The Bacteriology of Acute Cholecystitis: Comparison of Bile Cultures and Clinical Outcomes in Diabetic and Non-Diabetic Patients.

BACKGROUND: Acute cholecystitis is one of the most common acute surgical diseases. Diabetic patients have been shown to have an increased risk for gallbladder disease, but the correlation between the severity of gallstone disease and diabetes is still debated. The aim of this study is to examine the possible difference in the disease process between patients with diabetes mellitus (DM) and those without. PATIENTS AND METHODS: A retrospective study was conducted of all patients who underwent percutaneous cholecystostomy between 2005 and 2015 at Emek Medical Center, Afula, Israel. Demographic and medical history including data on bile and blood culture results, antimicrobial susceptibility, and clinical outcomes were retrieved from patient files. RESULTS: The cohort included 272 patients. Mean age was 68 years old, 50.74% were male and 43.75% had diabetes mellitus. Bile cultures were obtained from 252 (92.64%) patients and were positive in 134 (53.2%) patients. In 11 patients (4%) two pathogens were isolated. Blood cultures obtained from 231 patients and were positive in 35 (15.2%). Escherichia coli was the most common isolate, and was seen in 22.3% of positive bile cultures and 40% of blood cultures. Although diabetic patients had significantly more positive bile cultures, the severity of the disease, according to the Tokyo guidelines, was not higher. CONCLUSIONS: Acute cholecystitis was neither more severe nor had significant difference in bacteriological properties when comparing diabetic patients to non-diabetic ones.

Prefrontal Oxytocin is Involved in Impairments in Prefrontal Plasticity and Social Memory Following Acute Exposure to High Fat Diet in Juvenile Animals.

Juvenility represents a critical developmental phase during which exposure to a high fat diet (HFD) can severely modify cognitive and emotional functioning. The purpose of this study was to address how short and acute exposure to a HFD during juvenility affects social memory recognition and prefrontal long-term potentiation (LTP). As LTP and social memory depend on the neuromodulator oxytocin (OXY) and due to its role in metabolism, we also examined the effects of OXY in mediating HFD-induced alterations in social memory and LTP. Our results show that short exposure to a HFD during juvenility impairs social preference memory and prefrontal LTP. Interestingly, whereas systemic injections of OXY reversed the impairments in HFD-fed animals and impaired LTP and memory in control animals; prefrontal injections of the OXY agonist TGOT reversed the effects in HFD animals without affecting control animals. Exposure to HFD was associated with a reduction in the levels of OXY in the prefrontal compared to control animals. Interestingly, the restoration of social memory by TGOT in HFD animals was also associated with normalization of OXY in the prefrontal. These results point to a role that prefrontal OXY has in mediating the effects of HFD on memory and plasticity.

Different mechanisms underlie stress-induced changes in plasticity and metaplasticity in the prefrontal cortex of juvenile and adult animals: Emotional-induced metaplasticity in the prefrontal cortex.

Metaplasticity is the dynamic regulation of the ability to induce activity-dependent synaptic plasticity and is governed by the prior history of the synapses. Previous reports by others and us have shown that behavioral stress induces a form of emotional metaplasticity that affects the ability to induce LTP in the subiculum-medial prefrontal cortex pathway, which depends on NMDA receptors (NMDAr). However, studies addressing the effects of stress on LTP and metaplasticity have mainly focused on the adult animal. Here we compared the effects of exposure to stress on the induction of LTP in adult and juvenile animals and examined whether a low dose of NMDAr antagonist (MK801) that does not affect LTP per se would differentially affect stress-induced metaplasticity in adult and juvenile animals. Our findings show that exposure to the elevated platform differentially affects the induction of LTP in adult and juvenile animals. Specifically, whereas exposure to stress resulted in impaired LTP in adult animals, it resulted in enhanced LTP in juvenile animals. Similarly, while MK801 failed to inhibit the induction of LTP in both age groups, it resulted in inhibition of stress-induced enhanced LTP in juvenile animals, but did not affect stress-induced impaired LTP in adult animals. Taken together, these findings demonstrate that emotional metaplasticity is differently dependent on NMDAr in adult and juvenile animals that may stem from developmental differences in the NMDA receptor representation. These results further confirm that the mechanisms of plasticity following stress are distinctive in the two groups of age.

