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Acquired pyloric narrowing is a rare and poorly-documented condition in cats, but the endoscopic appearance of pyloric narrowing has never previously been reported. The objectives of this study were to describe the clinical, endoscopic and histological features in cats with gastrointestinal signs where the pylorus could not be passed during endoscopy, and to compare these data with a control group. Medical files of cats that underwent upper GI endoscopy by the same operator between 2006 and 2015 were reviewed. Cats for which the pylorus could not be passed were assigned to the case group, whilst those with an easily-passable pylorus were assigned to the control group. The case group comprised 27 cats and control group comprised 35 cats. Median age and weight were not different between groups, but there were more Siamese cats in the case group (6/27) compared with the control group (1/35; P = 0.04). Chronic vomiting was the main clinical sign in both groups, but the vomitus was more likely to contain food in case group (23/25) than in cats in control group (17/30; P < 0.01). Endoscopic findings confirmed gastric inflammation in both groups, whilst histological findings revealed similar lymphoplasmacytic infiltration of the gastric mucosa and the duodenum in most cases, neoplastic features being infrequent. Acquired pyloric narrowing is probably an underdiagnosed condition in adult cats. A possible association between pyloric narrowing and gastrointestinal inflammatory disease requires further study but, for now, it is recommended that multiple gastric, pyloric, and duodenal biopsies be acquired during the endoscopy., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Case Description: A 5-month-old 1.9-kg (4.2-lb) spayed female Siamese cat was evaluated because of a history of decreased appetite, regurgitation, vomiting, and lack of weight gain., Clinical Findings: Radiographic findings included a fluid- and gas-distended stomach with a small accumulation of mineral opacities. Ultrasonographic examination confirmed severe fluid distention of the stomach with multiple hyperechoic structures present and revealed protrusion of the thickened pylorus into the gastric lumen, with normal pylorogastric serosal continuity. Endoscopy of the upper gastrointestinal tract revealed an abnormally shortened pyloric antrum and stenotic pyloric outflow orifice. Pyloric stenosis resulting in pyloric outflow obstruction was diagnosed., Treatment and Outcome: A pylorectomy with end-to-end gastroduodenostomy (Billroth I procedure) was successfully performed, and a temporary gastrostomy tube was placed. Six days after surgery, the cat was eating and drinking normally, with the tube only used for administration of medications. The gastrostomy tube was removed 12 days after surgery. Results of follow-up examination by the referring veterinarian 3 weeks after surgery were normal. Occasional vomiting approximately 2 months after surgery was managed medically. Fifteen months after surgery, the owners reported that the cat seemed completely normal in appearance and behavior., Clinical Relevance: Pyloric stenosis should be considered a differential diagnosis for young cats with pyloric outflow obstruction. The cat of this report was treated successfully with a Billroth I procedure. Histologic examination and immunohistochemical analysis of the excised tissue showed the stenosis to be associated with hypertrophy of the tunica muscularis.

A 10-week old male Hovawart presented with acute renal failure. Based on clinical symptoms, blood analysis results and serology, a diagnosis of leptospirosis was made. Besides being acotemic, the puppy was initially also severely hypercalcemic. The dog was treated successfully, but developed widespread cutaneous and visceral calcifications. Severe pyloric calcification resulted in functional pyloric obstruction, which was successfully treated by pyloromyotomy. All skin lesions were cured with topical therapy within a few weeks. To the authors' knowledge, this is the first report of generalized intestinal and cutaneous calcification associated with acute renal failure due to Leptospirosis.

Atropine, an anticholinergic agent commonly used in human and veterinary medicine, is reported to cause toxicity associated with its antimuscarinic action. A juvenile pygmy sperm whale, Kogia breviceps, was treated with atropine in an attempt to relieve symptoms similar to pyloric stenosis, as has been used in humans. Two doses of 0.01 mg/kg were given i.m., 12 hr apart, followed by three doses of 0.005 mg/kg i.m. s.i.d. over the next 3 days. Symptoms associated with atropine toxicity developed gradually and included hyperexcitability, a generalized ascending paralysis of body musculature, shallow, rapid respiration, vomiting, aspiration of seawater, and pulmonary edema. Treatment with physostigmine salicylate (two doses of 2 mg i.m., I hr apart) was effective in counteracting the paralysis, as well as other symptoms, beginning in as little as 17 min after the first dose, and the whale was back to swimming on its own after 8 hr. All overt symptoms of atropine toxicity were gone in about 24 hr, but there were other possible sequella that lasted much longer.

