Colonic Wall Thickening Research Articles

Magnetic resonance colonography in rats with TNBS-induced colitis: A feasibility and validation study

Magnetic resonance colonography (MRC) has been recently developed to assess bowel inflammation in inflammatory bowel disease (IBD) patients. Evaluating animal models of inflammation with MRC may be important in new drug-screening processes. The aim of this study was to assess the feasibility of MRC in colitic rats and confront it with model characteristics. Colitis was induced by rectal injection of trinitrobenzene-sulfonic acid (TNBS) in 13 rats while six rats received the vehicle. MRC was performed at day 2. Colon inflammation and production of inflammatory mediators were evaluated. Image quality was assessed by wall and motion artifacts. MRC criteria were bowel wall thickness, wall signal intensity on T2-weighted (T2w) and T1w images, the appearance of a target sign pattern, and irregular patterns of mucosal surface. MRC quality was good or excellent in 16/21 examinations with no difference between groups. Colitis rats were significantly different from controls in terms of wall thickness (P = 0.004), the appearance of a target sign pattern (P = 0.02), irregular patterns of mucosal surface (P = 0.01), and hyperintensity on T1w images (P = 0.03). All MRC criteria except maximal bowel wall thickness were associated with colon weight:length ratio and inflammatory biomarkers (all P < 0.05). Minimal bowel wall thickness and wall signal intensity on T2w images were associated with histological score (P < 0.05). MRC is feasible and reliable in rats with TNBS-induced colitis. MRC criteria including colon wall thickness, wall signal intensity on T2w images, hyperintensity in T1w sequence, and the appearance of a target sign pattern may be potential targets for new IBD drugs.

Marked Colonic Wall Thickening in Lupus Enteritis

Marked Colonic Wall Thickening in Lupus Enteritis

Colonic bowel wall thickening: Is there a need for endoscopic evaluation?

Clinical relevance of colonic bowel wall thickening seen on abdominal CT scans is unknown. Recommendations for further diagnostic procedures are lacking. The aim of this retrospective study was to evaluate detecting of bowel wall thickening on CT scan and findings that were seen in case of endoscopical evaluation. The radiological database was retrospectively reviewed for all reports of CT scans from 2003 to 2009 at the University Hospital Regensburg, Germany. Patients with underlying diseases for suspected bowel wall thickening were excluded. Sixty-two patients with bowel wall thickening were detected. Twenty-one percent (13/62) had generalized bowel wall thickening. In 58%, bowel wall thickening was limited to one segment of the colon (36/62), mostly left sided (25/62). Forty-four percent of patients (27/62) were sent to endoscopy. In 15% (4/27), malignancy was suspected, and it could be histologically confirmed in two patients. Nineteen percent (5/27) had normal endoscopy, and 67% (18/62) showed benign findings. Colonic bowel wall thickening is not a common finding on CT scan in this study. Consequential endoscopic evaluation was performed in less than 50% of patients. Pathological findings were detected in 80% of these patients. We recommend endoscopical evaluation if bowel wall thickening is reported on CT scan.

Quantification and Monitoring of Inflammation in Murine Inflammatory Bowel Disease with Targeted Contrast-enhanced US

To evaluate ultrasonography (US) by using contrast agent microbubbles (MBs) targeted to P-selectin (MB(P-selectin)) to quantify P-selectin expression levels in inflamed tissue and to monitor response to therapy in a murine model of chemically induced inflammatory bowel disease (IBD). All procedures in which laboratory animals were used were approved by the institutional administrative panel on laboratory animal care. Binding affinity and specificity of MB(P-selectin) were tested in cell culture experiments under flow shear stress conditions and compared with control MBs (MB(Control)). In vivo binding specificity of MB(P-selectin) to P-selectin was tested in mice with trinitrobenzenesulfonic acid-induced colitis (n = 22) and control mice (n = 10). Monitoring of anti-tumor necrosis factor α antibody therapy was performed over 5 days in an additional 30 mice with colitis by using P-selectin-targeted US imaging, by measuring bowel wall thickness and perfusion, and by using a clinical disease activity index score. In vivo targeted contrast material-enhanced US signal was quantitatively correlated with ex vivo expression levels of P-selectin as assessed by quantitative immunofluorescence. Attachment of MB(P-selectin) to endothelial cells was significantly (P = .0001) higher than attachment of MB(Control) and significantly (ρ = 0.83, P = .04) correlated with expression levels of P-selectin on endothelial cells. In vivo US signal in mice with colitis was significantly higher (P = .0001) with MB(P-selectin) than with MB(Control). In treated mice, in vivo US signal decreased significantly (P = .0001) compared with that in nontreated mice and correlated well with ex vivo P-selectin expression levels (ρ = 0.69; P = .04). Colonic wall thickness (P ≥ .06), bowel wall perfusion (P ≥ .85), and clinical disease activity scoring (P ≥ .06) were not significantly different between treated and nontreated mice at any time. Targeted contrast-enhanced US imaging enables noninvasive in vivo quantification and monitoring of P-selectin expression in inflammation in murine IBD.

