Failure In Preterm Infants Research Articles

The Mapleson D continuous positive airway pressure system: a novel indication for the Mapleson circuit?

The Mapleson D continuous positive airway pressure system: a novel indication for the Mapleson circuit?

Development of an artificial placenta I: pumpless arterio-venous extracorporeal life support in a neonatal sheep model

Purpose Effective treatment of respiratory failure in premature infants remains an unsolved problem. The development of an artificial placenta, in the form of a pumpless arteriovenous extracorporeal life support (AV-ECLS) circuit that maintains fetal circulation, is an appealing alternative. Methods A near-term (140 d/term = 145 days) neonatal lamb model was used (n = 7). Fetuses were exposed by hysterotomy, and flow probes were placed on the ductus arteriosus, aorta, and carotid artery. Catheters were placed into the umbilical vessels, and pumpless AV-ECLS was initiated. Fetuses were submerged in a warm saline bath, and support was maintained for up to 4 hours. Results Mean initial device flow was 383 mL/min but steadily declined to 177 mL/min at 4 hours. Mean initial pO 2 was 24 mm Hg and 18 mm Hg at 4 hours. Initial mean pCO 2 was 60 mm Hg and declined to 42 mm Hg at 4 hours. Mean arterial pressure was initially 43 mm Hg and decreased to 34 mm Hg at 4 hours. Flow in the ductus arteriosus was maintained for 4 hours. Of 7 fetuses, 5 survived 4 hours of support. Conclusions Pumpless AV-ECLS can support gas exchange and maintain fetal circulation in a neonatal lamb model for a 4-hour period. Prolonged support (>4 hours) is hampered by high cannula resistance and declining device flow.

Surfactant Status in Preterm Neonates Recovering From Respiratory Distress Syndrome

The goal was to establish whether reduced amounts of pulmonary surfactant contribute to postextubation respiratory failure in preterm infants recovering from respiratory distress syndrome. We prospectively recruited preterm infants who needed mechanical ventilation and exogenous surfactant for treatment of moderate/severe respiratory distress syndrome and could not be extubated before day 3 of life. (13)C-labeled dipalmitoyl-phosphatidylcholine was administered endotracheally as tracer before extubation, for estimation of surfactant disaturated phosphatidylcholine pool size and half-life. Patients were retrospectively divided into 3 groups, that is, extubation failure if, after extubation, they needed reintubation or continuous positive airway pressure treatment of >or=6 cmH(2)O and fraction of inspired oxygen of >0.4, extubation success if they did not meet the failure criteria, and not extubated if they needed ongoing ventilation. Clinical and respiratory parameters were recorded hourly. Reliable kinetic data could be obtained for 63 of the 88 enrolled neonates. Sixteen, 23, and 24 neonates were categorized in the extubation failure, extubation success, and not extubated groups, respectively. Clinical and demographic characteristics did not differ between the extubation failure and extubation success groups. Disaturated phosphatidylcholine pool size was smaller in the extubation failure group than in the extubation success group (25 +/- 12 vs 43 +/- 24 mg/kg) and was 37 +/- 32 mg/kg in the not extubated group. Disaturated phosphatidylcholine half-life was 19 +/- 7, 24 +/- 12, and 28 +/- 18 hours in the extubation failure, extubation success, and not extubated groups, respectively. In a selected population of preterm infants with moderate/severe respiratory distress syndrome who could not be extubated in the first 3 days of life, infants who were reintubated or needed high continuous positive airway pressure settings after extubation had a smaller disaturated phosphatidylcholine pool size than did those who were successfully extubated or needed low continuous positive airway pressure settings.

The INNOVO multicentre randomised controlled trial: neonatal ventilation with inhaled nitric oxide versus ventilatory support without nitric oxide for severe respiratory failure in preterm infants: follow up at 4–5 years

Background:Trials of inhaled nitric oxide (iNO) used short term in preterm infants with severe respiratory failure have to date shown no evidence of benefit, and there have been no trials...

