Article, Toxicology

Systemic manifestations following ingestion of small amounts of acetic acid by a child

i An update to this article is included at the end

American Journal of Emergency Medicine (2007) 25, 738.e1 – 738.e2

Case Report

Systemic manifestations following ingestion of small amounts of Acetic acid by a childB,BB

Acetic acid ingestion can cause hemolysis, DIC, respi- ratory and renal insufficiency, and hepatic necrosis. Only a few cases of acetic acid ingestion have been described in the past, most of which caused hemolysis, and one description of hepatic necrosis. All of these were reported in adults, usually as a suicide attempt with ingestion of large amounts. Severe symptoms have not been reported so far in children following accidental ingestion of small amounts of acetic acid. We report of a 3-year-old child who ingested a minimal amount of 60% acetic acid and developed hemolysis and Hepatic dysfunction.

A 3-year-old child was brought to the emergency department 3 hours after ingestion of 60% acetic acid (AA). After placing the bottle in his mouth and spitting out shortly, the child vomited with some bloody content. On admission, the child appeared well, with no external signs of burns or erosions around and in the mouth, and without drooling or signs of dysphagia. arterial blood gases were pH 7.41, Pco2

28.8 mm/Hg, HCO3 18 mmol/L. No erosion or sign of

damage to the oropharynx and larynx were seen using a fiberoptic endoscope. A nasogastric tube was placed, and the patient was put on intravenous fluids. Twelve hours after ingestion, hematuria appeared. His blood tests showed signs of hemolysis, with Lactate dehydrogenase rising to 2478 U/L, bilirubin 4.06 mg/dL. Twenty-four hours after ingestion, his Liver enzymes were elevated: aspartate amino- transferase (AST) 444 U/L, alanine aminotransferase (ALT) 349 U/L. The coagulation function tests were normal, as well as the urine output and kidney function tests. The child was treated with intravenous fluids, augmentin, and nothing per Os (NPO) with resolution of the hematuria after 24 hours. Laboratory signs of hemolysis and hepatitis resolved after 3 days with no apparent residual dysfunction.

Acetic acid is the chemical compound responsible for the characteristic odor and sour taste of vinegar. Typically, vinegar is about 4% to 8% AA. Because vinegar is acidic,

B We report a case of a 3-year-old child who ingested a few drops of highly concentrated acetic acid, with no local damage to the oropharynx, who developed systemic manifestations a few hours later including hematuria, hemolysis, and hepatic dysfunction.

BB 19th Congress of the Israeli Society of Toxicology 10/2004, Ramat-

Gan, Israel.

it has a variety of properties useful around the house: removing mineral deposits formed on plumbing fixtures and in tea kettles; preserving foods, such as pickled vegetables; and as a mild disinfectant in cleaning. It is popular as a flavoring in cooking and in salad dressings. Because of the dangerous corrosive effects of AA, many countries have strict regulations concerning AA and many other toxic chemicals. The large Arab population in Israel use highly concentrated AA very commonly for pickled vegetables and for preserving meat. Highly concentrated AA is also generally available in the successor states of the former USSR, and its use in suicides is thus not uncommon. Hematotoxicity of alkoxy AAs is demonstrated in the past in different studies using rats. Early swelling of erythrocytes followed by hemolysis was demonstrated in vitro [1]. To date, multiple cases of acute AA ingestion were reported, all of which were suicide attempts of adults who ingested large amounts of highly concentrated AA. Most of the patients reported suffered severe oropharyngeal damage and hemolysis [2-4]. A few reports of renal insufficiency or failure [5,6], a few reports of disseminated intravascular coagulation [7,8], and a report of acute hepatic failure [9] were found.

This is a first report of a young child who accidentally ingested a few drops of AA, with no local damage but with systemic manifestations, including hemolysis, hematuria, and hepatitis.

Small amounts of AA, accidentally ingested by a child, may cause significant systemic abnormalities even in the lack of local damage to the upper gastrointestinal tract; therefore, discharge of children with no local damage but a history of AA ingestion should be postponed for a few hours, and later systemic manifestations should be taken into consideration. Laws banning sale of lye products should be encouraged worldwide.

Yeshayahu Yonatan MD, MHA

Engelhard Dan MD Department of Pediatrics Hadassah University Hospital Ein Karem, P.O.B. 12000

Jerusalem 91120, Israel E-mail address: [email protected]

doi:10.1016/j.ajem.2007.01.015

0735-6757/$ – see front matter D 2007

738.e2 Case Report

References

  1. Ghanayem BI, Burka LT, Matthews HB. Structure-activity relationships for the in vitro hematotoxicity of N-alkoxyacetic acids, the toxic metabolites of glycol ethers. Chem Biol Interact 1989;70(3-4):339 – 52.
  2. Davids PH, Bartelsman JF, Tilanus HW, van Lanschot JJ. Consequen- ces of caustic damage of the esophagus. Ned Tijdschr Geneeskd 2001;145(44):2105 – 8.
  3. Faller-Marquardt M, Bohnert M, Logemann E, et al. Combined suicide by drinking acetic acid with subsequent hanging. Arch Kriminol 2000;206(5-6):140 – 9.
  4. Boseniuk S. Rieger C Acute oral acetic acid poisoning–case report. Anaesthesiol Reanim 1994;19(3):80 – 2.
  5. Schardijn GH, Kastelein JJ, Statius van Eps LW. Kidney tubule dysfunction caused by acetic acid. Ned Tijdschr Geneeskd 1989;133(11):556 – 9.
  6. Sanguesa Molina JR, Macia Heras ML. Acute oliguric kidney failure secondary to acetic acid poisoning. An Med Interna 1999;16(9):461 – 2.
  7. Greif F, Kaplan O. Acid ingestion: another cause of disseminated intravascular coagulopathy. Crit Care Med 1986;14(11):990 – 1.
  8. Jurim O, Gross E, Nates J, et al. Disseminated intravascular coagulopathy caused by acetic acid ingestion. Acta Haematol 1993;89(4):204 – 5.
  9. Kamijo Y, Soma K, Iwabuchi K, et al. Massive noninflammatory periportal liver necrosis following concentrated acetic acid ingestion. Arch Pathol Lab Med 2000;124(1):127 – 9.

Update

American Journal of Emergency Medicine

Volume 28, Issue 4, May 2010, Page 534

DOI: https://doi.org/10.1016/j.ajem.2010.03.018

American Journal of Emergency Medicine (2010) 28, 534

Errata

In the article “Systemic manifestations following ingestion of small amounts of acetic acid by a child,” published in Am J Emerg Med 2007;25(6):738.e1-738.e2, the author names were listed incorrectly. The Correct byline is below.

Yonatan Yeshayahu MD, MHA, Dan Engelhard MD.

DOI of original article: 10.1016/j.ajem.2007.01.015. doi:10.1016/j.ajem.2010.03.018

The article, “Negative pressure Pulmonary hemorrhage induced by a candy,” published in Am J Emerg Med 2010;28(1): 112.e3-112.e5 had an error in the byline. The correct name of the last author is Venerino Poletti.

DOI of original article: 10.1016/j.ajem.2009.02.027. doi:10.1016/j.ajem.2010.03.019

0735-6757/$ – see front matter (C) 2010