Esophageal Varices due to a Probable Arteriovenous Communication in a Dog

Abstract

A 6-year-old 40-kg castrated male Samoyed dog was presented for evaluation of chronic remittent lameness of the right forelimb. The dog had a history of polyuria-polydipsia (PU/PD) and lethargy over the previous year. Physical examination was unremarkable except for a grade II systolic murmur at the apex of the heart on the left side. A 6-lead ECG was within normal limits. Arterial blood gas analysis indicated mild respiratory alkalosis (pH, 7.457, reference range, 7.370-7.450 Thoracic radiographs disclosed a generalized increase in the size of the cardiac silhouette and pulmonary vascular enlargement, suggesting pulmonary overcirculation. An ELISA for Dirofilaria immitis antigen was negative. Two-dimensional, M-mode echocardiography a (transducer frequency, 2.0-3.0 MHz) revealed left atrial enlargement, left ventricular eccentric hypertrophy, and impaired systolic function (end-diastolic dimension, 65.7 mm; end-systolic dimension, 44.2 mm; shortening fraction, 32.7%) with normal valves. Spectral and colorflow Doppler examination disclosed mild mitral, aortic, and pulmonic valve insufficiency. Both the tricuspid and the telediastolic pulmonic valvular peak regurgitant jet velocities were increased as follows: 3.26 m/s (normal, #2.5 m/s) and 2.44 m/s (normal, #2.0 m/s), respectively. According to the Bernoulli's equation modification, the systolic pulmonary artery pressure was estimated to be 42.5 mm Hg and the diastolic pulmonary artery pressure was estimated to be 23.9 mm Hg, values consistent with mild pulmonary hypertension.The dog was anesthetized and subjected to radiography of the right forelimb and total body multidetector computed tomography b (MDCT). The radiographs were negative for abnormalities, and synovial fluid examination of the shoulder and stifle joints did not indicate evidence of any inflammatory pathology. MDCT scans of the brain, thorax, and abdomen were obtained. For the thoracic and abdominal scans, the dog was positioned in dorsal recumbency, and we employed the following parameters: helical modality, 120 kV, 200 mA, 0.7-second rotation tube, 0.526 pitch, and 1.2-mm slice thickness. For the brain scan, the dog was positioned in sternal recumbency and the scanner parameters were as follows: axial modality, 120 kV, 310 mA, 2-second rotation tube, 0.625 slice thickness, and 10-mm intervals. For an enhanced series, 2-mL/kg iodixanol c 320 mg I/mL was injected via a 22-gauge catheter into the right cephalic vein at a 3 mL/second infusion rate, through a computed tomography injector system. d The brain and abdominal MDCT scans were normal. However, MDCT of the neck and chest revealed 12 pairs of ribs, an enlarged heart, and enlarged pulmonary vessels. Both of the bronchoesophageal arteries were enlarged and connected with an enormous network of homogeneously enhancing serpentine structures involving the thoracic esophagus (esophageal and paraesophageal varices). The bronchoesophageal vein was extremely dilated (Figs 1, 2). The right azygous and hemizygous veins were normal. The cranial vena ca...

Acquired Portal Collateral Circulation in the Dog and Cat

“…Some collaterals of the porta‐postcaval system have been described in dogs and cats with portal hypertension, either using conventional angiographic techniques or Doppler ultrasound 11,16–18 . Porta‐precaval collaterals include anastomosis between the cardial radicles of the left gastric vein and esophageal radicles of the azygos vein, and have only been described in experimental models and in a prior report 10–12 . In the dogs without portal hypertension in the present study, only varices were encountered.…”

“…Acquired collateral circulation also results from the cranial vena cava syndrome, caused by increased resistance or occlusion of the cranial vena cava. These collaterals may connect to the portal system as well 6–10 …”

“…However, when the obstruction occurs at or inferior to the azygos vein, the blood flows through the venous plexus of the esophagus and cardiac veins and continues into the portal circulation 9,31,32 . A dog with esophageal and paraesophageal varices resulting from increased cranial vena cava resistance due to an arteriovenous communication has been described 10 …”

Aspectos epidemiológicos, clínicos e anatomopatológicos da infecção por Gurltia paralysans em gatos

“…Os exemplos mais comuns de varizes em humanos incluem aquelas que afetam os membros inferiores e aquelas que ocorrem no plexo hemorroidal (hemorróidas), mas dezenas de outras localizações estão descritas na literatura médica, incluindo varizes de meninges (Moonis et al 2003, Paldor et al 2010, como visto nesse caso. As raras descrições de varizes na literatura veterinária incluem os olhos (Adkins et al 2005), a bexiga (Littman et al 1990) e o esôfago (Bertolini et al 2007) de cães, embora diferentemente de humanos, cães não desenvolvam varizes esofágicas associadas à hipertensão portal (Germain 1975), mas apenas experimentalmente (Tamiya & Thal 1960, Ross et al 1961, Jensen et al 1983). Outras descrições de varizes em animais incluem aquelas que afetam o trato genital, como as veias testiculares (varicocele) de garanhões, touros, carneiros e cães (Ezzi et al 1987, Foster et al 1989, as veias uterinas de éguas (Foster et al 1997) e coelhas (Bray et al 1992) e as veias vaginais de éguas (White et al 1984).…”

Hepatic Fibrosis in Dogs

“…In cirrhotic human patients, a hepatic venous pressure gradient >5 mmHg is defined as portal hypertension and a value above 10 mmHg is correlated with development of clinical consequences, including life‐threatening gastroesophageal varices . In dogs, gastroesophageal varices have been described, but their clinical importance is unclear . In addition, portal hypertension can contribute to the development of ascites and can lead to the opening of vestigial blood vessels that bypass the portal circulation (acquired portosystemic collaterals) .…”