Volume 44 | Issue 1 Article 3

1982 Canine Ascites W. Michael Peden Iowa State University

R. D. Zenoble Iowa State University

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Recommended Citation Peden, W. Michael and Zenoble, R. D. (1982) "Canine Ascites," Iowa State University Veterinarian: Vol. 44 : Iss. 1 , Article 3. Available at: https://lib.dr.iastate.edu/iowastate_veterinarian/vol44/iss1/3

This Article is brought to you for free and open access by the Journals at Iowa State University Digital Repository. It has been accepted for inclusion in Iowa State University Veterinarian by an authorized editor of Iowa State University Digital Repository. For more information, please contact [email protected]. Canine Ascites

by W. Michael Peden, DVM R. D. Zenoble, DVM*

INTRODUCTION cirrhosis, and cholangitis. Most of the cardiac Canine ascites is an infrequently seen and hepatic diseases are associated with por­ clinical sign which is often the primary com­ tal hypertension as the direct cause of ascites. plaint for presentation of an animal to a vet­ Another cause of fluid accumulation in the erinarian. As in all cases a good history is a peritoneal cavity is hypoproteinemia due to priority as further questions may reveal renal loss of protein. Diseases such as behavioral changes, vomiting, anorexia, and amyloidosis and glomerulonephritis may other clinical signs which may be important cause massive proteinuria. Other causes of in defining the primary problem. Ascites itself abdominal fluid accumulation include can physically interfer with respiration, cause neoplasia of an abdominal organ, ruptured general discomfort, and disturb fluid and urinary bladder, and hemorrhage from electrolyte metabolism. The underlying cause trauma or neoplasia. must be determined and treated. Simply re­ The following steps need not necessarily be moving the ascitic fluid will only give short performed in any certain sequence, but a term relief. logical procedure should be followed in order A diagnostic evaluation of an animal to arrive at a diagnosis. For example, blood presented with ascites may include a complete work and radiographs or analysis of ab­ blood count (CBC), biochemical evaluation, dominal fluid may be done in a different abdominal paracentesis and biocheIll,ical and order than presented here, but all work cytologic analysis of the fluid obtained, should be done with the idea of ruling out the radiographs, biopsy, and organ function easiest and most obvious diseases first. Ascites tests. A physical exam always precedes any is most often due to cardiac disease which can further diagnostic aids. be ruled out relatively easily by a physical ex­ Ascites is a sign that something serious has am and thoracic radiographs. If these find­ gone wrong with the animal and the client ings are normal, more involved diagnostic should be appraised that diagnosis could be aids may be required to rule out liver disease expensive, the prognosis may be poor, and or neoplasia. A urinalysis may reveal the treatment difficult or unrewarding. In causes of hypoalbuminemia to be via the general the two main causes of ascites are car­ kidneys. In short, a logical pattern should be diac problems and liver disease, with the kept in mind in order to arrive at a reasonable greater percentage caused by cardiac prob­ diagnosis with a reasonable amount of time lems. and effort. Common cardiac problems associated with ascites are heartworms, congestive cardiomy­ PHYSICAL EXAM opathy, right heart failure, and congenital The animal is often presented with a com­ pulmonic stenosis. Hepatic diseases which plaint of abdominal enlargement. The causes cause ascites and/or hypoalbuminemia are of distension (gas, liquid, organomegaly) liver insufficiency, chronic-active hepatitis, should be determined. Intraabdominal gas will give a sharp rebound to percussion and a *From Iowa State University College of Veterinary Medicine. Dr. Peden is a 1981 graduate. Dr. Zenoble is higher pitched resonance when ausculated an assistant professor in Veterinary Clinical Sciences. than fluid. The ascitic abdomen has a charac-

