Evaluation of Hepatobiliary Disorders PDF

Evaluation o f Hepatobiliary Disorders  Diagnosis???? History ✓Vaccination will decrease risk for viral affections. ✓Administration of some drug can affect liver for example glucocorticoids, mebendazole, paracetamol, and anticonvulsant. ✓Onset of signs correlated with disease...

Evaluation o f Hepatobiliary Disorders  Diagnosis???? History ✓Vaccination will decrease risk for viral affections. ✓Administration of some drug can affect liver for example glucocorticoids, mebendazole, paracetamol, and anticonvulsant. ✓Onset of signs correlated with disease process as in hepatic disease, acute signs seen in hepatic necrosis and drug induced hepatopathy, infection. Clinical presentation and physical findings Individual animals will show some but not all of these signs, and many animals with hepatobiliary disease will show no clinical signs at all.  GIT signs Vomiting, diarrhea, and anorexia are common clinical signs associated with liver disease. Vomiting in dogs and cats with liver disease can be as a result of local inflammation, portal hypertension, or HE. Animals with portal hypertension may have hematemesis and melena as a result of upper GI ulceration.  ABDOMINAL PAIN Some forms of liver disease also cause abdominal pain; the liver parenchyma is poorly supplied with pain fibers, but the liver capsule and biliary tract are well innervated. Biliary tract disease is particularly painful in dogs and cats; gallstones in cats, gallbladder mucoceles in dogs, and extrahepatic biliary obstruction in both species are particularly painful. Dogs and cats with hepatomegaly of any cause often show pain on cranial abdominal palpation, presumably due to stretching of the liver capsule.  POLYURIA AND POLYDIPSIA The underlying mechanisms are poorly understood, but several factors are suspected to contribute to polydipsia (PD) and polyuria (PU), which are seen primarily in dogs and rarely in cats. Altered sense of thirst may be a manifestation of HE. Changes in the function of portal vein osmoreceptors that stimulate renal water loss early after drinking, before a change in systemic osmolality, may also be partly responsible for PU in patients with liver disease, although studies have been published only for rodents and humans. Loss of the renal medullary-concentrating gradient for urea because of the inability to produce urea from ammonia may also be involved and would first cause PU and then compensatory PD.  ABDOMINAL EFFUSION It is much more common in dogs than in cats with liver disease. With the exception of liver disease associated with feline infectious peritonitis (FIP) or congenital ductal plate abnormalities, cats with liver disease rarely have ascites. A small amount of effusion is suspected when abdominal palpation yields a slippery sensation during physical examination. the general pathogeneses of third-space fluid accumulation (excessive formation by increased venous hydrostatic pressure, decreased intravascular oncotic pressure, or altered vascular permeability and insufficient resorption), singly or in combination, apply to cats and dogs with hepatobiliary diseases.  In parenchymal liver disease, the commonest cause of ascites formation is portal hypertension, which is a sustained increase in pressure in the portal system, with or without a contribution from reduced serum albumin concentration. A low protein transudate is occasionally seen in animals with liver disease and concurrent hypoalbuminemia. The pathogenesis of the development of ascites in portal hypertension is complex and has really been studied only in humans; it is assumed that the mechanisms of ascites are similar in dogs. Sodium retention by the kidneys is an important mechanism in the development of ascites in liver disease. Portal hypertension results in congestion of splanchnic vessels with pooling of blood in the splanchnic circulation. This results in a drop in systemic circulating blood volume and thus blood pressure that leads to increased renal sodium retention, partly as a result of reduced glomerular filtration rate and decreased sodium delivery to the tubules and partly as a result of increased release of renin-angiotensin-aldosterone (RAAS) that results in increased sodium retention in the distal tubules. This leads to an increase in circulating fluid volume, which precipitates the formation of ascites, which in turn reduces venous return because of increased pressure on the caudal vena cava and initiates a vicious cycle of renal sodium retention and ascites. This is the “over-fill” theory of ascites formation in liver disease. Therefore, aldosterone antagonists (e.g., spironolactone) are usually most effective in dogs with ascites secondary to portal hypertension, whereas loop diuretics, such as furosemide used alone, can be ineffective or even, in some cases, actually increase the volume of effusion by causing a further decrease in systemic blood pressure as a result of hemoconcentration and secondary increases in RAAS activation.  