Shock associated with endothelial dysfunction in omental microvessels.

BACKGROUND: Impaired microvascular function leads to a poor outcome in a variety of medical conditions. Our aim was to determine whether vasodilator responses to acetylcholine (Ach) are impaired in human omental arterioles from patients with severe trauma. MATERIALS AND METHODS: Patients with massive blood loss and severe shock requiring damage control procedures were included. Tissues were collected at the first (FEL) and the second explorative laparotomy (SEL). Control tissues were collected from nontrauma patients. Freshly isolated 50-200-µm-diameter omental arterioles were analysed using videomicroscopy. Dihydroethidine and DCF-DA fluorescence were used to assess reactive oxygen species (ROS) production. MnTBAP was used to determine the contribution of excess vascular superoxide contribution to endothelial dysfunction. RESULTS: After constriction (30-50%) with endothelin-1, dilation to graded doses of Ach (10-9 -10-4 M) was greater in control vessels compared to FEL and SEL (max dilation at 10-4 M (MD) = 25 ± 3%, n = 8; and 59 ± 8%, n = 8, respectively, and controls MD = 93 ± 10%, n = 6, P < 0·05). Fluorescence imaging of ROS production showed significant increases in superoxide (225·46 ± 12·86; 215·77 ± 10·75 vs. 133·75 ± 7·26, arbitrary units; P < 0·05) and peroxide-related ROS (240·8 ± 20·42; 234·59 ± 28·86, vs. 150·78 ± 15·65, arbitrary units; P < 0·05), in FEL and SEL microvessels compared to control, respectively. FEL pretreated with MnTBAP demonstrated significant improvement in Ach-induced vasodilation (25·5 ± 3·0% vs. 79·5 ± 8·2%; P < 0·05). CONCLUSIONS: Severe shock associated with microvascular endothelial dysfunction enhances production of ROS in human omental tissues. The altered flow regulation may contribute to a mismatch between local blood supply and demand, exacerbating abnormal tissue perfusion and function.

The intermediate-conductance calcium-activated potassium channel KCa3.1 contributes to atherogenesis in mice and humans.

Atherosclerosis remains a major cause of death in the developed world despite the success of therapies that lower cholesterol and BP. The intermediate-conductance calcium-activated potassium channel KCa3.1 is expressed in multiple cell types implicated in atherogenesis, and pharmacological blockade of this channel inhibits VSMC and lymphocyte activation in rats and mice. We found that coronary vessels from patients with coronary artery disease expressed elevated levels of KCa3.1. In Apoe(-/-) mice, a genetic model of atherosclerosis, KCa3.1 expression was elevated in the VSMCs, macrophages, and T lymphocytes that infiltrated atherosclerotic lesions. Selective pharmacological blockade and gene silencing of KCa3.1 suppressed proliferation, migration, and oxidative stress of human VSMCs. Furthermore, VSMC proliferation and macrophage activation were reduced in KCa3.1(-/-) mice. In vivo therapy with 2 KCa3.1 blockers, TRAM-34 and clotrimazole, significantly reduced the development of atherosclerosis in aortas of Apoe(-/-) mice by suppressing VSMC proliferation and migration into plaques, decreasing infiltration of plaques by macrophages and T lymphocytes, and reducing oxidative stress. Therapeutic concentrations of TRAM-34 in mice caused no discernible toxicity after repeated dosing and did not compromise the immune response to influenza virus. These data suggest that KCa3.1 blockers represent a promising therapeutic strategy for atherosclerosis.

Primary small cell type of non-Hodgkin lymphoma of the colon: a case report.

