Urinalysis and peritonitis

• Ascites
• Ultrasonography enables the examiner to detect very small amounts of fluid in the peritoneal cavity and to determine its location, amount, and sonographic features. The pathologic process responsible for the ascites, for example, ileus, hepatic fibrosis, thrombosis of the caudal vena cava, or traumatic reticuloperitonitis, often can be identified. Abdominocentesis and analysis of the aspirated fluid allow differentiation of inflammatory and noninflammatory ascites as well as the diagnosis of uroperitoneum, hemoperitoneum, chylous ascites, and bile peritonitis.
• The urea and creatinine concentrations are measured when uroperitoneum is suspected.   A typical exudate is defined as cloudy, watery to viscous, foul-smelling fluid that may clot quickly after collection. An exudate often contains flecks of fibrin and pus
• ** Goals of abdominocentesis **
• 1. Assessment of amount, color, odor, and consistency of a sample (eg, serous, bloody, purulent, urinelike, bilelike)
  • Poultry
  • Many turkeys on a poultry farm develop whitish “wart-like” nodules and scabs on the comb, wattles, feet, and vent. Which management intervention would help prevent spread of the disease?
  • The condition described here is the dry form of avian (fowl) pox. This is a relatively slow spreading disease that can be spread by contact or by mosquitoes that may harbor infective virus for greater than a month.
  • In the dry form of the disease, the main sign is raised, whitish wart-like lesions on unfeathered areas (head, legs, vent, etc.). The lesions heal in about 2 weeks. Unthriftiness, decreased egg production and retarded growth may be seen. Mortality is low with this form of the disease. The wet form mainly involves the oral cavity and upper respiratory tract. Lesions are diphtheritic and can ulcerate or erode mucous membranes. Marked respiratory involvement can lead to mortality.
  • A diagnosis is usually based on flock history and presence of these lesions. This is a pox virus and there is no specific effective treatment but there is a vaccine. Disease control is best accomplished by preventive vaccine as sanitation alone will not prevent spread of disease. Several vaccines are available and a single application results in permanent immunity.
  • There are not many tick borne poultry diseases but they may include spirochaetosis and Pasteurella infection.
  • Raising the temperature 5 degrees may be part of the treatment for infectious bronchitis in chickens. Disinfecting pens +/- quarantine is done for quail bronchitis, aspergillosis, and ulcerative enteritis. Antibiotics in the drinking water are most effective for preventing secondary bacterial infections and for mycoplasma but not preventing spread of the virus.
•  2. Determination of specific gravity and concentration of total protein (total solids) using a refractometer
• 3. California mastitis test for semiquantitative determination of cellular content of fluid
• 4. Cytologic, bacteriologic, and possibly biochemical evaluation of fluid
• 5. Comparison of urea and creatinine concentrations of peritoneal fluid and serum
• The specific gravity is greater than 1.015 and the protein content greater than 30 g/L. Smears made from exudates contain numerous leukocytes, but the number of cells may be reduced because of cytolysis.
• The proportion of eosinophils and neutrophils is used as a criterion for the diagnosis of peritonitis14; fewer than 10% eosinophils and greater than 40% neutrophils is highly suggestive of peritonitis. Sterile pus without bacteria may occur after antibiotic treatment of the animal, and the presence of bacteria in the absence of leukocytes may indicate contamination from accidental intestinal puncture.
• To improve the diagnostic usefulness of peritoneal fluid analysis, other variables, including albumin, glucose, fibrinogen, L-lactate, D-dimers, and the activities of lactate dehydrogenase and creatine kinase, were measured in serum and peritoneal fluid of 95 cows; the peritoneal-to-serum ratios of these variables were calculated.17 The glucose concentrations of blood and peritoneal fluid are usually similar, but bacteria in the peritoneal cavity metabolize glucose and cause a decrease in the peritoneal glucose concentration. The glucose concentration is, therefore, considered a very sensitive and specific criterion for the diagnosis of septic peritonitis in cattle.1
• ** Type of Intra-Abdominal Fluid  **
• ** Characteristics  **
• Inflammatory ascites Exudate
• Noninflammatory ascites. Transudate or modified transudate
• Chylous ascites Milky fluid
• Uroperitoneum -------Urine like fluid
• Hemoperitoneum------Bloody fluid
• Biliary ascites---------Bilious fluid
• ** Noninflammatory ascites** is the abnormal accumulation of serous fluid in the peritoneal cavity.2 An increase in intravascular hydrostatic pressure and/or a decrease in intravascular colloid osmotic (oncotic) pressure are the principal causes of
• noninflammatory ascites. It is most commonly caused by vascular congestion but can also be the result of hypoalbuminemia (decrease in oncotic pressure), retention of sodium accompanied by water retention in secondary aldosteronism, or peritoneal cancer, such as mesothelioma.19–22 Often the cause of noninflammatory ascites is multifactorial.
