Circulatory disorders of the liver in dogs and cats

Summary

This paper presents a review of the literature on hepatic circulation and circulatory disorders of the liver in the dog and cat, and also includes a number of our own not previously published data. Circulatory disorders of the liver are frequently observed in dogs and cats. These disorders can be divided into congenital portosystemic shunts, disorders associated with outflow disturbances, and disorders associated with portal hypertension. Outflow disturbances result in passive congestion of the liver and in both species are mainly due to cardiac failure. Portal hypertension with resultant portosystemic collateral circulation and ascites mainly results from chronic liver disease, particularly cirrhosis. The main vascular disorder resulting in portal hypertension and ascites in the dog is primary hypoplasia of the portal vein.     

A Syndrome Resembling Idiopathic Noncirrhotic Portal Hypertension in 4 Young Doberman Pinschers

We describe 4 young male Doberman Pinschers (3 littermates and 1 unrelated dog) with a syndrome resembling idiopathic or noncirrhotic portal hypertension of humans. Each dog was evaluated for a hepatopathy resulting in portal hypertension, development of portosystemic collateral vessels, and hepatic encephalopathy. These dogs differ from previous reports of young dogs with hepatic insufficiency associated with portal hypertension and acquired portal systemic shunting by their lack of intrahepatic arteriovenous fistulae, portal vein atresia, or intrahepatic fibrosis. Clinicopathologic features included erythrocyte microcytosis, normal to mildly increased liver enzyme activities, increased concentrations of serum bile acids, reduced plasma indocyanine green clearance, and normal total bilirubin concentration. Abdominal ultrasonography disclosed a small liver and portosystemic collateral vessels. Radiographic imaging studies confirmed hepatofugal portal circulation and discounted hepatic arteriovenous fistulae. Histopathologic features in liver tissue from each dog were similar and consistent in all sections examined. Common findings included increased cross-sectional views of hepatic arterioles; hepatic lobular atrophy; scanty increase in connective tissue around some large portal triads; and absence of inflammation, disturbed lobular architecture, bile duct proliferation, or intrahepatic cholestasis.     

SIMULTANEOUS CONGENITAL AND ACQUIRED EXTRAHEPATIC PORTOSYSTEMIC SHUNTS IN TWO DOGS

Two dogs with simultaneous congenital and acquired portosystemic shunts are reported. The first dog was an eight-month-old, male Golden Retriever with a history of peritoneal effusion, polyuria/polydipsia, and stunted growth. The dog had a microcytic, hypochromic anemia, a mildly elevated AST, and a moderate to severely elevated preprandial and postprandial serum bile acids. Transcolonic portal scintigraphy confirmed the presence of a portosystemic shunt. An intraoperative mesenteric portogram was performed. Two conjoined congenital extrahepatic portosystemic shunts and multiple acquired extrahepatic portosystemic shunts were identified. The second dog was a five-month-old, mixed breed with two week history of peritoneal effusion. Abdominal ultrasound and transcolonic scintigraphy were used to diagnose a portosystemic shunt. A single extrahepatic portosystemic shunt, portal hypertension, and multiple acquired collateral shunts were identified at surgery. The histologic alterations observed in these dogs were consistent with a portosystemic shunt. In these dogs, the presence of congenital and acquired portosystemic shunts and histopathologic findings are considered to represent a combination of congenital portosystemic shunts and noncirrhotic portal hypertension or portal vein hypoplasia.     

Obstructed portal venous flow and portal vein thrombus in a dog

A young adult Doberman Pinscher had clinical signs and laboratory data consistent with the copper-associated hepatopathy commonly found in Doberman Pinschers. Hepatic biopsy and hepatic copper analysis did not support this diagnosis. Furthermore, changes seen in the hepatic biopsy specimen did not explain the acquired portosystemic shunting or the portal hypertension that the dog had. A mesentery venoportagram revealed markedly delayed filling of one portal vein, and necropsy revealed a small thrombus partially occluding that hepatic vein. It was not determined whether obstructed portal venous flow caused the portal vein thrombus or vice versa; however, it was theorized that the portal vein thrombus, once formed, contributed to further portal hypertension and/or delayed portal vein filling.     

