Curcuma longa turmeric , Camellia sinensis green tea , and Glycyrrhiza glabra licorice are reviewed in this installment. A large portion of antibiotics are dispensed by pediatricians treating common outpatient infectious diseases. Ethical and medicolegal aspects of percutaneous endoscopic gastrostomy tube placement and provision of artificial nutritional therapy. We comply with the HONcode standard for trustworthy health information - verify here. Accessed 13 July
Enteral feeding is a mainstay of nutritional support in pediatric burn patients and is considered the ideal route for caloric and nutrient supplementation. Pediatric Critical Care Fourth Edition , Enteral feeding provides nutrients to support growth and metabolism but also, even in very small amounts, promotes intestinal development and function. Feeding stimulates secretion of gut hormones and regulatory peptides, motility, and intestinal growth.
These effects are most prominent with feeding of maternal milk, which also contributes to gut health by facilitating and augmenting the innate gut immune system and establishing a more normal gut microbiome, which is increasingly being recognized as essential for both short- and long-term health. Enteral feeding, even in small amounts, helps to prevent the cholestasis that often develops with TPN.
Enteral feedings are contraindicated in those infants with active NEC or hemodynamic instability marked hypotension. Caution must be exercised when considering enteral feeding of infants with poor intestinal motility or ileus, such as those who are postoperative, on extracorporeal membrane oxygenation, or heavily sedated with narcotics.
Use of paralytics, per se, is not an absolute contraindication to enteral feeding because nondepolarizing neuromuscular blocking agents block transmission at the neuromuscular junction in skeletal muscle but not in smooth muscle. Giannone, in Gastrointestinal Tissue , Enteral feeding, especially formula feeding, is one of the most important risk factors for NEC.
The exact relationship between enteral feeding and NEC remains unclear, but the volume and rate of feeding advancement may play a role . In a recent observational study, enteral feeding with human milk exclusively was shown to reduce the incidence of NEC . Multiple variables such as the nature of feeds human milk vs formula feeding , time of initiation of enteral feeds, and the rate at which feeds are advanced are thought to affect the immature GI tract and lead to the development of NEC .
However, currently there is no consensus among healthcare professionals on feeding practices in preterm infants and there are wide variations in such practices across NICUs in the United States. Early enteral feeding improves outcome in critically ill patients, whereas inappropriate parenteral nutrition is associated with infections and other complications such as immune dysfunction. Neonates with CHD are prone to necrotizing enterocolitis NEC perhaps in part due to reduced splanchnic blood flow in a low cardiac output state coupled with systemic venous hypertension.
Therefore, neonates often have enteral feedings introduced slowly because NEC usually does not occur before the beginning of oral feedings. Similarly, some physicians limit enteral feedings in adults with very significant right ventricular dysfunction.
There are no specific data to support this practice. Enteral feeding may reduce the incidence of overt GI bleeding due to stress ulceration, but there are conflicting data. Continuous infusion of commercially available enteral feeding solutions pH of 6 to 7 are reported to neutralize gastric acid and raise the gastric intraluminal pH and may encourage the redistribution of blood flow to the mucosal layer. Tolerance of enteral nutrition is often poor in the critical care setting, and this may be one reason that clinical trials have been inconsistent with regard to cytoprotection.
As a result, enteral nutrition cannot be recommended as the sole method of prophylaxis against stress ulceration. Enteral feeding is the preferred method. Critical illness frequently is associated with atrophy of intestinal mucosa and gut-associated lymphoid tissue GALT , disruption of normal intestinal flora by antibiotics, ileus induced by a variety of drugs, and decreased production of gastric acid caused by proton pump inhibitors.
All of these factors can lead to barrier dysfunction in the gut. The result of this breakdown in intestinal structure and barrier function can lead to malabsorption and bacterial translocation. The term bacterial translocation describes the migration of bacteria from the gut lumen to the lymph tissue or bloodstream and has been implicated in the pathogenesis of sepsis and the septic inflammatory response syndrome.
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