Rational use of gastroprotectants in cats: An evidence-based approach.

PRACTICAL RELEVANCE: Acid-related disorders including esophagitis and gastroduodenal ulceration are uncommon in the cat. However, when they occur, they can have devastating consequences and require targeted intervention, including the use of gastroprotectants. Careful consideration of the causes of esophagitis and gastroduodenal ulceration can help the clinician to determine which gastroprotectant to use, and when to begin and end gastroprotective therapy. CLINICAL CHALLENGES: Gastroprotectants remain one of the most misused classes of drugs in veterinary and human medicine. There are very few studies evaluating the efficacy of gastroprotective agents in cats. Furthermore, goals for the degree of gastric acid suppression are extrapolated from studies performed in dogs and humans. AIMS: This review provides a foundation for the logical approach to the choice of gastroprotectant as indicated by the disease process, and is aimed at all veterinarians who prescribe gastroprotectants for use in cats. EVIDENCE BASE: The guidance provided in this review is supported by current literature, including consensus opinion from the American College of Veterinary Internal Medicine. Gaps in evidence for use of gastroprotectants in cats are filled by extrapolations from studies performed in dogs and humans.

Primary repair of nonsteroidal anti-inflammatory drug-associated full thickness gastrointestinal ulcers in 11 dogs.

OBJECTIVE: To report the outcomes of dogs that underwent primary repair of gastroduodenal perforations associated with the administration of nonsteroidal anti-inflammatory drugs (NSAID). A secondary objective was to identify clinicopathological findings that predisposed dogs to postoperative death. STUDY DESIGN: Retrospective study. ANIMALS: Eleven dogs with complete gastric or duodenal perforation related to administration of an NSAID that underwent primary surgical repair. METHODS: Medical records were reviewed for dogs that presented with peritonitis due to a complete gastroduodenal perforation while receiving NSAIDs between November, 2011 and January, 2021. Data collected included patient characteristics, clinical signs, clinicopathological results, surgical details, and postoperative management and outcome. RESULTS: All dogs were large breeds (mean weight 42 kg; range 22-75 kg), with a mean age of 7.35 years. Nine dogs from a total of 11 (82 %) received a concurrent corticosteroid and NSAID, or a higher dose/frequency/length of NSAID administration than recommended by the manufacturer. All gastroduodenal perforations were found in the upper gastrointestinal tract. Eight of 11 (73%) dogs survived to discharge. The median postoperative duration of follow up was 444 days (range 2-1460 days). No association was detected between ulcer size or location and mortality. CONCLUSION: Most dogs who underwent primary repair of complete gastroduodenal ulcers survived. Gastroduodenal perforations were generally due to the administration of higher or longer doses of NSAIDs, or concurrent administration of another NSAID or corticosteroid. CLINICAL SIGNIFICANCE: Primary closure may be associated with a high success rate in dogs with full thickness gastroduodenal ulcers.

Continuous radiotelemetric monitoring of intragastric pH in a dog with peptic ulceration.

CASE DESCRIPTION A 6-year-old castrated male Boxer was evaluated for a 5-week history of frequent vomiting, melena, and signs of abdominal pain following accidental ingestion of 5 to ten 15-mg meloxicam tablets (approx ingested dose, 3.1 to 6.2 mg/kg [1.4 to 2.8 mg/lb]). CLINICAL FINDINGS Clinical signs persisted despite 3 weeks of treatment with sucralfate (41.8 mg/kg [19 mg/lb], PO, q 8 h) and omeprazole (0.8 mg/kg [0.36 mg/lb], PO, q 24 h). Results of a CBC and serum biochemical analysis were unremarkable. Abdominal ultrasonography revealed peptic ulceration, and esophagogastroduodenoscopy confirmed the presence of severe proximal duodenal ulceration. TREATMENT AND OUTCOME A radiotelemetric pH-monitoring capsule was placed in the gastric fundus under endoscopic guidance for continuous at-home monitoring of intragastric pH and response to treatment. Treatment was continued with sucralfate (as previously prescribed) and omeprazole at an increased administration frequency (0.8 mg/kg, PO, q 12 h). Intragastric pH was consistently ≥ 3.0 for > 75% of the day during treatment, with the exception of 1 day when a single dose of omeprazole was inadvertently missed. Ulceration and clinical signs completely resolved. CLINICAL RELEVANCE Continuous radiotelemetric monitoring of intragastric pH in the dog of this report was useful for confirming that treatment achieved a predetermined target pH and for demonstrating the impact of missed doses. Duodenal ulceration resolved with twice-daily but not once-daily omeprazole administration. Findings suggested that twice-daily administration of omeprazole may be necessary to achieve this target pH and that a pH ≥ 3.0 for 75% of the day may promote healing of peptic ulcers in dogs.

