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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 to the generation of electric current that occurs after prolonged contact with mucosal surfaces [10], and magnets can cause perforation secondary to tissue entrapment between two magnets or a magnet and metallic object [7,18–20].

Figure 5.1 Removal of solidified wood glue from the stomach of a dog. Note the length of incision necessary to remove a foreign body of this size.