INTRODUCTION: Primary lymphoma of the colon is exceedingly rare and comprises 0.2-1% of all colon tumors. The most common subtype of lymphoma in the colon is non-Hodgkin lymphoma. Symptoms are often nonspecific, and treatment varies between chemotherapy alone and a combination of surgery and chemotherapy. CASE PRESENTATION: We describe a case of a Ashkenazi Jew patient who presented in the typical way that carcinoma of the colon might present but turned out to have a very rare type of tumor in both its histology and its location. CONCLUSION: There was apparent discordance between the relative bulkiness and gross appearance of the tumor with the unrevealing result of the biopsies, demanding a high level of suspicion as to the actual presence and possible type of such a tumor in the future.

Preoperative Exclusive Total Parental Nutrition is Associated with Clinical and Laboratory Remission in Severe Active Crohn's Disease-A Pilot Study.

BACKGROUND: The effect of 1-3 months of preoperative exclusive total parental nutrition (TPN) in active Crohn's disease (CD) patients is not well established. We investigated the efficacy of exclusive TPN in active CD patients. METHODS: In a retrospective multi-visit study with data according to our standard care therapy, we assessed clinical and laboratory remission to refractory CD with exclusive preoperative TPN. Inclusion required exclusive preoperative home TPN without additional oral intake for 1-3 months prior to planning surgery. RESULTS: Twenty preoperative CD patients (65% male; 35% female) were on exclusive TPN. The mean age of the cohort was 30.8 ± 11.6 years. Mean duration of preoperative TPN treatment was 73 days (range: 24-142 days). Most patients had terminal ileal (35%) or ileocolonic CD (30%), and with stricturing (B2) phenotype. All 20 patients had significant clinical improvement in all disease activity indices at the end of preoperative TPN (baseline vs. post TPN): HBI 14.5 vs. 4.0 (p = 0.001); BMI 19.2 vs. 19.7 kg/m2 (p = 0.017); CRP 57.2 vs. 10.3 mg/L (p = 0.001); Fecal calprotectin (FC) 672 vs. 200 (µg/g); albumin 2.7 vs. 3.6 g/dL (p = 0.001). Two patients (10%) no longer required surgery after completion of exclusive TPN. CONCLUSION: Exclusive preoperative TPN was found to provide significant improvement in nutritional status, and clinical and laboratory remission in severe active Crohn's patients.

Acute exposure to a high-fat diet in juvenile male rats disrupts hippocampal-dependent memory and plasticity through glucocorticoids.

The limbic circuit is still undergoing maturation during juvenility and adolescence, explaining why environmental and metabolic challenges during these developmental periods can have specific adverse effects on cognitive functions. We have previously shown that long-term exposure (8-12 weeks) to high-fat diet (HFD) during adolescence (from weaning to adulthood), but not at adulthood, was associated with altered amygdala and hippocampal functions. Moreover, these HFD effects were normalized by treatment with glucocorticoid receptor (GR) antagonists. Here, we examined in male rats whether acute exposure (7-9 days) to HFD during juvenility [from postnatal day (PND) 21 to PND 28-30] or adulthood (from PND 60 to PND 67-69) is sufficient to affect hippocampal functions and whether it is also dependent on GRs activation. Juvenile HFD abolished both hippocampal synaptic plasticity, assessed through in vivo long-term potentiation (LTP) in CA1, and long-term hippocampal-dependent memory, using object location memory (OLM). No effect of HFD was observed in short-term OLM suggesting a specific effect on consolidation process. In contrast, adult HFD enhanced in vivo LTP and OLM. Systemic application of GR antagonist alleviated HFD-induced LTP and OLM impairments in juveniles. These results suggest that acute exposure to HFD during juvenility is sufficient to impair hippocampal functions in a GR-dependent manner. Interestingly, this effect depends on the developmental period studied as acute exposure to HFD at adulthood did not impair, but rather enhanced, hippocampal functions.