Objective: To determine the origin of the nonacid (nonparietal) component of gastric secretions in horses induced by pentagastrin infusion., Animals: 6 horses., Procedure: A Latin square design was used, involving 6 horses, 3 treatments, and 2 duodenal intubation conditions (catheter with balloon to obstruct pylorus [B] or without balloon allowing movement of contents between stomach and duodenum [NB]). Each horse had an indwelling gastric cannula and a catheter positioned in the duodenum. Gastric and duodenal contents were collected during 15-minute periods. Each experiment consisted of serial collection periods: baseline; infusion of pyrilamine maleate (1 mg/kg of body weight, IV); not treated; and IV infusion of saline (0.9% NaCl) solution alone, saline solution containing pentagastrin (6 microg/kg x h), or saline solution containing histamine (30 microg/kg x h). Volume of samples was recorded, and electrolyte concentrations were measured., Results: Pentagastrin and histamine stimulated maximal acid output; however, during NB conditions, pentagastrin-induced concentration of hydrogen ions was significantly less than during histamine or pentagastrin infusions during B conditions. The large volume produced in response to pentagastrin during NB conditions was accompanied by increased sodium ion output that was greater than for pentagastrin during B conditions, but both values were significantly greater than values for histamine during B or NB conditions., Conclusions and Clinical Relevance: Nonparietal secretions collected during IV infusion of pentagastrin are duodenal in origin. Reflux of duodenal contents into the stomach of horses is enhanced by pentagastrin. Flow of duodenal contents into the stomach could have implications in the pathogenesis of ulcers in horses.

An adult dog with pyloric obstruction was anesthetized with thiamylal and halothane for surgical revision. When an ECG was attached, the QRS-complex rate was noted to differ dramatically from the peripheral pulse rate. A dorsal pedal arterial catheter was introduced, and direct arterial pressure measurements revealed a blood pressure waveform that alternated in amplitude. Blood pressure and ECG traces were recorded, and the condition was diagnosed as pulsus alternans. The inhalation anesthetic was changed to isoflurane, and the condition was resolved.

The clinical findings, the autopsy and the histology of functional pyloric stenosis in three sheep between four and eight years old are described. A chronic ulcer with structural alterations of the pyloric protuberance was found in the first animal. In the second sheep there were several polyps in the pylorus, and in the third erosions throughout the whole pylorus, and a few hyperplastic areas of epithelium at the junction between pylorus and duodenum. The abomasum was moderately to extremely congested and the contents weighed between 6.7 and 13 kg. In addition to these findings chronic and unspecific abomaso-duodenitis was found in all three sheep. These three cases can be attributed to the distal functional pyloric stenosis (Hoflund syndrome).

Diagnosis and treatment of pyloric stenosis in the dog are described. The most common causes in 47 dogs were hypertrophic and functional pyloric stenosis. These conditions were mostly seen in young, male dogs of brachycephalic breeds. In contrast with the literature no indications were found for a predisposition in miniature breeds. Hypertrophic stenosis was treated successfully with the Fredet-Ramstedt pyloromyotomy. Functional stenosis and hypertrophic gastritis were mainly treated with the Heineke-Mikulicz pyloroplasty; good results were obtained in more than half of the cases.