12 Iowa State Veterz"narz"an teristic pear shape and percussion of the ab­ alerts the clinician to consider the heart more domen will result in a sharp fluid rebound on carefully. Specific examples include: 1) heart­ the opposite side. worm disease with enlarged right ventricle Fluid distensions may occur within the and enlarged pulmonary arteries, 2) biven­ gastrointestinal tract or any hollow organ. tricular enlargement with mitral and Palpation is used to rule out a palpable tricuspid insufficiency, 3) enlarged right ven­ obstruction such as an intussusception. tricle and poststenotic dilation of pulmonary However, the great volume of fluid may limit artery with congenital pulmonic stenosis, 4) a good physical examination. Ballotment marked generalized cardiomegaly with through the abdominal wall may indicate a idiopathic congestive cardiomyopathy of mass or enlargement of an organ. large breed dogs. Physical findings along with Since cardiac disease is a major cause of radiographic findings may add support to ascites, particular care should be paid to cardiac cause of ascites. auscultating the heart. Murmurs may be in­ If there is no indication for cardiac disease dicative of a number of problems and the as the cause of ascites, abdominal radio­ location of the murmur may be a clue to the graphs may be helpful. Abdominocentesis particular problem. A murmur on the right prior to radiographing the abdomen is benefi­ side, third to fifth intercostal space may in­ cial as the amount of fluid in the abdomen dicate a tricuspid insufficiency due to car­ will obscure any detail in most cases. Removal diomyopathy or valvular fibrosis. In con­ of the fluid will give better definition and gestive heart failure both mitral and tricuspid possibly enable visualization of the abdominal insufficiency may be noted. Severe heartworm organs and relative positions. For example, disease can cause right sided heart failure and caudal displacement of the stomach gas a positive Knott's test and characteristic shadow may indicate hepatomegaly. Dorsal thoracic radiographs will support the diagno­ displacement of the intestines may indicate a sis. Delayed heart sounds such as late closure splenic tumor or mass. Pneumoperitoneogra­ of the pulmonary valve may also indicate phy may help in visualizing the abdominal heartworms. organs. Cystography may be used to evaluate Congenital pulmonic stenosis may be in­ the bladder if paracentesis shows urine in the dicated by a murmur on the left side near the fluid. cranial sternum. This condition may lead to right ventricular enlargement and right heart CBC and BLOOD CHEMISTRY failure. A CBC should be done on all animals Idiopathic congestive cardiomyopathy may presented with ascites even though the in­ be suspected when a large breed dog with formation will not give a definitive diagnosis. ascites is showing a deficit between the heart An eosinophilia may be a further indication and pulse rate. If atrial fibrillation is present of heartworm disease. An inflammatory (> 80 %) the heart rate can be greater than leukogram may indicate an inflammatory 200 beats per minute. process such as peritonitis. Hepatomegaly or spenomegaly are often Protein levels should be determined and a noted with cardiac problems due to venous specific check for albumin levels should be congestion. These signs may also indicate made. Hypoalbuminemia rarely is the pri­ neoplasia or hyperplasia. It is important not mary cause of ascites but definitely con­ to be led astray by signs which may indicate tributes to the continuation of the problem. more than one disease. Icterus is another In order for hypoalbuminemia to cause clinical sign which could be confusing as it is ascites the albumin level must be less than 1.5 usually associated with hepatic disease or g/dl. Decreased hepatic synthesis will con­ hemolytic disease. tribute to hypoalbuminemia but a more likely cause is expansion of the plasma volume and 2 7 RADIOGRAPHS subsequent dilution of albumin • The most important ancillary test used in A Knott's test for D'ioroj'ilar'ia 'imm'itzs diagnosing the cause of ascites is radiography. should also be performed. It should be Cardiac causes of ascites are easy to rule out remembered that a significant percentage of with a thoracic radiograph. In most in­ animals suffering from heartworms are stances, cardiomegaly will be seen which negative with the Knott's test. If all other