A novel safe approach to laparoscopic colorectal cancer resection in patients with ventriculoperitoneal shunt: report of two cases and literature review.

There is ongoing challenges regarding the safety of performing laparoscopic surgery with the presence of ventriculoperitoneal (VP) shunts, especially in patients treated for cancer disease. To date, only one case has been reported in the English literature. Herein, we report an additional two cases of patients with previous insertion of a VP shunt, diagnosed with colon cancer. Both our patients underwent successful laparoscopic colectomies, without clamping or removal of the VP shunt, with no reported perioperative complications or postoperative neurological deficits. Laparoscopic bowel resection for cancer, in patients with a pre-existing VP shunt, could be considered a potentially safe and feasible procedure. Furthermore, due to the increasing number of patients with VP shunts, additional case reports and investigations are warranted to further confirm safety of this procedure.

Radiation induces endothelial dysfunction in murine intestinal arterioles via enhanced production of reactive oxygen species.

OBJECTIVE: Endothelial dysfunction and vascular dysregulation contribute to the pathological effects of radiation on tissues. The objectives of this study were to assess the acute effect of irradiation on acetylcholine (Ach)-induced dilation of gut submucosal microvessels. METHODS AND RESULTS: Rats were exposed in vivo to 1 to 9 cGy in 3 fractions per week on alternate days for 3 successive weeks for a total dose of up to 2250 cGy. Submucosal microvessels were isolated after varying levels of irradiation. Diameters of isolated vessels were measured using videomicroscopy, and the dose-response relationship to Ach was determined. Dihydroethidine and 2', 7'-dichlorodihydrofluorescein diacetate fluorescent probes were used to assess reactive oxygen species (ROS) production. After constriction (30% to 50%) with endothelin, dilation to graded doses of Ach (10(-9)-10(-4) M) was observed in control vessels (maximal dilation [MD] 87+/-3%; n=7). However, Ach-induced dilation was reduced in vessels from irradiated rats (MD=3+/-9%; n=7; P= or <0.05 versus controls). Significant increases in superoxide and peroxides were observed in irradiated microvessels. Irradiated microvessels pretreated with superoxide dismutase-mimetic demonstrated significant improvement in Ach-induced vasodilation compared with irradiation alone, suggesting that superoxide contributes to impaired dilation to Ach after irradiation. CONCLUSIONS: Radiation induces acute microvascular dysfunction in the resistance arterioles of the intestine. Enhanced ROS contribute to this dysfunction and therefore may represent a novel therapeutic target to minimize radiation toxicity in the gut.

Compression gastrointestinal anastomosis.

The creation of anastomoses between various parts of the GI tract is a major task in the daily practice of oncological, reconstructive and transplant surgery. The most widely used anastomosing techniques today involve the use of sutures or metal titanium staples. Both techniques involve foreign material penetrating the tissue and evoking localized inflammatory response, tissue injury and breaking of mucosal barriers that may facilitate bacterial growth within the anastomotic line, increasing the propensity to anastomotic-related morbidity. Different types of compression devices were successfully used clinically in the past. The history and evolving characteristics of this technology is reviewed. Nitinol-based solutions for the creation of compression anastomosis are evaluated as a possible potential for revolutionary impact on the current surgical methods and anastomosing technology in the alimentary tract and beyond.

Sentinel node detection in an animal study: evaluation of a new portable gamma camera.

We tested the capacity of a newly developed portable gamma camera to precisely locate sentinel nodes by injecting a radiotracer. Two sets of experiments were performed on eight pigs under general anesthesia. 99mTc-Nanocolloid and dye complex was injected in the submuscular layer of the small bowel in the first set and subcutaneously in the knee region in the second set of experiments. Image acquisition of the sentinel nodes was performed with the Camera placed at various angles. A mosaic of images was obtained encompassing the injection sites, lymphatic pathways, and sentinel lymph nodes. Three-dimensional visualizations were obtained, allowing the precise location and complete excision of these nodes. The use of the portable gamma camera allowed the rapid visualization of the lymphatic pathways leading from the injection sites to the sentinel nodes and precise location of these nodes. The Camera was also useful to verify the complete removal of the labeled target tissues.

