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Hernias involving the abdomen are seen when abdominal contents protrude through a natural or abnormal opening in the body wall. They may be congenital or acquired. In acquired hernias, there is usually a history of trauma. Congenital hernias may involve the diaphragm or the abdominal wall. Hernias involving the diaphragm are of 3 main types: peritoneopericardial, in which abdominal contents are found extending into the pericardial sac; pleuroperitoneal, in which abdominal contents are found within the pleural cavity; and hiatal, in which the abdominal esophagus, gastroesophageal junction, and/or portions of the stomach protrude through the esophageal hiatus of the diaphragm into the thoracic cavity. Clinical signs vary from asymptomatic to severe and depend on the amount of herniated tissue and its effect on the organ it is displacing. Hiatal hernias may be “sliding” and result in clinical signs of reflux esophagitis (anorexia, salivation, and/or vomition) that may be intermittent. Diagnosis is through radiology; contrast studies are often needed for confirmation. Fluoroscopy or endoscopy is useful in the diagnosis of sliding hiatal hernias. Correction of the aforementioned hernias is best accomplished through surgery. In the case of hiatal hernias, medical therapy, including the use of systemic antacid preparations and dietary modification, may control signs if mild.

Hernias involving the abdominal wall include umbilical, inguinal, or scrotal. Umbilical hernias are secondary to failure of the normal closure of the umbilical ring and result in protrusion of abdominal contents into the overlying subcutis. Size varies depending on the extent of the umbilical defect and the amount of abdominal contents contained within it. The etiology in both large and small animals is likely to have a genetic component; however, excess traction on an oversized fetus or cutting the umbilical cord too close to the abdominal wall are other possible causes. Diagnosis is usually straightforward, especially if the hernia is manually reducible. If irreducible, the hernia must be differentiated from an umbilical abscess, which is common in large animals. Umbilical hernia and umbilical abscess often are seen together, especially in cattle and swine. Exploratory puncture, such as via fine-needle biopsy with cytopathology, may be required for confirmation. Correction is surgical. In small animals, if the hernia is small, surgical correction is often done at the same time as sterilization procedures. In calves, some success has been achieved by applying a binder of broad adhesive bandage (10 cm width) for 3–4 wk. In horses, small hernias (<1–3 cm) may spontaneously resolve over time; however, if they persist for >6 mo, surgical correction is likely required. The owner should be advised that the weakness may be heritable.

Inguinal hernias in male pigs are common, and they usually extend into the scrotum. Suspending the piglet by the forelegs and gently shaking, which generally causes even a small hernial bulge to become visible can confirm the diagnosis. In female pigs, this defect is invariably accompanied by arrested genital development; such animals are sterile, and surgery is indicated only when the size of the defect is a threat to the growth of the pig to market weight. Inguinal hernias in male foals frequently resolve spontaneously during the first year of life, often assisted with repetitive manual reduction. For this reason, early corrective surgery is not indicated unless the hernia is strangulated or of such magnitude that it interferes with gait. Strangulated inguinal hernia in stallions is fairly frequent and is characterized by signs of constant and severe abdominal pain. It is readily recognized by rectal palpation and may be reduced, under general anesthesia, by rectal manipulation. If this fails, immediate surgery is necessary. Inguinal hernias in cattle are rare although sometimes seen in males. Surgical correction to preserve the breeding potential of the bull, when done, is not always successful.

Last full review/revision March 2012 by Walter Ingwersen, DVM, DVSc, DACVIM

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