Digestive System 3 PDF

grave prognosis; they should be repaired only if small and if treatment is instituted before the peritoneal cavity is grossly contaminated. Abomasal Disorders: Introduction Abomasal disorders include left displaced abomasum (LDA), right displaced abomasum (RDA), abomasal volvulus, ulcers,...

grave prognosis; they should be repaired only if small and if treatment is instituted before the peritoneal cavity is grossly contaminated. Abomasal Disorders: Introduction Abomasal disorders include left displaced abomasum (LDA), right displaced abomasum (RDA), abomasal volvulus, ulcers, and impaction. Displacement or volvulus occurs commonly in dairy cows, particularly high-producers, but also in bulls, calves, and small ruminants. They are rare in beef cattle. Left or Right Displaced Abomasum and Abomasal Volvulus Because the abomasum is suspended loosely by the greater and lesser omenta, it can be moved from its normal position on the right ventral part of the abdomen to the left or right side (LDA, RDA), or it can rotate on its mesenteric axis while displaced to the right (abomasal volvulus). Abomasal volvulus can develop rapidly or slowly from an uncorrected RDA. Etiology: The etiology is multifactorial, although abomasal atony and gas production contribute to development of displacement or volvulus. Atony is related to high-concentrate, low-roughage diets, which result in increased production of volatile fatty acids, high concentrations of which reduce abomasal motility. Other contributing factors include decreased abomasal motility associated with hypocalcemia, concurrent diseases (mastitis, metritis, and ketosis), changes in position of intra-abdominal organs, and genetic predisposition. About 80% of displacements occur within 1 mo of parturition; however, they can occur any time. LDA is much more common than RDA (8:1), and cases of volvulus are even less frequent (25 LDA to 1 volvulus). Pathogenesis: A mild metabolic alkalosis with hypochloremia and hypokalemia are common. The hypochloremic metabolic alkalosis is probably due to abomasal atony, continued secretion of hydrochloric acid into the abomasum, and the partial abomasal outflow obstruction, with sequestration of chloride in the abomasum and reflux into the rumen as a result. Hypokalemia is probably due to decreased intake of feeds high in potassium and to continued renal secretion of potassium. Secondary ketosis is common and may be complicated by development of fatty liver disease. A large quantity of fluid accumulates in the abomasum; chloride is sequestered there as well. Hypochloremic, hypokalemic metabolic alkalosis develops. The blood supply to the abomasum, and often the omasum, is compromised, eventually resulting in ischemic necrosis of the abomasum as well as dehydration and circulatory failure. As this progresses, a metabolic acidosis is superimposed on the metabolic alkalosis. Clinical Findings: The most important diagnostic physical finding is a ping on simultaneous auscultation and percussion of the abdomen, which should be performed in the area marked by a line from the tuber coxae to the point of the elbow, and from the elbow toward the stifle. The ping characteristic of an LDA is most commonly located in an area between ribs 9 and 13 in the middle to upper third of the abdomen; however, the ping can be more ventral or more caudal, or both. Pings associated with a rumen gas cap or rumen collapse are usually more dorsal, less resonant, and extend more caudally through the paralumbar fossa. Pings associated with pneumoperitoneum typically are less resonant, present on both sides of the abdomen, and inconsistent in location on repeated evaluation. The ping associated with RDA also is most commonly located in the area between ribs 9 and 13. Differentiation between various causes of a right-sided ping is difficult in some cases. A small ping underlying ribs 12 or 13 and extending as far forward as rib 10 is common in cows with functional ileus from a number of causes. It is most often associated with gas in the ascending colon and resolves with correction of the underlying condition. Palpation per rectum is helpful in differentiating an RDA from cecal dilatation or rotation. Other right-sided pings are produced by pneumoperitoneum or gas in the rectum, descending colon, duodenum, or occasionally in the ventral sac of the rumen (with chronic vagal indigestion). The characteristic rectal examination findings with LDA include a medially displaced rumen and left kidney. The abomasum is rarely palpable in LDA and only occasionally in RDA. An early abomasal volvulus is indistinguishable