Postnatal growth failure in preterm infants: Recovery of growth and body composition after term

Background Many preterm infants are significantly growth restricted at hospital discharge and are at increased risk for long-term growth failure. Aims To compare growth and weight gain composition after term between preterm infants who were growth retarded and those who were not. Study design An observational longitudinal study was conducted. Subjects 35 preterm infants who showed growth retardation at term (group 1) and 26 preterm infants who did not (group 2). Outcome measures Growth and body composition were assessed at term and at 1, 2, 3, 4 and 5 months of corrected age. Results At term, and at 1, 2, and 3 months of corrected age, growth-retarded infants showed significantly lower body weight and fat mass than infants who did not develop growth retardation. The mean energy and protein intakes did not differ significantly between the two groups. Daily increases in body weight and fat mass between term and three months did not differ between the groups. However, during the fourth and fifth months, daily gains of body weight and fat mass were significantly greater in growth-retarded than in non-growth-retarded infants, and as a result, body weight and fat mass were comparable between the two groups at 4 and 5 months of corrected age. Conclusions In terms of growth parameters and body composition, growth-retarded preterm infants recovered from postnatal growth failure within the fourth month of corrected age.

A trial of spontaneous breathing to determine the readiness for extubation in very low birth weight infants: a prospective evaluation

Extubation failure in premature infants is common. A spontaneous breathing trial (SBT) was prospectively evaluated to determine timing of extubation. Compared with historical controls, infants were extubated at significantly higher...

Aminophylline Compatibility with Neonatal Total Parenteral Nutrition

Aminophylline has proven useful for treating renal failure in preterm infants. Previous reports state that aminophylline is incompatible with some neonatal total parenteral nutrition (TPN) solutions. If this is correct, administration of aminophylline doses would be complicated by the need to hold TPN and provide flush solution after each aminophylline dose. Our experience with administering aminophylline over 30 minutes concurrently with TPN was that this was not problematic. We therefore examined the in vitro compatibility of aminophylline and TPN solutions used in our neonates over a 30-minute interval to see if our policy of allowing concurrent mixing of these products was appropriate. TPN solutions (2.5 mL) were mixed with 1 mL of intravenous aminophylline 2.5 mg/mL in a glass vial. Three different TPN solutions used in our NICU were collected for the study, and five samples of each combination were prepared. Samples were watched for 60 minutes to see if precipitation occurred. Although the aminophylline and TPN solutions were not miscible, no turbidity or precipitation was observed. This study supports that aminophylline is physically compatible with neonatal TPN for 60 minutes.

Factors associated with INSURE method failure in preterm infants with respiratory distress syndrome

Objective : To identify which factors can predict INSURE failure in preterm infants with respiratory distress syndrome. Study design : A retropective analysis of the prenatal histories, clinical courses and paraclinical data of all inborn infants (birth weight 4 with a positive predictive value equals to 80 % (adjusted odds ratio [95 % CI] = 14,81 [1.96-111.56]). Complication rates in INSURE failure group were worse than those in INSURE success group. Conclusion : CRIB score > 4 was the main factor of failure of INSURE method in preterm infants with RDS. However, a prospective randomised controlled trial is needed to determine whether or not infants at risk for INSURE failure are better off being treated with mechanical ventilation. Abbreviations : RDS : Respiratory distress syndrome, SUR : surfactant, INSURE : INtubation SURfactant Extubation, MV : mechanical ventilation, N-CPAP : Nasal continuous positive airway pressure, FiO2 : fraction of inspired oxygen

Nutrition of Preterm Infants After Hospital Discharge

Growth failure in preterm infants remains extremely common despite advances in neonatal care. Many, or even a majority, leave the hospital with weights below the 10th centile for age. Because of this, the possibility of nutritional interventions to improve postdischarge growth has been considered. A variety of interventions have been tested in randomized controlled trials in formula-fed infants. Although the studies vary in design and in the intervention used, on balance the evidence supports the use of fortified formulas in formula-fed preterm infants after hospital discharge. Specially designed postdischarge formulas and preterm infant formulas seem equally efficacious. The situation for infants fed human milk is much less clear. Although the postdischarge growth in human milk-fed infants is not as good as in formula-fed infants, no interventions have been examined in human milk-fed infants in a randomized study, to our knowledge. We are unaware of any evidence that any of the commonly proposed nutritional interventions in human milk-fed infants after hospital discharge are either safe or efficacious. In the absence of such evidence, it seems prudent to avoid untested interventions in this population and to concentrate our efforts on the encouragement of breast-feeding after hospital discharge.

