Prolonged Total Parenteral Nutrition Research Articles

Bone Status and Early Nutrition in Preterm Newborns with and without Intrauterine Growth Restriction.

Intrauterine growth restriction (IUGR) together with preterm birth could be harmful to bone health. The aim of the study was to examine bone status in IUGR versus non-IUGR preterms and to analyze the nutritional management best correlated with its improvement. Newborns < 34 weeks of gestational age (wGA), 75 IUGR and 75 non-IUGR, admitted to the Neonatal Intensive Care Unit of the University Hospital of Padova were enrolled and monitored from birth until 36 wGA through anthropometry (weight, length, head circumference, lower limb length (LLL)), biochemistry, bone quantitative ultrasound assessment of bone status (metacarpus bone transmission time, mc-BTT, us) and nutritional intakes monitoring during parenteral nutrition. IUGR compared to non-IUGR showed lower mean mc-BTT (0.45 vs. 0.51, p = 0.0005) and plasmatic phosphate (1.45 vs. 1.79, p < 0.001) at birth. Mc-BTT at 36 wGA, though equal between groups, correlated in IUGR newborns with basal phosphate, mean total energy of the first week and month (positively) and days to reach full enteral feeding (negatively). Lower i.v. vitamin D intake, LLL and prolonged total parenteral nutrition predicted worse mc-BTT at 36 wGA in the enrolled infants. These results suggest that preterms and in particular IUGR newborns need special nutritional care to promote bone development.

Twin Premature Infants With Riboflavin and Biotin Deficiency Presenting With Refractory Lactic Acidosis, Rash, and Multiorgan Failure During Prolonged Parenteral Nutrition.

We are reporting monochorionic, diamniotic twin premature infants born at 25 weeks and 6 days gestation with riboflavin (vitamin B2) and biotin (vitamin B7) deficiency, while on prolonged total parenteral nutrition (TPN) during vitamin shortage. They presented initially with skin rash, lactic acidosis, and thrombocytopenia. Both twins progressed to severe respiratory failure, severe lactic acidosis, with refractory vasodilatory shock, pancytopenia, ischemic bowel injury, acute kidney injury, liver injury, and capillary leak syndrome leading to death of twin A. The surviving twin B was diagnosed with riboflavin and biotin deficiency that presented with abnormal metabolic work up suggestive of maple syrup urine disease, glutaric acidemia type 2, and X-linked adrenoleukodystrophy. Twin B was started on riboflavin and biotin supplementation at 41 days of life, with rapid improvement in clinical findings and laboratory abnormalities within days of starting biotin and riboflavin supplementation. He was discharged home in stable condition at 49 weeks of postmenstrual age.

Challenges in hyperglycemia management in critically ill patients with COVID-19.

Hyperglycemia is commonly associated with adverse outcomes especially in patients requiring intensive care unit stay. Data from the corona virus disease 2019 (COVID-19) pandemic indicates that individuals with diabetes appear to be at similar risk for COVID-19 infection to those without diabetes but are more likely to experience increased morbidity and mortality. The proposed hypothesis for hyperglycemia in COVID-19 include insulin resistance, critical illness hyperglycemia (stress- induced hyperglycemia) secondary to high levels of hormones like cortisol and catecholamines that counteract insulin action, acute cytokine storm and pancreatic cell dysfunction. Diabetic patients are more likely to have severe hyperglycemic complications including diabetic ketoacidosis and hyperosmolar hyperglycemic state. Management of hyperglycemia in COVID-19 is often complicated by use of steroids, prolonged total parenteral or enteral nutrition, frequent acute hyperglycemic events, and restrictions with fluid management due to acute respiratory distress syndrome. While managing hyperglycemia special attention should be paid to mode of insulin delivery, frequency of glucose monitoring based on patient and caregiver safety thereby minimizing exposure and conserving personal protective equipment. In this article we describe the pathophysiology of hyperglycemia, challenges encountered in managing hyperglycemia, and review some potential solutions to address them.

