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Trauma Cases from Harborview Medical Center |
Department of Radiology, Harborview Medical Center, University of Washington School of Medicine, 325 Ninth Ave., Box 359728, Seattle, WA 98104-2499.
Received February 6, 2005; accepted after revision February 16, 2005.
Address correspondence to F. A. Mann
(famann{at}u.washington.edu).
A 29-year-old man with schizophrenia presented to the emergency department with abdominal pain immediately after ingesting approximately 200 mL of cleaning solution containing 36% hydrochloric acid. Initial unenhanced CT of the chest, abdomen, and pelvis showed an intact stomach and a small amount of free intraperitoneal fluid (Fig. 1A). Direct endoscopy showed mucosal injury in the oropharynx, hypopharynx, and supraglottic region, and diffuse caustic injury to the esophageal mucosa. Because of worsening clinical status, a contrast-enhanced CT of the abdomen was performed 2 days later, showing gastric necrosis and perforation (Fig. 1B). The patient died shortly thereafter.
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Caustic injury to the upper gastrointestinal tract from acid ingestion is less common in the United States than ingestion of alkaline liquids and usually occurs in young children or in adults attempting suicide [1]. In contrast to injury from alkali, which tends to affect the pharynx and esophagus with gastric sparing, caustic injury from acid ingestion typically affects the stomach and spares the esophagus. However, concurrent esophageal injury occurs in up to 20% of patients after acid ingestion [2].
The degree and location of the caustic injury depends on the quantity, concentration, and nature of the ingested acid, duration of mucosal contact, and contents of the stomach at the time of injury, as gastric contents can buffer the ingested acid [3]. Acute caustic injury is characterized by inflammation and coagulation necrosis of the gastric mucosa, leading to sloughing of the overlying eschar after several days [1]. This may be accompanied by gastric hemorrhage or perforation. Late sequelae include fibrosis and gastric outlet obstruction [1, 2, 4].
The initial clinical presentation may be misleading and underestimate the severity of caustic injury, because the patient may have a normal level of consciousness, normal vital signs, and no signs of injury to the mouth or pharynx. This can precede a rapidly developing coagulopathy, plasma volume depletion, renal failure, and metabolic acidosis [4].
Imaging, particularly CT, can help in the immediate and subsequent evaluation of the gastrointestinal tract after caustic ingestion when endoscopy is not available or is limited by a severe injury. CT has the potential to show abnormalities of the esophageal, gastric, and duodenal walls and signs of perforation, including extraluminal fluid, pneumomediastinum, pneumoperitoneum, or pneumoretroperitoneum. Findings on CT depend on the severity of injury and time from ingestion. As this case shows, early CT, like clinical examination, may underestimate extent of injury. However, when the normally enhancing gastric mucosa and the underlying submucosal and muscular layers are no longer apparent, necrosis should be suspected.
Treatment centers on correcting metabolic imbalances, coagulopathy, and surgical intervention for more severe injury and late sequelae. Partial or total gastrectomy may be necessary, particularly in the setting of transmural necrosis [1, 2, 4]. However, the prognosis is generally poor and worsens with increasing quantity of acid ingestion [4].
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