In vivo Dilatation of the Fetal and Postnatal Ductus Arteriosus by Inhibition of Phosphodiesterase 3 in Rats

Background: Clinically, it appears that phosphodiesterase 3 (PDE 3) inhibitors, which are used for acute cardiac failure in premature infants, dilate the ductus arteriosus (DA). Objectives: To clarify the ductus-dilating effects of PDE 3 inhibitors in near-term rat pups and their differential effects in near-term and preterm fetal rats, in in vivo studies. Methods: The in vivo ductal diameter of rat pups and fetuses was measured using a rapid whole-body freezing method, by cutting on a freezing microtome and measuring with a microscope and micrometer. Eight to twenty pups and fetuses were studied in each group. Milrinone and amrinone (specific inhibitors of PDE 3) were injected into 1-hour-old pups and the DA was studied 0.5 and 1 h later. The differential effects of these PDE 3 inhibitors on the near-term and preterm ductus were studied by injecting indomethacin (10 mg/kg) and PDE 3 inhibitors into 21D (21st day of pregnancy: term-21.5 days) and 19D dams and studying the fetal ductus 4 and 8 h later. Results: Milrinone and amrinone dilated the postnatal ductus dose-dependently. Large doses of these drugs dilated it completely, and clinically equivalent doses dilated it minimally. Milrinone and amrinone prevented constriction of the fetal ductus by indomethacin. Their ductus-dilating effects were more potent in the preterm than in the near-term fetuses, and clinically equivalent doses of these PDE 3 inhibitors dilated preterm ductus completely. Conclusion: In rats, PDE 3 inhibitors reopen the constricted postnatal DA slightly. PDE 3 inhibitors dilate the fetal DA constricted with indomethacin effectively and more sensitively in preterm than in near-term fetuses.

Repeat surfactant therapy for postsurfactant slump

To evaluate repeat surfactant therapy for the treatment of respiratory failure associated with postsurfactant slump in extremely low birth weight infants (ELBW) by characterizing the population of premature infants who develop postsurfactant slump and measuring their response to a secondary course of surfactant therapy. A retrospective analysis of a cohort of all patients admitted over a 3-year period with birth weights <1000 g (ELBW infants). Information was collected by chart review and the patients were categorized into three distinct groups for analysis. Initial surfactant only, patients who received surfactant replacement therapy only for respiratory distress syndrome (RDS); repeat surfactant, patients who received both initial surfactant replacement for RDS and repeat surfactant therapy for postsurfactant slump (defined as respiratory failure after 6 days of age), and no surfactant, patients in whom no surfactant was ever administered. A respiratory severity score (RSS) was used to measure the severity of lung disease and response to surfactant therapy. Over 3 years, there were 165 ELBW infants who could develop postsurfactant slump and be eligible for repeat surfactant therapy. There were 39 infants who never received any surfactant therapy estimated gestational age (EGA) 27.7 +/- 1.7, birth weight 856 +/- 109 g) either at birth or after 6 days of life. There were 126 patients treated for RDS with initial surfactant replacement therapy (EGA 25.6 +/- 1.9 weeks, birth weight 713 +/- 179 g). Out of these RDS patients, 101 improved with an initial course of surfactant therapy (EGA 26 +/- 1.8, birth weight 751 +/- 143 g), but 25 (20% of the patients with RDS) developed postsurfactant slump and received a repeat course of surfactant therapy (EGA 24.7 +/- 1.2, birth weight 647 +/- 120 g). The repeat surfactant group (postsurfactant slump) was significantly more premature and had significantly lower birth weights compared to both the initial surfactant only group and the no surfactant ever group. Logistic regression analysis revealed that lack of antenatal steroids, earlier gestational age, and the receiving of 2 or more doses of surfactant to treat the initial RDS were significantly associated with receiving repeat surfactant therapy for postsurfactant slump. Of the 25 patients treated with a repeat course of surfactant therapy more than 70% of patients (n = 18) had an improvement in their lung disease with a 15% reduction in their RSS. This improvement was significant at all time points evaluated (12, 24, and 48 h). We found that a repeat course of surfactant therapy, after day of life 6, led to a significant improvement in hypoxemic respiratory failure in premature infants with postsurfactant slump. Infants who received repeat surfactant therapy were born at a significantly earlier gestational age, had significantly smaller birth weight and had significantly worse lung disease. They were significantly less likely to have received antenatal steroids and were significantly more likely to have received multiple doses of surfactant to treat their initial RDS. A repeat course of surfactant therapy for patients with postsurfactant slump appeared beneficial in the short-term. These initial findings would support performing randomized control trials of repeat surfactant therapy for postsurfactant slump.