Difficulties in managing hyperglycemia in extremely low birth weight infants – case report

Introduction. Studies have shown that 60-80% of ex­tremely low birth weight (ELBW) newborns develop hy­per­gly­ce­mia in the first two weeks of life. The cause is usually iatrogenic, through high rates of exogenous glu­cose infusion from total parenteral nutrition (TPN). Other mechanisms are represented by insulin resistance due to the immaturity of enzyme systems, increased he­pa­tic pro­duc­tion of glu­cose, the inability to inhibit glu­co­neo­ge­ne­sis, and by the ef­fect of stressors through the action of cate­cho­la­mines. Hy­per­gly­cemia generates multiple harmful effects, which can be reduced with the help of insulin therapy, op­ti­mizing growth and avoiding fluid overload. Materials and method. We present the case of three ELBW newborns with neonatal respiratory distress, who required surfactant and invasive mechanical ventilation, along with prolonged TPN. The newborns developed persistent hyperglycemia in the first weeks of life (plasma glucose above 180 mg/dl) de­spite the decrease in glucose concentration and infusion rate, requiring insulin infusion. Results. In all three cases, it was relatively difficult to control the plasma glucose le­vels. Weight gain was satisfactory, but the patients pre­sen­ted multiple severe complications. Conclusions. The ma­nage­ment of metabolic complications of ELBW new­borns is im­portant due to the major implications in their prognosis and survival. A special interest has recently been given to the concept of cellular modulation in critical pe­riods of de­velopment and the influence in the subsequent oc­cur­rence of some diseases. Extrauterine adaptation in ELBW newborns involves biochemical and metabolic ad­just­ments, with immediate and long-term impact.

Vanishing gastroschisis with jejunal atresia and extreme short bowel syndrome: A case series

Background: Vanishing gastroschisis may occur due to spontaneous partial or complete closure of anterior abdominal wall defect around the viscera, leading to small bowel ischemia and resultant entry/exit level atresia and extremely short length of the remaining bowel. The prognosis is very poor, even after aggressive surgery, and requires prolonged total parenteral nutrition.&#x0D; Case Series: We report two female neonates, one with closed and another with closing vanishing gastroschisis, associated with jejunal atresia and extreme short bowel syndrome. In both patients, the antenatal scans showed gastroschisis without the evidence of vanishing gastroschisis. In both neonates, palliative surgeries were done. Both patients died after a few days due to short bowel syndrome and sepsis.&#x0D; Conclusion: When antenatally detected gastroschisis presents with closed or closing anterior abdominal wall defect, (vanishing gastroschisis), the parents/caregivers must be counseled about the poor prognosis of this condition. A tailored approach to either palliation or aggressive therapy is essential in this rare condition.

Wernicke Encephalopathy Due to Prolonged Total Parenteral Nutrition in A Child with Signet Ring Cell Gastric Carcinoma

Signet ring cell gastric carcinoma is extremely rare during childhood. One of the most important problems in these patients is nutritional difficulty and impairment, and these patients are often supported by total parenteral nutrition. Herein, the authors report a case of Wernicke encephalopathy due to prolonged total parenteral nutrition in a 13-year-old girl with diffuse gastric cancer with signet ring cell.

Retrospective Assessment of Selenium Status in High Risk Infants

Abstract Objectives Selenium (Se) is an essential trace mineral important in neonatal development that contributes to oxidative stress and the inflammatory response. Se deficiency in preterm infants is associated with late onset sepsis, bronchopulmonary dysplasia, poor neurodevelopmental outcomes, and retinopathy of prematurity. Current Se dosing in many US Neonatal Intensive Care Units is based on the amount of Se in term breastmilk. However, it is unclear if this is sufficient and higher levels may be needed to prevent or treat Se deficiency. Our goal was to evaluate if the current practice supplementing total parenteral nutrition (TPN) with sodium selenite 2 mcg/kg/d is sufficient at preventing Se deficiency in high risk infants. Methods This is a retrospective chart review of Se status at a level IV Children's Hospital NICU from January 1, 2017 to August 30, 2019. Infants were included if born from 22–42 weeks gestation and received TPN for &amp;gt;4 weeks. They were excluded if there was concern for active sepsis or bacterial illness at time of Se draw. Normal Se status was defined as 45–90 ng/mL for infants 0–2 months. Birth weight, IUGR status, gestational age, and % enteral feeds were evaluated. Se deficient infants received higher Se dosing at 5–7 mcg/kg/d. Repeat levels were evaluated after 4 weeks. Results are reported as mean ± SD. Results Se status was assessed for 39 infants. Average gestational age was 29.8 ± 5.36 weeks. Average birth weight was 1499 ± 837 g. At the time of first Se assessment, 78% of infants were Se deficient, with a mean Se level of 40.95 ± 12 ng/mL. Repeat Se levels on higher dosing was assessed in 23 infants. After &amp;gt;4 weeks of higher Se dosing, 35% of infants remained Se deficient, with a mean Se level of 54.04 ± 14 ng/mL. By t-test, statistically fewer infants were Se deficient on higher Se dosing (P &amp;lt; 0.0003). Conclusions Infants on prolonged TPN &amp;gt;4 weeks are at high risk for Se deficiency. Se dosing at 2 mcg/kg/day is insufficient in preventing deficiency for a majority of these babies. Higher Se dosing improved the percentage of Se sufficient infants, but a third remained deficient. Future studies are needed to prospectively determine if higher Se in TPN prevents Se deficiency. Funding Sources University of Colorado, Section of Neonatal-Perinatal Medicine.