HEPATIC ENCEPHALOPATHY HE describes neurologic dysfunction in patients with liver disease as a result of exposure of the cerebral cortex to toxins. In dogs with cirrhosis and acquired PSS secondary to portal hypertension, in dogs and cats with acute liver failure, and in cats with hepatic lipidosis (which is in effect a reversible acute liver failure). The most important toxin implicated is ammonia (NH3), which crosses the blood-brain barrier. Buildup of NH3 in the systemic circulation occurs as a result of diversion of portal flow from the liver by the development of PSS or as a result of a marked reduction in functional hepatic mass. In most cases of acquired portosystemic shunting, there is a combination of vascular and functional mechanisms leading to HE. The sources of increased blood ammonia levels in animals with liver disease include the following: Small intestinal enterocyte catabolism of glutamine as their main energy source Endogenous hepatic protein metabolism from excess dietary protein, GI bleeding, or breakdown of lean body mass Bacterial breakdown of undigested amino acids and purines that reach the colon Bacterial and intestinal urease action on urea, which freely diffuses into the colon from the blood. In many cases it is the precipitating factors (rather than the diet) that are most important in triggering HE.  Typical Clinical Signs of Hepatic Encephalopathy in Dogs and Cats Hepatic encephalopathy (HE) may wax and wane, though certain elements could exacerbate signs as high-protein diet, Sedatives or anesthetics, Azotemia, hypokalemia, constipation, GI hemorrhage and metabolic alkalosis.  CHANGE IN LIVER SIZE In normal cats and dogs, the liver is palpable just caudal to the costal arch along the ventral body wall, but it may not be palpable at all..  JAUNDICE, BILIRUBINURIA, AND CHANGE IN FECAL COLOR ✓ Jaundice in cats and dogs is the yellow staining of serum or tissues by an excessive amount of bile pigment or bilirubin. ✓ Jaundice may be prehepatic, due to very marked red cell breakdown; hepatic, due to primary liver disease; or posthepatic, due to biliary tract obstruction or rupture. Because the normal liver has the ability to take up and excrete a large amount of bilirubin, there must be either a large, persistent increase in the production of bile pigment (hyperbilirubinemia) or a major impairment in bile excretion (cholestasis with hyperbilirubinemia) before jaundice is detectable as yellow-stained tissues (serum bilirubin concentration ≥2 mg/dL) or serum (serum bilirubin concentration ≥1.5 mg/dL). Jaundice Acholic stool: result from the total absence of bile pigment in the intestine (Fig. 33.10). Only a small amount of bile pigment is needed to be changed to stercobilin and yield a normal fecal color; therefore, bile flow into the intestine must be completely discontinued to result in acholic feces. Bilirubinuria Canine renal tubules have a low resorptive threshold for bilirubin bilirubinuria (up to 2+ to 3+ reaction by dipstick analysis) may be a normal finding in canine urine specimens. Cats do not have this ability, and they have a ninefold higher tubular absorptive capacity for bilirubin than dogs. Bilirubinuria in cats is associated with hyperbilirubinemia and is always pathologic.  Coagulopathies Liver plays important role in hemostasis. The inability to form Vitamin K-dependent factors (II, VII, IX, X) as a result of absence of bile-acid-dependant fat absorption consequent to extrahepatic bile duct obstruction (EBDO) can cause bleeding. Severe liver diseases cause change in coagulation factors activities. DIC can play a role. Dogs with hepatic necrosis (acute) characterized by thrombocytopenia caused by increase usage or sequestration. Portal hypertension elicits vascular congestion and fragility causing hemorrhage especially in GIT. Though mechanism of GIT hemorrhage is poorly understood, it was presumed to be correlated with poor mucosal perfusion and reduction of epithelial turnover caused by portal hypertension and splanchnic blood pooling.  