Vol. 44, Issue No. 1 13 signs indicate heartworm disease, a negative hepatocellular necrosis, fibrosis, or Knott's test should not be the basis for biochemical lesions. Levels of significance for discarding that diagnosis. these enzymes can be found in most clinical Evaluation of the serum may reveal ab­ pathology references. It is important to normal chemical values which may be ex­ remember that the magnitude of the increase tremely helpful in diagnosing the primary in enzyme levels is proportionate to the problem after cardiac disease has been ruled damage, but no evaluation of the reversibility out. A urinalysis may yield information on of the damage can be made from these levels. bilirubin levels, urobilinogen, and renal loss The persistence of high levels of these enzymes of protein. is a poor prognostic sign, as the half-life is 2-4 In general, biochemical analysis of serum is days, and persistent high levels mean con­ primarily aimed at determining the status of tinuing damage. Other enzymes which can be the liver by 1) measuring substances excreted used to detect hepatocellular disease include or produced in the normal liver, 2) measuring isocitrate dehydrogenase, glutamate de­ enzymes which are associated with abnormal hydrogenase, and arginase.2 liver function, and 3) measuring the rate of Reduced functional hepatic mass can be removal of certain dyes such as BSP (sulfabro­ measured by a BSP excretion test or an am­ mophthalein).8 monia tolerance test. BSP is rapidly removed Bilirubin is a breakdown product of hemo­ from the blood and conjugated in the liver globin and measurements of total bilirubin, and ammonia is converted to urea in the liver. conjugated bilirubin, and unconjugated Both of these processes depend on an ade­ bilirubin are helpful in assessing hepatic func­ quate hepatic mass and blood flow. The tion, cholestasis, or hemolytic disease. A results for both tests may be affected by car­ marked rise in conjugated bilirubin as op­ diac disease (inadequate blood flow) which posed to unconjugated bilirubin is a strong in­ could lead to a false diagnosis of a primary dication of cholestasis. If the increase is pro­ liver problem if the results were used alone for portionately greater in the unconjugated a diagnosis. In addition BSP clearance is bilirubin, a hemolytic cause should be hastened by hypoalbuminemia and delayed suspected for the increase in bilirubin.2 by hyperbilirubinemia. For these reasons the Bilirubinuria is often noted before bilirubi­ results of such tests may be confusing and the nemia and may be the first indication of tests should be far down on the list of cholestasis. Urinary urobilinogen may help diagnostic aids. In general, increased am­ differentiate a partial or complete biliary monia concentration has been documented obstruction. A positive test for urobilinogen most frequently in animals with portocaval indicates that the bile duct is patent to some venous shunting and liver atrophy.2.8 degree.2 Serum alkaline phosphatase (SAP) is also a ABDOMINAL PARACENTESIS good indicator of cholestasis. Cholestasis Abdominal paracentesis is accomplished by s~imulates de novo synthesis of SAP and these advancing a needle into the most pendulous increased levels are reflected in the circula­ area of the abdomen while keeping a slight tion. Increased SAP levels often precede negative pressure in the syringe. This insures hyperbilirubinemia or bilirubinuria and any that fluid will be withdrawn as soon as the increase in the latter two should be ac­ needle enters the peritoneal cavity. Fluid companied by increased SAP levels if they are should be drawn into a container containing due to cholestasis. 2,8 anticoagulant. 6 Serum glutamic-pyruvate transaminase The fluid should be evaulated for cell (SGPT) and serum glutamic-oxalacetic tran­ counts and cytology, biomechanical para­ saminase (SGOT) are leakage enzymes in­ meters, and cultured. All degrees of tran­ dicative of hepatocellular damange. SGPT is sudates and exudates may be found in ascites, the only enzyme specific for hepatic damage. and examination of the fluid is a valuable A number of factors may induce hepatocellu­ diagnostic test. lar leakage including hypoxia, toxins, drugs, Cytologic examination of the fluid (direct hepatitis, fatty change and degeneration due smear or sediment) may indicate lymphosar­ to metabolic disorders. Lesions accompany­ coma or other neoplasia as the origin of the ing leakage of enzymes may be fatty change, fluid. Bloody or cloudy fluid often indicates