A dose response study of inhaled nitric oxide in hypoxic respiratory failure in preterm infants

Background Inhaled nitric oxide (iNO) is used widely in newborn infants with hypoxic respiratory failure, despite the known and theoretical toxicity of iNO, and a relative lack of information about appropriate doses. Aim To determine whether a dose–response relationship existed for iNO in preterm infants. Design A four-period, four-dose, cross-over design was used with iNO given for 15 min in a randomised sequence in concentrations of 5, 10, 20 and 40 parts per million (ppm), with a minimum 5 min wash-out period. Data on ventilatory, blood gas and other physiological measurements were recorded before and at the end of each period. The relationship of clinical response with iNO dose and period was analysed using multivariate regression. Subjects Infants with gestational age < 34 weeks and < 28 days postnatal age with hypoxic respiratory failure were recruited. Outcome measure A clinically significant dose–response was defined as a rise in the post-ductal arterial oxygen tension (PaO 2) of at least 3 kPa. Results Thirteen infants were recruited. At trial entry, ten were < 3 days of age; 11 were being treated with high frequency oscillatory ventilation; median (inter-quartile range) gestational age 27 (25–29) weeks; birthweight 983 (765–1120) g; oxygenation index 27.1 (21.8–28.8). Six infants (46%) showed a clinically significant response. After adjusting for period and patient effect, no evidence for an overall dose effect was identified (likelihood ratio test, p = 0.34). Conclusion No evidence of a dose–response relationship with iNO was found in this study of very preterm infants with respiratory failure.

Postnatal growth failure in preterm infants: ascertainment and relation to long-term outcome

Traditional measure of postnatal growth failure assessment has poor discriminatory power for long-term outcomes. Our objective was to identify measure of postnatal growth failure associated with long-term outcome in preterm infants born at < 28 weeks' gestation. Four measures of defining postnatal growth failure at 36 weeks corrected gestational age: (1) weight < 10(th) centile, (2) weight < 3(rd) centile, (3) z score difference from birth > 1 and, (4) z score difference from birth > 2; were compared for their predictive values and strength of association with adverse neurodevelopmental outcomes at 18-24 months. Postnatal growth failure defined as a decrease in z score of > 2 between birth and 36 weeks corrected gestational age had the best predictive values compared to other postnatal growth failure measures, however, it was significantly associated with psychomotor developmental (P=0.006) but not with mental developmental indices (P=0.379). Postnatal growth failure defined by z score change influenced psychomotor but not mental tasks in this cohort. This method of ascertainment could be useful to identify infants who might benefit from nutritional interventions.

