Intestinal obstructions are seen in all large animal species but are most common in horses. Cattle are the most commonly affected ruminants; diagnosis in sheep and goats is rare, except for intestinal volvulus in lambs. Other than inguinal hernias, intestinal obstructions are infrequently recognized in pigs.
Obstructions interrupt the flow of ingesta and can be mechanical or functional in nature. Mechanical intestinal obstructions are characterized as being luminal or extraluminal. Extraluminal obstructions include hemorrhagic strangulating obstructions in animals with volvulus of the GI tract, or simple extraluminal compression in animals with an expanding abdominal mass such as lymphosarcoma or fat necrosis. Functional obstructions have no gross abnormality but are characterized by a generalized hypomotility or ileus. In general, functional obstructions occur more often than mechanical obstructions, and they are commonly identified in horses after abdominal surgery.
The inciting cause of a functional intestinal obstruction often is not determined. Functional obstructions are associated with altered intestinal motility, often due to dietary or management factors, phytobezoars, parasite infection, enteritis, peritonitis, or electrolyte abnormalities. Mechanical obstructions (physical blockage of ingesta) occur due to abnormalities in the bowel lumen, in the wall, or outside the tract. Mechanical obstructions include congenital obstructions (atresia jejuni, coli, recti, and ani in calves; atresia ani in lambs and pigs) that result in the lack of passage of feces since birth.
In horses, transient functional obstructions are common, as are feed impactions, which usually involve the pelvic flexure of the left colon. Parasite infection or migration, dental abnormalities, and dietary or management factors are often implicated in the development of functional obstruction. Impactions and other luminal obstructions can result from coarse feeds, reduced water intake, enteroliths, or ingested foreign material. Sites of impaction other than the pelvic flexure are the small colon, transverse colon, right dorsal colon, cecum, and ileum. Other causes of intestinal obstruction in horses are volvulus (twist on the mesenteric axis), torsion (twist along the long axis of the bowel), displacement of the ascending (large) colon, and volvulus of part or all of the small intestine. Altered motility and possibly strenuous exercise and rolling may be initiating causes. Broodmares may be predisposed to volvulus, torsion, or displacement of the ascending colon during gestation and shortly after parturition. Obstruction occurs either due to incarceration of the intestine (usually small) by herniation through the inguinal canal, diaphragm, mesenteric defects, umbilicus, or epiploic foramen; or because of fibrous bands (adhesions, mesodiverticular bands, or stalks of pedunculated lipomas). Standardbred stallions and colts develop inguinal and scrotal hernias more commonly than other breeds. Diaphragmatic hernias and mesenteric defects may be congenital or traumatically induced. Adhesions in horses are most often the sequela of parasite migration or abdominal surgery; however, most adhesions are clinically silent. Pedunculated lipomas are common in older horses. Ileocecal, cecocecal, cecocolic, and small-intestinal intussusceptions also are seen. Lymphosarcoma and other abdominal neoplasms as well as abdominal abscesses can cause intestinal obstruction.
In cattle, specific causes of intestinal obstruction include volvulus of the duodenal sigmoid flexure; intussusception of the jejunum and ileum; volvulus of the jejunoileal flange of the small intestine; volvulus at the root of the mesentery; luminal occlusion of the jejunum due to a blood clot secondary to hemorrhagic jejunitis; obstruction of the small intestine or spiral colon due to phytobezoars; cecocolic volvulus; and atresia coli, recti, and ani. Intussusceptions are thought to be the result of irregular peristaltic movements related to enteritis, intestinal parasitism, dietary disorders, and mural masses. Altered intestinal motility due to ingestion of a rapidly fermentable substrate may cause intestinal volvulus. Obstructions of the small intestine can develop due to a variety of fibrous bands (eg, adhesions, parovarian bands, falciform ligament, spermatic cord retraction into the abdomen after surgical castration), mural thickening (eg, intestinal adenocarcinoma), extramural masses (eg, lymphosarcoma, fat necrosis, abdominal abscesses), herniation (omental, inguinal, or umbilical), or hemorrhagic jejunitis (which results in luminal blood clots and obstruction). Adhesions and abdominal abscesses can form subsequent to peritonitis, intraperitoneal injections, or previous abdominal surgery. Decreased motility caused by accumulation of volatile fatty acids, possibly related to high-concentrate rations or an abrupt increase in the concentrate:forage ratio, have been suggested as causes of cecocolic volvulus in cattle. They also are associated with advanced pregnancy and ileus from concurrent disease. Atresia coli develops most commonly in Holstein-Friesian calves secondary to in utero ischemia of the developing spiral colon.
Intestinal obstruction in horses generally manifests as abdominal pain, which is termed colic (see Colic in Horses). In cattle, signs of abdominal pain include treading of the hindlimbs, stretching, restlessness, and kicking at the abdomen; rolling and bellowing are rarely seen. The signs of intestinal obstruction in cattle are generally more subtle than in horses and are usually referable to small-intestinal distention, tension on the intestinal mesentery (by the weight of distended bowel), or vascular impairment. Signs of pain are relatively consistent but often transient with intussusceptions and are seen in some cases of cecocolic volvulus. Cattle with volvulus of the small intestine at the root of the mesentery are severely affected.
Usually, cattle with intestinal obstruction are anorectic and pass few or no feces, and milk production in lactating cows drops suddenly. The feces that are passed may be covered with mucus, or mixed or coated with blood. Thick, raspberry-colored blood mixed with scant feces is characteristic of small-intestinal bleeding, particularly that associated with intussusception or hemorrhagic jejunitis. Blood from the colon or rectum is generally brighter red. Melena is typical of abomasal bleeding. Calves with atresia coli are healthy at birth but have progressive abdominal distention and decreased appetite during the first few days of life. (Also see Congenital and Inherited Anomalies of the Digestive System.)