14 Iowa State Veterinarian an inflammatory or neoplastic process, and key hole technique will be the only technique the number and type of cells should be described here. evaluated. The animal should be fasted and fat should Specific gravity, the presence of bile or be given per os to contract the gall bladder. urine, and the protein level should all be Ascitic fluid should be removed before at­ checked. A specific gravity of greater than tempting a biopsy. The animal is placed in 1.030 with high numbers of red blood cells dorsal recumbency and general anesthesia or and white blood cells may indicate bleeding local anesthesia and sedation is employed. into the abdominal cavity. Urine in the fluid The area to be incised is on the ventral may indicate a ruptured bladder. Bile in­ midline, directly posterior to the xiphoid. A dicates a direct communication of the biliary small incision large enough to insert a finger tree and peritoneal cavity. 6 is made into the peritoneal cavity. The area is A low protein level (less than 2.0 gI dl) is in­ palpated and the left hepatic lobe is im­ dicative of a pure transudate, possibly due to mobilized. This is a larger lobe in the dog and hypoproteinemia caused by renal disease or biopsy of this lobe has less risk for gall bladder intestinal malabsorption. Most ascitic fluid is penetration as it lies on the right side of the a modified transudate with a protein level of animal. A separate skin incision is made to 2.5 to 5.0 g/dl. Modified transudates are seen the left of the first incision to permit entry of in many diseases such as congestive heart the biopsy needle into the peritoneal cavity. failure, portal venous obstruction, cirrhosis, The index finger is used to guide the biopsy hepatoma, and abdominal neoplasia. 2,6 needle to the biopsy site. The liver lobe is im­ mobilized by pinning it against other lobes or LIVER BIOPSY AND LAPAROTOMY the diaphragm with the index finger. The The results of various tests and physical needle is positioned so that it will not findings may suggest or rule out hepatic penetrate vital structures such as the large disease as the cause of ascites. A liver biopsy is vessels and gall bladder. If a Menghini needle one method which can be used to confirm is used for the biopsy a slight negative other findings and establish a specific pressure is maintained in the syringe and diagnosis. A liver biopsy should only be at­ needle as the needle is moved rapidly into and tempted when the information obtained will out of the liver in one smooth, continuous mo­ be beneficial to the patient, as the possibility tion. The biopsy needle is placed in fixative of serious iatrogenic complications is an ob­ and the negative pressure is released. The vious concern. Therefore if other findings can liver should be examined for bleeding and the establish a specific diagnosis there is little incision closed. 5 necessity for a liver biopsy. A liver biopsy may If neither neoplasia or hepatic disease can be the only way to diagnose neoplasia, toxic be ruled out a combined exploratory hepatitis, or cirrhosis and in these instances laparotomy and biopsy can be considered to histology is necessary to establish a specific arrive at a diagnosis. diagnosis, prognosis, and treatment regimen. Before attempting a liver biopsy the PATHOGENESIS OF HEPATIC AND animal's condition in regard to PCV, clotting CARDIAC ORIGIN ASCITES time, prothrombin time and platelet number Ascites due to cardiac problems is brought should be evaluated. If these values are ques­ about by a failing right heart leading to tionable the biopsy is contraindicated as splanchnic pooling and congestion. Hepatic massive hepatic bleeding may result. disease and fibrosis also lead to splanchnic There are many techniques for obtaining a pooling of blood. Both of these problems lead specimen of liver. These include a keyhold to portal hypertension. In ascites- due to por­ technique, percutaneous transthoracic or tal hypertension there is a derangement of transabdominal approach, and exploratory fluid and electrolyte metabolism of the laparotomy.3.5 The keyhole technique is the animal. With portal hypertension plasma safer of the two as it permits digital exam of proteins readily escape from the sinusoidal the liver and surrounding organs, the hepatic capillaries into the interstitial space of Disse. lobes can be immobilized, precise selection of From there only the hepatic capsule separates the biopsy site can be obtained, and any the proteins from the abdominal space. The hemorrhage can be easily ascertained. The increased hydrostatic pressure causes the

