Acute oral acetic acid intoxication 145

Acute Oral Acetic Acid Intoxication: A Case Report

Tien-Kuei Hsu1, Chi-Wen Jaun2, Chung-Chieh Huang3

Diluted acetic acid in the form of vinegar (5%) is safe for human consumption; however, intake
of weakly diluted or undiluted acetic acid can be deadly. A 49-year-old man presented to the emer-
gency department with acute acetic acid intoxication. Results from various tests revealed metabolic
acidosis, disseminated intravascular coagulopathy, acute liver dysfunction, acute renal failure, and acute
respiratory failure. Upper gastrointestinal panendoscopy revealed third-degree gastrointestinal corro-
sion. The signs of peritoneal irritation were noted. An emergency total gastrectomy was performed. After
aggressive treatment, the patient was discharged in critical condition 8 hours after having arrived at
the emergency department and died at home. In our review of the literature, no reports have been pub-
lished regarding surgery or the taking of biopsy specimens in patients with acetic acid intoxication. The
pathology of the biopsy specimens taken from revealed extensive necrotizing inflammation and massive
hemorrhage. Hemodialysis may be performed when severe metabolic acid and renal failure develop in pa-
tients with acute acetic acid intoxication.

Key words: acetic acid intoxication, metabolic acidosis, corrosive injury

Introduction intravascular coagulopathy, acute liver dysfunction,

Acetic acid is one of the most extensively used
organic acids. It is obtained either by the oxidation
of alcohol and aldehyde, or by the destructive
distillation of wood and carbohydrates. Pure, water-
free acetic acid (glacial acetic acid) is a colourless
liquid that absorbs water from the environment and
freezes below 16.7°C to a colourless crystalline
solid. Acetic acid is corrosive, and its vapour
causes irritation to the eyes, a dry and burning nose,
sore throat and congestion to the lungs. In dilute
solution (5%), acetic acid is known as vinegar(1).
In concentrated solution it is used to pickle food
and as a corrosive agent to etch metals(2). Acetic
acid intoxication may result gastrointestinal
corrosive injury, metabolic acidosis, disseminated
and acute renal failure. We report a case of severe
acetic acid intoxication in a 49-year-old man. The
patient died despite vigorous treatment including
emergency total gastrectomy. The pathology of
the biopsy specimen obtained during the operation
revealed extensive necrotizing inflammation and
massive hemorrhage.
Case History
A 49-year-old man who had drunk an unknown
amount of glacial acetic acid presented to the emer-
gency department with epigastric pain, hemetemesis
and dyspnea less than one hour after ingestion.
On admission, the patient’s blood pressure was
90/52mmHg, heart rate was 116/min, respiratory