Invited commentary

Since Dr Robert Gross performed the first surgical closure of a patent ductus arteriosus (PDA) in 1938, tens of thousands of operations have been performed. During these 67 years, tremendous advances have occurred in the field of neonatology, so that it is now commonplace to find 24-week gestation infants in a typical neonatal intensive care unit, commonly with a patent ductus. Unlike the term infant with a large PDA and resultant congestive heart failure, these tiny infants frequently have associated premature lung disease and elevated pulmonary artery pressures. Neonatologists, pediatric cardiologists, and cardiac surgeons now find themselves in a quandary of applying historical data from healthy infants and children to a population of patients with an entirely different set of issues. In this article, our French colleagues [1Jaillard S. Larrue B. Rakza T. Magnenant E. Warembourg H. Storme L. Consequences of delayed surgical closure of patent ductus arteriosus in very premature infants.Ann Thorac Surg. 2006; 81: 231-235Abstract Full Text Full Text PDF PubMed Scopus (54) Google Scholar] have nicely demonstrated that there is no advantage to delaying surgical closure after pharmacologic failure in premature infants in whom the PDA is documented to be hemodynamically significant. In fact their data suggests an advantage to earlier closure to allow earlier initiation of enteral nutrition. This is an important step in defining management strategies for this group of patients. However it is important to note that the entire series of patients had exclusively left to right shunting, and this rationale of early closure does not necessarily apply to all premature infants with PDAs. There is a spectrum of patients ranging from those who clearly benefit from ductal closure (as the authors in this article have described) to those who do very poorly after closure because of pre-existing pulmonary hypertension and the subsequent development of right ventricular failure. Within the center of the spectrum lies a group of preemies for whom we have even less data. Many of these infants have echocardiographic and clinical evidence of bidirectional shunting or intermittent right to left shunting associated with the pulmonary hypertension of premature lung disease, or transiently associated with sepsis. Closure of the PDA in these infants removes the potential pop-off effect preventing right ventricular failure during transient elevation of the pulmonary vascular resistance. Yet failure to treat the PDA may contribute to progression of the lung disease and worsening pulmonary hypertension. There is currently little to no data supporting any particular management strategy for these difficult infants. Therefore we must rely on common sense and clinical judgment to guide us. At our institution we do not attempt to address PDAs in the presence of significant right to left shunting. Repeated echocardiographic evaluations on various levels of FiO2 can often help determine the reactivity of the pulmonary vascular bed and the contribution of primary pulmonary disease to any observed hypoxemia. With documented response to O2, we have usually proceeded with ductal closure and maintained tighter postoperative ventilatory management to prevent respiratory acidosis, along with liberalizing the utilization of oxygen therapy and nitric oxide. This relatively conservative approach has minimized our incidence of postoperative right ventricular failure that others have seen more commonly. Clearly we need to continue to investigate these issues and develop guidelines for these most complex patients.

Óxido nítrico inhalado como rescate en insuficiencia respiratoria del recién nacido inmaduro

Inhaled nitric oxide (iNO) is indicated in near-term (> 34 weeks' gestation) and term newborns with hypoxemic respiratory failure and persistent pulmonary hypertension, decreasing the need for extracorporeal membrane oxygenation support in at least 40 %. Currently the use of iNO has not been approved for premature neonates, and its therapeutic efficacy in this group remains controversial. However, it has been suggested that iNO may be helpful by improving oxygenation and reducing the need for aggressive mechanical ventilation in some cases of severe hypoxemic respiratory failure in preterm infants with inadequate response to conventional treatment. We report the cases of three hypoxemic preterm neonates unresponsive to conventional treatment in whom the use of iNO was effective in the management of hypoxemic respiratory failure.

Prediction of extubation failure in preterm infants

Objective: To identify whether the results of assessment of respiratory muscle strength or respiratory load were better predictors of extubation failure in preterm infants than readily available clinical data. Patients:...

Inhaled nitric oxide for respiratory failure in preterm infants.

Inhaled nitric oxide has been proven effective in term infants with hypoxic respiratory failure. The pathophysiology of respiratory failure, and the potential risks, differ substantially in preterm infants. Analysis of the efficacy and toxicities of inhaled nitric oxide in infants born before 35 weeks is therefore necessary. To determine whether, in preterm newborn infants (<35 weeks gestation) who have hypoxic respiratory failure, treatment with inhaled nitric oxide improves oxygenation within 2 hours and reduces the rates of death, bronchopulmonary dysplasia, intraventricular hemorrhage, or neurodevelopmental disability Standard methods of the Cochrane Neonatal Review Group were used. We searched MEDLINE, EMBASE, Healthstar and the Cochrane Controlled Trials Register from the Cochrane Library, using the following keywords: nitric oxide, clinical trial, newborn, and covering years from 1985 to 2000. In addition, we searched the abstracts of the Pediatric Academic Societies. Randomized and quasi randomized studies in preterm infants with hypoxic respiratory failure. Administration of inhaled nitric oxide. Clinically relevant outcomes that were analysed included death, bronchopulmonary dysplasia (defined as oxygen dependence at 36 weeks postconceptional age), intraventricular hemorrhage, long term neurodevelopmental outcome and short term effects on oxygenation. Standard methods of the Cochrane Neonatal Review Group were used. Two investigators extracted, assessed and coded separately all data for each study. Any disagreement was resolved by discussion. Three randomised controlled trials of inhaled nitric oxide therapy in preterm infants were found. One study consisted of infants determined to have a high risk of developing bronchopulmonary dysplasia. The second study consisted of infants with a 50% predicted mortality. The third study included term and preterm infants who had an oxygenation index of between 12.5 and 30, but randomised and analysed separately the preterm infants. No significant effect of inhaled nitric oxide on mortality or bronchopulmonary dysplasia was demonstrated. One study showed a reduction in days receiving assisted ventilation in the nitric oxide group, which was a secondary outcome. There was no evidence of effect on intraventricular hemorrhage incidence. There are no data on long term neurodevelopmental outcome. There may be short term improvements in oxygenation. The currently published evidence from randomized trials does not support the use of inhaled nitric oxide in preterm infants with hypoxic respiratory failure. There is a possible reduction in the severity of chronic lung disease (shortened duration of assisted ventilation). Because of lack of power, it is not possible to eliminate the possibility of substantial improvements in outcome. Further studies should be performed.

