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

“…11,[16][17][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][11][12] In the dogs without portal hypertension in the present study, only varices were encountered. Large shunts were found only in two dogs with portal hypertension.…”

“…These collaterals may connect to the portal system as well. [6][7][8][9][10] Several patterns of acquired collateral portal circulation have been described in dogs, either angiographically [11][12][13] or sonograpically. [15][16][17][18][19][20] These reports mainly describe multiple small tortuous vessels in the renal region or a longer tortuous vessel between the splenic vein and left renal vein, draining into the caudal vena cava through a network connected to the left gonadal vein, and ultimately entering the left renal vein.…”

“…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 In human beings, varices draining into the inferior vena cava include abdominal wall varices, gallbladder and choledocal varices, duodenal, retroperitoneal, omental, and colic varices. [23][24][25][26][27][28][29] Spontaneous formation of these portal collaterals have not been fully described in dogs or cats.…”

Anomalies of the Portal Venous System in Dogs and Cats as Seen on Multidetector-Row CT: An Overview and Systematization Proposal

“…Varices may be subdivided according to their anatomic location and pathways into left gastric vein, gastrophrenic, omental, gallbladder, abdominal wall, duodenal, and colic varices. 10,76 Importantly, anomalous vascular connections between systemic and portal systems can also occur in case of chronic obstruction of the caudal vena cava (cavo-portal collaterals) allowing blood to return to the right atrium. 77 Special care should be taken to not misinterpret these vascular anomalies.…”

Hepatic Fibrosis in Dogs

“…[104][105][106][107] In dogs, gastroesophageal varices have been described, but their clinical importance is unclear. 104,108 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). 104 Ascites is the consequence of a combination of splanchnic arterial vasodilation, decreased cardiac output, and activation of the RAS, which leads to sodium and water retention.…”