Gastroduodenal Ulceration in Small Animals: Part 2. Proton Pump Inhibitors and Histamine-2 Receptor Antagonists.

In the first part of this review, we discussed the pathophysiology and epidemiology of gastric acid secretion and the epidemiology of gastroduodenal ulceration in dogs and cats. In this section, we discuss the pharmacology and evidence-based clinical use of histamine-2 receptor antagonists and proton pump inhibitors.

Gastroduodenal Ulceration in Small Animals: Part 1. Pathophysiology and Epidemiology.

Gastroduodenal ulceration in small animals is a complex and important comorbidity that occurs when the physiological homeostasis of the gastrointestinal tract is disrupted secondary to administration of medications or the presence of local or systemic diseases. The aim of this article is to provide a comprehensive review of the veterinary literature regarding the pathophysiology, epidemiology, and risk factors associated with gastroduodenal ulceration in small animals. Pertinent concepts from the human literature will be integrated into the discussion. This article serves as an introduction to the second part of this series, which will review current evidence regarding the use of H2-receptor antagonists and proton pump inhibitors in small animals.

An unusual clinical presentation of a dog with gastrinoma.

Gastrinoma is a rare malignant neuroendocrine neoplasia that results in autonomous gastrin secretion that stimulates hypersecretion of gastric acid, resulting in severe gastric and proximal small intestinal ulcerations. The principal clinical manifestation of gastrinoma is persistent vomiting. This report describes an uncommon manifestation of pancreatic gastrinoma in a dog.

Successful surgical management of spontaneous gastric perforations in three cats.

BACKGROUND: In the veterinary literature, feline gastroduodenal ulcer disease has been described only in individual case reports or retrospective studies reporting small numbers of cats. Although its canine counterpart is commonly encountered, less is known about factors predisposing cats to gastroduodenal ulceration and potentially perforation. Similarly the outcome following treatment is not well reported in this species. REPORTED RISK FACTORS: In dogs, hepatic disease and administration of non-steroidal anti-inflammatory drugs (NSAIDs) have been reported as the two most common causes of gastroduodenal ulceration. In cats, only one clinical report so far has implicated an NSAID as a risk factor for spontaneous gastroduodenal perforation. FINDINGS AND PRACTICAL RELEVANCE: This report describes the historical and physical findings, as well as the treatment and outcome, in three cats with spontaneous gastric perforation that were receiving anti-inflammatory medication immediately prior to presentation. It highlights the importance of thorough patient evaluation in any cat presenting with non-specific clinical signs and a history of anti-inflammatory drug administration.

Assessment of necropsy findings in sled dogs that died during Iditarod Trail sled dog races: 23 cases (1994-2006).

OBJECTIVE: To describe the character and frequency of causes of death and associated lesions in long-distance racing sled dogs. DESIGN: Retrospective case series. ANIMALS: 23 dogs. PROCEDURES: Medical records of dogs that died during or soon after competition in the Iditarod Trail sled dog races (1994 through 2006) were examined for fi ndings of gross necropsy and histologic evaluation of tissue samples. From the data, descriptive and comparative statistics were obtained. RESULTS: Recognized causes of death included aspiration of gastric contents (n = 4), aspiration pneumonia (4), acute blood loss secondary to gastric ulceration (3), and sled dog myopathy (2). A cause of death was not established for 7 dogs. Prevalent lesions among the study population included rhabdomyolysis (n = 15), enteritis (10), gastritis (10), aspiration pneumonia (8), and gastric ulceration (8). All dogs with aspiration pneumonia had concurrent gastric mucosal lesions. Subjective biventricular cardiac hypertrophy was evident in most dogs; other lesions detected frequently included centrilobular hepatic fibrosis, gastric dilatation, and mild cardiac myodegeneration and necrosis. CONCLUSIONS AND CLINICAL RELEVANCE: Unexpected death is a rare event among conditioned sled dogs during competition in endurance races. Potentially life-threatening conditions of dogs that are associated with periods of long-distance physical exertion include aspiration pneumonia, gastric mucosal lesions, and severe rhabdomyolysis. Dogs that develop clinical signs suggestive of these conditions should be excluded from strenuous activities. Epidemiologic investigations are required to clarify the risk for death associated with these lesions in dogs competing in endurance races.

