Small Animal Surgical Emergencies. Группа авторов

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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 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].

Photo depicts removal of solidified wood glue from the stomach of a dog.

      Young (mean 2.5–4.5 years), medium to large‐breed dogs are most commonly reported to have GI foreign bodies [2, 4, 11, 21, 22], although this is not consistent in all studies [23]. Most reported cats are also young [2] with the mean age of 1.8–2.7 years [2, 13]. Clinical signs depend on the duration since ingestion and the type, extent, and location of obstruction. Animals with acute or complete obstruction often present with lethargy, anorexia, vomiting, and abdominal pain. Dehydration may also be present due to a combination of vomiting and lack of water intake. Vomiting tends to be more common with upper GI obstructions and has been reported to be present for 0.04–60 hours before presentation [2]. Chronic or partial obstruction, particularly distal in the intestinal tract, may include the same signs in addition to weight loss and diarrhea; and hemorrhagic diarrhea has also been reported subsequent to ingestion of contaminated foreign bodies, such as used feminine hygiene products [2, 24, 25]. Animals may also present with seemingly unrelated clinical signs, such as respiratory distress subsequent to intrathoracic migration of a foreign body [26]. Animals presented immediately after witnessed ingestion of a foreign body or those with small or inconsequential foreign bodies frequently have no clinical signs [2, 4, 21, 24].

      Foreign objects may or may not be identified on physical examination. Evans et al. reported that only 6% (2 of 32) of dogs with linear foreign bodies had the object visible under the tongue [11]. A second study showed that 3% of objects were visible in the oral cavity or at the anus, while 76% of the foreign bodies or the intestinal abnormalities resulting from such were palpable in either the awake (60%) or anesthetized patient [2]. Additional clinical signs such as fever, lethargy, abdominal pain, and abdominal distention may also be seen in patients with perforation and septic peritonitis, induced by a foreign body.

      Laboratory abnormalities depend on the type and extent of obstruction, as well as the duration and severity of clinical signs. Many of the clinicopathologic abnormalities result from dehydration and hypovolemia that accompany the obstruction. Dehydration may result in an elevated hematocrit, total protein, and urine specific gravity, as well as prerenal azotemia. Hypoproteinemia and hypoalbuminemia may occur in animals with GI perforation‐induced septic peritonitis or in those with chronic obstructions marked by long‐standing protein‐losing diarrhea. Elevations in hepatic enzymes, particularly alanine transaminase, may be seen as a consequence of hypovolemic shock and reduced hepatic perfusion. Preoperative hypoalbuminemia has sometimes been associated with postoperative dehiscence of anastomotic sites or mortality [23,27–31], but in other studies hypoalbuminemia had not increased these risks [32–34]. Toxic effects of some foreign bodies, such as those composed of zinc or lead, may precipitate toxin‐specific laboratory abnormalities.

      Acid–base abnormalities are common in animals with foreign body obstruction. In a study of animals by Boag et al. [4], it was found that 74.6% had elevated bicarbonate, 51% had hypochloremia, 45.2% had metabolic alkalosis (base excess greater than reference range), and 40–45% had hyperlactatemia. There was no statistical association between biochemical abnormalities and location of the foreign body at surgery (proximal or distal to the duodenal papilla). Hypochloremic, hypokalemic metabolic alkalosis was identified in 12% of dogs with proximal GI obstructions and 13.7% of dogs with distal GI obstruction [4].

      Radiographs

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