Prolonged versus short course of indomethacin for the treatment of patent ductus arteriosus in preterm infants.

Indomethacin is a prostaglandin inhibitor used to treat patent ductus arteriosus (PDA) in preterm infants. Although indomethacin produces ductal closure in the majority of cases, it is ineffective in up to 40% of patients. Furthermore, the ductus will re-open in up to 35% of infants who initially respond to the drug. A more prolonged course of indomethacin has been studied regarding the potential to achieve higher rates of ductal closure. To determine if a prolonged course of indomethacin (compared to a short course) reduces the rate of treatment failure in preterm infants with PDA without unwanted side-effects. The search included review of personal files, abstracts of conferences, and the following electronic databases: MEDLINE (1966 to April 2003), EMBASE (1974 to April 2003), and Oxford Database of Perinatal Trials, Cochrane Central Register of Controlled Trials (The Cochrane Library, Issue 3, 2003). No language restrictions were applied. 1) DESIGN AND POPULATION: Randomized or quasi-randomized controlled trials including preterm infants with PDA diagnosed on clinical and/or echocardiographic examination.2) INTERVENTION: Indomethacin treatment by any route given as a long course (four or more doses) vs a short course (three or fewer doses). 3) OUTCOMES: Report of at least one of the following outcomes: failure of PDA to close, need for re-treatment, PDA re-opening, PDA ligation, mortality, duration of assisted ventilation, chronic lung disease (CLD), duration of supplemental oxygen dependence, intraventricular hemorrhage (IVH) (all and severe), diminished urine output, increased serum creatinine, necrotizing enterocolitis (NEC), bleeding diathesis, retinopathy of prematurity (ROP), and duration of hospital stay. The three reviewers independently abstracted data from each study. Relative risk (RR) and Risk Difference (RD) with 95% confidence intervals (CI) using the fixed effect model for meta-analysis are reported. When a statistically significant RD was found, the number needed to treat (NNT) or number needed to harm (NNH) was also calculated with 95% CIs. A chi-square test was used to test for heterogeneity of results among included trials. Prolonged indomethacin treatment when compared to the short course resulted in a borderline statistically significant difference in PDA re-opening rate favoring the prolonged course [RR 0.54 (95% CI 0.3, 0.99); RD -0.12 (95% CI -0.24, -0.01); NNT = 8 (4, 100). There was no statistically significant treatment effect on PDA closure, re-treatment, or ligation rates. The prolonged course was associated with a decreased incidence of severe IVH [RR 0.49 (95% CI 0.25, 0.98); RD -0.12 (95% CI -0.24, -0.01); NNT 8 (4, 100)] and renal function impairment, as evidenced by a lower proportion of infants having an increased creatinine level [RR 0.52 (95% CI 0.34, 0.81); RD -0.20 (95% CI -0.33, -0.08); NNT 5 (3, 13)]. However, there was a trend for the prolonged course to increase the proportion of infants with CLD in the one trial reporting this outcome [RR 2.24 (95% CI 0.98, 5.12); RD 0.24 (95% CI 0.01, 0.47)]. Prolonged as compared to short course of indomethacin for the treatment of PDA in preterm infants has a borderline effect on reducing the rate of PDA re-opening and it may be associated with an increased risk for CLD. However, prolonged course of indomethacin appears to reduce the risk of severe intracranial hemorrhage and renal impairment in this population. Definitive recommendations about the preferred duration of indomethacin therapy, i.e. prolonged versus short course, for the treatment of PDA in premature infants cannot be made based on the current findings of this review. There is a paucity of data on optimal duration of indomethacin therapy for the treatment of PDA, in particular for ELBW premature infants. Future randomized clinical trials should include this high risk population and investigate the premature infants. Future randomized clinical trials should include this high risk population and investigate the possibility of tailoring duration of therapy (prolonged versus short) to individual response in terms of echocardiographic findings and/or prostaglandin levels, focusing on clinically significant outcomes and potential complications associated with either strategy. In addition, factors which may influence treatment effect need to be taken into account when designing such studies.