Ultrasonographic diagnosis of unusual portal vascular abnormalities in two cats

Two cases of ascites secondary to portal vascular abnormalities associated with portal hypertension are described. In the first case a five-month-old cat was presented with recurrent ascites and investigations showed that the underlying cause was a hepatic arteriovenous fistula. Ultrasonography showed direct communication of the coeliac artery and right branch of the portal vein. There was also hepatofugal flow in the main portal vein consistent with portal hypertension. The ultrasonographic features were similar to those seen in dogs with hepatic arteriovenous fistulae. In the second case, ascites, portal hypertension and an intraluminal mass in the main portal vein was diagnosed in a 16-year-old cat that had been presented with hyperthyroidism and hepatomegaly. Acquired portosystemic collaterals involving the left renal vein were present. Additional diagnostic investigations were not permitted. Ultrasonography was useful in both cases to document portal hypertension and the underlying cause.     

克伦特罗对绵羊肝脏血流量和氮代谢的影响

在4头门静脉、肝静脉、肠系膜静脉和股动脉上安装血管导管的绵羊中研究了克伦特罗（CL,0.8 mg/kgBW,肠系膜静脉给药,每天2次,连续5 d）对其肝脏生长代谢的影响。结果表明:CL对肝脏血流量影响较小。而在CL作用下绵羊血浆中尿素氮水平明显下降,肝静脉和门静脉血液尿素氮流量分别减少16.86％（P<0.01）和15.51％（P<0.05）。肝静脉多肽流量在CL处理期也较对照期下降38.71％（P<0.01）,门静脉处多肽水平处理期则与对照期相当。克伦特罗还增加绵羊肝脏IGF-I的合成和分泌,门静脉和肝静脉中的增加幅度分别为38.84％（P<0.01）和33.18％（P<0.01）。提示CL可通过增强对绵羊肝脏氮的储留及肝脏IGF-I的合成和分泌从而促进机体的生长代谢。     

Concentrations of free steroids in the jugular and hepatic portal veins of pigs after ingestion of testosterone, estrogen, or progesterone or transplantation of ovaries to the intestine.

Estrogen, progesterone or testosterone were administered orally to ovariectomized gilts fitted with indwelling catheters. Blood samples were taken from the jugular and hepatic portal veins at intervals varying from a few minutes to daily over periods that varied from 1 d to several months. Concentrations of free steroids rose dramatically in the hepatic portal vein within a few min of feeding steroids and remained high for 3-8 hr before declining to base levels. Concentrations in the jugular vein sometimes rose very slightly for the same period. At 48 hr after administration the concentrations remained at baseline in the hepatic portal vein, but rose several-fold in the jugular and remained elevated for several days. Autotransplantation of the ovaries to the intestine resulted in very large ovaries consisting of many large, heavily luteinized cystic follicles. Concentrations of progesterone and estrogen in the hepatic portal vein were very high, but were low in the jugular vein. The gut wall allows for passage of some orally administered free steroids to the liver via the hepatic portal vein. The free steroids are essentially metabolized before they reach the jugular vein, but can be recirculated via the enterohepatic route.     