from an RDA except by the anatomic position identified at surgery. In contrast with cases of displacement, an animal with abomasal volvulus has tachycardia proportional to the severity of the condition. Diagnosis: For displacement or volvulus, diagnosis is based on the presence of the characteristic ping on simultaneous auscultation and percussion and ruling out other causes of left- or right-sided pings. Recent parturition, partial anorexia, and decreased milk production suggest displacement. A ketosis that is only temporarily responsive to treatment is consistent with abomasal displacement, which may be intermittent. The typical signs on physical examination (in addition to the ping), rectal examination, and laboratory evaluation also support the diagnosis. Melena or signs of peritonitis (eg, fever, tachycardia, Merck Veterinary Manual - Summary 35 localized abdominal pain, pneumoperitoneum) with an LDA may indicate a bleeding or perforated abomasal ulcer, respectively. Treatment: Closed (percutaneous) or open (surgical) techniques can be used to correct displacements. Rolling a cow through a 70°arc after casting her on her right side corrects most LDA; however, recurrence is likely. LDA can be corrected surgically using right paramedian abomasopexy, right paralumbar fossa omentopexy, or left paralumbar abomasopexy. Toggle-pin fixation or the blind-stitch technique, both performed in the right paramedian area, are percutaneous methods for correction of LDA. With toggle-pin fixation, the pH can be checked to confirm that the pin is in the abomasum, which reduces the likelihood of attaching rumen, small intestine, or omentum to the body wall rather than the abomasum. RDA and abomasal volvulus are corrected surgically (right paralumbar fossa omentopexy or right paramedian abomasopexy) when economically feasible. Calcium borogluconate SC helps restore normal abomasal motility in many cases. Occasionally, animals with abomasal displacement or volvulus will have atrial fibrillation, thought to be of metabolic or neurogenic origin. It is characterized by an irregularly irregular cardiac rhythm with pulse deficits. Correction of the displacement or volvulus results in correction of the atrial fibrillation, although some cases do not resolve for ≥1 mo. The prognosis after correction of simple LDA or RDA is good, with reported success of 75-95%. Volvulus has a variable and less favorable prognosis; a large quantity of fluid in the abomasum, a high anion gap, a high heart rate, a low plasma chloride concentration, and metabolic acidosis are associated with a poor prognosis. Prevention: feeding a complete ration rather than feeding grain twice daily, maintaining adequate roughage in the diet, avoiding postparturient hypocalcemia, and minimizing and promptly treating concurrent disease. Abomasal Ulcers Abomasal ulcers affect mature cattle and calves and have several different manifestations. Etiology and Pathogenesis: Except for lymphosarcoma of the abomasum and the erosions of the abomasal mucosa that occur with viral diseases such as bovine viral diarrhea, rinderpest, and bovine malignant catarrhal fever, the causes of abomasal ulceration are not well understood. Many different causes have been suggested. Although abomasal ulcers can occur any time during lactation, they are common in high-producing, mature dairy cows within the first 6 wk after parturition. This has led to speculation that the cause is a combination of the stress of parturition, the onset of lactation, and heavy grain feeding. Abomasal ulcers are common in hand-fed calves after they are weaned from milk or milk replacer and begin to eat roughage. Most of these are subclinical and nonhemorrhagic. They may be due to consumption of dry food. Occasionally, milk-fed calves 7 yr old. Finally, there is a natural space between the dorsal aspect of the spleen and the left kidney. This space is bounded by the nephrosplenic ligament, a strong band of tissue that connects the dorsomedial aspect of the spleen with the fibrous capsule of the left kidney. This ligament provides a “shelf” over which large colon can be displaced. Colonic Motility Patterns: Normograde peristalsis in the left ventral colon moves ingesta toward the left dorsal colon, and the muscles in the wall of the left dorsal colon contract to move the ingesta toward the diaphragmatic flexure. Clinical Findings and Diagnosis: Numerous clinical signs are associated with colic. The most common include pawing repeatedly with a front foot, looking back at the flank region, curling the upper lip and arching the neck, repeatedly raising a rear leg or kicking at the