Upper gastrointestinal hemorrhage is associated with poor outcomes among patients with acute cholangitis: a nationwide analysis.

Acute cholangitis (AC) and upper gastrointestinal hemorrhage (UGIH) are common emergencies encountered by gastroenterologists. We aimed to evaluate the impact of UGIH on in-hospital mortality, morbidity and resource utilization among patients with AC. Adult admissions with a principal diagnosis of AC were selected from the National Inpatient Sample 2010-2014. The exposure of interest was significant UGIH (requiring red blood cell transfusion). The primary outcome was in-hospital mortality. Secondary outcomes were significant UGIH's incidence, morbidity (shock, prolonged mechanical ventilation and total parenteral nutrition), and resource utilization (length of hospital stay and total hospitalization charges and costs). Confounders were adjusted for using propensity matching and multivariate regression analysis. A total of 50 375 admissions were included in the analysis, 747 of whom developed significant UGIH. After adjusting for confounders, the adjusted odds ratio (aOR) of in-hospital mortality for patients who developed UGIH was 7.1 (95% confidence interval: 2.1-23.9, P<0.01) compared with those who did not. Significant UGIH was associated with substantial increase in morbidity [shock: aOR: 4.1 (2.1-9.3), P<0.01, prolonged mechanical ventilation: aOR: 5.8 (2.2-12.4), P<0.01, total parenteral nutrition: aOR: 4.7 (1.9-10.7), P<0.01], and resource utilization [mean adjusted difference in: length of hospital stay: 7.01 (4.72-9.29), P<0.01 and total hospitalization charges: $81 818 ($58 109-$105 527), P<0.01 and costs: $25 230 ($17 805-$32 653), P<0.01]. Similar results were obtained using multivariate regression analysis. Onset of significant UGIH among patients hospitalized with AC has a detrimental effect on in-hospital mortality, morbidity and resource utilization.

Direct hyperbilirubinemia in newborns with gastroschisis.

Patients with gastroschisis and prolonged total (or partial) parenteral nutrition (PN) commonly develop direct hyperbilirubinemia (DH). To quantify the prevalence and severity of DH in newborns with gastroschisis and characterize the diagnostic work-up for DH in this patient population. Retrospective chart review of patients born with gastroschisis between 2005 and 2015 for the first 6 months of life. 29 patients were identified with gastroschisis. Mean gestational age and birthweight were 36.4 (± 1.8) weeks and 2.5 (± 0.6) kg. 41% were treated with primary reduction versus staged closure. Peak total and direct bilirubin (DB) levels were 10.17 ± 6.21mg/dL and 5.58 ± 3.94mg/dL, respectively. 23 patients (79.3%) were diagnosed with DH and 78.2% underwent additional work-up for hyperbilirubinemia consisting of imaging and laboratory studies, none of which revealed a cause for DH other than the presumed PN-associated cholestasis. In all patients, DB began to decline within 1-10 days of initiation of enteral feeds. DH is common in patients with gastroschisis and is unlikely to be associated with pathology aside from PN. Additional work-up may lead to unnecessary resource utilization. Case series with no comparison group, Level IV.