Received: July 2, 2008 Accepted for publication: September 11, 2008

From the 1Department of Emergency, Chang-Bing Show Chwan Memorial Hospital, 2Department of Emergency, Yuanli Lee's
General Hospital, Lee's Medical Corporation, 3Surgery, Show Chwan Memorial Hospital
Address reprint requests and correspondence: Dr. Chi-Wen Juan
Department of Emergency, Yuanli Lee's General Hospital, Lee's Medical Corporation
168 Heping Road, Yuanli Town, Miao-Li County 358, Taiwan (R.O.C.)
Tel: (037)862387 Fax: (037)851919
E-mail: juanchiwen@yahoo.com.tw
146 J Emerg Crit Care Med. Vol. 20, No. 3, 2009
rate was 18/min and body temperature was 36.0℃.
He was in acute distress. Skin erosion was noted
over the anterior neck and chest wall. The abdomen
was tender with rebounding pain and guarding.
A complete blood cell count disclosed the fol-
lowing values: white blood cell count, 43100/uL;
hemoglobin, 14.9g/dL; and platelet, 744000/μL.
The serum sample showed acute hepatitis and acute
renal failure. Prolonged prothrombin time, pro-
longed activated partial thromboplastin time and
prolonged D-dimer were indicative of coagulopathy.
An upper gastrointestinal panendoscopy re-
vealed severe corrosive injury: grade III corrosive
injury in bilateral piriform fossae, grade III corro-
sive injury in the fundus and high body of the stom-
ach, and grade II to III corrosive injury in the first
and second portions in the duodenum.
Svere gastrointestinal corrosive injury,
metabolic acidosis, acute respiratory failure, acute
renal failure, acute liver dysfunction, disseminated
intravascular coagulation (DIC), and shock were
diagnosed. An emergency total gastrectomy was
performed. Transmural bleeding and necrosis of the
duodenum and stomach were found during surgery.
The patient was admitted to the intensive care unit
for further treatment after the operation; however,
his condition rapidly deteriorated despite aggressive
management and resuscitation, and the patient
was discharged in critical condition 8 hours after
admission due to the custom of death at home. The
pathology of the stomach and duodenum showed
extensive necrotizing inflammation and massive
hemorrhage consistent with corrosive injury.
Discussion
Acetic acid at high concentrations is a
hazardous substance that may cause severe
burns, permanent disabilities and even death (2-7).
In Taiwan, acetic acid can be purchased easily
in supermarkets and is widely used as regular
vinegar. Ingestion of as little as 60mL of substances
containing 99% acetic acid can lead to death. And
even if a person survives, treatment for esophageal
stricture is necessary. Studies on animals have
reported that 10% acetic acid can cause permanent
eyesight loss(8). Furthermore, a report by the US
Consumer Protection Safety Commission stated that
10% acetic acid can cause strong skin abrasions and
that ingesting acetic acid at concentrations > 20%
can be fatally toxic to humans(8). The oral acetic
acid lethal dosage is 20 to 50 grams.
S u b s t a n c e s c o n t a i n i n g 9 9 % a c e t i c acid
may be used in pharmaceutical products, dyes,
cosmetics and spices(2). The local effect of ingesting
concentrated acetic acid includes corrosive injury
to the upper gastrointestinal tract, skin, and
airway (3). Systemic complications of oral acetic
acid intoxication include metabolic acidosis,
renal failure caused by hemoglobinuria following
hemolysis, DIC(4), and massive noninflammatory
periportal liver necrosis(3). In one study, computed
tomography of a patient who had ingested pure
glacial acetic acid showed low-density, diffuse, and
marked wall thickening from the upper esophagus
to the stomach and multiple wedge-shaped low
densities in the liver (6). Acetic acid intoxication
even by rectal administration may present with
necrosis of the colon, acute renal failure, acute liver
dysfunction, DIC and sepsis (7). A few reports on
burns induced by acetic acid have been published,
including first degree chemical burns in a febrile
newborn infant, first degree facial chemical burn
in an adult by vinegar, and third degree burns in
a 18 month-old infant which caused upper airway
obstruction and required skin grafting(2).
In a meta-analysis of 517 patients admitted
to hospital for acute poisoning due to corrosive
substances, 62 patients (12%) had ingested con-
centrated acetic acid. Among these 62 patients, 37
(60%) developed acute renal failure and 4 patients
(7%) died(9). In another study, it was reported that

