Soham Dasgupta

Amniotic fluid: Source of trophic factors for the developing intestine

The gastrointestinal tract (GIT) is a complex system, which changes in response to requirements of the body. GIT represents a barrier to the external environment. To achieve this, epithelial cells must renew rapidly. This renewal of epithelial cells starts in the fetal life under the influence of many GIT peptides by swallowing amniotic fluid (AF). Development and maturation of GIT is a very complex cascade that begins long before birth and continues during infancy and childhood by breast-feeding. Many factors like genetic preprogramming, local and systemic endocrine secretions and many trophic factors (TF) from swallowed AF contribute and modulate the development and growth of the GIT. GIT morphogenesis, differentiation and functional development depend on the activity of various TF in the AF. This manuscript will review the role of AF borne TF in the development of GIT.

Protective effects of amniotic fluid in the setting of necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is the most common life threatening condition affecting preterm infants. NEC occurs in 1–5% of all neonatal intensive care admissions and 5–10% of very low birth weight infants. The protective role of human breast milk (BM) has been well established. It has also been shown that amniotic fluid (AF) and BM have many similarities in terms of presence of growth and other immune-modulatory factors. This finding led to the initial hypothesis that AF may exert similar protective effects against the development of NEC, as does BM. Multiple studies have elucidated the presence of growth factors in AF and the protective effect of AF against NEC. Studies have also described possible mechanisms how AF protects against NEC. At present, research in this particular area is extremely active and robust. This review summarizes the various studies looking at the protective effects of AF against the development of NEC. It also provides an insight into future directions, the vast potential of AF as a readily available biologic medium, and the ethical barriers that must be overcome before using AF.

Dilated Cardiomyopathy Induced by Chronic Starvation and Selenium Deficiency

Protein energy malnutrition (PEM) has been rarely documented as a cause of cardiovascular abnormalities, including dilated cardiomyopathy. Selenium is responsible for antioxidant defense mechanisms in cardiomyocytes, and its deficiency in the setting of PEM and disease related malnutrition (DRM) may lead to exacerbation of the dilated cardiomyopathy. We report a rare case of a fourteen-year-old boy who presented with symptoms of congestive heart failure due to DRM and PEM (secondary to chronic starvation) along with severe selenium deficiency. An initial echocardiogram showed severely depressed systolic function consistent with dilated cardiomyopathy. Aggressive nutritional support and replacement of selenium and congestive heart failure medications that included diuretics and ACE inhibitors with the addition of carvedilol led to normalization of the cardiac function within four weeks. He continues to have significant weight gain and is currently completely asymptomatic from a cardiovascular standpoint.

NTproBNP as a surrogate biomarker for early screening of pulmonary hypertension in preterm infants with bronchopulmonary dysplasia

ObjectivePulmonary hypertension (PH) is a known complication of bronchopulmonary dysplasia (BPD). This study aimed to determine the utility of serial N-Terminal pro-Brain Natriuretic Peptide (NTproBNP) levels in the screening of BPD associated PH (BPD-PH) in preterm infants.Study designInfants with birth weight <1500 g and <30 week corrected gestational age (CGA) were followed with serial NTproBNP levels and echocardiograms (ECHO). They were divided into control, BPD and BPD-PH groups. Statistical analyses included repeated measures analysis of variance and receiver operator curve (ROC) generation.ResultsInfants in the BPD-PH and BPD group had significantly elevated NTproBNP levels as compared to the control group. ROC curves for NTproBNP at 28 weeks CGA provided a cut-point of 2329 pg/ml and 578.1 pg/ml for detection of BPD-PH and BPD, respectively.ConclusionsNTproBNP appears to be a good screening tool to determine the onset of BPD-PH as early as 28 weeks CGA.

Case 2: Progressive Abdominal Pain in a 3-year-old Boy with Repaired Congenital Diaphragmatic Hernia