INDIRECT AND DIRECT DETERMINATION OF THE PORTAL VEIN PRESSURE IN NORMAL AND ABNORMAL DOGS AND NORMAL CATS1

Portal hypertension resulting in ascites and portosystemic shunts leading to hepatoencephalopathy are major clinical manifestations of hepatic circulatory disease. Diffuse liver disease impairing sinusoidal blood flow can induce portal hypertension, portosystemic shunts, or both. The liver may also be involved secondarily in posthepatic hypertension and become the site of ascitic fluid formation. Portosystemic shunts may or may not be associated with portal hypertension. Selective catheterization of the hepatic and portal veins permits one to record pressures and to outline gross and subgross vascular anomalies by injecting contrast medium. Sequential pressure recordings in the caudal vena cava, in a free and wedged hepatic vein position, in the splenic pulp, and directly in the portal vein are the bases for the differentiation of prehepatic, liver-induced, and posthepatic portal hypertension. In addition to localizing the disease process along the postcaval-portal vein axis, pressure measurements are a reliable basis for the prognosis and selection of the most appropriate therapy. In dogs with portacaval shunts, wedge hepatic vein pressure recordings assist in the detection of hepatic sinusoidal anomalies that limit blood flow and preclude surgical ablation of the shunts. The various technics and their suitability for direct and indirect portal vein pressure recording are described and evaluated. Normal portal vein pressure values in 11 dogs and two cats, using different technics, are provided. The clinical usefulness of the various technics of pressure recording and angiography was illustrated in ten dogs with ascites, hepatoencephalopathy, or both.     

Dual-phase CT Angiography of the Normal Canine Portal and Hepatic Vasculature

A dual-phase computed tomography (CT) angiographic technique was developed to image the hepatic and portal vascular systems using a nonselective peripheral injection of contrast medium. The arterial phase of the dual-phase scan imaged the hepatic arteries and veins, and the portal phase imaged the portal vein as well as its tributaries and branches. There were three steps involved in acquiring the dual-phase scan: a survey helical scan for orientation, a dynamic scan for timing, and finally the dual-phase helical scan. Five normal dogs were imaged using a helical scan technique. The timing of the arterial and portal phases of the scan was calculated using time vs. attenuation graphs generated from a dynamic scan. The median time of appearance of contrast medium in the cranial abdominal aorta was 8.6 s and the median time of appearance of contrast medium in the hepatic artery occurred 0.4 s later. The median time of peak enhancement in the cranial abdominal aorta was 12.0 s. The median time of appearance of contrast medium in the portal vein was 14.6 s and median time of peak enhancement was 33.0 s. The dual-phase scans provided excellent vascular opacification. The hepatic arteries, hepatic veins, cranial and caudal mesenteric veins, splenic vein, gastroduodenal vein, and portal vein branches were all consistently well defined. Dual-phase CT angiography is a minimally invasive technique which provides an excellent three-dimensional representation of portal and hepatic vascular anatomy.     

A method for chronically quantifying net absorption of nutrients and gut metabolites into hepatic portal vein in conscious swine

Surgical procedures are described for chronic cannulation of portal vein, ileal vein, abdominal aorta, and carotid artery in pigs. Silastic or Micro-Renathane tubing was used for cannulating portal vein and ileal vein, while carotid artery was cannulated with Micro-Renathane tubing. The lumen of Micro-Renathane tubing was coated with tri-dodecylmethyl ammonium chloride (TDMAC)-heparin complex. The abdominal aorta was cannulated via saphenous artery with vinyl tubing. This allows simultaneous collection of blood samples from hepatic portal vein and systemic artery (carotid or abdominal aorta) and continuous infusion of p-aminohippuric acid (PAH) into ileal vein. The constant PAH infusion provided an indicator-dilution method for estimating the blood flow rate in portal vein. In 13 pigs weighing 54 +/- 2.8 kg, the mean portal vein blood flow rate during the 8-h postprandial period was estimated to be 1,979 ml X min-1 X pig-1 or 37.8 ml X min-1 X kg-1 body weight. By simultaneously measuring the concentration of nutrients and metabolites in the portal and systemic arterial blood and multiplying porto-arterial differences by the estimated portal vein blood flow rate, the net absorption of nutrients (except long-chain fatty acids) and metabolites into hepatic portal system in conscious swine can be quantified.     

Gross Anatomy of the Canine Portal Vein

The gross anatomy of the portal vein of 21 dogs was studied by venous portography, corrosion casting, and gross dissection. The portal vein in all specimens originated by confluence of the cranial and caudal mesenteric veins. Its large tributaries were the splenic and gastroduodenal veins, which entered the portal vein between its origin and the hepatic porta. At the hepatic porta, the portal vein divided into a short right branch and a larger left branch. The right branch ramified in the caudate process of the caudate lobe and in the right lateral lobe of the liver. The left branch was essentially the continuation of the portal vein from which successive branches passed to each of the remaining lobes of the liver and the papillary process of the caudate lobe.     

