Plasmapheresis

Hong in acetic
Kong Journal acid poisoning
of Nephrology
2000;2(2):110-112.

C A S E
R E P O R T

Successful treatment of oral acetic acid poisoning with

plasmapheresis
Gensy MW TONG1, Siu-Ka MAK1, Ping-Nam WONG1, Kin-Yee LO1, Sheung-On SO2, Chi-Leung
WATT2, Andrew KM WONG1
1
Renal Unit, Department of Medicine, 2Intensive Care Unit, Kwong Wah Hospital, Hong Kong.

Abstract
Injudicious use of acetic acid can result in acute or chronic poisoning. Chronic ingestion of large
amount of 5% acetic acid has been reported to be a cause for hypokalemia, hyper-reninemia and
osteoporosis. Acute poisoning can occur after percutaneous treatment of hepatocellular carcinoma
or after oral ingestion. Most of the reported cases are from Russia before 1980s. We report an adult
with acute accidental poisoning with 30% acetic acid leading to severe intravascular hemolysis,
hemoglobulinuria, acute hepatitis, coagulopathy, and acute gastrointestinal bleeding and acute
renal failure. Plasmapheresis was started soon after intoxication with good recovery and we discuss
its possible role in the management of acetic acid poisoning.

Key words: Acetic acid, Plasmapheresis, Poisoning

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CASE REPORT Examination of the abdomen was unremarkable. The

In Chinese tradition, on the wedding day, the bridegroom
or the best man is often required to finish difficult tasks
before the bridegroom is allowed to bring the bride from
her house to their new home. In our case, a 27-year-old
best man drank 100 mL of 30% acetic acid (vinegar)
under the request of a bridesmaid. The bridesmaid bought
the high concentration acetic acid from a drug store,
without knowing that it was for industrial use. The best
man developed intense throat and epigastric pain
immediately and presented with coffee-ground vomiting
on arrival at the Emergency Department.
On admission, his blood pressure was 130/80 mmHg and
pulse rate was 80 per minute. There was a strong sour
smell from his breath. His throat was congested.
urine output was around 50 mL per hour and dark-
colored.
His hemoglobin was 16.5 g/dL, WBC 35.2 x 109/L and
platelet 171 x 109/L. Serum sodium was 148 mmol/L
and potassium 4.4 mmol/L. Serum urea was 6.1 mmol/
L, creatinine 121 µmol/L, calcium 1.84 mmol/L, and
phosphate 1.1 mmol/L. He had metabolic acidosis with
pH 7.28 and bicarbonate 17.5 mmol/L. Serum total
bilirubin was 36 µmol/L, alkaline phosphatase 46 IU/L,
aspartate aminotransferase 716 IU/L and alanine
aminotransferase 541 IU/L. The International
Normalized Ratio was 2.2 and activated partial
prothrombin time was 86 seconds. Serum creatine kinase
was 218 IU/L and lactate dehydrogenase 1843 IU/L. He

Correspondence: Dr. Siu-Ka MAK, Renal Unit, Department of Medicine, Kwong Wah Hospital, 25 Waterloo Road, Kowloon, Hong
Kong. Fax: (852) 2783 9902, E-mail: skmak@medi.net.hk