Toxic megacolon in patients with severe acute colitis: computed tomographic features

Objective The objective of the study was to evaluate computed tomography (CT) in the differential diagnosis of patients with toxic megacolon (TM) complicating severe acute colitis (SAC) and patients with SAC but no TM. Materials and methods We identified 16 patients who presented clinically complicated SAC and CT examination before surgery. The CT scans of these patients were retrospectively evaluated in consensus by two abdominal radiologists blinded to the clinical and pathological results for CT findings of SAC, i.e., diffuse colonic wall thickening, submucosal edema, pericolonic fat stranding and ascites, and CT findings of TM reported in the literature, i.e., segmental colonic wall thinning, air-filled colonic distension over 6 cm with abnormal haustral pattern, nodular pseudopolyps and associated small bowel distension. Fisher's Exact Test was used for all statistical analyses. Results Segmental colonic wall thinning with abnormal haustral pattern was noted in TM only ( P=.001). As compared to patients with SAC but no TM as a complication, patients with TM showed statistically more frequent air-filled colonic distension over 6 cm ( P=.001) and nodular pseudopolyps ( P=.001). Diffuse colonic wall thickening ( P=.036) and submucosal edema ( P=.036) were more present in cases of uncomplicated SAC. Pericolonic fat stranding ( P=.12), ascites ( P=.6), and small bowel and gastric distension ( P=1) were not distinctive criteria. Conclusion Computed tomography is useful in distinguishing patients with TM from patients with SAC but no TM as a complication. The association of air-filled colonic distension >6 cm, abnormal haustral pattern and segmental colonic parietal thinning seems pathognomonic of TM and should lead to rapid surgery.

Antagonism of Protease-Activated Receptor 2 Protects against Experimental Colitis

Many trypsin-like serine proteases such as β-tryptase are involved in the pathogenesis of colitis and inflammatory bowel diseases. Inhibitors of individual proteases show limited efficacy in treating such conditions, but also probably disrupt digestive and defensive functions of proteases. Here, we investigate whether masking their common target, protease-activated receptor 2 (PAR2), is an effective therapeutic strategy for treating acute and chronic experimental colitis in rats. A novel PAR2 antagonist (5-isoxazoyl-Cha-Ile-spiro[indene-1,4'-piperidine]; GB88) was evaluated for the blockade of intracellular calcium release in colonocytes and anti-inflammatory activity in acute (PAR2 agonist-induced) versus chronic [2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced] models of colitis in Wistar rats. Disease progression (disease activity index, weight loss, and mortality) and postmortem colonic histopathology (inflammation, bowel wall thickness, and myeloperoxidase) were measured. PAR2 and tryptase colocalization were investigated by using immunohistochemistry. GB88 was a more potent antagonist of PAR2 activation in colonocytes than another reported compound, N¹-3-methylbutyryl-N⁴-6-aminohexanoyl-piperazine (ENMD-1068) (IC₅₀ 8 μM versus 5 mM). Acute colonic inflammation induced in rats by the PAR2 agonist SLIGRL-NH₂ was inhibited by oral administration of GB88 (10 mg/kg) with markedly reduced edema, mucin depletion, PAR2 receptor internalization, and mastocytosis. Chronic TNBS-induced colitis in rats was ameliorated by GB88 (10 mg/kg/day p.o.), which reduced mortality and pathology (including colon obstruction, ulceration, wall thickness, and myeloperoxidase release) more effectively than the clinically used drug sulfasalazine (100 mg/kg/day p.o.). These disease-modifying properties for the PAR2 antagonist in both acute and chronic experimental colitis strongly support a pathogenic role for PAR2 and PAR2-activating proteases and therapeutic potential for PAR2 antagonism in inflammatory diseases of the colon.