DOPPLER ULTRASONOGRAPHIC DIAGNOSIS AND ANATOMY OF CONGENITAL INTRAHEPATIC ARTERIOPORTAL FISTULA IN A PUPPY

A dilated, tortuous blood vessel was identified sonographically in the right medial liver lobe in a puppy with severe ascites. This vessel was thought to represent the dilated right medial portal vein branch. Using pulsed wave Doppler ultrasonography, retrograde, abnormally pulsatile flow was detected in both the dilated right medial portal vein branch and the main portal vein. The right medial liver lobe was surgically resected then fixed in formalin. Silicon rubber was injected and outlined the connection between the portal vein and hepatic artery.     

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.     

克伦特罗对绵羊肝脏挥发性脂肪酸和糖代谢的影响

在 4头门静脉、肝静脉、颈静脉、肠系膜静脉和股动脉上安装血管导管的绵羊中研究了克伦特罗 (CL ,0 8mg/kgBW ,肠系膜静脉给药每天 2次 ,连续 5d)对其肝脏物质代谢的影响。结果表明 :CL可增加绵羊肝脏中的VFA流量 ,其中门静脉处乙酸、丙酸和丁酸的流量分别较对照期增加 19 4 9% (P <0 .0 1)、2 0 2 % (P >0 .0 5 )和4 5 5 % (P >0 .0 5 ) ,而肝静脉处VFA流量两期水平接近。CL也提高肝脏中葡萄糖的异生作用 ,在肝静脉处血中葡萄糖流量上升了 2 5 96 % (P <0 .0 1)。门静脉处血中葡萄糖循环水平也相应提高。此外在CL作用下肝静脉处胰岛素水平也较对照期有所下降。提示CL可增加进入绵羊肝脏中VFA的流量并促进肝脏对VFA的吸收和利用。通过降低胰岛素水平或对肝脏的直接作用CL还可增加绵羊血中葡萄糖的水平     

ANGIOGRAPHY OF THE HEPATIC AND PORTAL VENOUS SYSTEM IN THE DOG AND CAT: AN INVESTIGATIVE METHOD*

The investigators studied the hepatic angiographic technics used in human medicine with respect to their applicability for the investigation of circulatory liver diseases in the dog and cat. The technics were performed in 11 normal dogs and 2 normal cats, and the normal radiographic anatomy of the hepatic portal system and its tributaries was described. The potential indications for the angiographic technics were defined and their respective advantages and disadvantages discussed. Splenoportography was a valuable method for outlining the intrahepatic portal vein branches and for percutaneous prehepatic portal vein pressure determination. Percutaneous transhepatic portography was more difficult to perform, but it provided better detail of the intrahepatic portal veins than splenoportography. Transjugular transhepatic portography was the most versatile but also the most cumbersome of all technics tested. Percutaneous kinetic hepatography proved impractical in dogs and cats. The mesenteric tributaries to the hepatic portal system were best outlined by cranial mesenteric arterial portography or by operative mesenteric venous portography. Operative mesenteric venous portography, in contrast to cranial mesenteric arterial portography, was also useful for prehe-patic portal vein pressure determination. Free and wedged hepatic venography provided an opportunity for the functional and morphologic investigation of the hepatic sinusoid circula-tion.     

Standard planes for ultrasonographic examination of the portal system in dogs

A scanning protocol for the systematic ultrasonographic examination of the portal system in dogs was developed. Seven planes were used to image the portal system. With the dogs in left lateral recumbency, 3 transverse planes obtained via the right intercostal spaces were used to visualize the portal vein and right portal branch, and a longitudinal plane obtained with the transducer caudal to the last right rib was used to visualize the portal bifurcation. With the dogs in dorsal recumbency, a longitudinal plane was used as an alternative method of visualizing the portal vein and its bifurcation. Finally, with the dogs in right lateral recumbency, longitudinal planes obtained with the transducer in the left flank were used to visualize the hepatic artery, the left renal vein, and the left testicular or ovarian vein. To diagnose or rule out portosystemic shunting, the right portal branch, the left testicular or ovarian vein, the portal vein immediately caudal to the portal bifurcation, and the portal vein at the level of the celiac artery should be examined with this scanning protocol.     

