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- A Case of Cement Hardening Agent Intoxication with Acute Kidney Injury
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Young Woo Seo, Tae Chang Jang, Gyun Moo Kim, Seung Hyun Ko
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J Korean Soc Clin Toxicol. 2018;16(2):157-160. Published online December 31, 2018
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DOI: https://doi.org/10.22537/jksct.2018.16.2.157
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Abstract
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- Chronic silica nephropathy has been associated with tubulointerstitial disease, immune-mediated multisystem disease, chronic kidney disease, and end-stage renal disease. On the other hand, acute intentional exposure is extremely rare. The authors' experienced a 44-year-old man who took rapid cement hardener (sodium silicate) in a suicide attempt whilst in a drunken state. He visited the emergency department approximately 1 hour after ingestion. Information on the material was obtained after 3 L gastric lavage. The patient complained of a sore throat, epigastric pain, and swollen to blood tinged vomitus. Proton pump inhibitors, hemostats, steroid, and fluids were administered. Nine hours after ingestion, he was administered 200 mL hematochezia. Immediately after, a gas-troenterologist performed an endoscopic procedure that revealed diffuse hyperemic mucosa with a color change and variable sized ulceration in the esophagus, whole stomach, and duodenal $2^{nd}$ portion. Approximately 35 hours later, persistent oligouria and progressive worsening of the renal function parameters (BUN/Cr from 12.2/1.2 to 67.5/6.6 mg/dL) occurred requiring hemodialysis. The patient underwent 8 sessions of hemodialysis for 1 month and the BUN/Cr level increased to 143.2/11.2 mg/dL and decreased to 7.6/1.5 mg/dL. He was discharged safely from the hospital. Follow up endoscopy revealed a severe esophageal stricture and he underwent endoscopic bougie dilatation. Acute cement hardener (sodium silicate) intoxication can cause renal failure and strong caustic mucosal injury. Therefore, it is important to consider early hemodialysis and treatment to prevent gastrointestinal injury and remote esophageal stricture.
- The Clinical Characteristics and Risk Factors of Upper Digestive Lesions that are due to Ingestion of Caustic Material
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Young-Sin Kim, Se-Min Choi, Hyung-Min Kim, Chun-Song Youn, Kyu-Nam Park
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J Korean Soc Clin Toxicol. 2009;7(2):113-120. Published online December 31, 2009
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Abstract
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- Purpose: Though caustic injury of the upper digestive tract can lead to severe sequelae, there are few clinical studies on this subject. This study was undertaken to evaluate the clinical characteristics, the endoscopic findings and the risk factors of the upper digestive lesions in patient with caustic ingestion injury. Methods: We retrospectively reviewed the medical records of 137 patients who ingested caustic materials and who visited to our emergency room from January, 2000 to June, 2009. Results: The most common ingested agent was sodium hypochlorite (44.5%), followed by acetic acid (19.7%), hydrochloric acid (11.7%) and lye (8.0%). Ingestion for suicidal attempt (62.0%) was more frequent than accidental ingestion (30.7%). Grade IIa injury was the most frequent finding on endoscopy of the esophagus and Grade 1 injury was the most frequent finding on endoscopy of the stomach. For the late sequelae, there were 9 cases (6.6%) of esophageal stricture and 2 cases (1.5%) of gastric outlet obstruction. The initial signs and symptoms did not correlate with the development of stricture, but leukocytosis, and grade III injury were related to the risk of developing stricture. Conclusion: Caustic injury of the upper gastrointestinal tract is frequently observed on early endoscopy and it can cause significant late sequelae such as stricture. Therefore, it is necessary to evaluate these patients with regular follow up endoscopic examinations for the management of late sequelae.
- Esophageal Stricture and Acute Renal Failure after Formic Acid Poisoning: - A Case Report -
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Kyung-Il Song
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J Korean Soc Clin Toxicol. 2009;7(1):32-37. Published online June 30, 2009
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Abstract
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- Formic acid or formate is a common industrial compound used in the production of ensilage, disinfectants, decalcifying agents and mainly as a precursor in industrial chemical synthesis. It is also a well-known toxic metabolite produced in methanol poisoning. Thus, formate is a potential source of both accidental and deliberate poisoning. Very few reports have been published thus far, on the toxicology of direct formic acid poisoning. Here, we report a case of a 74-year-old man without a history of depression, who ingested about 30 gm of formic acid. The patient presented with profound high anion gap metabolic acidosis, acute renal failure and esophageal stricture. The patient was successfully treated with hemodialysis and supportive measures. But permanent esophageal stricture was complicated by formic acid burns in the gastrointestinal tract. We discuss the pathophysiology and treatment of this case.
- A Case of Pyloric Obstruction Developed after Upper GI Barium Study in Patients with Caustic Injury on Gastrointestinal Tract
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Jeong-Goo Kim, Hye-Jin Cho, Seung-Hee Lee, Pum-Soo Kim, Hyung-Keun Roh
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J Korean Soc Clin Toxicol. 2003;1(1):51-55. Published online June 30, 2003
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Abstract
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- Caustic ingestion can produce a progressive and devastating injury to the esophagus and stomach, In the acute stage, perforation and necrosis may occur. Long-term complications include esophageal stricture, antral stenosis and the development of esophageal cancer. Endoscopy should be performed as soon as possible in all cases to evaluate the extent and severity of damage, unless there is evidence of perforation. Endoscopy is the diagnostic procedure of choice. However, when the endoscopy cannot be passed through due to esophageal stricture, upper GI barium studies may be useful as a follow-up measure and in the evaluation of complications. A 44-year-old man visited our hospital complaining frequent vomiting 1 hour after ingestion of unknown amount of hydrochloric acid. At the time of arrival, the patient's oral cavity was slightly swollen and erythematous. On the endoscopic examination fourteen hour after the caustic ingestion, marked swelling of the arytenoids and circumferential ulceration with brown and black pigmentation at the upper esophagus were observed. Four weeks after the caustic injury, upper esophageal narrowing was observed and then the scope could not be advanced to the stomach. Upper GI barium study performed at that time revealed diffuse luminal narrowing of the esophagus and concentric luminal narrowing from prepyloric antrum to pylorus with disturbance of barium passage. At a week after the Upper GI study, through endoscopic examination after bougie dilatation of the esophagus, barium impaction in the stomach and the pylorus was noticed.
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Korean Society of Clinical Toxicology