The findings of ultrasonography of the gastrointestinal (GI) tract of 265 dogs with GI disorders were analysed retrospectively. The sonographic changes associated with various inflammatory and neoplastic conditions and mechanical obstruction of the GI system were recorded and discussed. Sonographic alterations of the pancreas and the tissues adjacent to the GI tract were also included in the study. Ultrasonographic alterations of the GI tract were classified into three main categories: thickening of the GI wall, changes in peristalsis and dilation of the lumen. Localised thickening of the GI wall with disruption of its structure was caused by both neoplastic diseases and by inflammatory disorders. However, diffuse thickening with retained wall structure was generally associated with inflammatory diseases. The criteria previously established for the ultrasonographic diagnosis of intestinal obstruction were successfully applied to a large number of GI disorders. Pancreatitis was most often associated with hyperechoic mesentery and hypoechoic pancreas mass, but similar alterations were encountered in some cases of gastric or duodenal ulceration. Except in cases of invaginations and intestinal obstructions, the observed ultrasonographic changes were not specific enough for a definitive diagnosis. Nevertheless, ultrasonography proved to be a valuable technique in the diagnostic process of GI disorders of the dog.
Percutaneous ultrasound-guided cholecystocentesis was performed on 13 healthy beagle dogs to determine whether percutaneous ultrasound-guided cholecystocentesis in the dog was a feasible and safe procedure. Clinical, laboratory and ultrasonographic examinations were done at 0 and 10 minutes, in the 2nd and 16th hour, and on the 7th day. They included a detailed physical examination of the mucous membranes, cardiorespiratory system and abdominal organs. Laboratory examinations of the blood consisted of a complete blood count, determination of packed cell volume (PCV), haemoglobin (Hb), total plasma protein (TPP), parameters of haemostasis including prothrombin time (PT), activated partial thromboplastin time (APTT), and enzyme activities reflecting hepatobiliary function, i.e. aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gamma-glutamyltransferase (GGT). Ultrasonographic findings of the gallbladder (size, shape, wall, content) and appearance of the biliary tract and the surrounding cranial intraabdominal organs were also evaluated. Percutaneous ultrasound-guided cholecystocentesis was performed easily during the study, and dogs tolerated well the procedure performed without anaesthesia. All laboratory parameters of the blood remained within normal limits throughout the study. However, some follow-up values, i.e. PCV, TPP, APTT and ALT, demonstrated statistically significant differences when compared to baseline measurements, which might reflect the effect of 24-hour fasting before the experiment, as well as day-to-day metabolic fluctuations due to feeding and water supply during the study. There were no visible signs of bleeding from the liver, bile leakage from the gallbladder or accumulation of free peritoneal fluid during repeated ultrasonographic examinations. Percutaneous ultrasound-guided cholecystocentesis seems to be an important diagnostic procedure in canine gallbladder diseases and can be used safely and easily to gain gallbladder bile for diagnosis of bacterial cholecystitis or for investigating hepatobiliary function in the dog.
The aim of this study was to characterise the development of cardiac dilatation induced by chronic volume overload in 12 dogs. Bilateral arteriovenous fistulas were created between the common femoral arteries and the femoral veins, and the animals were serially studied with transthoracic echocardiography for a period of 12 weeks after the operation. Compared to the measurements obtained before the operation (week 0), the data obtained at the end of the experimental period showed significantly increased left ventricular volume measured by 2D-echocardiography (from 25.1 cm
to 43.8 cm
, p < 0.0001 in diastole and from 8.6 cm
to 16.8 cm
, p < 0.001 in systole), and left ventricular diameter measured by M-mode echocardiography (from 26.2 mm to 32.6 mm, p < 0.0001 in diastole and from 17.1 mm to 20.6 mm, p < 0.001 in systole). The size of the left atrium also increased in transversal (from 29.2 mm to 33.6 mm, p < 0.01) but not in longitudinal diameter. In spite of a significant cardiac chamber dilatation over the 12-week period, left ventricular systolic functional variables (fractional shortening, FS % and ejection fraction, EF %), and also the left ventricular systolic and diastolic free wall thickness remained unchanged. In this study we demonstrated that chronic progressive volume overload resulted in gradual dilatation of the canine heart, and that the pathological process can be monitored successfully by serial echocardiography. We found that left atrial dilatation occurred without the development of mitral regurgitation and/or detectable left ventricular dysfunction.
In this study one spleen-intact dog (A) and two splenectomised dogs (BSE, CSE) were infected with Babesia canis. All animals developed an acute disease characterised by fever, haemoglobinuria and anaemia, the latter being more severe in the splenectomised dogs. Fever and parasitised red blood cells were detected for three days after imidocarb treatment in the splenectomised animals. Haematological abnormalities included regenerative anaemia, thrombocytopenia and leukopenia (due to neutropenia and lymphopenia) in the acute phase, soon followed by leukocytosis, neutrophilia and left shift a few days later. Acute hepatopathy was detected in all dogs with elevated ALT activity, which was more seriously altered in the splenectomised dogs. Diffuse changes in liver structure and hepatomegaly were seen by ultrasonography. Liver biopsy and histology revealed acute, non-purulent hepatitis in the splenectomised dogs. Both splenectomised dogs were successfully cured after collection of 400 ml highly parasitised blood, proving that large-amount antigen production is possible with rescuing the experimental animals. Whole blood transfusion, imidocarb and supportive care with infusions, antipyretics, glucocorticoids and diuretics were applied. The spleen-intact dog clinically recovered after receiving supportive treatment, with no imidocarb therapy. Microbial infections developed in both splenectomised animals (BSE: haemobartonellosis, CSE: osteomyelitis caused by Escherichia coli), probably as a consequence of immunosuppression after splenectomy and glucocorticoid therapy.
Findings of hepatic and gallbladder ultrasonography were analyzed in 12 dogs with gallbladder and/or extrahepatic biliary tract obstruction and compared with the results of exploratory laparotomy. Hepatic ultrasonography demonstrated normal liver in 2 dogs and hepatic abnormalities in 10 animals. The following ultrasonographic diagnoses were established compared to surgical findings: gallbladder obstruction caused by bile sludge (correct/incorrect: 1/2, surgical diagnosis: choleliths in one case), gallbladder obstruction caused by neoplasm (0/1, surgical diagnosis: mucocele), gallbladder and extrahepatic biliary tract obstruction due to choleliths (3/3), extrahepatic biliary tract obstruction caused by pancreatic mass (1/1) and small intestinal volvulus (1/1). Bile peritonitis caused by gallbladder rupture (4/4) was correctly diagnosed by ultrasound, aided with ultrasonographically-guided abdominocentesis and peritoneal fluid analysis. Rupture of the gallbladder should be suspected in the presence of a small, echogenic gallbladder or in the absence of the organ together with free abdominal fluid during ultrasonography. Laparotomy was correctly indicated by ultrasonography in all cases. However, the direct cause of obstruction could not be determined in 2 of the 12 dogs by ultrasonography alone.