A Case of Pseudomembranous Collagenous Gastritis

Purpose: A 51-year old woman presented with a two-month history of watery diarrhea and 20-pound weight loss. Stools occurred 8-10 times a day and were without blood or features of steatorrhea. She had a part history of type I diabetes and was on insulin. Physical examination was unremarkable. Initial investigations showed WBC 13.3 (ANC 11.2), Hb of 143 g/dL, platelet count of 331. Albumin was 19 g/L (normal 33-53 g/L) and C-reactive protein was elevated at 15.4 mg/L. TTG was 0 with a normal IgA level. Stool studies were negative for C. difficile toxin and bacterial pathogens. CT scan of the abdomen and pelvis demonstrated a fluid-filled colon but without colonic wall thickening and normal small intestine. Gastroscopy revealed numerous, white, plaque-like pseudomembranes throughout the stomach and first portion of the duodenum. On colonoscopy, pseudomembranes were seen in the right colon, rectosigmoid and also in the terminal ileum. Biopsies from all sites showed thickened subepithelial collagen and lymphocytic inflammation. A diagnosis of collagenous gastritis, enteritis and colitis was made. The patient was treated with Entocort 9 mg daily and her symptoms improved within days. Follow-up gastroscopy after 12 weeks of therapy showed normal mucosa. Gastric and duodenal biopsies showed resolution of the collagen band but residual lymphocytic inflammation. The albumin and C-reactive protein normalized to 40 g/L and 1.8 mg/L, respectively. Discussion: Collagenous gastritis is a rare disorder, first described in 1989. It is usually associated with collagenous colitis and sometimes, collagenous enteritis. It is associated with type I diabetes as well as celiac disease. Response to steroid therapy is typical although relapse is common. This case was unique in that the patient had endoscopically visible pseudomembranes, which has not been previously described in collagenous gastritis. Most cases of pseudomembranous gastritis have been related to infection, such as aspergillosis, in an immune-compromised host. This case indicates that collagenous gastritis should be in the differential of pseudomembranous gastritis.

Metastatic Colorectal Adenocarcinoma Presenting with Dyspeptic Symptoms

Purpose: A 58-year-old man presented with refractory dyspeptic symptoms and evaluation of an abnormal findings on CT scan of the abdomen and pelvis. A positive serology for H. pylori was noted with no documented prior treatment and a prior CT scan showed right colonic wall thickening. No change in bowel habits, hematochezia, melena, weight loss, dysphagia, or loss of appetite. An EGD and colonoscopy were performed. Upper endoscopy showed erythematous mucosa in the antrum and body of the stomach, and a few localized areas of white granular mucosa in the second portion of the duodenum suggestive of lymphangiectasia. Colonoscopy showed a large irregular friable mass in the ascending colon. Biopsy of the colonic mass showed moderately differentiated adenocarcinoma. The biopsies from the upper endoscopy were positive for H. pylori, chronic gastritis and complete focal intestinal metaplasia. The duodenal biopsy showed metastatic adenocarcinoma in the lymphatics of the small intestine mucosa. Colorectal cancer (CRC) is a common and lethal disease. In the United States, more than 140,000 new cases are diagnosed each year, and approximately 51,000 deaths due to CRC occur each year. Despite the decrease in the mortality of CRC over the past two to three decades, it still remains the second most common cause of cancer death in the U.S. Approximately 20 percent of patients have metastatic disease at the time of presentation. CRC can spread by hematogenous, lymphatic, contiguous, and transperitoneal routes. The most common sites of metastasis are lymph nodes, liver, lungs, peritoneum, and brain. The small intestine is a rare site for CRC metastasis. Our case is unusual, as the patient presented with refractory dyspeptic symptoms, which led to the diagnosis of metastatic colorectal cancer despite a CT scan without evidence of metastatic disease.Figure: Duodenal metastatic lesions.Figure: Metastatic lymphatic invasion.

