Chronic hypertrophic pyloric gastropathy as a cause of pyloric obstruction in the dog

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.     

Perforated gastric ulcer v associated with pyloroplasty for chronic hypertrophic pyloric gastropathy in a dog

A six-year-old male silkie terrier presented with a history of chronic vomiting. A diagnosis of gastric outflow obstruction was made using contrast radiography of the upper gastrointestinal tract. Surgical examination of the stomach revealed thickened pyloric antral mucosa. A Heineke-Mikulicz pyloroplasty combined with resection of the hypertrophic pyloric mucosa were performed to increase the patency of the pyloric lumen. The dog recovered well from surgery and his condition remained stable until the sixth day postoperatively when his condition deteriorated rapidly resulting in his death that night. At autopsy a perforated gastric ulcer was found in the cardiac region of the pylorus with evidence for a generalised peritonitis. An association between gastric outflow obstruction and gastric ulceration has been reported in human clinical literature and in canine experimental models. No such association has been previously documented in the veterinary clinical literature.     

Chronic hypertrophic pyloric gastropathy in 14 dogs

SUMMARY Ten mate and 4 female dogs with chronic hypertrophic pyloric gastropathy were seen at the Sydney University 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 complications 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.     

Uremic gastropathy in the dog.

Stomachs of four dogs with uremia and four normal dogs were examined. Uremic stomachs represented four types of disease: atrophic, amyloidotic, ulcerative and necrotic gastropathy. Pathologic changes common to all uremic stomachs were expansion of the lamina propria, atrophy of gastric glands, and submucosal arteriopathy; lesions were limited to body and fundic zones. Lamina propria was markedly expanded by edema, mastocytosis, deposition of acidic mucosubstances, fibroplasia and mineralization. Capillaries in lamina propria had swollen endothelium and calcium salts were present extracellularly as amorphous granular laminae. Gastric glands were distorted and irregular and had fewer cells per unit of tissue. Parietal cells were swollen and had fragmentation of cytocavitary network and mitochondrial swelling with calcification. Chief cells were shrunken, agranular and atrophic with foci of glycogen and dilation of endoplasmic reticulum. Argentaffin cell content was diminished. Muscular arteries of submucosae had segmental degenerative lesions characterized by myocyte necrosis, calcification, and deposition of acidic mucosubstances and fibrin; thrombosis and obstructive arteriopathy were common. These studies suggest that uremic gastropathy is a disease of mucosal lamina propria and that lesions were due to anoxia caused by diffuse vascular injury and to altered parietal cell function.     

Focal cystic endometrial hyperplasia in a bitch

Rapid abdominal enlargement and weight gain occurred in a four-year-old Rhodesian ridgeback bitch in late oestrus. The bitch was nulliparous. Severe cardiovascular dysfunction followed and an exploratory laparotomy was performed. A large, single, spheroid mass weighing 17 kg was located in the middle section of the left uterine horn. A diagnosis of sterile, focal, cystic endometrial hyperplasia was made from gross pathology, histopathol-ogy and bacteriology. The bitch made a complete recovery following an ovariohysterectomy.     

Focal myasthenia gravis in a dog.

A 10-month-old American cocker spaniel was evaluated for megaesophagus, aspiration pneumonia, but no appendicular muscle weakness. During hospitalization, weakness of the facial muscles developed, this resolved with anticholinesterase administration. Serum antibodies against acetylcholine receptors were documented, confirming the diagnosis of focal myasthenia gravis. Diagnosis, management, and medical treatment are discussed.     

Cerebellar cystic meningioma in a dog

A 21-kg, seven-year-old, male, mixed-breed Labrador retriever was admitted for incoordination and a head tilt of approximately three months' duration. Ataxia was noted of the trunk and limbs, and there was a head tilt to the right side. Conscious proprioceptive deficits were present in the left thoracic and pelvic limbs (i.e., hemiparesis). These abnormalities were consistent with paradoxical vestibular syndrome and a lesion involving the caudal cerebellar peduncle. A mass lesion consisting primarily of fluid was present on magnetic resonance imaging and at craniectomy. Histopathological diagnosis was a cystic meningioma. Based upon previous reports and experience, the location of this tumor was unusual.     

Massive cystic tetrathyridiosis in a dog

This report describes a case of massive cystic tetrathyridiosis in a four-year-old female dobermann. The larvae were distributed in both the peritoneal and pleural cavities, as well as in the lumen of the small intestine along with adult Mesocestoides species. These parasites were identified as tetrathyridia. Numerous cysts were dispersed on the peritoneal, pleural and mesenteric surfaces. The same cysts were seen both on subcapsular surfaces and within sections of the spleen, liver, kidneys and lungs. Histopathological examination also revealed characteristics of tetrathyridium of Mesocestoides species.     