Paralysis Due to Thiamine and Copper Deficiencies Following Sleeve Gastrectomy Complicated by Oral Intolerance With Recurrent Pancreatitis

Worsening obesity and widespread availability of laparoscopic surgery has led to an increase in bariatric weight loss procedures with long term consequences including nutritional deficiencies more common after malabsorptive procedures such as gastric bypass and biliopancreatic diversion. This is a case of a restrictive procedure that led to unexpected nutritional deficiencies with lasting disability. A 30 year old woman with a history of vertical sleeve gastrectomy 16 months prior had complications of oral intolerance due to several bouts of pancreatitis with prolonged hospitalization and total parenteral nutrition (TPN). Five weeks after surgery she developed ascending numbness and tingling of the feet leading to falls and inability to walk. She was treated for multiple vitamin deficiencies including Dry Beriberi and had several balloon dilations of her sleeve eventually tolerating enteral feeding again. She was improving with physical therapy but recurrence of oral intolerance led to progression of numbness, tingling, and weakness to include her face, hands, and abdomen causing her to present to the ED. Labs revealed deficiencies of copper and riboflavin with borderline thiamine levels as well as toxic levels of pyridoxine. Exam revealed motor and sensory polyneuropathies with an escutcheon sign to the umbilicus and weakness of lower extremities with loss of vibration and proprioception. Nystagmus and memory loss were consistent with Wernicke's Encephalopathy as well. Endoscopy was unrevealing and gastrointestinal symptoms resolved prior to discharge six days later with improvement of the neuropathy of the hands and face after IV and oral thiamine and copper supplementation. Although not often associated with sleeve gastrectomy, copper deficiency is associated with zinc supplementation and use of TPN as in this case. Currently, the ASMBS (American Society of Metabolic and Bariatric Surgery) only recommends checking levels in patients with suggestive symptoms who have had malabsorptive procedures, but not in restrictive. But in 2017, a small retrospective study of patients with gastric sleeves showed those with neuropathy displayed a pattern of low thiamine, copper, and riboflavin with toxic levels of pyridoxine which also causes neuropathy. Perhaps copper levels should be routine post-operatively in restrictive bariatric procedures. Consistent vitamin toxicities also speaks to the need for reevaluation of vitamin supplementation regimens.

A Case of Iatrogenic Wernicke Encephalopathy Following Prolonged Total Parenteral Nutrition

Thiamine is a water-soluble vitamin that plays a role in the metabolism of glucose. Thiamine deficiency affects cardiovascular and nervous systems. Wernicke encephalopathy is characterized by oculomotor abnormalities, ataxia and cognitive deterioration caused by thiamine deficiency. It is most commonly observed in chronic alcoholics. It may also occur in patients who receive long-term total parenteral nutrition. In this study, we present the case of a 50-year-old male patient who underwent surgery for laryngeal cancer, who stayed in the intensive care unit for a prolonged period and received total parenteral nutrition because of the inability of oral intake.

The Effect of Hepatocyte Growth Factor on Intestinal Adaption in an Experimental Model of Short Bowel Syndrome

Introduction Short bowel syndrome (SBS) is a relatively uncommon syndrome which is defined as the functional loss of the 75% of normal short bowel length at least. To date, the standard therapy is the administration of total parenteral nutrition (TPN). However, long-term complications in patients with protracted PN are occurred. Intestinal transplantation is a potentially life-saving treatment for patients with severe SBS; its increased morbidity and mortality rates imply a careful preoperative consideration though. Moreover, the lack of compatible donor organs may delay significantly the transplantation. As a result, alternative therapies, like the administration of growth factors, in order to enhance intestinal adaptation acting as a bridge to transplantation have been emerged. The purpose of the present study is to evaluate the effect of hepatocyte growth factor (HGF) on structural intestinal adaptation, cell proliferation and apoptosis in a rat model of short bowel syndrome (SBS). Materials and Methods Thirty Sprague-Dawley female rats were divided into three groups, sham rats underwent bowel transection (group A); SBS rats underwent a 75% bowel resection (group B); and SBS/HGF rats underwent bowel resection and were treated with HGF (75 μg/kg/d) (group C) starting at fourth postoperative day. All rats were sacrificed at 15th postoperative day. Parameters of intestinal adaptation (body weight, villus height and crypt depth in jejunum and ileum), enterocyte proliferation and enterocyte apoptosis were determined. A microarray analysis of RNA extracted from ileal samples was also carried out. Statistical analysis was performed using ANOVA test, with P<0.05 considered statistically significant. Results Treatment with HGF (group C rats) resulted in significant increase in body weight compared to SBS rats (group B). The histopathologic analysis showed that jejunal and ileal villus height and crypt depth were significantly increased in HGF/SBS rats compared to SBS rats (36%, P<0.05 and 27%, P<0.05 respectively), showing that treatment with HGF enhanced the intestinal adaptation making intestinal absorption more efficient. Enterocyte proliferation was also significantly increased in HGF rats (21% P<0.05) compared to SBS rats; however we did not found any significant differences in enterocyte apoptosis rate between HGF/SBS and SBS rats. These findings indicate the augmentation of intestinal hyperplasia through HGF therapy. Microarray analysis of 22 genes showed that 12 genes were significantly up-regulated, and four genes were down-regulated in HGF/SBS rats compared to SBS rats; of note, some of these genes are involved in enterocyte proliferation/apoptosis pathway, indicating also that HGF therapy induces cell proliferation. Conclusion HGF emerges as a growth factor that enhances intestinal adaptation in patients with short bowel syndrome. A future use of HGF may facilitate the prolonged TPN therapy while patients wait for intestinal transplantation.

