CLINICAL TOXICOLOGYy 22(6), 585-588 (1984-85)

"MASSIVE COPPER SULFATE INGESTION RESULTING IN HEPATOTOXICITY"

William Jantsch, MD
Resident, Emergency Department
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Denver General Hospital

Denver, Colorado 80204-4507

Kenneth Kulig, MD
Associate Director
Rocky Mountain Poison and Drug Center
University of Colorado School of Medicine
Denver General Hospital

Barry H. Rumack, MD
Associate Professor of Pediatrics
University of Colorado School of Medicine
Director, Rocky Mountain Poison and Drug Center
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Denver General Hospital

ABSTRACT:

Intentional overdosage of copper salts is seen infrequently in the TJ.S.,

but is fairly common in other countries (1). Toxic blood levels can be seen
after oral ingestion of as little as one gram of copper sulfate in an adult (2).
We report a case of a patient who ingested 250 grams of copper sulfate,
developed transient hepatic dysfunction, and recovered after the prompt
administration of c helat ion therapy.

CASE REPORT

A forty-two year old black male presented to the emergency

department 90 minutes after ingesting approximately 250 gm of crystalline

5 85

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 586 JANTSCH, KULIG, AND RUMACK

copper sulfate in a suicide attempt. Within 1 0 minutes of ingestion he

developed severe epigastric pain and Vomiting, along with a metallic taste in
the mouth.
On physical exam, blood pressure was 130/100 m m Hg, pulse 100/min,

respirations 28/min and temperature 37.00C. He was actively vomiting, but

awake and alert. The lips and fingers were stained with greenish-blue
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material. The abdomen demonstrated diffuse epigastric tenderness, but was

without signs of peritoneal inflammation. There was no neurologic deficit.
Laboratory investigations revealed a blood alcohol level of 222 mg/dl, white
blood count of 12,200 with a normal differential, hematocrit 56.1 percent,
and an arterial blood gas demonstrating pH 7.29, pC02 32 and pop 153 m m
Hg, on oxygen supplementation. EKG revealed sinus tachycardia only, and
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the chest X-ray was normal. Examination of the urine revealed microscopic
hematuria without renal tubular cells or casts. The patient was treated
initially with a single injection of BAL (Dimercaprol), 4 mgkg. The
patient's vomiting subsided within 1 0 hours of ingestion. At that point
activated charcoal and magnesium sulfate were given in addition to oral d-
penicillamine 250 mg p.0. every 6 hours. Throughout the patient's hospital
course vital signs were normal and he remained awake and alert. Within

three days of ingestion, the serum bilirubin rose to 6.5 mg/dl along with 100-
fold elevations of the hepatic enzymes (see table). CPK peaked a t 5,620
IU/h. These abnormalities subsided spontaneously within a week. There was
no hemolysis or oliguria. Serum copper level was 1423 mcg/dl (normal value
less than 100) on the day after ingestion. Twenty-four hour urinary copper
excretion after initiation of chelation therapy was 8,160 mcg (nl 15-50).
The patient was discharged on d-penicillamine, and is presently being

followed in our clinics.

 COPPER SULFATE AM) HEPATOTOXICITY 587

TABLE
Day Post SGOT Bilirubin LDH CPK
Ingestion -
U/L mg96 -
U/L -
IU/L
- 0.5 444 -
5,500 6.5 6,460 5,620
2,320 7.0 6,580 5,075
360 3.4 1,520 -
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COMMENT:

Oral ingestion of copper sulfate produces profound vomiting. Its use

as an emetic has been curtailed since death has been reported after

administration of as little as two grams (2). Central nervous system

depression and shock account for immediate deaths, but hepatic and renal
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failure are implicated in deaths more than 2 4 hours after ingestion. In

addition, hemolysis has been seen after acute ingestion (3). Our patient

demonstrated transient jaundice and rhabdomyolysis as well. Treatment

consists of chelation to increase urinary excretion of copper, and d-

penicillamine is the preferred agent. However, intramuscular dimercaprol is

an alternative in a patient who is actively vomiting. An abnormal 24 hour

urinary copper level after reinstitution of d-penicillamine therapy is an

indication for continued treatment. Our patient recovered after a massive

ingestion, probably on the basis of brisk emetic response and prompt

chelation therapy.

REFERENCES:

1. M.D. Singh and G. Singh, Biochemical Changes in Blood in Cases of

Acute Copper Sulfate Poisoning, J. Indian. Med. ASSOC.,
(1968).
so,
549-554

2. R.S. Stein, D. Jenkins, and M.E. Korns, Death After Use of Cupric
Sulfate as Emetic, --
JAMA, 235, 801 (1976).
 588 JANTSCH, KULIG, AND RUMACK

3. M. Walsh, F.J. Crosson, M. Bayley, Acute Copper Intoxication, Am. J.

-
Dis. Child., 131, 149-151 (1977).
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