Nonperforated Ulcers Research Articles

S2872 A Case of CMV Enteritis Resulting in Severe Obscure GI Bleeding

INTRODUCTION: Small bowel (SB) bleeding accounts for less than 5% of gastrointestinal (GI) bleeds, in non-IBD patients, with an even smaller portion originating from the jejunum [1]. Locating SB bleeds poses great challenges, frequently resulting in delay in diagnosis. Although SB arteriovenous malformations (AVMs) are most common, other rare etiologies such as infectious enteritis should be considered. CASE DESCRIPTION/METHODS: A 62 year old male was diagnosed with T-cell lymphoma with EBV positivity and placed on high-dose steroids for one month. Staging CT chest, abdomen, and pelvis incidentally revealed intraperitoneal free air with concerns for a gastric wall neoplasm. EGD revealed a 4cm, deep, non-bleeding, non-perforated ulcer in the gastric body (Image 1). Two weeks after, he had painless melanotic stools, requiring multiple transfusions. Emergent arteriography of the celiac and mesenteric arteries did not identify a source of bleeding. Repeat CT imaging was negative for worsening free air. His course continued to worsen, requiring high-dose vasopressors and continued transfusions. Emergent EGD and colonoscopy were performed. EGD revealed a known, non-bleeding gastric ulcer. Colonoscopy showed bright red blood to the cecum with scattered, non-bleeding, ischemic-appearing ulcers (Image 2). Repeat celiac angiogram was performed two more times, eventually revealing active bleeding from small jejunal artery branches which were embolized. Due to concern for ongoing bleeding, surgical resection of the distal jejunum and proximal ileum was performed. Gross pathology demonstrated extensive ulcerations, with biopsies negative for malignancy (Image 3). Serum testing for Cytomegalovirus (CMV) was positive for strongly elevated quantitative levels and the patient was started on Valganciclovir. DISCUSSION: Delays in diagnosing SB bleeds are not uncommon and can frequently be fatal. Our case presents a complex diagnostic scenario where bleeding was presumed to be from the known gastric lesion, but complicated by inability to perform EGD safely with pneumoperitoneum. Ultimately, the patient’s immunocompromised state and steroids predisposed him to opportunistic infections such as CMV, resulting in bleeding ulcers in the jejunum and ileum. Upon literature review, CMV enteritis is exceedingly rare and accounts for under 5% of all CMV infections in the GI tract [2]. Though rare, CMV enteritis has been reported to cause massive hemorrhage requiring emergent surgery and is often associated with high mortality.Figure 1.: 4cm non-bleeding ulcer in the gastric body seen on the initial EGD.Figure 2.: Scattered ischemic-appearing colonic ulcers.Figure 3.: Gross specimen of resected and ulcerated jejunum.

Prevalence of abomasal lesions in Danish Holstein cows at the time of slaughter

Abomasal lesions in cattle are challenging to diagnose because the clinical signs are often subtle and nonspecific. An increasing number of studies suggests that abomasal lesions are commonly found in cattle of all ages, but the number of recent prevalence studies in dairy cows is limited. The main objective of this study was to estimate the prevalence of abomasal lesions in a population of Danish Holstein dairy cattle in Denmark. An abattoir survey of 1,327 dairy cows apparently suitable for slaughter was performed in 2016 and 2017. Abomasal lesions are usually classified using a standardized protocol with the following types: abomasal ulcer type I: erosions and nonperforating ulcers; type II: ulcers with arterial bleeding; type III: perforating ulcer with localized peritonitis; and type IV: perforating ulcer with diffuse peritonitis. A further subdivision of the nonperforating abomasal ulcers type I were classified as subtype Ia: erosions; subtype Ib: small ulcers with localized hemorrhage; subtype Ic: ulcers with a crater-like appearance; and subtype Id: retention of the mucosa due to tissue loss with either radial wrinkles converging at a central point or perforations of the spiral folds. Type I abomasal lesions were found in 84% of the examined cows. No ulcers with arterial bleeding (type II) or perforating ulcers with diffuse peritonitis (type IV) were found, but one perforating abomasal ulcer (type III) was observed. The total number of lesions found was 7,418 and when the lesion subtypes were evaluated individually the majority of subtypes Ia and Ic were found in the pyloric area (85 and 94%, respectively), whereas lesion subtypes Ib and Id dominated the fundus/corpus area (71 and 67%, respectively). When considering lesion subtypes according to parity, there was a high prevalence of subtype Ib across the 3 groups of parity (51, 58, and 55% for parity 1, 2, and ≥3, respectively). The prevalence of lesion subtype Id seemed to increase with increasing parity, and the prevalence of lesion subtype Ia seemed to decrease with increasing parity. The prevalence of abomasal lesions was higher than that shown in similar studies of cattle at the time of slaughter. However, the expectedly most painful cases were rare, with only one perforating and no arterial bleeding ulcers found. The etiology of the different subtype I lesions is still unknown, and further investigations are needed to establish the possible influence these lesions might have on welfare and production.