Vol. 44, Issue No. 1 15 movement of large amounts of fluid and pro­ urine in the peritoneal cavity. tein into the abdominal cavity. The Hepatic origin ascites requires the most peritoneal lymphatics are unable to return definitive diagnosis and treatment in order to the volume of fluid to the normal circulation. be adequately resolved. If chronic-active The loss of fluid into the abdominal cavity hepatitis is diagnosed the treatment will leads to a decrease in effective plasma volume revolve around arresting the inflammation, and in cardiac output. This causes a decrease correcting nutritional derangements, resolv­ in glomerular filtration, which leads to the ing fibrosis and resolving any complications. release of renin and the conversion of Corticosteriods will decrease inflammation angiotensinogen to angiotensin II, and secre­ but may increase protein catabolism and in­ tion of aldosterone by the adrenal gland. The crease ammonia production which is undesir­ kidney saves more sodium and water to try able. A high quality, low protein diet in and increase effective plasma volume and numerous small feedings is desirable to does increase total plasma volume. 7 diminish bacterial conversion of excess pro­ Only 20% of the blood is in the high pres­ tein to ammonia in the colon. Adequate sure arterial side of the circulation and all energy should be included to minimize conservation mechanisms operate on the low catabolism of proteins. Eggs, milk, lean meat, pressure side. Increasing total volume may glucose, and B complex vitamins are ex­ not necessarily increase effective plasma amples of high quality foods to be included in volume and return the arterial side to normal such a diet. Corticosteriods and colchicine function. An animal with ascites has its cir­ may help resolve fibrosis. Antibiotics should culatory system working at maximum com­ be used to minimize bacterial infection via the pensation and any disruption of fluid or elec­ portal circulation. Confining the animal is trolyte beyond what has already happened beneficial as blood flow to the liver is in­ may throw the animal into circulatory failure creased and the work load of the liver is or collapse. decreased. In normal animals expansion of the ex­ Ascites itself is usually managed with tracellular fluid compartment will result in diuretics and a low sodium diet. A loop diuresis due to a poorly understood phenome­ diuretic such as furosemide is the diuretic of non known as Third Factor. This is believed choice unless there is already an electrolyte to be a hormone mediated action on renal mi­ imbalance. If potassium values are low the crocirculation but is not well understood. The potassium sparing diuretics such as ascitic animal will not respond to volume ex­ triamterene may be indicated. Removal of pansion as a normal animal will, thus making large quantities of fluid at anyone time is not Third Factor very important in the mecha­ generally recommended because of the albu­ nism offluid retention in animals with ascites. min loss and possibility of circulatory col­ In addition, aldosterone is metabolized by the lapse. The removal of fluid over several days liver, and in hepatic insufficiency the effect of is a better plan, and even that may not benefit aldosterone may be prolonged. 7 the animal as intraabdominal pressure may have a role in the rate of ascites formation, TREATMENT such that decreasing pressure may only in­ Treatment of ascites will depend upon the crease the rate offormation of ascites. underlying cause. If cardiac failure is the primary cause the standard treatment of diuretics and digitalis may help resolve the REFERENCES ascites as cardiac function is improved. 1. Agosti, M; Malvezi, A; Pozza, 0: New Techniques in Paracentesis and removal of fluid may be the Treatment of Ascites in the Dog (Abstract). Arti beneficial, but the loss of protein in the fluid della Scocieta Italiana delle Scienze Veterinarie, 29:317-322, 1975. is undesirable. In addition the sudden 2. Duncan JR; Prasse, KW: VeteTZ'nary Laboratory removal of large quantities of flu.id may Med'icz'ne-Clz'nz'cal Pathology, ISU Press, Ames, IA. further compromise the animal. 1977. 3. Feldman, EC; Ettinger, SJ: Percutaneous Surgical treatment and removal of fluid Transthoracic Liver Biopsy in the Dog, JAVMA, will be the obvious choice for treating 169:805-810, 1976. 4. Furneaux, RW; Mero, KN: End to Side Portocaval operable neoplasia and traumatic injuries Anastomosis for the Correction of Ascites in a Terrier leading to accumulation of bile, blood, and Dog, JAAHA, 9:562-566,1973.