Pathomorphological study on gastroduodenal ulceration in horses: localisation of lesions.

Gastroduodenal ulceration is a prevalent disease in foals and adult horses. Decreased performance as well as fatal complications relate to this syndrome. The objective of our study was to determine the prevalence of gastric ulceration in a mixed population of horses by postmortem examination and to evaluate a possible association between equine gastric ulcer syndrome (EGUS) and sex or age of the examined horses, to evaluate the localisation of lesions in the proximal part of the gastrointestinal tract and to determine the occurrence of gastric parasites. Postmortem examinations were performed on 71 horses over a period of 24 months. Gastric ulcers were found in 52 horses (73.2%). There was no significant association between age or sex and occurrence of gastric ulcers. In all horses the squamous mucosa lesions were localised near the margo plicatus (100% of the cases), whereas in 23 horses the lesions were near the margo plicatus and lesser curvature and in 7 horses at the greater curvature. In 18 horses the mucosa was affected in the whole extent of the margo plicatus and in 1 horse diffuse lesions of the squamous mucosa were noted. Lesions of the glandular mucosa were localised in 11 horses at the fundic area, in 1 horse they occurred in the pylorus, and in 10 horses diffuse lesions of the glandular mucosa were recorded. A low prevalence of Gasterophilus intestinalis infection was detected (1 horse, 1.4%). We have confirmed that gastric ulcers are a common problem in horses and duodenal or oesophageal ulceration is rare (not a single case of the latter was found in this study). Lesions in the glandular mucosa of the stomach are more frequent in suckling foals than in older animals. Lesions of the glandular mucosa are also common in adult horses, and a complete gastroscopic examination including examination of the pylorus is advisable to evaluate this syndrome.

Cholangiohepatitis and pancreatitis secondary to severe gastroduodenal ulceration in a foal.

A 2-month-old foal was presented with clinical signs of colic. Gastroduodenal ulceration was suspected. A poor response to medical treatment and signs of gastroduodenal obstruction led to celiotomy and an attempted bypass procedure. The foal was euthanized and postmortem examination revealed gastric ulceration, segmental duodenal stenosis, and severe chronic cholangiohepatitis and pancreatitis.

Bile acids in gastric fluids from llamas and alpacas with and without ulcers.

To investigate the relationship between duodenogastric reflux and ulceration, gastric fluid was collected from the 1st (n = 26) and 3rd (n = 45) gastric compartments of llamas and alpacas during postmortem examination. Gastric fluids were analyzed for the presence of bile acids. Additionally, the 3rd compartment was examined grossly for the presence of erosions or ulcers, and the intestines were examined for evidence of fluid distention. Detectable bile acids were found in the 3rd compartment fluid of 1 of 28 camelids without ulcers, 7 of 14 camelids with ulcers, and 3 of 3 camelids with intestinal distention. Third compartment bile content was significantly higher in camelids with ulcers (median = 2.9 micromol/L) or intestinal distention (median = 371.5 micromol/L) than those with neither (median = 0 micromol/L). Bile acids were detected in the 1st gastric compartment in only 2 camelids. These findings suggest a reflux of duodenal contents, including bile acids, into the 3rd compartment in camelids with ulcers, similar to what is seen in camelids with poor intestinal emptying. Whether bile reflux was the cause of the ulcers or occurred after or concurrent to their development remains unknown.

The effect of dosing interval on the efficacy of misoprostol in the prevention of aspirin-induced gastric injury.

The effect of twice-daily administration of misoprostol on aspirin-induced gastric injury was evaluated. Twenty-four random-source dogs were divided into groups that received aspirin and misoprostol as follows: group I, aspirin 25 mg/kg PO q8h and placebo PO q8h; group II, aspirin 25 mg/kg PO q8h and misoprostol 3 microg/kg PO q8h; group III, aspirin 25 mg/kg PO q8h, misoprostol 3 microg/kg PO q12h, and placebo PO q24h; and group IV, aspirin 25 mg/kg PO q8h, misoprostol 3 microg/kg PO q24h, and placebo PO q12h for 28 days. Gastroscopy was performed on days -9, 5, 14, and 28. Visible lesions were scored on a scale of 1 (mucosal hemorrhage) to 11 (perforating ulcer). No difference in total score was identified between groups I and IV on any day. Median total scores for groups II and III were significantly (P < or = .05) lower compared to groups I and IV on day 5. Group III had a significantly lower score (P < or = .05) than groups I, II, and IV on day 28. This study suggests that misoprostol 3 microg/kg PO q12h is as effective as misoprostol 3 microg/kg PO q8h in preventing aspirin-induced gastric injury in this model. However, misoprostol 3 microg/ kg PO q8h was less effective in preventing aspirin-induced gastric injury on days 14 and 28 than in previous studies. No difference among numbers of dog-days of vomiting, diarrhea, or anorexia was detected among groups.