Ischemic Injury of the Stomach and Colon Mimicking Crohnʼs Disease in a Patient with ESRD

Purpose: A 37-year-old African-American female with ESRD on hemodialysis presented with a 3 day history of sharp abdominal pain, nausea and vomiting. She had multiple prior admissions for similar symptoms with repeated EGDs that revealed multiple malignant-appearing gastric ulcers. Her exam was significant for epigastric and right lower quadrant tenderness and rectal exam was hemoccult positive. An EGD was done that revealed several cratered gastric ulcers, largest measuring 15 mm, unchanged endoscopically from 1 month prior despite BID PPI use. Biopsies that were taken from ulcer margins revealed acute and chronic inflammation with multifocal calcifications, negative for malignancy. For further workup of her persistent abdominal pain, CT of the abdomen/pelvis was done that showed colonic wall thickening of her ascending and transverse colon. Colonoscopy to further evaluate showed severely congested, erythematous, friable and ulcerated mucosa in the cecum, ascending, transverse colon in a skipped pattern. The terminal ileum was also involved with ulcerated and friable mucosa. Biopsies were taken throughout the colon. Based on the colonoscopic findings in conjunction with previous upper endoscopy findings, a presumptive diagnosis of Crohn's disease was made and the patient was placed on mesalamine and steroids. The patient's symptoms did not improve after 48 hours. Colonoscopy biopsies revealed focal acute inflammation with scattered neutrophils and areas of submucosal hemorrhage consistent with ischemic injury. Ischemic injury to the colon is a common finding and the endoscopic findings can often mimic inflammatory bowel disease. However, ischemic injury with ulcer formation in the stomach is quite rare and this patient was likely predisposed to calcification of small vessels secondary to her history of ESRD. Specifically, isolated right sided colonic ischemia has been shown to occur more frequently in ESRD patients. These patients have a more course and higher mortality compared to those with colonic ischemia without chronic renal failure. Missing the diagnosis of ischemic injury can have significant consequences. Management for these patients is supportive.Figure: No Caption available.

MANEC: Case Report of a Rare and Newly-Defined Tumor

Purpose: Introduction: Mixed adenoneuroendocrine carcinoma (MANEC) is newly defined within the World Health Organization's classification of gastrointestinal tumors. Limited experience precludes guidelines for diagnostic approach and clinical management. We present a case of MANEC in a 55 year old male. Case Report: A 55 year old Caucasian male presented with sharp, epigastric pain. Previous medical history included Childs-Pugh Class A cirrhosis, ischemic dilated cardiomyopathy with an ejection fraction of 30%, diabetes, and hypertension. Physical exam revealed tenderness to palpation, with maximal discomfort at the epigastrium and no guarding or peritoneal rigidity. Initial laboratory values were significant for a WBC of 12.1, lipase 23, and lactic acid 1.3. CT abdomen showed colon wall thickening and pericolic inflammation, especially in the hepatic flexure and transverse colon. Colonscopy revealed dark, hemorrhagic bullae and ulcerations; biopsies were consistent with ischemic colitis. General Surgery performed an exploratory laparotomy with right hemi-colectomy, and pathology specimens incidentally demonstrated an appendiceal tumor infiltrating beyond the muscularis propria. Staining was positive for cytokeratins 20 and AE 1/3; synaptophysin; and chromogranin. Ki67 stain showed a proliferation index of 30%. Mucicarmine stain demonstrated intracytoplasmic mucin. The tumor was 75% adenocarcinoma and 25% carcinoid. Discussion: Newly defined in the GEP-NET class by the World Health Organization, MANECs are considered a progression of Goblet Cell Carcinoid (GCC), and are typed either as signet-ring cell or poorly differentiated adenocarcinoma. They typically affect older patients (average age 52 years), and like their GCC precursors, grow concentrically in the submucosa. They must display both endocrine and exocrine components, with one exceeding 30%. MANECs stain positive for mucin, and their cells express p53 and MUC1, though no MUC2. MANECs produce somatostatin, serotonin, and carcinoembyronic antigen. Their diagnosis is usually incidental during immunohistochemical staining of surgical specimens. MANEC size averages 2cm, with a range of 1-5cm, and gross specimen appearance is described as whitish and mucoid, without dilation of the appendiceal lumen. Specific prognostic data for MANECs is unavailable, necessitating further inquiry into the characterization of this nascent sub-classification.