Contrast‐enhanced ultrasonography is a feasible technique for quantifying hepatic microvascular perfusion in dogs with extrahepatic congenital portosystemic shunts

Extrahepatic‐congenital portosystemic shunt is a vascular anomaly that connects the portal vein to the systemic circulation and leads to a change in hepatic microvascular perfusion. However, an assessment of hepatic microvascular perfusion is limited by conventional diagnostic modalities. The aim of this prospective, exploratory study was to assess hepatic microvascular perfusion in dogs with extrahepatic‐congenital portosystemic shunt using contrast‐enhanced ultrasonography (CEUS) using perfluorobutane (Sonazoid^®). A total of 17 dogs were included, eight healthy dogs and nine with extrahepatic‐congenital portosystemic shunt. The time‐to‐peak (TTP), rising time (RT), and rising rate (RR) in the hepatic artery, portal vein, and hepatic parenchyma, as well as the portal vein‐to‐hepatic parenchyma transit time (ΔHP‐PV) measured from time‐intensity curve on CEUS were compared between healthy and extrahepatic‐congenital portosystemic shunt dogs. The RT of the hepatic artery in extrahepatic‐congenital portosystemic shunt dogs was significantly earlier than in healthy dogs (P = 0.0153). The TTP and RT of the hepatic parenchyma were significantly earlier in extrahepatic‐congenital portosystemic shunt dogs than in healthy dogs (P = 0.0018 and P = 0.0024, respectively). ΔHP–PV was significantly shorter in extrahepatic‐congenital portosystemic shunt dogs than in healthy dogs (P = 0.0018). CEUS effectively revealed changes in hepatic microvascular perfusion including hepatic artery, portal vein, and hepatic parenchyma simultaneously in extrahepatic‐congenital portosystemic shunt dogs. Rapid hepatic artery and hepatic parenchyma enhancements may reflect a compensatory increase in hepatic artery blood flow (arterialization) caused by a decrease in portal vein blood flow and may be used as an additional diagnostic test to distinguish extrahepatic‐congenital portosystemic shunt dogs from healthy dogs.     

Gross Anatomy of the Portal Vein and its Tributaries in the Opossum (Didelphis albiventris)

The gross anatomy of the portal vein (V. portae) and its tributaries was studied through anatomical methods, i.e. dissection, corrosion and diaphanization, in 45 opossums (Didelphis albiventris). In all animals the portal vein was formed by the junction of the cranial mesenteric, caudal mesenteric and lienal veins (V. mesenterica cranialis, V. mesenterica caudalis and V. lienalis, respectively). Many collateral tributaries were observed running into the portal venous trunk.     

Splanchnic Surface Oximetry during Experimental Portal Hypertension and Surgical Manipulation of Portosystemic Shunts in Dogs

Surface oxygen tension (PSO2) was measured in dogs during experimental manipulation of the portal vein and hepatic artery, and during surgery to correct portosystemic shunting. There was no alteration in PSO2 of liver, pancreas, duodenum, or jejunum during partial (50%) or complete reduction of hepatic artery flow. After 100% reduction in portal vein blood flow, PSO2 was lower in jejunum, duodenum, and liver. With 50% reduction in portal flow, PSO2 was significantly decreased only in jejunum. In six dogs with single extrahepatic shunts, there was a significant correlation between portal pressure and jejunal PSO2. It was concluded that measurement of visceral organ PSO2 represents an accurate noninvasive means of obtaining objective data on the effect of reduction in hepatic blood flow on perfusion of other select splanchnic organs.