acetic acid was the most common caustic substance
ingested by Arab children(10).
In medical practice, acetic acid may be used
to treat adrenocortical adenoma and hepatocellular
carcinoma(11-17). The sensitivity of visual inspection
with acetic acid equaled or exceeded reported rates
for conventional cervical cytology in cervical caner
screening(18,19). Acetic acid is also used for treating
the sting of the box jellyfish by disabling the
stinging cells, and is used in the form of Vosol for
treating outer ear infections.
Strong corrosive acid is sometimes ingested by
children accidentally or by psychiatric patients for
the purpose of committing suicide. Late complica-
tions of the ingestion of corrosive acids include
chemical burns to pharynx, perforation and stricture
of the upper gastrointestinal tract, respiratory insuf-
ficiency and renal failure caused by hemoglobinuria
following hemolysis (20). First-degree lesions are
characterized by acute inflammation with edema,
hyperaemia and aggregations of mucosa and lay-
ers of destroyed epithelium. Additions of fibrin
aggregates, erosions and mild bleeding character-
ize second-degree lesions. Third-degree lesions
are associated with the presence of ulcers, severe
fibrin clots and acute necrosis. Emergency upper
gastrointestinal panendoscopy gave us the possibil-
ity to confirm or exclude the presence of corrosive
destruction of the stomach, and to determine cor-
rectly the extent of the chemical destruction(21). It
has been reported that the grade of mucosal injury
determined during endoscopy was the strongest pre-
dictive factor for the occurrence of systemic and GI
complications and mortality(22). Most experts agree
that the timing of endoscopy should be within the
first several hours after ingestion and that follow-up
exams should be avoided between days 5 and 15.
The indications for emergency laparotomy
include peritoneal signs or free intraperitoneal air.
Esophageal perforation diagnosed by mediastinal
air on plain films or by endoscopy is also an indi-
Acute oral acetic acid intoxication 147
cation for emergency surgery. More controversial
is the management of severe esophageal injuries,
third-degree lesions, without obvious perforation (23).
The case presented herein illustrates the rapid
progression of acetic acid intoxication. The com-
plications of intoxication in our patient included
severe gastrointestinal corrosive injury, acute renal
failure, metabolic acidosis, acute liver dysfunction,
and DIC. Besides the gastrectomy, the patient
underwent aggressive treatment including blood
transfusion, intravenous proton pump inhibitor,
fluid resuscitation, sodium bicarbonate supplement,
and cardiopulmonary resuscitation.
Histologically, the acute esophageal injury
showed necrosis and acute inflammation of the
mucosa and perivascular inflammation and edema
of the submucosa (24). In our case, a pathologic
diagnosis was obtained during the surgical pro-
cedure; however, in most cases, a pathologic di-
agnosis is made at autopsy. The pathology of the
surgical specimens revealed extensive necrotizing
inflammation and massive hemorrhage, findings that
are compatible with acid corrosive injury.
Hemodialysis was not performed in our pa-
tient because of intractable hypotension with shock
after cardiopulmonary resuscitation following the
operation. The family refused for the patient to
undergo further invasive management. However,
hemodialysis may play a role in metabolic acidosis
and renal failure(5,9). It has been reported that a pa-
tient who suffered from acetic acid intoxication fol-
lowing a manifold lethal dose of acetic acid (200ml
80% acetic acid) survived after being treated with a
complex application of hemodialysis and intensive
care therapy(25). It has, therefore, been suggested
that continuous renal replacement therapy, such as
continuous venous-venous hemodialysis, be applied
to patients with hypotensive status.
In conclusion, acetic acid intoxication may
cause severe complications. Upper gastrointestinal
panendoscopy is indicated when corrosive injury
148 J Emerg Crit Care Med. Vol. 20, No. 3, 2009
is suspected. Laparotomy should be considered if
third-degree corrosive injury with peritoneal signs
is noted. Hemodialysis should be considered when
severe metabolic acid and renal failure develop.
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150 J Emerg Crit Care Med. Vol. 20, No. 3, 2009

急性口服醋酸中毒：一個案例報告

許添貴1　阮祺文2　黃重傑3

稀釋的醋酸以食用醋(5%)的形式對於人們消費使用上是安全的，然而，誤食只有微弱稀釋或甚至未
稀釋的醋酸卻可能造成死亡。一位49歲的男性因為誤食醋酸而送到醫院急診室，一連串的檢驗顯示酸中
毒、瀰漫性血管內凝固病變、急性肝臟受損、急性腎臟衰竭、以及急性呼吸衰竭。上胃腸道內視鏡顯現
第3級的胃腸腐蝕性傷害且病人有腹膜刺激的現象，胃切除手術被緊急實施，經過積極治療，病人在入
院8小時內病危出院而病逝於家中。在我們的文獻回顧中，並沒有因為醋酸中毒而實施手術或切片檢體
病理報告。病理報告呈現廣泛的壞死性發炎及大量的出血，與腐蝕性的傷害表現一致。血液透析法在嚴
重的酸中毒及腎衰竭形成時應該採取。

關鍵詞：醋酸中毒，代謝性酸中毒，腐蝕性傷害

收件：97年7月2日　接受刊載：97年9月11日
1
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