110 Hong Kong Journal of Nephrology, October 2000

Hong Kong J Nephrol 2000;2(2):110-112.
had 4+ hemoglobinuria but not proteinuria nor hematuria.
Another significant finding was the repeated failure to
obtain cross matching as a result of the active hemolysis.
Prompt fluid resuscitation was accompanied by mannitol
infusion in an attempt to increase urine output. Sodium
bicarbonate infusion was given to correct the metabolic
acidosis. However, his serum creatinine rose from 121
µmol/L to 145 µmol/L six hours after admission whereas
serum bicarbonate remained at 18 mmol/L. Hemoglobin
dropped from 16.5 g/dL to 13.8 g/dL within 24 hours.
Meanwhile, he remained hemodynamically stable but
was passing dark-colored urine at 50 mL per hour.
Plasmapheresis was started 10 hours after the ingestion
of acetic acid (infusion of 50 mL of 5% plasma protein
fraction and fresh frozen plasma per kilogram of body
weight per exchange). All filtrate was dark-colored. After
one session of plasmapheresis, the acidosis was corrected
and there was no further hemolysis detected.
On the second day of admission, he suffered from severe
epiglottic edema associated with arterial desaturation,
requiring intubation and mechanical ventilation. He also
developed hypotension and required inotropic support.
On the third day, he developed peritonitis. Emergency
laparotomy revealed ischemic small bowel requiring
resection of 50 cm of proximal jejunum and creation of
jejunostomy and ileostomy. His serum creatinine rose
to 181 µmol/L on day two and returned to 90 µmol/L
after the operation. From day three onward, his renal
function remained stable and no more hemolysis was
detected. His liver function became normal 4 weeks after
admission. He resumed normal oral diet in the sixth week
when anastomosis of the jejunostomy and ileostomy was
successfully performed. He had no dysphagia but
remained apprehensive with any sour smell.
DISCUSSION
Acetic acid, or vinegar, has a diversity of clinical and
industrial uses depending on its concentration. Dietary
vinegar ranges from 2% to 6%. Thirty-percent acetic acid
is used in food preservation. Sixty-percent acetic acid is
used in hat making, printing, dyeing and rayon
manufacturing. Two- to three-percent acetic acid is used
as an anti-fungal and anti-bacterial agent in otitis media
and vaginal douching. Application of 3% to 4% acetic
acid is found to be a useful diagnostic tool in detection
of cervical cancer (1). Endoscopic application of 1.5%
acetic acid improves identification of remnant of Barrett's
epithelium after endoscopic therapy (2). Thirty- to fifty-
percent acetic acid can be injected percutaneously for
the treatment of small hepatocellular carcinoma (3-5).
GMW TONG, et al
Injudicious use of acetic acid can result in acute or
chronic poisoning. Chronic ingestion of large amount of
5% acetic acid has been reported to be a cause for
hypokalemia, hyper-reninemia and osteoporosis in a 28-
year-old female (6). Acute poisoning can occur after
percutaneous treatment of hepatocellular carcinoma
(HCC) (7) or after oral ingestion. Most of the reported
cases are from Russia before 1980s' (8-14). Sporadic
cases have been reported: two cases from Japan (15-16);
one from Thailand (17); one from Spain (18) and one
from Germany (19).
In all cases of acute poisoning, the victims suffered from
hemolysis, acute renal failure, acute liver failure,
coagulopathy and shock to different extents following
systemic absorption of acetic acid. It is believed that once
the acid is absorbed, red blood cells are the first sufferers.
The acid induces hemolysis resulting in hemoglobinuria
(20). The liver is the second organ suffering from
devastating damage, followed by the kidneys and the
heart. Kamijo Y reported that hemolysis, disseminated
intravascular coagulation, and liver dysfunction occurred
45 minutes after oral glacial acetic acid poisoning (16).
The autopsy finding of that case revealed massive hepatic
necrosis in periportal distribution without significant
inflammation. A direct effect of acetic acid on
hepatocytes involving portal circulation was thus
suggested.
The exact mechanism of renal toxicity in acetic acid
poisoning is largely unknown. Zimina examined the
morphological changes of kidneys in 118 patients who
died of acetic acid poisoning (21). Lesion of the kidneys
was similar to those in acute hemoglobinuric nephrosis.
Schardijn found an elevated urinary excretion of ß2-
microglobulin, alanine-aminopeptidase and N-acety-
glucosaminidase in acetic acid poisoning (22). Thus,
acute renal failure has been suggested to be related to
the direct toxic action of acetic acid to renal tubules,
indirect damage by hemoglobinuria, or as a combination
of both together with concurrent hypotension.
There is no specific detoxification procedure or antidote
for acetic acid poisoning. Lysenko suggested partial
replacement of blood in 1966 (14). In 1994, Boseniuk
reported his success in treatment of acetic acid poisoning
by plasma separation done within 2 hours of poisoning
(19). Our patient underwent plasmapheresis during the
early period of poisoning with good recovery from the
acute massive hemolysis, renal and liver dysfunction.
Plasmapheresis is believed to be a quick and effective
way of removal of the water-soluble acetic acid and the
hemolyzed products from the patient. In the case of our
patient, one single session was employed. However, the
111
Plasmapheresis in acetic acid poisoning
choice over this or multiple successive sessions still needs
to be further studied, particularly for cases with
continuous hemolysis.
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