Intoxication by Lornoxicam in Two Dogs

Background: The indiscriminate use of drugs is routinely observed in the field of veterinary medicine. Nonsteroidal antiinflammatory drugs (NSAIDs) are the class of drugs that most commonly cause intoxication in pet animals. Lornoxicam, an NSAID, is a cyclooxygenase COX-1 and COX-2 inhibitor and is only recommended for human treatment. Here we present cases involving two dogs who presented with Lornoxicam intoxication following administration without veterinary prescription.Cases: 1) - A 1-year-old female Rottweiler was presented for clinic with claudication, profuse vomiting, and fetid blackish diarrhea. The owner reported administer two tablets of oral Lornoxicam. Physical examination revealed lethargy, a bulging abdomen and pale mucous membranes. Contrast-enhanced imaging of the gastrointestinal tract revealed decreased stomach flow. The ultrasound revealed predominantly gaseous contents in the stomach with normal walls, a large amount of accumulated gas in the pyloric region. Therefore, exploratory laparotomy was held and a nonperforated ulcer was observed in the pyloric region. There were hemorrhagic areas in the stomach mucosa and enlarged lymph nodes in the duodenum. The ulcer was resected without complications. Medications included after surgery were intravenous fluid, antibiotic, analgesic, antiemetic, histamine H2-receptor antagonist and Cytoprotective drugs. The day after the surgical procedure, no episode of vomiting or diarrhea was observed and the food and water were introduced gradually in the following days. 2) - An 11-yearold male Old English Sheepdog came to the clinic with a history of vomiting, blackish diarrhea, and loss of appetite. The owner reported that first was administered deltamethrin for tick infestation and approximately 3 days after, the amitraz. The animal began vomiting, limping, and lost its appetite. Because of the limping, the owner administered Lornoxicam in a single dose and the animal start vomiting and manifested fetid, blackish diarrhea. On physical examination, the patient showed 7.0% dehydration and tenderness on palpation in the epigastric region. For diagnostic screening was performed: hematological and biochemical evaluation; the Canine Test SNAP 4DX; and total abdominal ultrasound. The results only showed leukocytosis and predominantly gaseous contents in the stomach. Then, pyrethroid and formamidine intoxication with hemorrhagic gastroenteritis secondary to Lornoxicam administration was suspected. Intravenous fluid therapy was performed with Ringer’s lactate solution. In addition, metoclopramide, ranitidine, sucralfate and sulfamethoxazole/trimethoprim were administered along the gradual insertion of food and water. The patient showed complete clinical recovery after 7 days of hospitalization and was discharged.Discussion: The clinical signs presented by the both cases were similar to those described in the literature on NSAID intoxication in animals. In the two cases, none of the exams confirmed the presence of the ulcer, but they helped to suspect. Blood tests performed for the second animal revealed findings similar to previously reported nonspecific laboratory findings for gastric ulcers. In both cases, ultrasound did not identify any changes that proved the existence of gastric ulcers. However, this test is necessary to rule out complications such as perforation or peritonitis. In the first case, exploratory laparotomy was required for a definitive diagnosis because of suspected obstruction in the pyloric region. For the second animal, surgery was not planned because all the performed tests only raised a suspicion of hemorrhagic gastritis, and the suspected diagnosis was confirmed by the positive response to the treatment. The underlying etiology in both cases was identified as Lornoxicam intoxication due to administration without veterinary medical prescription.Keywords: nonsteroidal anti-inflammatory drug, gastritis, gastric ulcer.

