Gastroduodenal ulceration in dogs with liver disease.

BACKGROUND: Liver disease is frequently cited as a cause of gastroduodenal ulceration (GDU) in dogs but studies regarding GDU and liver disease are limited. OBJECTIVES: To document the presence of GDU in dogs with liver disease. ANIMALS: Forty dogs that underwent liver biopsy, computed tomographic (CT) angiography or both at the University of Florida Small Animal Hospital to diagnose congenital or acquired liver disease. METHODS: Cross-sectional study. Dogs had gastroduodenoscopy performed with photographic and video documentation in a standardized fashion. Lesions (hemorrhage, erosions, ulcers) in the esophagus, stomach, and duodenum were scored based on a grading scale. Presence of esophageal varices was recorded. Dogs were categorized into 4 groups according to cause of liver disease (inflammatory disease, cirrhosis, congenital, other). Presence or absence of ulcers, erosions or both as well as total endoscopic scores were compared among groups. RESULTS: Forty dogs were enrolled with the following distribution: 13 congenital, 13 inflammatory, 3 cirrhosis, and 11 other. Four dogs had GDU (10%; 95% confidence interval [CI], 3%-24%) and 6 dogs had erosions (15%; 95% CI, 6%-30%). No difference was found in total endoscopic score (P = .21) or in the proportion of dogs with ulcers, erosions or both versus those without (P = .25) among the groups. CONCLUSIONS AND CLINICAL IMPORTANCE: Gastroduodenal ulceration was found in 10% of dogs with liver disease in this population. Additional studies are warranted to confirm these findings in larger numbers of dogs with specific disease etiologies.

Esophageal varices in dogs: A retrospective case series.

BACKGROUND: Esophageal varices (EV) are abnormally dilated veins in the esophagus caused by alterations of blood flow or pressure. Esophageal variceal hemorrhage is a major complication of hepatic disease in humans, but a lack of information exists regarding associated adverse events in dogs. OBJECTIVE: To describe the clinical manifestations and associated etiologies and outcomes of dogs with EV. ANIMALS: Twenty-five client-owned dogs with EV diagnosed via computed tomography (CT), endoscopy, or fluoroscopy. METHODS: Retrospective case series. Cases were identified by review of the hospital imaging records database between 2010 and 2020. Signalment, clinical signs, and outcomes were documented. When present, additional collateral vasculature was also recorded. Cases were subcategorized into suspected etiology based upon the anatomic location or absence of an attributable underlying disease process, as well as the direction of blood flow. RESULTS: Twenty-four of 25 cases were identified via CT, with a prevalence of 0.012% (24/1950 total studies). Presenting clinical signs were nonspecific, and more likely because of the underlying cause as opposed to complications secondary to EV themselves. Etiologic anatomic locations were similar in occurrence between the abdomen (N = 14) and thorax (N = 11). All cases with an abdominal etiologic location had presumed or confirmed portal hypertension and 9/11 cases with a thoracic etiologic location had pulmonary, caval, or systemic hypertension. No cases died or were euthanized as a direct result of EV or associated hemorrhage. CONCLUSIONS AND CLINICAL IMPORTANCE: Esophageal varices are rarely reported in dogs and commonly identified concurrently with portal, pulmonary, and caval hypertension. Hemorrhage is not a common clinical manifestation of EV.

Presumptive non-cirrhotic bleeding esophageal varices in a dog.

An 8-year-old male American Staffordshire terrier was admitted for evaluation of chronic episodes of ptyalism and hematemesis after exercise. Abnormalities were not detected on routine clinicopathological tests, thoracic radiography, and abdominal ultrasonography. Endoscopic examination revealed a labyrinthine network of severely distended, hemorrhagic esophageal blood vessels. Computed tomography angiography demonstrated a network of para-esophageal vessels that communicated with the celiac artery caudally and the brachiocephalic trunk cranially, consistent with a diagnosis of non-cirrhotic esophageal varices. This is a report of exercise, ptyalism, and hematemesis secondary to presumptive, non-cirrhotic, bleeding esophageal varices in a dog.

MULTIDETECTOR-ROW COMPUTED TOMOGRAPHY PATTERNS OF BRONCHOESPHAGEAL ARTERY HYPERTROPHY AND SYSTEMIC-TO-PULMONARY FISTULA IN DOGS.