Ten male and 4 female dogs with chronic hypertrophic pyloric gastropathy were seen at the Sydney Veterinary Teaching Hospital in the period 1982-88. The most commonly affected breeds were the Shihtzu and Maltese. The mean age was 8.2 yr and the mean body weight 6.5 kg. The most common clinical signs were vomiting, weight loss, polydipsia and depression. Hypokalaemia was present in 11 of 12 dogs examined and hypochloraemia in 10 of 11 dogs examined. Five of the six dogs that had blood gases measured were found to have a metabolic alkalosis. Surgery was performed on 13 dogs; pyloromyotomy 7, pyloroplasty 4, gastroduodenostomy 2. There was a recurrence of symptoms in one pyloromyotomy dog, and fatal ulceration and perforation of the cardia occurred in one pyloroplasty case. The remaining 11 dogs had a mean known symptom-free survival time of 20 mo. This study confirms the preponderance of affected males, identifies electrolyte and blood gas disturbances as significant complication of chronic hypertrophic pyloric gastropathy, and suggests that relatively minor surgery (pyloromyotomy) may have a place in the treatment of a selected subgroup of cases.

The clinical features and changes in blood and rumen fluid, and the results of therapy are described in 10 cows suffering from acute functional pyloric stenosis. The general condition of the cows was moderately to severely disturbed. The abdomen of most of them was distended on one or both sides and the rumen was excessively full. Defecation was reduced or absent. In most of them there was moderate or severe abomasal reflux-syndrome. Exploratory laparotomy or slaughter revealed a grossly distended abomasum which was filled with ingesta but not displaced. The omasum, reticulum and rumen of most of the cows were dilated secondarily and filled with ingesta. Six of the cows were treated by the administration of a solution of sodium chloride, glucose and potassium chloride intravenously, and metoclopramide intramuscularly. Five cows recovered within a short time, general condition, appetite and defecation were again normal and the abomasal and ruminal function returned within three days.

In the complex called vagal indigestion two main types of stenosis can be distinguished, pyloric stenosis and stenosis between the reticulum and omasum or reticulo-omasal stenosis. Laboratory examinations of blood and rumen fluid were carried out in 10 cows with reticulo-omasal stenosis. The results are discussed with respect to the differential diagnoses of pyloric stenosis. In the cows with reticulo-omasal stenosis no metabolic alkalosis occurred and consequently dehydration and uraemia did not develop. For the clinician valuable points of difference were a more prolonged and chronic course and, on physical examination, the absence of serious circulatory disturbances and the absence of an ammoniacal-uraemic odour in the expired air. The clinical picture of reticulo-omasal stenosis strongly resembles a syndrome described as failure of omasal transport.

Partial pyloric obstruction causing gastric retention is described in 2 young female horses. Gastric retention was confirmed by contrast radiography of the upper gastrointestinal tract. In both horses a large mass was palpated in the wall of the pyloric antrum at exploratory laparotomy. Post-mortem examination of the first case confirmed that this mass was associated with chronic gastric ulceration. Gastric ulceration was not confirmed in the second case but this horse recovered after the pylorus and duodenum were bypassed by gastro-jejunostomy.

In a 2 year period at Children's Hospital of Philadelphia, seven human infants and a baby orangutan all presented with a previously unreported association of a prepyloric membrane and hypertrophic pyloric stenosis. In the humans, the pyloric stenosis was the obstructive lesion, and in the orangutan, the web. We also report a 6-year-old patient with previous pyloromyotomy who presented because of prolonged retention of a marble in the stomach by an associated antral membrane.

Gastric outlet disease in the dog and cat can be successfully managed by various surgical techniques. Diagnosis is based upon clinical history, radiographic, fluoroscopic and endoscopic studies, and histological examination of excised tissue. Procedures that can improve gastric outflow include pyloromyotomy, various pyloroplasties, and antrectomy with gastroduodenostomy or gastrojejunostomy. Complications are both perioperative and long-term. A successful outcome is dependent upon proper diagnosis, complete assessment of both related and concurrent disease states, proper selection of surgical procedure, careful surgical technique, and attention to postoperative and long-term complications.

A two month old Thoroughbred filly was presented with signs of depression, grinding of the teeth, frothing of the mouth and abdominal pain. These signs had persisted for two weeks despite treatment with mineral oil, dioctyl sodium sulfosuccinate, meperidine and antibiotics. A variety of diagnostic tests were done, the only abnormal finding was a stress leukon. On exploratory laparotomy the stomach was dilated with fluid and gas and the pyloric canal was constricted. Pyloroplasty resulted in correction of the condition. The etiological possibilities are discussed. This is believed to be the first report of pyloric stenosis in the horse.