Late gastrointestinal tissue effects after hypofractionated radiation therapy of the pancreas.

BackgroundTo consolidate literature reports of serious late gastrointestinal toxicities after hypofractionated radiation treatment of pancreatic cancer and attempt to derive normal tissue complication probability (NTCP) parameters using the Lyman-Kutcher-Burman model.MethodsPublished reports of late grade 3 or greater gastrointestinal toxicity after hypofractionated treatment of pancreatic cancer were reviewed. The biologically equivalent dose in 1.8 Gy fractions was calculated using the EQD model. NTCP parameters were calculated using the LKB model assuming 1–5 % of the normal tissue volume was exposed to the prescription dose with α/β ratios of 3 or 4.ResultsA total of 16 human studies were examined encompassing a total of 1160 patients. Toxicities consisted of ulcers, hemorrhages, obstructions, strictures, and perforations. Non-hemorrhagic and non-perforated ulcers occurred at a rate of 9.1 % and were the most commonly reported toxicity. Derived NTCP parameter ranges were as follows: n = 0.38–0.63, m = 0.48–0.49, and TD50 = 35–95 Gy. Regression analysis showed that among various study characteristics, dose was the only significant predictor of toxicity.ConclusionsPublished gastrointestinal toxicity reports after hypofractionated radiotherapy for pancreatic cancer were compiled. Median dose was predictive of late grade ≥ 3 gastrointestinal toxicity. Preliminary NTCP parameters were derived for multiple volume constraints.

Hornhautulzera bei systemischen Autoimmunerkrankungen

Keratolysis is a rare severe complication following systemic autoimmunologic diseases. Despite of complex therapeutic treatments, the prognosis is very poor. Ten eyes from seven patients with corneal ulcers were reported (age 45 - 73 years, mean 63 years; 6 women, 1 man). The corneal ulcer was perforated in 7 eyes. Five patients suffered from rheumatoid arthritis, and one patient developed a Sjögren's syndrome. Besides, one patient had shown both autoimmunologic diseases. After clinical attendance, visual acuity in the eyes with nonperforated ulcers was between 0.1 and 0.4, and in the eyes with perforated ulcers between light perception and 0.2. In 7 eyes with perforated corneal ulcers an emergency tectonic conjunctival plasty and, 1 - 2 days later, a keratoplasty had been performed. Postoperatively, local therapies had been initiated with antibiotic and immunosuppressive eyedrops as well as with conventional drops for dry-eye symptoms. Because of the autoimmunologic diseases of the patients, a systemic immunosuppressive therapy had been arranged. Follow-up period had been between 4 weeks and 3,5years (mean 16 months). In the three eyes with nonperforated ulcers which received an antibiotic and immunosuppressive treatment, visual acuity was found at 1 / 20 and 0.4. However, in spite of stabilized findings in the 5 eyes with perforated ulcers, the visual acuity was in this case only between light perception and 0.05. One patient with a perforated ulcer and one patient with a recurrent corneal perforation after keratoplasty refused further operative procedures. Finally, both eyes had to undergo evisceration. Despite of intensive local and systemic immunosuppressive as well as operative therapies, corneal ulcers associated with autoimmunologic diseases (rheumatoid arthritis, Sjögren's syndrome) may cause a marked decrease of visual acuity or the loss of an eye. With regard to the healthy eye, an immunosuppressive therapy for life is most important.

