypotension (group III). The cortical activity decreased significantly due to severe hypotension alone (group IV) and combined hypotension and hypoxemia (group V and VI). Hypotension has a more potent effect on cortical electrical activity than hypoxemia in the newborn piglet. Cerebral electrical activity does not change during severe hypoxemia and moderate hypotension possibly due to cerebral flow regulation. CFM recorded decreased cerebral electrical activity during severe hypotension and hypotension with hypoxemia. CFM could provide invaluable data in severely ill newborns.