16 Iowa State Veterinarian 5. Osborne, EA; Hardy, RS; Stevens, JB; and Perman, 7. Strombeck, DK; Introduction to Diseases of the Liver, V: Liver Biopsy, Veterinary Clinics of North In: Small Animal Gastroenterology, Stonegate America, 4:333-350, 1974. Publishing, Davis, CA. 1979. 6. Scott, RC; Wilkins, RJ; and Green RW; Abdominal 8. Tennant, BC; Hornbuckle, WE: Diseases of the Paracentesis and Cystocentesis, Veterinary Clinics of Liver, In: Veterinary Gastroenterology, Anderson North America, 4:423-417, 1974. NV: Lea and Febiger, Philadelpha, PA. 1980.

Porcine Intestinal Adenomatosis: A Clinical Review

by Craig Rowles* Dr. J. Kunesh**

INTRODUCTION to strike 6 mo. - 1 yr. old gilts and boars as Porcine Intestinal Adenomatosis (PIA) is a they enter the breeding herd. disease affecting the alimentary tract of pigs. i Previous literature has described several syn­ ETIOLOGY dromes relating to PIA, including Regional Early observations of the disease were often 2 4 S 7 hampered by other concurrent infections. Ileitis - (RI), Necrotic Enteritis - (NE), and Hence, an etiologic agent was difficult to Proliferative Hemorrhagic Enteropathy8-10 (PHE). However, it wasn't until recently that identify. In 1972, however, a minimal disease morphologic evidence was found, linking all herd broke with several cases of PIA. 8 four syndromes with a single etiologic Through the use of special culturing tech­ 3 8 agent. 11-12 niques and immunofluorescence, Cam­ A clinical review of PIA, including in­ pylobacter sputorum var mucosalis was iden­ cidence and prevalence, etiology, lesions, tified. To date, this organism has not satisfied diagnosis, treatment and control, follows. Koch's postulates. Yet, it is universally agreed that the disease would not occur without this INCIDENCE AND PREYALANCE vibrioid organism. 8.18 PIA is reported to be worldwide in distribu­ Campylobacter sputorum var mucosalis is a tion. Cases have been documented in gram negative, short, irregularly curved rod, Australia, Canada, Denmark, Finland, In­ 0.25 urn wide and 0.95-2.8 urn long. Sea gull, dia, Sweden, the United Kingdom, and the spiral and comma forms occur. Coccal forms United States. 13 Two substantial slaughter­ also occur but are less prominent. 13 house studies have been conducted to deter­ Colonies grow on many solid nutrient mine the percentage of swine showing lesions media with 5-7% added blood. Microaero­ 2 14 philic conditions are necessary for growth. at slaughter. • Each indicated a low but ap­ preciable level of lesions, .25% and < 1% Colonies are 1. 5- 2.0 urn in diameter after 48 respectively. hrs. and can be differentiated from other No literature exists relating the number or vibriones by the production of a yellow pig­ percentage of herds infected with PIA. ment and by tube aggulutination tests. 12.13 However, it is generally agreed that this Because this is an intracellular organism af­ disease does pose a significant economic loss fecting the intestinal crypt cells, special for swine producers. culturing techniques must be used to isolate 12 Any age group may show clinical signs. the organism from intestinal samples. Most However, it appears that at two different practitioners are not equipped to use this times a pig may be more likely to show clinical method of diagnosis. signs. During the post weaning period, pigs * Mr. Rowles is .curr~ntly a senior veterinary student at the Iowa State University College of Veterinary Medicine. seem to show clinical signs relating to PIA, .* ~ Dr. ~unesh is currently a professor of Veterinary RI, and NE. 1s PHE, on the other hand, seems ClInIcal SCIences at Iowa State University.

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