Necrotizing enterocolitis (NEC) is a devastating intestinal disease that affects premature or very low birth weight infants. Symptoms may include poor feeding, bloating, decreased activity, blood in the stool, vomiting of bile, bowel death, multiorgan failure, and even death.The exact cause is unclear. However, several risk factors have been identified. Consistently described risk factors include formula feeding, intestinal dysbiosis, low birth weight, and prematurity. Maternal factors such as chorioamnionitis, cocaine abuse, in utero growth restriction, intrahepatic cholestasis during pregnancy, increased body mass index, lack of prenatal steroids, mode of delivery, placental abruption, preeclampsia, and smoking have not been consistently implicated with the development of NEC. Other risk factors potentially implicated include congenital heart disease, birth asphyxia, exchange transfusion, and prelabor rupture of membranes. The underlying mechanism is believed to involve a combination of poor blood flow and infection of the intestines. Diagnosis is based on symptoms and confirmed with medical imaging.Prevention includes the use of breast milk and probiotics. Treatment includes bowel rest, orogastric tube, intravenous fluids, and intravenous antibiotics. Surgery is required in those who have free air in the abdomen. A number of other supportive measures may also be required. Complications may include short-gut syndrome, intestinal strictures, or developmental delay.About 7% of those who are born prematurely develop NEC; however the odds of an infant developing this illness is directly related to the intensive care unit they are placed in. Onset is typically in the first four weeks of life. Among those affected, about 25% die. The sexes are affected with equal frequency.
V2 receptors maintain plasma osmolality and are coupled to aquaporin channels in the collecting ducts of kidneys where they regulate AVP levels. Conivaptan hydrochloride functions by antagonizing V2 receptors in the renal collecting ducts and thus causing aquaresis or water secretion. Typical pharmacodynamic effects of the drug are an increase in  net fluid loss, increase in  urine output, and decrease in the osmolality of urine. Conivaptan inhibits its own metabolism in the body, displaying non-linear pharmacokinetics. About 99% of conivaptan found is bound to human plasma proteins over the range of 10 ng/mL to 1000 ng/mL. The mean half-life of the drug is 5 hours and mean clearance is 15.2 L/hr. Adverse effects
Most adverse reactions to conivaptan are found at the site of infusion. Other complications include blood and lymphatic system disorders, gastrointestinal disorders, metabolism and nutrition disorders, psychiatric disorders as well as vascular disorders. There is risk of too rapid correction of hyponatremia causing fatal osmotic demyelination syndrome. Chemistry
Conivaptan hydrochloride is an off-white or a pale yellow power with a solubility of 0.25 mg/mL in water at 23 °C. The injectable formulation consists of 20 mg conivaptan hydrochloride, 0.4 g ethanol, 1.2 g propylene glycol and water. Development and commercialization
Conivaptan hydrochloride was discovered by Yamanouchi Pharmaceuticals and marketed by Astellas. Yamanouchi Pharmaceuticals filed a new drug application to the FDA for conivaptan hydrochloride to treat hyponatremia on 2 February 2004. On 1 December, Yamanouchi received approval for investigational hyponatremia treatment using conivaptan hydrochloride.