1. Soham Dasgupta, MD* 2. Ha Nguyen, MD* 3. Buria Naeem, MD* 4. Olivia Ginnard, MD* 5. Vidit Bhargava, MD* 6. Lane Shirley, MD* 1. *Department of Pediatrics, University of Texas Medical Branch at Galveston, Galveston, TX A 3-year-old boy presents to the emergency department (ED) with abdominal pain. His medical history includes a left congenital diaphragmatic hernia (repaired shortly after birth) and a small atrial septal defect. The generalized abdominal pain started 3 days ago and is associated with several episodes of nonbloody and nonbilious emesis. Evaluation at an outside ED 3 days ago included abdominal radiography (showing a large stool burden) and abdominal ultrasonography (showing a normal appendix). He was discharged with medication for constipation. However, he continues to have pain, emesis, and progressive abdominal distention. Radiographs at our ED today reveal unchanged stool burden as well as an incidental left-sided pleural effusion and lower lobe opacification (Fig 1), for which he is immediately admitted to the hospital for further evaluation. Figure 1. Chest radiograph shows left-sided pleural effusion, lower lobe opacification, and dilated loops of bowel. Initial vital signs include a temperature of 96.6°F (35.9°C) (axillary), respiratory rate of 30 breaths/min, heart rate of 140 beats/min, blood pressure of 108/56 mm Hg, and oxygen saturation of 98% on room air. He exhibits respiratory distress, with grunting, subcostal retractions, and diminished air entry in the left lung base. There is significant abdominal distention, with diffuse tenderness, normal bowel sounds, and tympanic percussion from the …

Mother With Diabetes Mellitus and Infant With Hypertrophic Obstructive Cardiomyopathy: Milrinone Precluded Need for Extracorporeal Membrane Oxygenation

A female infant was born at 38 weeks to a mother with gestational diabetes mellitus (Hemoglobin A1c 6.7%) via an elective C-section for fetal macrosomia (birth weight 5560 g; >99.9%). The prenatal ultrasound was only significant for a large for gestational age fetus without any structural cardiac anomalies. Within the first 2 hours, the infant developed hypoglycemia and required respiratory support (nasal cannula) for respiratory distress and hypoxemia. Neonatal hyperinsulinemia (297 uIU/mL [1.9–23 uIU/mL]) confirmed maternal gestational diabetes mellitus as the cause of the hypoglycemia (growth hormone and cortisol levels were normal for age). The infant was electively intubated for worsening respiratory status. A transthoracic echocardiogram showed severe biventricular hypertrophy, especially the interventricular septum (1.2 cm at the end of systole; z score=4.55) causing left ventricular outflow tract (LVOT) obstruction with a gradient of 22 mm Hg (Figure 1; Movies I and II in the Data Supplement). The left ventricular cavity size was remarkably diminished. A color Doppler showed a …

An Unusual Mechanism of Closure of Muscular Ventricular Septal Defects

Ventricular septal defects (VSDs) are the most common congenital heart defects. Most of the small or moderate size (<6 mm) muscular VSDs close spontaneously within the first two years of life. The usual mechanism of spontaneous closure involves muscular tissue encroachment with superimposed fibrosis or primary fibrous tissue formation around the margins of the defect. We describe an unusual mechanism of spontaneous closure of a muscular VSD.

Coarctation of the Aorta as a Complication of Surgical Ligation of Patent Ductus Arteriosus in a Premature Infant

Surgical ligation of a patent ductus arteriosus (PDA) is a commonly performed procedure. Complications are infrequent and most commonly include recurrent laryngeal nerve injury and rarely ligation of left pulmonary artery. We report a case of accidental ligation of the descending thoracic aorta leading to a clinically significant coarctation.

Junctional Bradycardia as Early Sign of Digoxin Toxicity in a Premature Infant with Congestive Heart Failure due to a Left to Right Shunt

Introduction Congestive heart failure due to left to right cardiac shunt is usually managed medically with diuretics, angiotensin converting enzyme inhibitors, and, in some cases, with the addition of digoxin. Case We report a 31-week gestation premature male infant who did not respond to such treatment and developed hyperaldosteronism and severe hypokalemia secondary to activation of the renin angiotensin aldosterone system. The hypokalemia was not responsive to intravenous KCL supplementation and induced digoxin toxicity despite a relatively normal digoxin level. The earliest signs of digoxin toxicity in the patient were junctional rhythm and bradycardia. The discontinuation of digoxin and the administration of digoxin specific immunoglobulin fragments (Fab) reversed those changes. The addition of spironolactone (an aldosterone antagonist) had a dramatic effect, resulting in clinical improvement of the patient coupled with normalization of Q4 serum and urine electrolytes. Conclusion Serum Digoxin level alone may fail as an independent guide in the diagnosis of digoxin toxicity when hypokalemia is present. In premature infants with congestive heart failure and hypokalemia, addition of an aldosterone antagonist should be considered.