Massive Bleeding from a Stercoral Ulcer in a True Colonic Diverticulum

Purpose: 28 year-old male with history of small internal hemorrhoids presented with multiple episodes of painless bleeding and clots per rectum for one day. He denied nausea, vomiting, abdominal pain, diarrhea, weight loss or use of NSAIDs. He was orthostatic and abdominal exam was unremarkable. A rectal exam revealed frank blood without any palpable mass. Hemoglobin was 8.9 gm/dL and did not respond appropriately to blood transfusions. An upper endoscopy showed mild nonerosive gastritis and an incomplete colonoscopy showed old and new blood clots up to the splenic flexure. A Meckel's scan was negative and a CT scan showed a round, heterogeneous, calcified mass in the proximal colon without surrounding fatty infiltration or definite colonic wall thickening. A repeat colonoscopy showed blood clots throughout colon with scant fresh blood on the right side and terminal ileum, but no definite bleeding source. An exploratory laparotomy identified a round, firm mass in the proximal ascending colon and intra-operative ileoscopy showed dark bile without evidence of bleeding. Right hemicolectomy with primary anastomosis was performed. The specimen was dissected and a large, firm fecal mass was dislodged from a diverticulum in the proximal ascending colon. Pathology specimen showed a 0.7 cm true diverticulum containing a fecalith, measuring 2 cm in diameter. The mucosa of the diverticulum was ulcerated with acute inflammation and granulation tissue abutting a blood vessel on histology. Patient ceased to bleed post-operatively, and was discharged home uneventfully. Acute lower GI bleeding has an incidence of 20 to 27 episodes per 100,000 persons annually. Most common colonic bleeding sources are pseudodiverticulosis, angioectasias, colitis, neoplasms and hemorrhoids. Stercoral ulceration is rare and almost always develops within the rectosigmoid colon in elderly, chronically constipated patients. The pressure necrosis of the bowel wall due to overlying firm and usually large fecalith is thought to be the main mechanism of injury. Only rarely stercoral ulcers and complications such as bleeding and perforation have been reported in anatomic locations other than the rectosigmoid. The incidence of true colonic diverticulum is much lower than that of pseudodiverticulum. A true diverticulum contains all three layers of the colonic wall and is thought to be congenital. Clinical course can parallel that of pseudodiverticulosis with inflammation, bleeding and perforation. This is the first reported case of massive bleeding from a stercoral ulcer inside a true colonic diverticulum.

The Correlation Between Colonic Wall Thickening and Abnormal Colonoscopy

The Correlation Between Colonic Wall Thickening and Abnormal Colonoscopy

Analysis of intestinal fibrosis in chronic colitis in mice induced by dextran sulfate sodium

Fibrogenic mesenchymal cells including fibroblasts and myofibroblasts play a key role in intestinal fibrosis, however, their precise role is largely unknown. To investigate their role in intestinal fibrosis, we analyzed the lesions of chronic colitis in C57BL/6 (B6) mice induced by dextran sulfate sodium (DSS). B6 mice exposed to single cycle administration of DSS for 5 days developed acute colitis that progressed to severe chronic inflammation with dense infiltrates of mononuclear cells, irregular epithelial structure, thickening of colonic wall, and persistent deposits of collagen. Increased mRNA expressions of proinflammatory cytokines are correlated with extensive cellular infiltration, and the mRNA expressions of collagen 1, transforming growth factor (TGF)-β, and matrix metalloproteinases were also enhanced in the colon. In the colon of chronic DSS colitis, fibroblasts (vimentin(+), α-smooth muscle actin (α-SMA)(-)) were increased in both mucosal and submucosal layers, while myofibroblasts (vimentin(+), α-SMA(+)) were increased in mucosal but not in submucosal layers. Primary mouse subcutaneous fibroblast cultures experiments revealed that exogenously added TGF-β 1 substantially augmented the expressions of both vimentin and α-SMA proteins with increased production of collagen. In conclusion, profibrogenic mesenchymal cells play an important role in the development of intestinal fibrosis in this chronic DSS-induced colitis model.