Growth Failure in Preterm Infants with Cerebral Palsy

Developmental and Behavioral Pediatrics| April 01 1999 Growth Failure in Preterm Infants with Cerebral Palsy AAP Grand Rounds (1999) 1 (4): 34. https://doi.org/10.1542/gr.1-4-34 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation Growth Failure in Preterm Infants with Cerebral Palsy. AAP Grand Rounds April 1999; 1 (4): 34. https://doi.org/10.1542/gr.1-4-34 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search toolbar search search input Search input auto suggest filter your search All PublicationsAll JournalsAAP Grand RoundsPediatricsHospital PediatricsPediatrics In ReviewNeoReviewsAAP NewsAll AAP Sites Search Advanced Search Topics: cerebral palsy, infant, premature Source: Rogers B, Andrus J, Msall ME, et al. Growth of preterm infants with cystic periventricular leukomalacia. Dev Med & Child Neuro. 1998;40:580–586. The cause of growth failure in children with cerebral palsy is poorly understood. Rogers and colleagues studied the growth patterns of an unselected cohort of 51 preterm infants with cystic periventricular leukomalacia (CPVL) with a gestational age of <33 weeks admitted to Children’s Hospital of Buffalo from 1988 to 1993. Of 41 survivors, 39 developed CP. Twenty-four infants had oral feeding impairments which included requiring over 30 minutes to complete a feeding, coughing and gagging while feeding, abnormal chewing, or failure to drink from a cup by 2 years of age. Eighteen subjects developed growth failure during infancy. Of these, the majority (13 of 18) had signs of protein-calorie undernutrition using the Waterlow1 criteria and a growth pattern suggestive of chronic malnutrition in which body mass is gradually lost until linear growth is compromised. The presence of an oral feeding impairment was found to be the sole risk factor for the occurrence of growth failure (p<0.005). Birth weight, gestational age, sex, multiple birth and selected neonatal complications were not significantly associated with growth failure. The authors call for close, early monitoring of feeding abilities and growth in preterm infants, particularly when risk factors for CP such as CPVL are present. This study supplies compelling evidence that undernutrition is associated with growth failure in preterm infants with CPVL and CP, and underscores the need for systematic monitoring of growth and feeding. Despite the relatively small study cohort, a retrospective design, and the lack of raw data on nutritional intake or body composition, this study is noteworthy for its methodological strengths including a well-defined population, inclusion of head circumference data, longitudinal evaluations in the earliest months of life, and the use of well-established norms for undernutrition. The authors note that nutritional disorders are not as frequently recognized and treated in children with CP as they are in children with Crohn’s disease or cystic fibrosis.2 In children with CP, nutritional deficiencies can often be corrected and result in improved growth and cognitive, behavioral and social outcomes.3,4 The authors studied former preemies with CP due to cystic periventricular leukomalacia. While their conclusion cannot be extrapolated to all children with CP, their results do argue for a careful assessment of feeding and protein-calorie intake in any child with CP before growth failure is evident. A larger, equally rigorous study of children with CP from other causes is needed. You do not currently have access to this content.

Growth of preterm infants with cystic periventricular leukomalacia.

Etiology of the high rates of growth failure in children with cerebral palsy (CP) remains unclear. The purpose of this study was to evaluate the relation between growth failure in preterm infants with cystic periventricular leukomalacia (CPVL) and neonatal health complications. The population consisted of all preterm infants (51) with a gestational age of <33 weeks who were admitted to the Children's Hospital of Buffalo from 1988 to 1993 and who had CPVL. Out of the 41 survivors with CPVL who were followed, 39 developed CP and 18 developed growth failure during infancy. At the time of greatest growth failure, the majority (72%) of infants had signs of undernutrition as defined by the Waterlow (1972) classification. Oral feeding impairment was the sole risk factor for the occurrence of growth failure. Undernutrition appears to be important in the occurrence of growth failure in preterm infants with CPVL and CP.