Outcomes of Therapeutic Deep Lamellar Keratoplasty and Penetrating Keratoplasty for Advanced Infectious Keratitis: A Comparative Study

To compare the therapeutic success, visual outcomes, complications, and graft survival rates of therapeutic deep anterior lamellar keratoplasty (TDALK) and therapeutic penetrating keratoplasty (TPK) for advanced infectious keratitis.Retrospective, comparative study.One hundred twenty-three patients (126 eyes) with medically uncontrolled infectious keratitis of bacterial, fungal, or acanthamoeba etiologies who underwent TDALK (n = 26) or TPK (n = 100 eyes; 80 nonperforated ulcers; 20 perforated ulcers; mean follow-up in TDALK, 12.9 months; in TPK, 21.3 months).We performed TDALK for infections confined to the corneal stroma and the technique used was either manual lamellar dissection or Anwar's big bubble technique for total stromal removal. Therapeutic penetrating keratoplasty was performed for either nonperforated or perforated ulcers. Comparison with respect to recurrence of infection, visual acuity, graft survival, and complications was made. Baseline characteristics of the patients were analyzed using the chi-square test. Kaplan-Meier survival analysis was used to evaluate graft survival.Therapeutic success (eradication of infection) or therapeutic failure (recurrence of original infection in cornea or sclera, or as endophthalmitis), graft survival (clarity), and best-corrected visual acuity (BCVA).Therapeutic success rate of 84.6% was achieved in the TDALK group and 88% in the TPK group (P = 0.74); of the 12 eyes with recurrence of infection in the TPK cohort, 6 developed endophthalmitis with poor outcomes. A BCVA of > or =6/9 was achieved in 50% of patients in the TDALK group and 20.2% in the TPK group (P = 0.01). Mean improvement of acuity was 7.27 lines in the TDALK group and 4.76 lines in the TPK group (P = 0.01). Kaplan-Meier survival analysis at 1 year showed better graft survival for TDALK (90%) compared with TPK (78.4%).For medically unresponsive infectious keratitis, TDALK may be considered instead of TPK yielding similar graft survival, without an increased risk of disease recurrence.

Outcome of Therapeutic Penetrating Keratoplasty in Infectious Keratitis

To study the outcome of therapeutic penetrating keratoplasty in eyes with microbial keratitis. A prospective database on 134 therapeutic cornea transplants in 134 patients recorded demographic details on age and gender of the patient, indication for surgery, size of the donor and recipient bed, graft clarity, complications, and residual morbidity. Patients included in this analysis had a minimum follow-up of 1 year. All patients underwent therapeutic penetrating keratoplasty by a similar method that involved a donor button that was oversized by 0.5 mm and 16 bites of interrupted sutures. Most of the 134 ulcers needing therapeutic grafts were bacterial (n = 54) or fungal (n = 54). One hundred eighteen eyes had perforation at presentation. One hundred six (90%) of the therapeutic grafts achieved anatomical success. The most common complication of glaucoma occurred in 22% of eyes with presurgical perforated ulcers and 1% of nonperforated ulcers. Persistent epithelial defects were significantly more frequent in grafts of 9 mm or more (P = .05). Our results confirm that therapeutic penetrating keratoplasty for infections is successful in restoring anatomic integrity in most eyes.

Type 1 Abomasal Ulcers in Dairy Cattle*

Abomasa from 912 randomly selected cows were examined; specimens were obtained at the local slaughter house on 35 days spread over one year. Abomasal lesions were assessed macroscopically and histologically. Additionally, haematological and blood chemistry (urea, aspartate aminotransferase, potassium, chloride, calcium) evaluations and the determination of rumen chloride concentration were performed. Of the 912 abomasa examined, 187 (20.5%) had ulcerative lesions of the mucosa. Lesions were classified from 1 to 4 based on severity as described by Whitlock (1980). All ulcers were classified as type 1 (erosions and non-perforating ulcers); thus, further division into four subtypes 1 a, 1 b, 1 c and 1 d was carried out. Fifty-six abomasa had minimal mucosal defects which were classified as type 1 a. Deeper erosions combined with local hemorrhage, classified as type 1 b, were observed in 54 abomasa. Type 1 c were crater-like ulcers and were seen in 61 abomasa. Sixteen abomasa had type 1 d ulcers which included two forms: ulcers with radial wrinkles converging on a central point, and ulcers with perforated folds. Types 1 a and 1 c occurred mainly in the pyloric region, and types 1 b and 1 d were observed mainly in the fundic region. Type 1 abomasal ulcus could not be diagnosed based on alterations in haematological or blood and rumen chemistry values.

Non-Perforating Ulcers of the Stomach and Duodenum

Non-Perforating Ulcers of the Stomach and Duodenum