Prevalence of gastric lesions in racing Alaskan sled dogs.

Human and equine athletes are reported to have a high prevalence of gastric disease, and anecdotal evidence suggests a similar phenomenon applies to racing sled dogs. To investigate the prevalence of gastric disease in racing sled dogs, we conducted 2 gastroscopy studies on dogs competing in the annual Iditarod Sled Dog Race. A pilot study of dogs that were either dropped from the 2000 Iditarod Sled Dog Race because of illness or that finished the race indicated that, approximately 5 days after competing, 10 of 28 dogs (35%) had endoscopic evidence of gastric ulceration, erosion, or hemorrhage. The next year, an endoscopic study of 73 dogs participating in the 2001 Iditarod race was performed in order to evaluate a larger population of dogs. Data from 70 of these dogs could be used; 34 (48.5%) had ulceration, erosion, gastric hemorrhage, or some combination of these findings. When this group of 70 dogs was compared retrospectively to a control group of 87 dogs presented to the Texas A&M University (TAMU) Veterinary Medical Teaching Hospital, the Iditarod sled dogs had a significantly higher prevalence (P = .049) of gastric lesions. These findings suggest that, similar to athletes of other species, elite canine athletes have an increased prevalence of gastric disease compared to the canine population at large.

Primary epitheliotropic intestinal T-cell lymphoma in a horse.

A 17-year-old Quarterhorse gelding with a clinical diagnosis of protein-losing enteropathy was submitted for necropsy following a 4-5-month duration of weight loss, decreased appetite, and hypoproteinemia. Gross findings included multiple 1-2-cm diameter ulcers on the luminal surfaces of the duodenum and ileum. Histologic examination revealed individual large, round cells infiltrating much of the mucosal epithelium of the duodenum, jejunum, ileum, and colon in addition to multifocal areas of ulceration. Similar round cells infiltrated Brunner's glands and expanded the submucosa beneath the foci of ulceration. Immunohistochemical staining indicated the round cell population was of T-lymphocyte origin. Several features of this equine neoplasm bear similarities to enteropathy-associated T-cell lymphoma in humans.

Gastroduodenal ulceration in cats: eight cases and a review of the literature.

Gastroduodenal ulceration (GU) and blood loss was diagnosed in eight cats and compared with 25 previously reported cases of feline GU. Cats with GU presented in a critical condition. Clinical signs consistent with gastrointestinal bleeding were infrequently identified although anaemia was a common finding. Non-neoplastic causes of feline GU tended to have a shorter clinical course with ulcers confined to the stomach. Conversely, cats with tumour-associated GU usually had a more protracted clinical course, weight loss, and ulcers located in the stomach for gastric tumours and the duodenum for extra-intestinal tumours. In this series, definitive diagnosis was possible for cats with neoplasia (gastric tumours and gastrinoma), however, it was difficult to precisely identify the underlying aetiology in cats with non-neoplastic GU. Prompt stabilisation with a compatible blood transfusion, surgical debridement or resection, antibiotic and antiulcer therapy, and treatment of the underlying disease, if identified, was successful in the majority of cases. The prognosis for cats with appropriately managed GU depended on the underlying aetiology, but even cats with neoplasia could be successfully palliated for prolonged periods.

The clinical, cerebrospinal fluid, and histopathologic effects of epidural ketorolac in dogs.