• ** Clinical Signs of Noninflammatory Ascites  **
• A tentative diagnosis can be made in severe cases when symmetric ventral abdominal enlargement causing a pear-shaped abdomen, a flaccid abdominal wall, and sloshing of fluid on abdominal succussion are evident (Fig. 1). When the condition is missed or allowed to continue, the contour of the animal may progress to barrel shaped (Fig. 2). Abdominal enlargement caused by ascites is generally more pronounced in calves and other young cattle than in mature cattle. However, even in cases with  considerable intra-abdominal fluid accumulation, the pear-shaped abdominal appearance may be missed. Ultrasonography is the method of choice for diagnosis of ascites.
• ** Ultrasonographic Findings of Noninflammatory Ascites   **
• The typical ultrasonographic finding of noninflammatory ascites is accumulation of anechoic fluid of varying extent in the peritoneal cavity. It may be limited to the ventral abdomen or the fluid level may extend dorsally or involve the entire peritoneal cavity. Large amounts of fluid surround the organs so that they are suspended in it. On the right side, intestines enclosed by the greater omentum are seen from the flank and intercostal spaces (Fig. 3). The surrounding fluid renders the greater omentum echoic; both walls of the omental bursa, each consisting of 2 serous layers, can often be seen (Fig. 4). The liver is displaced dorsally by the fluid and seen in the costal part of the abdomen. However, with mild or moderate ascites, only the ventral part of the liver including the gall bladder is surrounded by fluid (Fig. 5). With severe ascites, the liver is displaced from the abdominal wall creating an anechoic seam between the parietal peritoneum and the liver. Hepatic ligaments are often seen as fine echoic strands between the liver and the abdominal wall. On the left side, the rumen is displaced from the abdominal floor by anechoic fluid (Fig. 6). Likewise, the reticulum is displaced dorsally by fluid (Fig. 7). Owing to the acoustic properties of peritoneal fluid, the  different layers of the reticular wall are often very distinct: the tunica serosa appears as a thin echoic line on the outside and the tunica muscularis as a thin hypoechoic line in the middle, and the tunica mucosa combined with the tela submucosa on the inside are distinct. In contrast to reticuloperitonitis, there are no signs of inflammation, such as echoic fibrin deposits or abscesses. Furthermore, an anechoic seam of varying width is evident between the reticulum and spleen because the capillary space between these two organs is enlarged by the fluid.
• ** Causes of Noninflammatory Ascites **
• The most common causes of noninflammatory ascites attributable to vascular congestion include chronic right-sided cardiac insufficiency, mediastinal masses, chronic liver and kidney diseases, small intestinal ileus and enteropathies, tumors of the peritoneum, and caudal vena cava thrombosis or compression
• ** Right-Sided Cardiac Insufficiency **as the Cause of Ascites Ascites caused by right-sided cardiac insufficiency (traumatic pericarditis, valvular endocarditis, idiopathic cardiomyopathy, cardiac lymphosarcoma) is accompanied by abnormal auscultatory findings, such as tachycardia, pericardial or endocardial heart sounds, or cardiac arrhythmia (summation gallop heart sound in cardiomyopathy).23 The jugular veins are distended; there is submandibular, presternal, and ventral edema. Pleural effusion, dilation of the caudal vena cava, and a change in its crosssectional appearance from triangular to oval or circular are consistent and specific ultrasonographic findings of right-sided cardiac insufficiency.2 The activities of liver enzymes are increased because of liver congestion.