Necrotic stercoral colitis: Importance of computed tomography findings

To study the computed tomography (CT) signs in facilitating early diagnosis of necrotic stercoral colitis (NSC). Ten patients with surgically and pathologically confirmed NSC were recruited from the Clinico-Pathologic-Radiologic conference at Chang Gung Memorial Hospital, Taoyuan, Taiwan. Their CT images and medical records were reviewed retrospectively to correlate CT findings with clinical presentation. All these ten elderly patients with a mean age of 77.1 years presented with acute abdomen at our Emergency Room. Nine of them were with systemic medical disease and 8 with chronic constipation. Seven were with leukocytosis, two with low-grade fever, two with peritoneal sign, and three with hypotensive shock. Only one patient was with radiographic detected abnormal gas. Except the crux of fecal impaction, the frequency of the CT signs of NSC were, proximal colon dilatation (20%), colon wall thickening (60%), dense mucosa (62.5%), mucosal sloughing (10%), perfusion defect (70%), pericolonic stranding (80%), abnormal gas (50%) with pneumo-mesocolon (40%) in them, pericolonic abscess (20%). The most sensitive signs in decreasing order were pericolonic stranding, perfusion defect, dense mucosal, detecting about 80%, 70%, and 62.5% of the cases, respectively. Awareness of NSC and familiarity with the CT diagnostic signs enable the differential diagnosis between NSC and benign stool impaction.

Possible Role of Early Transabdominal Ultrasound in Patients Undergoing Cytapheresis for Active Ulcerative Colitis

Cytaphresis (CAP) is an effective modality in the treatment of active ulcerative colitis (UC), but the time lag before a notable clinical response on scheduled therapy frequently causes a significant delay in the modification of treatment. We previously reported that the clinical response after CAP was predicted by early application of transabdominal ultrasound (TAUS), but the predictability of long-term outcome after CAP still remains uncertain. METHODS PATIENTS: Twenty-six patients with active UC who received CAP were followed for 1 year. In addition to CAP they received pharmaceutical regimens, such as corticosteroid, 5-aminosalicylic acid, and immunomodulator, as indicated clinically. The mean UC-DAI score was 9.7 before CAP, and 3.2 at 1 year after CAP. Prognostic factor: Total colonic wall thickness was measured by TAUS at 2 to 3 weeks after the initiation of the treatment, and decrement from baseline was calculated. Early ultrasonographic response (EUR) was defined as a decrement statistically. UC-DAI score of 2 or less at 1 year was defined as sustained clinical remission. Score of 6 or more was defined as clinical relapse. EUR was defined as a decrement in wall thickness by at least 2.5 mm from the baseline. EUR was noted in 11 patients, and the remaining 15 did not attain EUR. In the UC-DAI score measured at 1 year after initiation of treatment 90.9% of patients with EUR, whereas 40.0% with non-EUR (p<0.05) showed sustained clinical remission. Regarding relapse, within 1 year 9.1% of patients with EUR relapsed whereas 46.7% with non-EUR (p<0.05) relapsed. Early application of TAUS may predict the long-term clinical outcome after CAP in patients with active UC.

En bloc right hemicolectomy and pancreaticoduodenectomy for HNPCC with simultaneous mutations of MSH-2 and MSH-6

Dear Editor: Hereditary nonpolyposis colon cancer (HNPCC or Lynch syndrome) is a multisystemic disorder, affecting the colon and rectum in up to 70% of cases. It is characterized by autosomal dominant inheritance and the development of multiple neoplasms including colorectal, endometrial, ovarian, pancreatic, small bowel, and urinary tract tumors. HNPCC is the leading cause of hereditary colorectal cancers (CRC) with an incidence of 2–5%. The genetic defects associated with this disorder arise from errors in the mismatch repair genes (MMR). Currently, five different genetic mutations have been identified (hMLH1, hMSH2, hMSH3, hMSH6, hPMS1) that lead to accelerated carcinogenic transformation, some of which show distinct phenotypic features like inflammatory component or expansive growth. Herein, we describe the first case report of an HNPCC patient with simultaneous loss of expression of MSH-2 and MSH-6 genes in the setting of a T4N0 colon cancer invading the duodenum and the head of the pancreas. A 38-year-old man presented to the emergency department of a tertiary referral center complaining of right-sided abdominal pain, nausea, vomiting, skinny stools, and weight loss (20 lbs) for the past 6 weeks prior to admission. He had no significant past medical history. However, he reported that his father died at the age of 50 of colon cancer. Physical exam was significant for mild discomfort in the right upper quadrant. His stool guaiac test was positive for occult blood, but no frank blood was seen and no mass was palpated on rectal digital exam. Laboratory tests were significant for mild transaminitis and a CT scan of the abdomen and pelvis revealed a 7.6-cm mass arising from the hepatic flexure of the right colon and extending into the second and third portion of the duodenum and pancreatic head. An upper and lower GI endoscopy with biopsy of the mass showed moderately differentiated adenocarcinoma of the colon. A subsequent PET scan showed no metastatic focus of fludeoxyglucose uptake. The patient underwent an exploratory laparotomy with an extended right hemicolectomy and pancreaticoduodenectomy. No contraindication to resection was encountered in the exploratory phase. The patient had an uneventful postoperative course and was discharged home on POD#14. Upon follow-up in the clinic 2 weeks later, he was eating a regular diet, having normal bowel movements, and was back to regular activities. The surgical specimen consisted of the resected colon, duodenum, and the head of the pancreas. Microscopic examination revealed a high grade (G3), poorly differentiated adenocarcinoma of the hepatic flexure, with mild to moderate lymphocytic invasion, infiltrating the full thickness of the colonic wall into the duodenum. The authors declare no conflict of interest and/or relationships with people or businesses that could influence or bias the outcome of this paper.