abdomen, lying down, rolling from side to side, sweating, stretching out as if to urinate, straining to defecate, distention of the abdomen, loss of appetite, and decreased number of bowel movements. It is uncommon for a horse with colic to exhibit all of these signs. Although these clinical signs are reliable indicators of abdominal pain, the particular signs do not indicate which portion of the GI tract is involved or whether surgery will be needed. In most instances, colic occurs for one of four reasons: 1) The wall of the intestine is stretched excessively either by gas, fluid, or ingesta. This stimulates the stretch-sensitive nerve endings located within the intestinal wall, and pain impulses are transmitted to the brain. 2) Pain develops if there is excessive tension on the mesentery. 3) Ischemia develops, most often as a result of incarceration or severe twisting of the intestine. 4) Inflammation develops and may involve either the entire intestinal wall (enteritis) or the covering of the intestine (peritonitis). Under such circumstances, proinflammatory mediators in the wall of the intestine decrease the threshold for painful stimuli. The list of possible conditions that cause colic is long, and it is reasonable first to determine the most likely type of disease and begin appropriate treatments and then to make the more specific diagnosis, if possible. The general types of disease that cause colic include excessive gas in the intestinal lumen (flatulent colic), simple obstruction of the intestinal lumen, obstruction of both the intestinal lumen and the blood supply to the intestine (strangulating obstruction), interruption of the blood supply to the intestine alone (nonstrangulating infarction), inflammation of the intestine (enteritis), inflammation of the lining of the abdominal cavity (peritonitis), erosion of the intestinal lining (ulceration), and “unexplained colic.” In general, horses with strangulating obstructions and certain simple obstructions require emergency abdominal surgery, whereas horses with the other types of disease can be treated medically. The diagnostic approach must be thorough and systematic. The history of the present colic episode and previous episodes, if any, must be ascertained to determine if the horse has had repeated or similar problems, or if this episode is an isolated event. The duration of the episode, the rate of deterioration of cardiovascular status, the severity of the pain, whether feces have been passed, and the response to treatment are important information. The physical examination should include assessment of the cardiopulmonary and GI systems. The oral mucous membranes should be evaluated for color, moistness, and capillary refill time. The mucous membranes may become cyanotic or pale in acute cardiovascular compromise and eventually hyperemic or muddy as peripheral vasodilation develops later in shock. The capillary refill time (normal ~1.5 sec) may be shortened early but usually becomes prolonged as vascular stasis (venous pooling) occurs. The membranes will become dry as the horse becomes dehydrated. The heart rate increases due to pain, hemoconcentration, and hypotension; therefore, higher heart rates have been associated with more severe intestinal problems (strangulation obstruction). However, not all conditions requiring surgery are accompanied by a high heart rate. An important aspect of the physical examination is passing a nasogastric tube. Because horses can neither regurgitate nor vomit, adynamic ileus, obstructions involving the small intestine, or distention of the stomach with gas or fluid may result in gastric rupture. Passing a stomach tube may, therefore, save the horse's life and assist in diagnosis of these conditions. If fluid reflux occurs, the volume and color of the fluid should be noted. The abdomen and thorax should be ausculted, and the abdomen percussed. The complete lack of sounds is usually associated with adynamic ileus or ischemia. Percussion will assist in identifying a grossly distended segment of intestine (cecum on right, colon on left) that may need to be trocarized. The respiratory rate may be increased due to fever, pain, acidosis, or an underlying respiratory problem. Diaphragmatic hernia is also a possible cause of colic. The most definitive part of the examination is the rectal examination. A sample of peritoneal fluid (obtained via paracentesis performed aseptically on midline) often reflects the degree of intestinal damage. The color, cell count and differential, and total protein concentration should be evaluated. Normal peritoneal fluid is clear to straw-colored, contains