Endothelium-derived microparticles induce endothelial dysfunction and acute lung injury.

Acute lung injury (ALI) carries a high mortality in critically ill patients. Recent reports correlate elevated concentrations of endothelium-derived microparticles (EMPs) with diseases of endothelial dysfunction. Many of these diseases have ALI sequelae. We hypothesize that EMPs contribute to endothelial cell (EC) dysfunction and development of ALI. To test this hypothesis, we treated isolated vessels with EMPs and examined changes in vasodilation. Endothelial cell cultures were incubated with EMPs and examined for changes in stimulated nitric oxide (*NO) production and nitric oxide synthase (eNOS) activation. Finally, EMPs were injected into rats and mice and lungs examined for ALI. In both mouse and human ex vivo vessel preparations, we found a marked attenuation of endothelium-mediated vasodilation after EMP treatment (4 x 10(6)/mL). This dysfunction was not corrected by pretreatment of EMPs with free radical scavengers. Coincubation of EMPs with EC cultures yielded a three-fold reduction in A23187-stimulated *NO release. Western analysis of these cells showed a corresponding decrease in eNOS phosphorylation at Ser1179 and a decrease in hsp90 association. Measurements of lung permeability, myeloperoxidase activity, and histology of EMPs-treated Brown Norway rats demonstrated pulmonary edema, neutrophil recruitment, and compromise of the endothelial-alveolar barrier as a second hit phenomenon. In C57BL/6 mice, exogenous EMPs caused a significant rise in pulmonary capillary permeability both as a primary and secondary injury. These findings demonstrate EMPs are capable of inducing significant lung injury at pathophysiologically relevant concentrations. Endothelium-derived microparticles inhibit endothelium-mediated vasodilation and *NO generation from eNOS. Once elucidated, EMP mechanisms of inducing ALI and endothelial dysfunction may present new therapeutic targets.

The intestinal microvasculature as a therapeutic target in inflammatory bowel disease.

Chronic inflammation is a complex biologic process which involves immune as well as non-immune cells including the microvasculature and its endothelial lining. Growing evidence suggests that the microvasculature plays an integral role in the pathophysiology of inflammatory bowel disease (IBD; Crohn's disease and ulcerative colitis). The microvasculature contributes to chronic inflammation through altered leukocyte recruitment, impaired perfusion, and angiogenesis leading to tissue remodeling. These diverse areas of IBD microvascular biology represent therapeutic targets that are currently undergoing investigation.

Novel mechanism of vasodilation in inflammatory bowel disease.

OBJECTIVE: Endothelium-dependent dilation to acetylcholine (Ach) is reduced in mucosal arterioles from patients with inflammatory bowel disease (IBD). The contributions of both nitric oxide (NO) and endothelial-derived hyperpolarizing factor (EDHF) are decreased. We hypothesized that the remaining dilation results from products of cyclooxygenase. METHODS AND RESULTS: High-performance liquid chromatography (HPLC) was used to isolate eicosanoid vasodilator products and videomicroscopy was used to examine vasomotor responses in human mucosal arterioles from subjects with or without IBD undergoing bowel resection surgeries. In subjects without IBD, Ach constricted (-52%+/-10%) arterioles devoid of endothelium. Indomethacin (INDO) (cyclooxygenase inhibitor) had no effect. In contrast, Ach dose-dependently dilated both intact and endothelial denuded arterioles from patients with IBD. The dilation was converted to constriction by INDO (-54%+/-9%; P<0.05 versus non-IBD) or by BWA868C (PGD2 receptor antagonist). Only in arterioles from subjects with IBD did Ach produce an arachidonic acid metabolite that comigrated on HPLC with PG D2 (PGD2). Exogenous PGD2 dilated (max=66%+/-4%) IBD arterioles. CONCLUSIONS: In arterioles from IBD patients, Ach-mediated dilation shifts from endothelial production of NO and EDHF to nonendothelial generation of a PG, likely PGD2. This is a novel dilator mechanism arising from nonendothelial vascular tissue that compensates for loss of endothelium-dependent dilation. PGD2 appears to be important in regulating mucosal blood flow in patients with IBD, implicating potentially detrimental effects from nonsteroidal antiinflammatory drugs.