The passage of a colonic cast

A 50-year-old alcoholic woman presented with periumbilical pain, mucoid diarrhoea, fever, and dysuria for 3 days. Abdominal ultrasonography showed thickening of the entire colonic wall. Abdominal MRI showed mucosal hypoperfusion confi ned to the descending colon without vascular thrombosis (fi gure A). Colonoscopy showed a diff use greenish mucosa with numerous black spots; biopsy samples confi rmed ischaemic colitis. Escherichia coli urosepsis with multi-organ dysfunction was diagnosed. 2 weeks later, after antibiotics and total parenteral nutrition administration, she excreted per anus a 120 cm tubular mucosa (fi gure B). Repeat colonoscopy showed a demucosed colon (fi gure C). She recovered uneventfully after conservative management. Colonic cast passage is a rare manifestation of ischaemic colitis. Our patient passed a colonic cast most likely because of mucosal infarction caused by urosepsis and disseminated intravascular coagulation with resultant diff use microthrombi formation over the colonic microvasculature. Most patients require surgical resection of the involved segments because of conservativetreatment failure.

S1549: Association Between Serum Albumin Levels and Computed Tomography (CT) Findings of Colon Wall Thickening (CWT)

CWT is a common finding on CT scans. Incidental findings of CWT often prompt further evaluation by colonoscopy. Endoscopic evaluation of CWT in the setting of abdominal pain has proven useful for diagnosis of colorectal carcinoma and IBD (J Clin Gastroenterol, Wolff JH 2008). Albumin, the major plasma protein, is essential for maintaining oncotic pressure in the vascular system. Decreased oncotic pressure allows fluid to leak from interstitial spaces and may be responsible for incidental CWT reported on CT.

W1445: Regional Differences in Colon Circumference and Wall Thickness

W1445: Regional Differences in Colon Circumference and Wall Thickness

NORMAL CANINE PEDIATRIC GASTROINTESTINAL ULTRASONOGRAPHY

The normal sonographic appearance of the adult canine gastrointestinal tract has been described. Interpretation of abdominal ultrasonographic findings in puppies is difficult due to the lack of information on normal ultrasonographic findings. The gastrointestinal tract, jejunal lymph node size and the presence and appearance of abdominal fluid were investigated in 23 normal, 7-12-week-old Beagle puppies. The duodenal wall thickness was greater than in other parts of the gastrointestinal tract (mean 3.8 +/- standard deviation [SD] 5 mm, range 3.2-4.8 mm). The mean stomach wall thickness was 2.7 +/- SD 0.4 mm (range 2.2-3.7 mm), the mean jejunal wall thickness was 2.5 +/- SD 0.5 mm (range 1.2-3.4 mm), and the mean colonic wall thickness was 1.3 +/- SD 0.3 mm (range 0.7-2.0 mm). In addition, mean duodenal and jejunal mucosal layer thicknesses measured 2.7 +/- SD 0.5 mm (range 2.0-3.8 mm) and 1.5 +/- SD 0.4 mm (range 0.6-2.5 mm), respectively. Homogenous, hypoechoic jejunal lymph nodes were easily found and the mean thickness was 7.1 +/- SD 2.2 mm (range 1.5-12.5 mm). A mild amount of anechoic free peritoneal fluid was present in all puppies.