Abdominal distention, usually with a ping on simultaneous auscultation and percussion, in the upper right caudal abdominal quadrant occurs with cecocolic volvulus. Cecal dilatation does not produce abdominal distention, but a ping is generally present in the caudal dorsal paralumbar fossa. In cecocolic volvulus, one or more large, distended loops of large intestine are identified on palpation per rectum. Rumen hypomotility is usually present, and metabolic and cardiovascular derangement tend to be mild except in cecocolic volvulus of long duration.
Abdominal distention in the lower right abdominal quadrant is sometimes seen with small-intestinal distention. Distended loops of bowel may be palpable on rectal examination, and fluid may be heard on simultaneous ballottement and auscultation of the right side of the abdomen. Small areas of tympanic resonance may be heard on simultaneous auscultation and percussion. Intussusceptions and fibrous bands that cause small-intestinal obstruction can be palpated per rectum in ~25% of cases. Ultrasonographic examination of the abdomen via the right paralumbar fossa or per rectum may help identify the presence of small-intestinal distention, ileus, and an increased peritoneal fluid volume. Occasionally, ultrasonography can identify an intussusception.
Profound changes in cardiovascular parameters, such as tachycardia, abnormal color of the mucous membranes, prolonged capillary refill time, and dehydration, are most commonly associated with hemorrhagic strangulating obstructions such as volvulus of the jejunal-ileal flange of the small intestine. Volvulus of the jejunal-ileal flange and volvulus at the root of the mesentery are characterized by acute onset and rapid cardiovascular deterioration. This is in contrast with cecocolic volvulus or intussusception, which can continue for several days in cattle.
Metabolic derangements range from hypokalemic, hypochloremic metabolic alkalosis in longstanding small-intestinal and duodenal obstructions to severe metabolic acidosis with hemorrhagic strangulating obstructions. Usually, there are no metabolic derangements in mild functional obstructions and early (simple) mechanical obstructions, particularly if a relatively distal part of the intestinal tract is involved. Hypocalcemia can develop, presumably due to decreased calcium absorption from the duodenum.
Peritoneal fluid changes reflect the degree of peritonitis and may aid in the diagnosis in both cattle and horses, although results are more variable in cattle. Hemorrhagic strangulating obstructions are characterized by an increase in the total protein concentration and nucleated cell counts of peritoneal fluid due to extravasation through the bowel wall. Neutrophils become degenerative, and intracellular gram-positive and gram-negative bacteria are seen in peritoneal fluid as the integrity of the bowel wall is lost. Plant material in the peritoneal cavity is indicative of bowel rupture or inadvertent enterocentesis. Peritoneal fluid analysis is normal with most simple mechanical and functional obstructions. When neoplasms are present and causing an extraluminal obstruction, neoplastic cells are sometimes identified in peritoneal fluid.
Treatment of intestinal obstruction in horses is covered elsewhere (see Colic in Horses). Treatment of functional intestinal obstruction in cattle is generally symptomatic and supportive after identifying and eliminating the inciting cause (eg, hypocalcemia, hypokalemia, excessive grain intake) and allowing time for normal intestinal motility to return. If present, dehydration and electrolyte imbalances should be corrected by appropriate fluid therapy (PO or IV). Lactating cows often benefit from calcium chloride gels administered orally or calcium borogluconate or calcium gluconate administered SC, and oral potassium chloride (120–240 g twice at 12-hr intervals). Secondary ketosis should be treated if present. Erythromycin (10 mg/kg, IM, bid) is the most effective pharmacologic method to increase abomasal emptying rate in cattle (and presumably increasing intestinal motility), but studies documenting efficacy in functional intestinal obstruction are lacking. Prokinetics should not be administered to cattle with a mechanical obstruction because of the increased risk of intestinal rupture proximal to the obstruction. The prognosis with most functional obstructions is good with appropriate supportive therapy, particularly if the inciting cause is identified and eliminated.
Mechanical obstructions almost always require surgery. Antimicrobial therapy should be started preoperatively; supportive therapy, such as fluids, electrolytes, and calcium, should be administered as needed.
Horses that require exploratory laparotomy to correct an intestinal obstruction have an overall longterm survival rate of 50%. The survival rate is lower for horses with hemorrhagic strangulating obstructions and small-intestinal lesions than for horses with simple obstructions, but early surgical intervention can improve the prognosis.
In cattle, 70%–80% of those with cecocolic volvulus survive, although 10% of cases recur. For cows with small-intestinal obstruction amenable to resection and anastomosis, 30%–40% survive and lead a productive life. For cows with volvulus of the jejunal-ileal flange of the small intestine or at the root of the mesentery, ~50% survive if surgical correction is performed within a few hours of onset. Less than 30% of calves with atresia coli survive to adulthood. Surgical correction of atresia coli is not recommended in Holstein-Friesian calves because the condition is probably inherited in this breed, although vascular damage secondary to amniotic vesicle palpation in the first 6 wk of embryonic development can also lead to intestinal ischemia and atresia in calves.
Prevention of all, or even most, cases of intestinal obstruction is not possible. However, abrupt changes in feeding and management; inadequate water intake; parasite infection; dental abnormalities; and access to coarse feeds, highly fermentable feedstuffs, and foreign material should be avoided or corrected.