Polyostotic cystic bone lesions in a dog

The clinical, radiological, and pathological features of a polyostotic cystic bone lesion in a 9-month-old Doberman Pinscher are described. The patient was diagnosed as having nutritional secondary hyperparathyroidism at 6 weeks of age and after dietary correction it remained clinically normal until 9 months when there was sudden left hind-limb lameness due to a pathological fracture through a cystic lesion in the distal femur. Radiography revealed additional cystic structures in the metaphyses of the left radius, and left and right tibia. Pseudofractures were associated with two of the cystic lesions.
In some areas the cysts were crossed by trabeculae and in others there were bony ridges on the inner cystic wall. The cavities were lined with flesh-coloured fibrillar material which formed a lacy network extending into cavities. Histologically, multiple small cysts were present adjacent to the larger cavities noted radiographically. The secondary spongiosa and the metaphyseal periosteum were the major abnormal tissue sites. The small cysts appeared to arise in an oedematous and congested metaphyseal spongiosa. The cysts were accompanied by small foci of intense osteoclasis but unattended by compensatory bone production, and the consequent possibility of pseudofractures is an important clinical consideration. Earlier reports demonstrated that resolution of the lesions will follow surgical drainage and curettage of the cystic cavity. Of six cases of polyostotic cystic bone lesions observed in the dog, five were in the Doberman Pinscher breed.     

Regression of hypertrophic osteopathy following pneumonectomy in a dog

Hypertrophic osteopathy was diagnosed clinically and radiographically in a 6-year-old English Bulldog. Pneumonectomy to remove a primary pulmonary fibrosarcoma resulted in rapid regression of clinical signs and soft tissue enlargement of the limbs and gradual but incomplete regression of periosteal new bone formation over a 15-month postoperative course.     

Focal mastocytosis in lymph nodes from a Beagle dog.

An 11-year-old Beagle dog had focal mastocytosis in the midtracheobronchial and left tracheobronchial lymph nodes. The cells were well-differentiated and were arranged in well-defined follicles. There were neither skin tumors nor mast-cell accumulations in other tissues.     

Endoscopic management of a cystic naso-lacrimal obstruction in a dog

A young adult Dachshund was presented with a cystic obstruction of the nasolacrimal duct causing maxillo-turbinate destruction but no epiphora. The lesion was demonstrated by dacryocystorhinography and identified on nasal endoscopy which also permitted the successful creation of a permanent fistula without resort to invasive surgery. Histological examination of the cystic wall of the duct showed normal turbinate structures replaced by chronic inflammatory tissue.     

Hypertrophic gastropathy associated with gastric sarcoma in a dog

A 14-y-old spayed female Labrador Retriever was presented with an 8-mo history of chronic vomiting. Abdominal ultrasound and gastrointestinal endoscopy revealed a mass protruding into the gastric lumen, with cytologic features suggestive of sarcoma. A partial gastrectomy was performed; the gastric body and antrum were thickened, with a cerebriform appearance of the mucosal surface. Histologic examination revealed a submucosal neoplastic proliferation of fusiform cells variably arranged in irregular bundles and scattered whorls. Fusiform cells strongly reacted to antibodies against vimentin, S100, and neuron-specific enolase; glial fibrillary acidic protein was moderately and multifocally expressed. Pancytokeratin, KIT, α–smooth muscle actin, and desmin were nonreactive. Histologic and immunohistochemical findings suggested a diagnosis of gastric sarcoma with features referable to a non-GIST (gastrointestinal stromal tumor), non–smooth muscle NIMT (non-angiogenic, non-lymphogenic intestinal mesenchymal tumor). The overlying gastric mucosa was thickened by elongated and dilated gastric glands, predominantly lined by intensely periodic acid-Schiff–stained mucous cells. This altered mucosal architecture was suggestive of Ménétrier-like disease. Although this disease has been hypothesized to predispose to gastric adenocarcinoma in dogs, an association with gastric sarcoma has not been documented previously in the veterinary literature, to our knowledge.     

Escherichia coli bacteremia associated with hypertrophic osteodystrophy in a dog.

Escherichia coli bacteremia was detected in a dog that had hypertrophic osteodystrophy. The dog improved after treatment with cephalothin sodium, iv fluid therapy, and cage rest. The cause of hypertrophic dystrophy has not been determined, although an infectious cause has been suggested. Dogs that are suspected of having hypertrophic osteodystrophy should be monitored closely for evidence of septicemia, and the administration of prophylactic antibiotics may be advisable.     

Cardiogenic hypertrophic osteopathy in a dog with a right-to-left shunting patent ductus arteriosus

A 5-year-old castrated male Shetland Sheepdog was examined because of progressive bilateral hind limb thickening. Cyanosis of the preputial mucous membranes was evident, whereas the oral mucous membranes had a normal color. A well-structured, palisade-like periosteal reaction with no underlying bone destruction was evident on radiographs of the hind limbs. The radiographic changes were consistent with hypertrophic osteopathy (HO). Severe right-sided cardiomegaly was seen on thoracic radiographs, and a diagnosis of patent ductus arteriosus with right-to-left shunting was made by means of echocardiography and contrast echoaortography. The cyanotic heart disease was believed to be the cause of the HO. Hypertrophic osteopathy has been associated with a number of diseases in animals and humans. In humans, congenital heart defects that cause cyanosis are among the most common causes of HO.