Magnetic resonance-guided focused ultrasound surgery using an enhanced sonication technique in a pig muscle model.

THE PURPOSE OF THIS STUDY: To evaluate the safety and efficacy of an enhanced magnetic resonance-guided focused ultrasound (MRgFUS) emission protocol that results in more extensive treatment by increasing the volume of each focal ablation using the same energy. MATERIALS AND METHODS: Six pigs were treated with an MRgFUS system combined with real-time MR, for imaging and temperature mapping, with 102 "enhanced" and 97 "regular" focal ablations performed on both buttock muscles. Real-time imaging, temperature mapping, and acoustic reflected spectrum data enabled immediate evaluation of the results. MR contrast-enhanced images and pathology examinations were used for confirmation. RESULTS: The location of the ablated volume by "enhanced" sonication is predictable, with a maximum possible shift of 6 mm toward, and 3 mm away, from the transducer. The ablated volume after enhanced sonication was, on average, 1.8 times larger than after a regular sonication of the same energy. Pathology results showed the same thermally induced damage patterns in the enhanced sonications and the regular sonications. CONCLUSION: Accelerated MRgFUS with enhanced sonication is a safe, controllable, and more effective tissue ablative modality than standard sonication. This new technology may significantly reduce the length of tumor ablation procedures. (Isn't the new technology you're talking about MRgFUS? If so, you don't need to repeat it at the end of this sentence.).

L-4F, an apolipoprotein A-1 mimetic, dramatically improves vasodilation in hypercholesterolemia and sickle cell disease.

BACKGROUND: Hypercholesterolemia and sickle cell disease (SCD) impair endothelium-dependent vasodilation by dissimilar mechanisms. Hypercholesterolemia impairs vasodilation by a low-density lipoprotein (LDL)-dependent mechanism. SCD has been characterized as a chronic state of inflammation in which xanthine oxidase (XO) from ischemic tissues increases vascular superoxide anion (O2*-) generation. Recent reports indicate that apolipoprotein (apo) A-1 mimetics inhibit atherosclerosis in LDL receptor-null (Ldlr-/-) mice fed Western diets. Here we hypothesize that L-4F, an apoA-1 mimetic, preserves vasodilation in hypercholesterolemia and SCD by decreasing mechanisms that increase O2*- generation. METHODS AND RESULTS: Arterioles were isolated from hypercholesterolemic Ldlr-/- mice and from SCD mice that were treated with either saline or L-4F (1 mg/kg per day). Vasodilation in response to acetylcholine was determined by videomicroscopy. Effects of L-4F on LDL-induced increases in endothelium-dependent O2*- generation were determined on arterial segments via the hydroethidine assay and on stimulated endothelial cell cultures via superoxide dismutase-inhibitable ferricytochrome c reduction. Effects of L-4F on XO bound to pulmonary arterioles and content in livers of SCD mice were determined by immunofluorescence. Hypercholesterolemia impaired vasodilation in Ldlr-/- mice, which L-4F dramatically improved. L-4F inhibited LDL-induced increases in O2*- in arterial segments and in stimulated cultures. SCD impaired vasodilation, increased XO bound to pulmonary endothelium, and decreased liver XO content. L-4F dramatically improved vasodilation, decreased XO bound to pulmonary endothelium, and increased liver XO content compared with levels in untreated SCD mice. CONCLUSIONS: These data show that L-4F protects endothelium-dependent vasodilation in hypercholesterolemia and SCD. Our findings suggest that L-4F restores vascular endothelial function in diverse models of disease and may be applicable to treating a variety of vascular diseases.

