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Ingestion of concentrated mineral (hydrochloric and sulfuric) acid frequently results in severe damage to the stomach but only minor and infrequent damage to the esophagus. This is surprising since the general conception is that corrosive ingestion leads predominantly to esophageal injury and stenosis. This is true of concentrated alkalis but apparently not for concentrated acids. This report of two cases with almost complete pyloric obstruction without permanent esophageal injury is prompted by the paucity of such reports in the English literature, by the excellent results following gastroenterostomy, and by the occurrence of homologous serum hepatitis after surgical convalescence.Case 1.\p=m-\A 26-year-old white salesman was admitted to the hospital 45 days after the ingestion of muriatic acid. On that occasion the patient was inebriated and he ingested a small amount of acid in the mistaken belief that it was whiskey. He immediately spat the fluid out, induced vomiting, and then drank a glass of milk. Except for a slight "rawness in the throat," he felt well until the following day when he noted nausea and vomiting after the ingestion of food or liquids. This continued for eight days, and he was hospitalized elsewhere after two episodes of hematemesis. Supportive therapy was instituted with good results, and the patient was discharged without a diagnostic check-up. A similar episode with hospitalization occurred one week later. The third episode of nausea and vomiting without epigastric distress, but this time with dysphagia, occurred four days before admission to the hospital. The patient stated that he had lost 50 lb. (22.7 kg.) in weight in this 45 day period.The physical examination on admission was essentially nega¬ tive except for evidence of recent weight loss, moderate dehydra¬ tion, and tachycardia of 120 beats per minute. The initial hemogram showed only slight leukocytosis with a normal differential count. Urinalysis was essentially negative. Blood chemistry determinations, including non-protein-nitrogen, blood urea nitrogen, blood chlorides, carbon dioxide combining power, and total proteins with the albumin globulin ratio, were within normal limits. Histamine fractional analysis of gastric contents on two occasions failed to show any free hydrochloric aeid. The upper gastrointestinal x-ray series, done soon after admission, was reported as follows: "Examination of the esophagus with both thick and thin barium revealed some delay in the passage of the barium through the cardiac sphincter. However, there is no appreciable dilatation of the esophagus. The barium passes into the stomach which does not fill out and repeated attempts to secure filling of the stomach were not successful as the patient was not able to tolerate the barium. Barium remained suspended within what appeared to be the fundus of the stomach; however, there was some slight irregularity in the region of the fundus just above the suspended barium. Radiographs confirm the fluoroscopic findings and reveal a normal esophagus ( fig. 1)....