A Rare Complication Developing After Hematopoietic Stem Cell Transplantation: Wernicke's Encephalopathy.

Thiamine is a water-soluble vitamin. Thiamine deficiency can present as a central nervous system disorder known as Wernicke’s encephalopathy, which classically manifests as confusion, ataxia, and ophthalmoplegia. Wernicke’s encephalopathy has rarely been reported following hematopoietic stem cell transplantation. Herein, we report Wernicke’s encephalopathy in a patient with acute myeloid leukemia who had been receiving prolonged total parenteral nutrition after haploidentical allogeneic hematopoietic stem cell transplantation. To the best of our knowledge, this is the first case reported from Turkey in the literature.

Oligohydramnios and growth restriction do not portend worse prognosis in gastroschisis pregnancies

Objectives: Gastroschisis is a common abdominal wall defect. While most neonates have an excellent prognosis, complications do occur. Several risk factors for adverse neonatal outcomes have been identified, however, the impact of intrauterine growth restriction (IUGR) and oligohydramnios on neonatal morbidity and mortality has not been fully elucidated. Methods: In this retrospective cohort study of pregnancies complicated by gastroschisis at two tertiary-care centers during an eight-year period, maternal, fetal and neonatal data were analyzed to estimate the impact of IUGR and oligohydramnios upon neonatal outcomes. Adverse outcomes were defined as five-minute Apgar score <7, umbilical cord pH <7.12, neonatal sepsis, prolonged ventilator support, prolonged total parenteral nutrition, extended NICU stay, death and a composite of the above. Results: Among the 179 cases of gastroschisis, there were no differences in maternal demographics between cases with and without IUGR or oligohydramnios. Fetuses with oligohydramnios demonstrated a trend toward lower birthweight (p = 0.06). Small for gestational age infants showed a trend toward prolonged ventilator support (p = 0.06). Oligohydramnios and IUGR were otherwise not associated with adverse neonatal outcomes. Conclusions: While risk factors for adverse neonatal outcomes have been identified in pregnancies complicated by gastroschisis, IUGR and oligohydramnios do not appear to be among them.

Wernicke's encephalopathy after total parenteral nutrition in patients with Crohn's disease.

Micronutrient deficiencies in Crohn's disease (CD) patients are not uncommon and usually result in a combination of reduced dietary intake, disease-related malabsorption, and a catabolic state. Decreased serum thiamine levels are often reported in patients with CD. Wernicke's encephalopathy (WE) is a severe form of thiamine deficiency that can cause serious neurologic complications. Although WE is known to occur frequently in alcoholics, a number of non-alcoholic causes have also been reported. Here, we report two cases of non-alcoholic WE that developed in two severely malnourished CD patients who were supported by prolonged total parenteral nutrition without thiamine supplementation. These patients complained of sudden-onset ophthalmopathy, cerebellar dysfunction, and confusion. Magnetic resonance imaging allowed definitive diagnosis for WE despite poor sensitivity. The intravenous administration of thiamine alleviated the symptoms of WE dramatically. We emphasize the importance of thiamine supplementation for malnourished patients even if they are not alcoholics, especially in those with CD.

Micronutrient deficiencies in inflammatory bowel disease: trivial or crucial?