Continuous fluid resuscitation for treatment of uncontrolled hemorrhagic shock following massive splenic injury in rats.

We have previously observed that bolus fluid resuscitation in uncontrolled hemorrhagic shock induced by solid organ injury leads to increased blood loss and mortality. In the present investigation, we studied the effect of continuous fluid resuscitation on the hemodynamic response and survival following massive splenic injury (MSI) in rats. The animals were randomized into 11 groups: group 1, sham-operated; group 2, MSI untreated; group 3, MSI treated with 17.5 mL/kg/h of Ringers lactate (RL) solution (RL-17.5); group 4, MSI treated with 35 mL/kg/h RL (RL-35); group 5, MSI treated with 70 mL/kg/h RL (RL-70); group 6, MSI treated with 7.5 mL/kg/h of 7.5% NaCl (HTS-7.5); group 7, MSI treated with 15 mL/kg/h of 7.5% NaCl (HTS-15); group S, MSI treated with 30 mL/kg/h of 7.5% NaCl (HTS-30); group 9, MSI treated with 7.5 mL/kg/h 6% hydroxyethyl starch (HES-7.5); group 10, MSI treated with 15 mL/kg/h 6% hydroxyethyl starch (HES-15); and group 11, MSI treated with 30 mL/kg/h 6% hydroxyethyl starch (HES-30). MSI in untreated group 2 was followed by a fall of mean arterial pressure (MAP) to 50.1 +/- 6.7 mmHg (P < 0.001) in 15 min. Mean survival time (MST) was 99.5 +/- 16.6 min, and total blood loss (TBL) was 37.8% +/- 2.6% of blood volume. Fluid treatment with increasing volumes of RL in groups 3, 4, and 5 was followed by a gradual increase in TBL compared with untreated animals, and MST remained unchanged. Increasing volumes of HTS infusion in groups 6, 7, and 8 was also followed by incease in TBL, but MST remained unchanged except for an increase to 123.0 +/- 20.5 min (P < 0.05) in group 6. Increasing volumes of HES in groups 9, 10, and 11 was also followed by increase in TBL, but MST remained unchanged. In conclusion, continuous infusion of LR, HTS, and HES following massive splenic injury resulted in a significant increase in intra-abdominal bleeding, but survival time in the first hour following injury remained unchanged in contrast to bolus fluid infusion, which increases early mortality.

Radiographic underestimation of small bowel stricturing Crohn's disease: a comparison with surgical findings.

BACKGROUND: The purpose of this study was to determine the accuracy of barium radiography compared with intraoperative evaluation with passage of a balloon catheter for assessment of stricturing Crohn's disease (CD). METHODS: After institutional review board approval, we retrospectively reviewed a tertiary inflammatory bowel disease center's consecutive records of surgical patients between 1998 and 2003 with small intestinal CD to compare the number of strictures found at surgery with those identified preoperatively by barium imaging. Age, gender, prior surgical procedures, and steroid usage were recorded. By decision of the surgeons, all patients were treated with an identical approach that utilized intraluminal sizing with passage of a balloon-tipped catheter. RESULTS: In 118 patients, 230 strictures were identified by barium examination; 365 strictures were identified using the balloon catheter technique. Barium examination overestimated or underestimated the number of strictures in 43 of 118 patients (36%). Overall, barium radiography was least accurate in patients with strictures amenable to strictureplasty. Prior surgery and multiple strictures identified preoperatively by barium studies were found to decrease the accuracy of the barium examination, but the decrease did not reach statistical significance. After successful surgery for stricturing small intestinal CD, more than 90% of patients can successfully be weaned from their steroids within 3 months. Failure to be able to wean from steroids may suggest a missed stricture. CONCLUSIONS: Our data suggest that careful exploration and intraoperative, intraluminal testing of intestinal patency identify additional strictures compared with barium radiographs in a significant number of patients with CD undergoing small bowel surgical intervention.