OBJECTIVE: To evaluate the clinical, cerebrospinal fluid (CSF), and histopathologic effects of epidural ketorolac. STUDY DESIGN: Blinded, randomized, placebo controlled study. ANIMALS: Twenty-two adult mixed breed dogs with 16 treatment and 6 control dogs, weighing 14.4 to 29.8 kg. METHODS: Dogs were anesthetized and epidural catheters were placed at the lumbosacral space. Catheter placement was evaluated fluoroscopically. Ketorolac (0.4 mg/kg) or placebo (5% ethanol) was administered epidurally over a 52-hour period, with 5 injections given at 12-hour intervals. At 1, 2, 4, or 8 hours after the first and last injection of ketorolac, dogs were anesthetized and CSF was obtained. Control dogs had CSF sampled 1 hour after the first and last ethanol injection. Neurologic function and pain responses were evaluated before and during the study. Selected dogs were then killed and necropsies performed. RESULTS: None of the dogs exhibited any clinical or neurologic abnormalities during the study. No statistical difference was noted in pain response or CSF analysis between treatment and control dogs. Gross necropsy revealed gastrointestinal ulceration of varying degrees in all treatment dogs. Histopathologic analysis of the spinal cord and meninges revealed minimal focal leptomeningeal phlebitis in 2 of 8 treatment dogs and minor subdural inflammation in 1 control dog. No changes to the neural structures were noted in any dogs. CONCLUSIONS: Epidural administration of ketorolac did not cause clinical signs, alteration in CSF values, or pathologic changes to the spinal cord when used for short duration. Gastrointestinal ulceration was common when ketorolac was administered epidurally at 0.4 mg/kg every 12 hours for 5 treatments. CLINICAL RELEVANCE: This study documented the neurologic safety of epidural ketorolac in dogs before an efficacy trial can be performed. Gastrointestinal ulceration may limit use to short duration or a single injection.

Abomasal bloat, haemorrhage and ulcers in young Norwegian lambs.

An abomasal syndrome affecting mainly three- to four-week-old lambs was studied by using a case-control design involving 88 cases and 85 controls. The principal clinical signs were tympany and colic. The cases were divided into three groups according to the main gross pathological findings in 82 of them. The 28 lambs in group 1 had abomasal tympany, the 29 lambs in group 2 had severe damage to the abomasal mucosa, and the 25 lambs in group 3 consisted mainly of lambs with various other diseases in combination with abomasal changes. The lambs in group 1 had a significantly (P<0.05) lower mean (se) abomasal pH (2.7 [0.19]) than those in group 2 (4.1 [0.32]), group 3 (3.7 [0.39]) or the controls (3.3 [0.13]). The ruminal pH values ranged from 3.5 to 7.4 but there were no significant differences between the groups. Lambs with ulcers had a significantly (P<0.05) higher frequency of trichophytobezoars, than the cases without ulcers or the controls. The tympanic lambs in group 1 had a significantly higher mean packed cell volume, and higher mean red and white blood cell counts, and a significantly lower mean cell volume and mean cell haemoglobin concentration than the healthy control lambs.

Sarcina -like bacteria, Clostridium fallax and Clostridium sordellii in lambs with abomasal bloat, haemorrhage and ulcers.

A study of abomasal disease in lambs aged 2-5 weeks, made during the period 1993-1998, included 67 cases and 45 non-affected controls. Gross pathological findings included various combinations of bloat, haemorrhage and ulcers in the abomasum. Sarcina -like bacteria were found in sections and smears from the abomasum of 79% (53/67) of the cases. From one case, a lamb with abomasal bloat, the anaerobic "packet"-forming Sarcina ventriculi was cultivated from the abomasal contents and identified by biochemical reactions and sequencing of the 16S rRNA gene. Sarcina -like bacteria were observed microscopically in specimens from 94% (44/47) of the lambs with abomasal gas and in 45% (9/20) of those with ulcers or haemorrhage or both but little gas. On culture, abomasal contents from 41 cases yielded Clostridium fallax from 16 (39%) and Clostridium sordellii from eight (20%); abomasal cultures from 30 control lambs were negative for the three bacterial species. Quantitative cultivation, carried out on abomasal contents from live lambs and lambs dead

Pathological alterations caused by Anoplocephala perfoliata infection in the ileocaecal junction of equids.

The pathological alterations caused by Anoplocephala perfoliata in the ileocaecal junction of 28 equids slaughtered in an abattoir in Madrid (Central Spain) are described. The lesions were scored in grades based on the intensity of the damage and were related to the tapeworm number observed. The first grade (grade I) of alterations consisted of a slight enteritis associated with focal erosions observed in 43% of parasitized animals with low parasitic burden (1-26 tapeworms). The second grade (grade II) was a focal pseudomembranous enteritis, present in the ileocaecal junctions of 36% infected animals with moderate to high burden (23-188 tapeworms), and the third grade (grade III) was a regional necrotizing enteritis, present in the animals (21%) with the highest burden (72-248 tapeworms). The possible role of the lesions caused by this parasite in the aetiology of colic is discussed.