Patients with IBD, especially those with CD, are at a risk for a variety of nutritional deficiencies because of reduced nutrient intake or absorption, or increased nutrient losses.1 Nutritional deficiencies in IBD patients can be divided into those involving macronutrients (nutrients needed in large amounts) and those involving micronutrients (nutrients required in small quantities).2 In adults, deficiencies of micronutrients, including several water- and fat-soluble vitamins, and minerals including calcium, iron, and other trace minerals, are a common problem.3 Although the nutritional issues in IBD have become less common with advances in treatment and the greater proportions of patients attaining clinical remission, micronutrient deficiencies are still relatively common, particularly in CD patients with active small bowel disease or multiple resections. The major micronutrient deficiencies in IBD patients are associated with anemia (iron, folate, and vitamin B12), bone disease (calcium, vitamin D, and possibly vitamin K), hypercoagulability (folate, vitamin B6, and vitamin B12), wound healing (zinc, vitamin A, and vitamin C), and colorectal cancer risk (folate and possibly vitamin D and calcium).3 There are multiple mechanisms that can contribute to micronutrient deficiencies in IBD, such as decreased nutrient intake, increased intestinal loss, malabsorption, hypermetabolic state, drug interactions, and long-term total parenteral nutrition (TPN).4 Numerous vitamin and mineral deficiencies have been reported in IBD patients, with varying degrees of clinical significance.2 Vitamins and minerals are naturally occurring compounds that are required for diverse bodily functions, and must be obtained from the diet as they are not sufficiently synthesized by humans. Vitamins are organic compounds that can be classified as either water-soluble or fat-soluble. Water-soluble vitamins include thiamine (B1), riboflavin (B2), nicotinic acid/niacin (B3), pyridoxine (B6), cobalamin (B12), biotin, pantothenic acid, folic acid, and vitamin C (ascorbic acid). The fat-soluble vitamins (A, D, E, and K) are hydrophobic substances that are dissolved within fat droplets and must be broken down by lipases and combined with bile salts in the duodenum to form mixed micelles.3 In the current article, the authors reported two patients with CD who developed Wernicke's encephalopathy (WE) after prolonged TPN.5 WE is a serious neurologic complication due to vitamin B1 (thiamine) deficiency. Thiamine deficiency also can cause peripheral neuropathy and cardiomyopathy. Thiamine is found in multiple dietary sources (eggs, meats, bread, and nuts), and its absorption mainly occurs in the jejunum through varying degrees of active and passive transport, depending on body stores and the luminal concentrations of the vitamin.3 A recent study showed that thiamine deficiency may be more common in CD patients than in controls.6 This study was performed on 54 CD patients whose disease was in clinical remission, and were compared with 25 healthy controls. In CD patients, dietary thiamine intake was significantly lower than that in controls and low serum vitamin B1 was found in around one-third of CD patients. Both of the two cases of the present report had extensive small bowel involvement and severe malnutrition state, with a very low BMI.5 Although multiple factors contribute to micronutrient deficiencies in IBD, some nutrients are digested and absorbed within specific locations in the gastrointestinal tract, and the activity and location of a patient's intestinal disease determines the risk for specific micronutrient deficiencies. Normally, more than 95% of vitamins and minerals from food are absorbed in the proximal small bowel, usually by the mid-jejunum.3 Patients who had undergone small bowel resection are also at a risk for micronutrient deficiencies, the nature of which depends on the extent and location of the resected bowel.7 The two patients of the present report had a relatively short duration of fasting and peripheral TPN (3 weeks and 17 days, respectively).5 As the authors mentioned, despite the relatively short period of fasting, the active inflammation caused by active CD, underlying malnourished state, infection, and surgery led to an increased thiamine requirement and to the development of WE. The use of long-term parenteral nutrition can lead to deficiencies in any micronutrient not added in sufficient quantities, and the reported deficiencies include those of vitamins, minerals, and trace elements such as Zn2+, Cu2+, selenium, and chromium.3 Fortunately, the symptoms in the two patients of the current report resolved without any neurologic sequelae after thiamine replacement.5 As the authors also mentioned, WE is diagnosed clinically and is a disease with no characteristic and pathognomonic abnormalities in diagnostic studies. Thus, the development of neurologic disability in IBD patients with malnutrition should raise the suspicion of thiamine deficiency. Micronutrient deficiencies, especially those of vitamins and essential trace elements, in IBD patients are common and associated with a complicated course of disease. IBD patients usually do not present overt symptoms of vitamin or micronutrient deficiency. Therefore, a high suspicion for micronutrient deficiencies is advocated for the timely treatment and prevention of irreversible complications.

