The economic burden of gastroschisis: costs of a birth defect.

Background: Intestinal dysfunction and feeding intolerance are comorbidities associated with the abdominal wall birth defect of gastroschisis (GS). These factors contribute to prolonged hospitalization in this population of patients. The purpose of this study was to evaluate the economic burden on a state and national level.

Improving gastroschisis outcomes: does birth place matter?

Purpose: Babies born in the hospital where they obtain definitive surgical care do not require transportation between institutions and may have shorter time to surgical intervention. Whether these differences result in meaningful improvement in outcomes has been debated. A multi-institutional retrospective study was performed comparing outcomes based on birthplace.

Effects of nonocclusive mesenteric hypertension on intestinal function: implications for gastroschisis-related intestinal dysfunction.

Introduction: Infants with gastroschisis (GS) have significant morbidity from dysmotility, feeding intolerance, and are at increased risk of developing intestinal failure. Although the molecular mechanisms regulating GS-related intestinal dysfunction (GRID) are largely unknown, we hypothesized that mechanical constriction (nonocclusive mesenteric hypertension (NMH)) from the abdominal wall defect acts as a stimulus for GRID. The purpose of this study was to determine the effect of NMH on intestinal function and inflammation.

Strategies for modulating the inflammatory response after decompression from abdominal compartment syndrome.

Background: Management of the open abdomen is an increasingly common part of surgical practice. The purpose of this review is to examine the scientific background for the use of temporary abdominal closure (TAC) in the open abdomen as a way to modulate the local and systemic inflammatory response, with an emphasis on decompression after abdominal compartment syndrome (ACS).

Methods: A review of the relevant English language literature was conducted.

An evidence-based review of a Lentinula edodes mushroom extract as complementary therapy in the surgical oncology patient.

The purpose of this review is to present the currently published evidence regarding the use, efficacy, potential mechanisms of action, and results of published clinical trials regarding the use of a Lentinula edodes mushroom-derived extract (active hexose correlated compound) as complementary therapy in patients with cancer. The authors explore the current preclinical and clinical evidence as it relates to this topic and its potential use in the surgical oncology patient. There has been a growing interest in stimulation of the immune system in trauma, cancer, and surgical patients in general.

Evaluating the potential role of nitric oxide as a mediator of hydrostatic edema mediated intestinal contractile dysfunction.

Background: Administration of L-nil, a selective inhibitor of inducible nitric oxide synthase (iNOS), improves ileus in an animal model of resuscitation induced intestinal edema. The purpose of this study was to elucidate the iNOS/nitric oxide (NO) signal transduction pathway in intestinal edema.

Materials And Methods: Male Sprague Dawley rats were divided into two groups; CONTROL and RESUS+VH (edema, 80 cc/kg normal saline (resuscitation) with mesenteric venous hypertension).

Hydrostatic intestinal edema induced signaling pathways: potential role of mechanical forces.

Background: Hydrostatic intestinal edema initiates a signal transduction cascade that results in smooth muscle contractile dysfunction. Given the rapid and concurrent alterations in the mechanical properties of edematous intestine observed with the development of edema, we hypothesize that mechanical forces may serve as a stimulus for the activation of certain signaling cascades. We sought to examine whether isolated similar magnitude mechanical forces induced the same signal transduction cascades associated with edema.

Intestinal ischemic preconditioning after ischemia/reperfusion injury in rat intestine: profiling global gene expression patterns.

Objective: Intestinal ischemia/reperfusion (IR) injury involves activation of inflammatory mediators, mucosal necrosis, ileus, and alteration in a variety of gene products. Ischemic preconditioning (IPC) reduced all the effects of intestinal injury seen in IR. In an effort to investigate the molecular mechanisms responsible for the protective effects afforded by IPC, we sought to characterize the global gene expression pattern in rats subjected to IPC in the setting of IR injury.

Intestinal edema: effect of enteral feeding on motility and gene expression.

Objective: Edema formation, inflammation, and ileus in the intestine are commonly seen in conditions like gastroschisis, inflammatory bowel disease, and cirrhosis. We hypothesized that early enteral feeding would improve intestinal transit. We also wanted to study the impact of early enteral feeding on global gene expression in the intestine.

