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Small Animal Surgical Emergencies


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4.15 Radiograph demonstrating a needle embedded in the esophageal wall of a dog.

Image described by caption.

      Needles

Photo depicts a splinter of wood being retrieved during a ventral midline exploration of a dog's neck.

       Amie Koenig and Mandy L. Wallace

       College of Veterinary Medicine, University of Georgia, Athens, GA, USA

      Gastrointestinal (GI) foreign bodies are common in dogs and cats; therefore, the need for surgical removal of foreign bodies is frequent in veterinary practice. In a pet insurance company report, $3.4 million in claims related to foreign body ingestion in dogs and cats were made in 2014 [1]. Discrete foreign bodies have been reported in all areas of the GI tract, with reports of the most common location being inconsistent [2–4]. Some authors hypothesize that location of the foreign body at the time of required intervention is correlated with owner awareness of ingestion. Lacking owner awareness, intervention occurs when the foreign body moves into a location that results in clinical signs.

      GI foreign bodies may be classified by clinical impact, for example, partial or complete obstruction, or by the nature of the foreign body, such as a discrete or linear foreign body. In addition, the foreign body may be classified by the location of the obstruction it creates within the GI tract into high (stomach or proximal duodenum), mid (jejunum), and low (ileocecocolic junction) obstruction and whether it has resulted in perforation.

      The underlying pathophysiology of GI foreign body obstruction is the result of failure of forward flow of GI contents secondary to the physical presence of the foreign material. The foreign body has a primary impact on local perfusion at the site of the physical obstruction and a secondary, often more serious, impact on fluid and electrolyte balance and intestinal motility [14, 15]. Proximal to the obstruction, the intestine dilates and distends with secretions and swallowed air. Dehydration results from subsequent vomiting, development of edema of the bowel wall, and loss of absorptive capacity [16]. Metabolic alkalosis results if vomiting is sufficient to result in loss of gastric chloride, potassium, and hydrogen ions or if obstruction sequesters GI contents proximally. Bacterial overgrowth occurs in the static intestinal tract. This overgrowth combined with the compromised bowel wall may lead to bacterial translocation and subsequent bacteremia. As intraluminal pressure increases, venous pressure is exceeded and loss of venous drainage occurs. Loss of arterial flow may occur in severe cases resulting in ischemia and necrosis of the intestinal wall [17]. Additionally, disk batteries can cause tissue necrosis and perforation subsequent