Bone metabolism in very preterm infants receiving total parenteral nutrition: do intravenous fat emulsions have an impact?

Very preterm infants (<32 weeks' gestation) are at high risk for impaired skeletal development because of factors that limit the provision of extrauterine nutrients. Cumulative net deficiencies of calcium, phosphorus, docosahexaenoic acid (DHA), and arachidonic acid (ARA) are evident in these infants after prolonged administration of total parenteral nutrition (TPN). This is significant because minerals as well as metabolites of DHA and ARA are important modulators of bone cell differentiation, lengthening of bone, and bone matrix deposition. Furthermore, diets containing only precursors of DHA and ARA result in suboptimal skeletal growth. With the emergence of new intravenous lipid emulsions, it is important to understand the impact of fatty acids on bone metabolism in the third trimester in order to optimize the provision of TPN in very preterm infants. The purpose of this review is to evaluate current evidence regarding intravenous lipid emulsions and bone metabolism in very preterm infants receiving prolonged TPN and to identify areas of research needed.

Delivery planning for pregnancies with gastroschisis: findings from a prospective national registry

The purpose of this study was to determine the influence of planned mode and planned timing of delivery on neonatal outcomes in infants with gastroschisis. Data from the Canadian Pediatric Surgery Network cohort were used to identify 519 fetuses with isolated gastroschisis who were delivered at all tertiary-level perinatal centers in Canada from 2005-2013 (n = 16). Neonatal outcomes (including length of stay, duration of total parenteral nutrition, and a composite of perinatal death or prolonged exclusive total parenteral nutrition) were compared according to the 32-week gestation planned mode and timing of delivery with the use of the multivariable quantile and logistic regression. Planned induction of labor was not associated with decreased length of stay (adjusted median difference, -2.6 days; 95% confidence interval [CI], -9.9 to 4.8), total parenteral nutrition duration (adjusted median difference, -0.2 days; 95% CI, -6.4 to 6.0), or risk of the composite adverse outcome (relative risk, 1.7; 95% CI, 0.1-3.2) compared with planned vaginal delivery after spontaneous onset of labor. Planned delivery at 36-37 weeks' gestation was not associated with decreased length of stay (adjusted median difference, 5.9 days; 95% CI, -5.7 to 17.5), total parenteral nutrition duration (adjusted median difference, 3.2 days; 95% CI, -7.9 to 14.3), or risk of composite outcome (relative risk, 2.3; 95% CI, 0.8-5.4) compared with planned delivery at ≥38 weeks' gestation. Infants with gastroschisis who were delivered after planned induction or planned delivery at 36-37 weeks' gestation did not have significantly better neonatal outcomes than planned vaginal delivery after spontaneous onset of labor and planned delivery at ≥38 weeks' gestation.

The outcomes of a standardized approach to managing metabolic bone disease of prematurity

Metabolic bone disease (MBD) of prematurity is an increasingly well-recognized complication of pre-term birth. Despite this, there is limited evidence for the optimum method for assessing and monitoring bone health and appropriate supplementation. This study assesses the effectiveness of the MBD protocol at Monash Health nurseries (Clayton, Dandenong and Casey) in infants born under 32 weeks’ gestation between November 2012 and January 2014. Preliminary data of 93 infants (mean gestational age (GA) 29 weeks (24-32.3weeks), birth weight (BW) 1279.4g (553-2512g)) were assessed. Risk factors assessed include 8.8% IUGR infants (n=56), 12.9% maternal pre-eclampsia, 7.5% necrotising enterocolitis (NEC) episodes and exposure to medications as follows:caffeine (84.9%; mean 42 days), diuretics (23.7%; mean 13.8 days) and steroids (2.2%). Preterm infants received 14.3 days of total parenteral nutrition (TPN) on average, with the majority on fortified expressed breast milk once enteral feeding was established. Initial MBD screen was performed for 80.6% infants (mean age 36.6 days) with only 24.7% having repeated monitoring (mean age 67.9 days). 6.5% had Alkaline phophosphatase (ALP) levels >500U/I initially (range 143827U/l), reducing to 1.1% (range 173-573U/I). Average Tubular Resorption of Phosphate (TRP) was 79.7% (n=71). The majority of infants were on Vitamin D 400units/day. 23.6%(n=22) commenced phosphate supplements (mean duration 41 days) and 15.1%(n=14) commenced calcium supplements (mean duration 53.2 days). Average birth length was 38cm (10-50centile) with evidence of slowing growth velocity (mean follow up length 49cm (<3centile) at mean age 79.9 days). Five infants were identified with fractures however two were from birth trauma and two suspected non-accidental injury. One patient had an incidental finding of fractured femur with multiple risk factors for MBD including very low birth weight (700g), NEC episodes requiring prolonged antibiotic therapy (69 days), TPN (48 days), caffeine (88 days) and diuretic use (22 days). Significant difference (p<0.001) is noted between phosphate-treatment and untreated groups for both GA and BW: Median 27weeks and 929g for treated subjects versus 29.6weeks and 1343g if untreated. In the phosphate-treatment group, ALP levels improved (mean pretreatment414U/l and post-treatment264U/l, p=0.0006) and difference in phosphate levels were also significant with p=0.003. Between phosphate-treatment group versus untreated group, differences were insignificant for ALP (p=0.05) and phosphate levels (p=0.09), though this may reflect insufficient subsequent MBD screens (treatment group, n=15 versus untreated group, n=7). Further evaluation is anticipated to help improve MBD understanding in this high-risk cohort particularly given morbidity associated with MBD occult fractures. In addition, secondary outcomes would include cost efficiency of MBD surveillance and identifying optimal supplemental therapy.