Pretreatment with bone morphogenetic protein-7 (BMP-7) mimics ischemia preconditioning following intestinal ischemia/reperfusion injury in the intestine and liver.

Intestinal ischemia/reperfusion (I/R) injury has been shown to cause intestinal mucosal injury and adversely affect function. Ischemic preconditioning (IPC) has been shown to protect against intestinal I/R injury by reducing polymorphonuclear leukocyte infiltration, intestinal mucosal injury, and liver injury, and preserve intestinal transit. Bone morphogenetic protein 7 (BMP-7) has been shown to protect against I/R injury in the kidney and brain.

Hypertonic saline reverses stiffness in a Sprague-Dawley rat model of acute intestinal edema, leading to improved intestinal function.

Introduction: Acute edema induced by resuscitation and mesenteric venous hypertension impairs intestinal transit and contractility and reduces intestinal stiffness. Pretreatment with hypertonic saline (HS) can prevent these changes. Changes in tissue stiffness have been shown to trigger signaling cascades via stress fiber formation.

Measurement of intestinal edema using an impedance analyzer circuit.

Background: Acute intestinal edema adversely affects intestinal transit, permeability, and contractility. Current resuscitation modalities, while effective, are associated with development of acute intestinal edema. Knowledge of levels of tissue edema would allow clinicians to monitor intestinal tissue water and may help prevent the detrimental effects of edema.

Hypertonic saline resuscitation prevents hydrostatically induced intestinal edema and ileus.

Objective: We have shown that acute edema induced by mesenteric venous hypertension (MV-HTN) impairs intestinal transit and reduces the standardized engineering measures of intestinal stiffness (elastic modulus) and residual stress (opening angle). We hypothesized that hypertonic saline (7.5%) would reverse these detrimental effects of acute edema.

Peroxisome proliferator-activated receptor gamma mediates protection against cyclooxygenase-2-induced gut dysfunction in a rodent model of mesenteric ischemia/reperfusion.

Cyclooxygenase (COX)-2 has been identified as an important mediator elaborated during ischemia/reperfusion, with pro- and anti-inflammatory properties having been reported. As the role of COX-2 in the small intestine remains unclear, we hypothesized that COX-2 expression would mediate mesenteric ischemia/reperfusion-induced gut injury, inflammation, and impaired transit and that these deleterious effects could be reversed by the selective COX-2 inhibitor, N-[2-(cyclohexyloxy)-4-nitrophenyl] methanesulphanamide (NS-398). Additionally, we sought to determine the role of peroxisome proliferator-activated receptor gamma (PPARgamma) in mediating protection by NS-398 in this model.

Ketamine inhibits lipopolysacharide (LPS) induced gastric luminal fluid accumulation.

Introduction: Lipopolysacharide (LPS) causes gastrointestinal ileus and gastric luminal fluid accumulation. Ketamine, an anti-inflammatory anesthetic agent attenuates accumulation of luminal fluid. However, its effects on gastrointestinal transit induced by endotoxemia are unknown.

Effects of primary and secondary intra-abdominal hypertension on mesenteric lymph flow: implications for the abdominal compartment syndrome.

Intra-abdominal hypertension leading to abdominal compartment syndrome complicates trauma resuscitation. The purpose of this study was to determine the effect of primary (1 degrees) and secondary (2 degrees) intra-abdominal hypertension (IAH) on hemodynamics, intestinal fluid balance, and mesenteric lymph flow. Anesthetized dogs were instrumented with vascular catheters, intra-abdominal manometer, and mesenteric lymphatic fistulae.

Ischemic preconditioning protects against gut dysfunction and mucosal injury after ischemia/reperfusion injury.

Mesenteric ischemia/reperfusion (IR) damages the gastrointestinal epithelia and impairs gut function. Ischemic preconditioning (IPC) has been shown to protect organs against IR injury. We hypothesized that IPC protects the gut from IR injury.

Resuscitation-induced gut edema and intestinal dysfunction.

Background: Mesenteric venous hypertension and subsequent gut edema play a pivotal role in the development of intra-abdominal hypertension. Although gut edema is one cause of intra-abdominal hypertension, its impact on gut function is unknown. The purpose of this study was to create a model of acute hydrostatic gut edema and to evaluate its effect on gut motility and barrier function.