• ** Mediastinal Masses as the Cause of Ascites** Compression of the caudal vena cava by a mediastinal mass, such as an abscess or tumor, also results in a change in its cross-sectional shape to oval or circular, which  can be detected sonographically in the 11th and 12th intercostal spaces. Jugular distension is not a feature of this condition.2
• ** Liver Disease as the Cause of Ascite**s Ascites is common in liver disease and occurs when hepatic perfusion is compromised by liver cirrhosis, fascioliasis, or a tumor or abscess causing intrahepatic congestion. Hypoalbuminemia from impaired albumin synthesis is responsible for a decrease in intravascular oncotic pressure in liver cirrhosis and fascioliasis.2 In addition, an increase in pressure in the venous part of the splanchnic circulation because of impaired liver perfusion causes transudation of fluid into the peritoneal space. In cattle, severe hypoalbuminemia is always accompanied clinically by edema. Prehepatic portal hypertension caused by portal vein thrombosis alone in the absence of liver disease is not associated with ascites, which underlines the crucial role of decreased oncotic pressure in the pathogenesis of ascites24; the oncotic pressure remains unchanged because arterial perfusion compensates for lost venous perfusion. In addition to ascites, characteristic ultrasonographic features of portal hypertension include focal changes with abscesses or tumors, calcification of bile ducts with fascioliasis, and dilation of the portal vein. Blood analysis shows hypoalbuminemia and increased activity of liver enzymes, and microscopic examination of bile collected under ultrasound guidance shows common liver fluke ova.25 Fascioliasis is commonly complicated by concurrent peritonitis, and analysis of peritoneal fluid may show a modified transudate or even an exudate with an elevated eosinophil count. The principal ultrasonographic finding in cows with hepatic fibrosis attributable to Senecio alpinus poisoning was severe noninflammatory ascites.26 The liver parenchyma of all cows appeared heterogeneous and often had nodular changes; all cows had portal hypertension caused by intrahepatic changes, dilation of the portal vein, and a decrease in the diameter of the caudal vena cava lumen because of reduced liver perfusion. Portal hypertension also resulted in edema of the gall bladder wall, small intestines, and greater omentum. Cows with hepatocellular carcinoma had severe focal or diffuse hepatic changes but no ascites.2
• The standard treatment to reduce splanchnic portal hypertension in people is nonselective β-blockade using propranolol, administered to control or reduce risk of spontaneous bleeding from APSSs
• Therapeutic strategies for control of ascites include dietary sodium restriction, administration of diuretics to increase urinary sodium elimination, and therapeutic abdominocentesis (when necessary). The first step is dietary sodium restriction to an intake of ≤100 mg sodium/100 kcal diet (25 mg/kg/day; <0.1% dry-matter basis in food). However, sodium-restriction alone is often insufficient and too slow in onset for efficient management. Thus, diuretics are usually also recommended. Diuretic therapy should slowly reduce ascites without causing dehydration, metabolic alkalosis, or hypokalemia. Reducing ascites by ≤1%–1.5% of total body wt/day is recommended by initially using combined treatment with furosemide (1–2 mg/kg, PO, bid) and spironolactone (loading dosage 2–4 mg/kg × 2–3 doses, then 1–2 mg/kg, PO, bid). Reevaluation every 7–10 days allows for careful upward titration of diuretic dosages. Combining a loop diuretic (furosemide) with spironolactone (aldosterone antagonist) reduces risk of iatrogenic hypokalemia.
• If ascites is slow to mobilize, measuring the urinary fractional excretion of sodium can help determine whether dietary restriction and diuretic dosing are adequate. If ascites causes tense abdominal distention compromising ventilation, appetite, or patient comfort, therapeutic abdominocentesis may be undertaken. In people, 8 g of human albumin is administered for every 5 L of effusion removed to offset the development of postdiuresis circulatory dysfunction developing ~12 hr after effusion removal. Postdiuresis circulatory dysfunction reflects reequilibration of body fluids and worsened hypoalbuminemia (removed by abdominocentesis)