Ascites is the abdominal accumulation of fluid.
The pathogenesis of abdominal effusion is diverse; causes associated with liver disease can be categorized according to cause as prehepatic, hepatic, or posthepatic. This categorization is relative to the normal directional flow of from the portal vein to the liver (portal tracts), across the sinusoids, with egress through the hepatic vein into the vena cava. (See figure Liver structure and function.)
Ascites due to liver disease often implicates the presence of portal hypertension and typically is associated with development of acquired portosystemic shunts (APSSs), which are macroscopic medusalike vascular plexi (see also congenital portosystemic shunts). APSSs are aberrant vascular communications between the portal vein and systemic veins, usually the caudal vena cava. APSSs reflect the physiologic adaptation for decompressing portal hypertension, providing a pathway of lesser resistance that mitigates portal pressure.
With development of APSSs, directional circulation to the liver (hepatopetal) deviates to flow around the liver (hepatofugal). Both congenital and acquired disorders can evolve APSSs. Congenital disorders include the following:
portal vein atresia (critical failure to develop functional portal vein vasculature within or external to the liver causing portal hypertension (note this is distinct from portal vein hypoplasia)
arteriovenous malformations (high arterial pressure flows retrograde into the portal vein) causing high pressure with flow blood into the normally low-pressure splanchnic portal vein
ductal plate malformations (DPM) with a chronic hepatic fibrosis phenotype
Acquired causes of APSSs due to liver disease include the following:
severe sinusoidal fibrosis and remodeling causing intrahepatic sinusoidal hypertension (usually reflects chronic hepatitis, occasionally reflects severe fulminant hepatic injury)
thromboembolism (impacting a major branch of the portal vein, with the external or prehepatic portion of the portal vein being more common)
neoplasia compromising perfusion to the liver via the portal vein
Chronic necroinflammatory liver disease evolving ascites typically is associated with critical loss of functional hepatic mass. Affected patients often become hypoalbuminemic, which escalates ascites accumulation. Ascites formation associated with liver disease and severe hypoalbuminemia generally indicates a poor longterm prognosis.
Hepatic encephalopathy (HE) denotes neurobehavioral dysfunction secondary to liver failure or severe portosystemic shunting. When hepatic encephalopathy develops in animals due to acquired liver disease, it typically is associated with diffuse liver fibrosis and remodeling, portal hypertension, and APSSs.
However, HE also may develop secondary to acute decline in functional hepatic mass in acute fulminant liver failure. Most commonly, HE is encountered in small companion animals with congenital portosystemic shunts (congenital macroscopic single communications that join the portal vein with the systemic circulation). Development of HE does not occur in dogs with only microvascular dysplasia (MVD).
Fecal color may change in animals with liver disease with enteric bile flow disruption (eg, complete bile duct obstruction, disorders leading to severe bile duct loss [ductopenia]). Complete mechanical bile duct obstruction or critical small bile duct ductopenia causes acholic pale-colored feces.
On the other hand, jaundice not associated with obstructive bile flow may be associated with increased flux of bilirubin pigments causing orange- or green-colored feces.
Alteration of hepatic size from subnormal to large can reflect a number of disorders.
The liver is a capacitance organ that adjusts in response to altered vascular volume. As a large compensatory vascular structure, the liver can engorge subsequent to systemic fluid retention, iatrogenic overload with polyionic fluids or blood component transfusions, or congestion due to heart failure or pericardial disease. Conversely, it may appear small in the case of hypovolemia.
Assessment of hepatomegaly or microhepatia must consider influential vascular volume accommodation: size of heart, width of the cranial vena cava, presence or absence of hepatic vein distention (on hepatic ultrasonography), macroscopic portosystemic shunting, or evidence of abdominal effusion.
Size assessment on ultrasonography is subjective, whereas estimates based on radiographic or CT imaging are more objective and should be considered relative to vena caval distention, to judge for hepatic venular congestion or hypovolemia.
Microhepatia or microhepatica can reflect severe vascular volume depletion (eg, as occurs in an Addisonian crisis due to severe hypovolemia and hypotension); however, more often it reflects chronic portal venous hypoperfusion (PVHP) causing hepatocyte atrophy.
PVHP provokes a remarkable increase in hepatic arterial blood flow (hepatic arterial buffer response) such that hypovolemic circulation to sinusoids is not causal. PVHP denotes persistently impaired portal venous sinusoidal perfusion, depriving hepatocytes of enterically derived hepatotropic factors, essential for normal hepatocyte and liver lobule size.