Anomalies involving arterial branches in the lungs are one of the causes of hemoptysis in humans and dogs. Congenital and acquired patterns of bronchoesophageal artery hypertrophy have been reported in humans based on CT characteristics. The purpose of this retrospective study was to describe clinical, echocardiographic, and multidetector computed tomography features of bronchoesophageal artery hypertrophy and systemic-to-pulmonary arterial communications in a sample of 14 dogs. Two main vascular patterns were identified in dogs that resembled congenital and acquired conditions reported in humans. Pattern 1 appeared as an aberrant origin of the right bronchoesophageal artery, normal origin of the left one, and enlargement of both the bronchial and esophageal branches that formed a dense network terminating in a pulmonary artery through an orifice. Pattern 2 appeared as a normal origin of both right and left bronchoesophageal arteries, with an enlarged and tortuous course along the bronchi to the periphery of the lung, where they communicated with subsegmental pulmonary arteries. Dogs having Pattern 1 also had paraesophageal and esophageal varices, with the latter being confirmed by videoendoscopy examination. Authors conclude that dogs with Pattern 1 should be differentiated from dogs with other congenital vascular systemic-to-pulmonary connections. Dogs having Pattern 2 should be evaluated for underlying pleural or pulmonary diseases. Bronchoesophageal artery hypertrophy can be accompanied by esophageal venous engorgement and should be included in the differential diagnosis for esophageal and paraesophageal varices in dogs.

Acquired portal collateral circulation in the dog and cat.

We describe patterns of acquired portal collateral circulation in dogs and in a cat using multidetector row computed tomography angiography. Large portosystemic shunts included left splenogonadal shunts in patients with portal hypertension. Small portal collaterals were termed varices; these collaterals had several patterns and were related either to portal vein or cranial vena cava obstruction. Varices were systematized on the basis of the venous drainage pathways and their anatomic location, namely left gastric vein varix, esophageal and paraesophageal varices, gastroesophageal and gastrophrenic varices, gallbladder and choledocal varices, omental varices, duodenal varices, colic varices, and abdominal wall varices. As reported in humans and in experimental dog models, esophageal and paraesophageal varices may result from portal hypertension that generates reversal of flow, which diverts venous blood in a cranial direction through the left gastric vein to the venous plexus of the esophagus. Blood enters the central venous system through the cranial vena cava. Obstructions of the cranial vena cava can lead to esophageal and paraesophageal varices formation as well. In this instance, they drain into the azygos vein, the caudal vena cava, or into the portal system, depending on the site of the obstruction. Gallbladder and choledocal varices, omental varices, duodenal varices, phrenico-abdominal varices, colic varices, abdominal wall varices drain into the caudal vena cava and result from portal hypertension. Imaging plays a pivotal role in determining the origin, course, and termination of these vessels, and the underlying causes of these collaterals as well. Knowledge about these collateral vessels is important before interventional procedures, endosurgery or conventional surgery are performed, so as to avoid uncontrollable bleeding if they are inadvertently disrupted.

Equid herpesvirus 2-associated oral and esophageal ulceration in a foal.

A case of a 1-month-old Thoroughbred foal with dysphagia, salivation, pyrexia, oral mucosal pustules, and esophageal ulceration is reported. Swabs from the ulcerated lesions yielded Equid herpesvirus 2 (EHV-2) in virus isolation assays, and histopathology of a biopsy from the esophageal lesion identified nuclear inclusions suggestive of herpesviruses. Immunohistochemical staining with antibodies specific for EHV-2 was positive for epithelial cells in the vicinity of the ulcer but not in more distant mucosa. Electron microscopic evaluation of the biopsy showed herpesviral particles in epithelial cells. The foal recovered over 5 days of supportive and gastroprotective therapy, and the esophageal ulcers healed. Serology and immunohistochemistry indicated that this foal likely had lesions associated with EHV-2 and not EHV-1, -4, or -5.

A reproducible canine model of esophageal varices.

One of the most promising nonoperative techniques for control of variceal hemorrhage is sclerosis via the fiberoptic endoscope. Many questions remain, however, about sclerosing agents, guidelines for effective use, and limitations of endoscopic techniques. A reproducible large animal model of esophageal varices would facilitate the critical evaluation of techniques for variceal hemostasis or sclerosis. Our purpose was to develop a large animal model of esophageal varices. Studies in pigs and dogs are described which led to the development of a reproducible canine model of esophageal varices. For the final model, mongrel dogs had laparotomy, side-to-side portacaval shunt, inferior vena cava ligation, placement of an ameroid constrictor around the portal vein, and liver biopsy. The mean (+/- SE) pre- and postshunt portal pressure increased significantly from 12 +/- 0.4 to 23 +/- 1 cm saline. Weekly endoscopies were performed to grade the varix size. Two-thirds of animals developed medium or large sized esophageal varices after the first operation. Three to six weeks later, a second laparotomy with complete ligation of the portal vein and liver biopsy were performed in animals with varices (one-third of the animals). All dogs developed esophageal varices and abdominal wall collateral veins of variable size 3-6 wk after the first operation. After the second operation, the varices became larger. Shunting of blood through esophageal varices via splenic and gastric veins was demonstrated by angiography. Sequential liver biopsies were normal. There was no morbidity or mortality. Ascites, encephalopathy, or spontaneous variceal bleeding did not occur. We have documented the lack of size change and the persistence of medium to large esophageal varices and abdominal collateral veins in all animals followed for more than 6 mo. Variceal bleeding could be induced by venipuncture for testing endoscopic hemostatic and sclerosis methods. We suggest other potential uses of this reproducible canine model of esophageal varices.