Diagnostic Tests for the Hepatobiliary System ❑ A battery of tests must be used to assess the hepatobiliary system. A reasonable package of screening tests recommended for an animal suspected of having hepatobiliary disease includes a complete blood count (CBC), serum biochemical profile, urinalysis, fecal analysis, and survey abdominal radiography or ultrasonography (US). ❑ Results of these tests may suggest evidence of hepatobiliary disease that can be confirmed by other, more specific tests, which would usually be some form of tissue sample. It is important at this stage to rule out secondary hepatopathy as much as possible because, with hepatopathies secondary to other diseases, time and resources should be devoted as soon as possible to identify and treat the underlying cause rather than investigate the liver.  Serum biochemistry COMPLETE BLOOD COUNT There are few changes in blood cells that suggest hepatobiliary disease: Microcytosis (mean corpuscular volume [MCV] < 60 fL in canine breeds other than the Japanese Akita or Shiba Inu), with normochromasia or slight hypochromasia (mean cell hemoglobin concentration, 32-34 g/dL), is a common finding in dogs with congenital PSS. A marked microcytic anemia greatly increases the index of suspicion for chronic GI blood loss. Strongly regenerative anemia, with macrocytosis, high reticulocyte count, and normal to slightly increased serum protein concentration in a jaundiced dog, especially if spherocytes are also identified, indicates hemolytic anemia. COAGULATION TESTS ABDOMINOCENTESIS—FLUID ANALYSIS—IN LIVER AND PANCREAS DISEASE Characteristics of Abdominal Effusion in Hepatobiliary Disease  DIAGNOSTIC IMAGING SURVEY RADIOGRAPHY: Survey radiographs provide subjective information regarding the size and shape of the liver. Lateral abdominal radiographs demonstrating gastric axis (white line) as an indication of liver size. (A) Lateral abdominal radiograph of a normal cat with normal liver size. (B) Lateral abdominal radiograph of a cat with diffuse hepatic amyloidosis demonstrating hepatomegaly and caudal displacement of the gastric axis. (C) Lateral abdominal radiograph of a middle-aged English Springer Spaniel with cirrhosis demonstrating microhepatica and cranial displacement of the gastric axis.  ULTRASONOGRAPHY Abdominal US is the preferred diagnostic modality for evaluating the hepatobiliary system in dogs and cats Subcostal approach with a dog or a cat in dorsal recumbency: liver (L); The gallbladder (GB), located to the right of the midline, is a useful landmark; Branching portal veins (PV) with hyperechoic boundaries. The normal hepatic parenchyma is uniformly hypoechoic, with a coarser echotexture, when compared with the spleen. Its echogenicity relative to the renal cortices is more variable, although usually hyperechoic to isoechoic Liver, spleen, and kidney relative echogenicities and echotextures. A: Sagittal image obtained in the left cranial abdomen of a normal dog. The liver (L) is in contact with the spleen (S), and is relatively hypoechoic and more granular in echotexture. B: Sagittal image obtained in the right cranial abdomen of a normal dog. The liver (L) appears relatively isoechoic to the cortex of the right kidney (RK). Acoustic shadowing (arrow) is caused by one of the last ribs. B: Leptospirosis. Ultrasonographic image of a portion of the liver in a dog with acute leptospirosis. The liver is diffusely hypoechoic, and its portal walls are prominent, appearing as double lines and “donuts” throughout the parenchyma. These findings are common in dogs with leptospirosis C: Chronic suppurative hepatitis. In this 6-year-old Labrador, the liver (L) is heterogeneously hyperechoic. St, stomach. Liver biopsy is usually needed to establish definitive diagnosis. It could be performed blind percutaneous method (without ultrasound guidance), ultrasound guided or during laparoscopy. The acronym DAMNIT includes a large number of broad etiological categories and is useful for the generation of an initial list of potential diagnoses that can then be used in making diagnostic plans. Not all etiological categories will apply to all problems. Potential etiologies for hepatomegaly using this system include: Degenerative/Developmental – No relevant diagnoses Anomalous/Autoimmune – Cysts (may be associated with polycystic kidney disease) Metabolic/Mechanical – Vacuolar hepatopathiesm – Glycogen accumulation (i.e., steroid hepatopathy, diabetes mellitus) – Fat accumulation – Venous congestion (mechanical), (i.e., right-sided heart failure) – Nodular hyperplasia Neoplastic/Nutritional – Primary neoplasia – Hepatocellular carcinoma – Hemangiosarcoma – Biliary carcinoma – Secondary/Systemic neoplasia – Lymphosarcoma – Mast cell tumor – Metastasis (i.e., Hemangiosarcoma) Infectious/Idiopathic/Inflammatory/Ischemic/Iatrogenic – Parasitic cysts (i.e., Echinococcus) – Liver lobe torsion (Ischemic, congestion) – Granulomas Toxic/Traumatic – Hematoma