Microhepatia may also reflect liver lobe atresia, most often encountered as a congenital deformity in animals with DPM.
A small liver also may reflect advanced-stage liver disease (old nomenclature: cirrhosis) associated with regenerative nodules and parenchymal extinction (scarred areas with loss of viable hepatic mass due to chronic liver disease).
Acquired microhepatia also may reflect ischemic injury (thromboembolism, liver lobe torsion) or can result from severe acute panlobular liver necrosis (fulminant hepatic failure).
Ultimately, the diagnosis requires consideration of history, routine blood test interpretation, imaging studies (radiography, ultrasonography, CT with contrast angiography, possible colorectal scintigraphy), and ultimately, liver biopsy.
Hepatomegaly occurs as an adaptive response to diverse disorders. The liver is essentially a network of low-pressure sinusoidal vasculature lacking valves, and hepatomegaly is the result of a compensatory accommodation to increased vascular volume or failure of forward flow.
Disorders causing hepatic congestion and hepatomegaly include conditions critically disrupting blood flow from sinusoids through hepatic venules and veins craniad to the level of and including the heart and pericardium, such as the following:
severe heart failure
pericardial disease (restricted right atrial-ventricular filling)
cranial vena caval-right atrial obstruction (due to mass lesions, congenital or acquired kinking or stricture of the vena cava, thromboembolism, or heartworm vena caval syndrome)
rare congenital cardiac defects (eg, cor triatriatum dexter)
Iatrogenic overload of polyionic fluids or overtransfusion of blood components also may provoke hepatomegaly, usually accompanied by acute onset small-volume abdominal effusion.
Hepatomegaly also may reflect expansion of nonparenchymal cell populations. Such disorders include extreme reticuloendothelial hyperplasia (expansion of tissue-fixed macrophages secondary to infection, pyogranulomatous hepatitis, histiocytic inflammation, neoplasia, or persistent immune stimulation), and rarely, extreme extramedullary hematopoiesis restricting centrilobular perfusion. Neoplastic disorders provoking hepatomegaly include massive hepatocellular carcinoma in dogs, cholangiocarcinoma (cats), diffuse lymphosarcoma (dogs, cats), or diffusely disseminated metastatic mass lesions (eg, hemangiosarcoma in dogs).
A diverse number of nonneoplastic infiltrative disorders also can cause hepatomegaly. Most common in dogs is a glycogen-type vacuolar hepatopathy (VH; steroid hepatopathy); this is rare in cats. Most common in cats is diffuse hepatocyte vacuolation with triglyceride (feline hepatic lipidosis [HL]), which is uncommon in dogs.
Rare genetic mutations provoke hepatomegaly due to accumulation of metabolic storage products; some of these lead to extreme, painful hepatomegaly. Recognized inborn errors of metabolism leading to hepatomegaly are certain lysosomal storage disorders, a form of glycogen storage disease, and cholesterol ester storage disease. A defect in activity of lipoprotein lipase also has caused severe hepatic lipid vacuolation in affected cats.
Rarely, idiopathic amyloidosis leads to diffuse sinusoidal amyloid accumulation causing massive painful hepatomegaly. This is more commonly encountered in cats where hepatomegaly is associated with spontaneous liver lobe rupture and hemoabdomen. Although nodular hyperplasia is commonly encountered as a randomly distributed singular lesion in dogs, rare diffuse hepatic involvement is occasionally encountered (one or two large liver lobes).
Acute complete common bile duct obstruction can cause mild hepatomegaly in the early stages of obstruction (10–14 days). Animals with chronic necroinflammatory liver disorders disturbing centrilobular perfusion can develop hepatomegaly in the early stages. Most pernicious are disorders disrupting zone 3 perfusion that cause a veno-occlusive-like or sinusoidal occlusion-like injury. Such lesions often develop subsequent to centrilobular toxin or copper-mediated liver damage.
Lastly, ductal plate malformations (DPM) occasionally develop one notably enlarged liver lobe as an apparent compensatory response to atresia or hypoplasia of another liver lobe or lobes. Rarely, dogs and cats with diffuse fibropolycystic liver disease develop remarkable hepatomegaly, where diffuse cystic lesions litter hepatic lobe structure.