Six small-breed, middle-age dogs with a history of chronic intermittent vomiting had benign pyloric lesions causing gastric outlet obstruction. Marked similarities were found in clinical signs, pathologic changes, and treatment results. The condition was classified as a syndrome and was named chronic hypertrophic pyloric gastropathy. The appearance of the obstructive lesions at surgery were various forms of mucosal hypertrophy. Microscopically, the syndrome was characterized by mucosal foveolar and glandular hyperplasia, cystic glandular dilatation, superficial mucosal ulcerations, and various cellular infiltrates. The affected dogs were successfully treated by surgical correction of the gastric outlet obstruction.

Intestinal surgery in the foal is seldom necessary but some conditions in which it is essential are well recognized. The foal is a good surgical subject but success depends mainly on operating promptly before irreversible degenerative changes take place. Exploratory laparatomy is recommended whenever mechanical obstruction is suspected. Indications fall broadly into two main categories: 1. Cases arising from congenital defects. These form a miscellaneous group and present considerable difficulties in diagnosis and effective treatment. 2. Cases related to acute onset of obstruction, mainly due to volvulus or torsion. By far the most important condition in this category is volvulus of the ileum close to the ileocaecal valve. Aetiological factors are discussed, and the value of resection of affected small intestine and creation of a new jejuno-caecal opening is indicated. It is suggested that with improvement of such techniques it will be possible to save a higher proportion of foals suffering from mechanical intestinal obstruction.

One potential complication of blind abomasopexy techniques, including the toggle-pin technique, is the possibility of creating pyloric outflow obstruction. Cows that have had left displaced abomasum corrected by this method should be observed closely for the first 48 postsurgical hours for signs of deterioration. If pyloric obstruction is suspected and the securing sutures are cut before fibrous adhesions have formed, permanent damage may be minimized.

Hypertrophic pyloric stenosis was observed to occur naturally in laboratory rabbits. Three cases in juvenile and adult rabbits and their antemortem histories were examined. The gross and microscopic pathology were studied. It was shown that not only the pylorus, but the stomach as a whole was increased in size both relatively and absolutely. The thickness of the pylorus was doubled, but its circumference was not increased, in hypertrophic stenosis. The chief histologic finding was hypertrophy of circular and longitudinal smooth muscles and their enveloping fascia. The myenteric plexi were essentially normal in appearance. The literature on a similar condition in man, dog, and cat was reviewed.

Paraesophageal hiatal herniation and pyloric obstruction were diagnosed in a pup with a history of vomiting. Findings of contrast radiography included esophageal reflux, delayed gastric emptying time, and paraesophageal herniation. Exploratory celiotomy revealed increased firmness of the pylorus and a primary defect in the esophageal hiatus, which allowed gastric herniation. Nissen fundoplication was performed following reconstruction of the esophageal hiatus, and pyloroplasty was performed to relieve the gastric outlet obstruction. Pyloric biopsy findings were consistent with a diagnosis of chronic gastritis. Recovery from surgery was initially unremarkable; however, the dog died suddenly 3 weeks after surgery. Necropsy revealed a large diaphragmatic hernia adjacent to the esophageal hiatus; the hernia had resulted in incarceration of the abdominal organs. The hiatal hernia reconstruction remained intact and was not the cause of the diaphragmatic disruption.

In 23 cows suffering from a secondary indigestion, in most cases with septicaemia, the syndrome of functional pyloric stenosis or vagal indigestion developed. The signs were anorexia, ruminal distension with fluid material, abomasal reflux into the ruminoreticulum, dehydration, hypochloraemic, hypokalaemic metabolic alkalosis and uraemia. These signs often disappeared after treatment of both the primary causative disease and the secondary indigestion. The importance of recognising this condition is emphasised, because the serious signs of the secondary indigestion may dominate the causative disease. The prognosis depends upon the causative disease and is not necessarily bad.