The outcomes of a standardized approach to managing metabolic bone disease of prematurity

Metabolic bone disease (MBD) of prematurity is an increasingly well-recognized complication of pre-term birth. Despite this, there is limited evidence for the optimum method for assessing and monitoring bone health and appropriate supplementation. This study assesses the effectiveness of the MBD protocol at Monash Health nurseries (Clayton, Dandenong and Casey) in infants born under 32 weeks’ gestation between November 2012 and January 2014. Preliminary data of 93 infants (mean gestational age (GA) 29 weeks (24-32.3weeks), birth weight (BW) 1279.4g (553-2512g)) were assessed. Risk factors assessed include 8.8% IUGR infants (n=56), 12.9% maternal pre-eclampsia, 7.5% necrotising enterocolitis (NEC) episodes and exposure to medications as follows:caffeine (84.9%; mean 42 days), diuretics (23.7%; mean 13.8 days) and steroids (2.2%). Preterm infants received 14.3 days of total parenteral nutrition (TPN) on average, with the majority on fortified expressed breast milk once enteral feeding was established. Initial MBD screen was performed for 80.6% infants (mean age 36.6 days) with only 24.7% having repeated monitoring (mean age 67.9 days). 6.5% had Alkaline phophosphatase (ALP) levels >500U/I initially (range 143-827U/l), reducing to 1.1% (range 173-573U/I). Average Tubular Resorption of Phosphate (TRP) was 79.7% (n=71). The majority of infants were on Vitamin D 400units/day. 23.6%(n=22) commenced phosphate supplements (mean duration 41 days) and 15.1%(n=14) commenced calcium supplements (mean duration 53.2 days). Average birth length was 38cm (10-50thcentile) with evidence of slowing growth velocity (mean follow up length 49cm (<3rdcentile) at mean age 79.9 days). Five infants were identified with fractures however two were from birth trauma and two suspected non-accidental injury. One patient had an incidental finding of fractured femur with multiple risk factors for MBD including very low birth weight (700g), NEC episodes requiring prolonged antibiotic therapy (69 days), TPN (48 days), caffeine (88 days) and diuretic use (22 days). Significant difference (p<0.001) is noted between phosphate-treatment and untreated groups for both GA and BW: Median 27weeks and 929g for treated subjects versus 29.6weeks and 1343g if untreated. In the phosphate-treatment group, ALP levels improved (mean pre-treatment414U/l and post-treatment264U/l, p=0.0006) and difference in phosphate levels were also significant with p=0.003. Between phosphate-treatment group versus untreated group, differences were insignificant for ALP (p=0.05) and phosphate levels (p=0.09), though this may reflect insufficient subsequent MBD screens (treatment group, n=15 versus untreated group, n=7). Further evaluation is anticipated to help improve MBD understanding in this high-risk cohort particularly given morbidity associated with MBD occult fractures. In addition, secondary outcomes would include cost efficiency of MBD surveillance and identifying optimal supplemental therapy.