Pharm Chem 32 – B (Lab)

Arsenic Toxicity Case Report

Case Report Summary

The patient was a 36-year-old man who had been diagnosed as having peptic ulcer disease and
the presence of helicobactor pylori in an EGD biopsy specimen 3 months earlier. He was
admitted to the hospital because of an acute onset of epigastric pain that began that morning.
The patient was admitted to the regular medical ward and the gastroenterologist who had been
following the patient for his PUD was consulted. The gastroenterologist recommended medical
therapy empirically for the ulcers. He believed the patient required a stat EGD since a follow-up
EGD done 2 weeks earlier had been negative for ulcers. An H2 blocker medication for
helicobactor pylori was started. He required 75 mgs of meperidine i.m. for his severe abdominal
pain. The abdominal pain persisted; further work-up included an upper GI series, which showed
no ulcers but did show some evidence of duodenitis, and a CT scan of the abdomen that was
negative. Laboratory work-up included stool cultures, pancreatic enzymes, sickle cell screen,
hepatitis screen, porphyria screen, liver function tests, and ESR, all of which were negative. The
patient described his abdominal pain as being intermittent, excruciating, either localized in the
epigastric region, the left lower quadrant, or sometimes everywhere; it was associated with
nausea but no vomiting. On physical examination, there was no rebound or guarding but mild
to moderate tenderness to palpation could be demonstrated. He continued to complain of
abdominal pain throughout his hospital course, and he required a constant regimen of pain
control including Demerol, Dilaudid, Darvocet, Percocet, and even a PCA pump with low-dose
morphine. The patient's abdominal pain work-up was completed without any significant
findings. He was discharged to outpatient care with pain medication, an H2 blocker, and
medica- * Kaiser Permanente Medical Center Department of Medicine 3288 Moanalua Road
Honolulu, HI 96819 Reprints can be requested from Dr. Craig H. Nakatsuka Kaiser Permanente
Medical Center 258 tion for helicobactor prophylaxis. He was instructed to return for follow-up
in a clinic in a couple of days. When he reported to the clinic, he still complained of severe
abdominal pain and had taken all of the pain medicine given at discharge. During this visit, a 24-
hour urine heavy-metal screen was obtained. The report came back negative for lead and
mercury but was positive for arsenic at 865 meg/liter (normal < 100). To confirm this urine
arsenic finding, pubic hair analysis for arsenic was done and it also returned positive at 5.6
microgram/gram of hair (* 75% have less than 0.03 to 0.3 mcg/gm hair, 20% are between 0.3 to
3mcg/gm hair, 5 % are up to 4 mcg/gm hair.) A more detailed diet and work history was
obtained. He was treated as an outpatient for arsenic toxicity with penicillamine. However, he
presented himself again to the clinic with the same, severe abdominal pain before penicillamine
therapy. He was again admitted to the hospital for treatment with dimercaprol or BAL (British
Anti-Lewisite), which entails intramuscular injections every 4 hours. The patient improved
clinically, the repeat 24-hour urinearsenic level was < 35 meg/liter, and the arsenic content in
the hair was down to 1.3 meg/gram of hair. The patient continued to be followed closely as an
outpatient. His abdominal pain reoccurred with a fluctuating course. Additional work-up
revealed a negative colonoscopy, a negative nerve conduction test and electromyelogram and
negative lab tests, including urine and hair arsenic levels
Management
A carefully detailed history regarding the possible source of the exposure is extremely
important when considering arsenic toxicity as a diagnosis. In addition to the history and
physical, laboratory tests are useful-some more than others. Serum arsenic level is often not
helpful because of rapid clearance. A 24-hour urine collection is useful, especially for
documenting acute arsenic intoxication. Arsenic is excreted through the kidney at a rate of 30%
to 70% in a 24-hour period21. Toxic levels might be missed if there is a delay between the time
of exposure and the time of evaluation. In acute ingestion, abdominal radiographs might be
useful because arsenic, a heavy metal, will show up radiographically22
In chronic exposure, analysis of nails and/or hair is helpful though the arsenic content of hair is
affected by nutritional and environmental factors. Arsenic is present in hair and nails 2 to 4
weeks after ingestion5• One paper reported analysis of arsenic in other biological fluids, such
as gastric and vesicular fluids that accumulate higher levels as compared to pleural and
pericardia! fluids 23 . There is no standardized value or a definitive test that diagnoses the
arsenic toxicity absolutely, although urine arsenic levels greater than 200 mcg/1 and hair
arsenic levels greater than 65mcg/1 00 grams of hair can be used as a presumptive evidence of
an increased arsenic load21
 Treatment should be directed in 2 ways: Chelation therapy to increase excretion of arsenic and
supportive and symptomatic therapy for the organ systems involved in the toxicity, The
Poisindex24 at the Hawaii Poison Center recommends the following treatment: "For acute
massive arsenic ingestion, cardiac and respiratory support using compressors and ventilators, as
in any other critical patient is recommended. This should be followed by gastric
decontamination with gastric lavage and an absorbent such as activated charcoal, or a cathartic
magnesium citrate or a sorbitol solution. Alkalinization of the urine might be helpful in
preventing deposition of red blood cell breakdown products in renal tubular cells when
hemolysis is occurring.
Chelation therapy is recommended in symptomatic patients known to have ingested arsenic
and in asymptomatic patients who have a documented urinary arsenic level greater than 200
mcg/1. Dimercaprol is the first line of treatment. The dose ranges from 3 to 5 mgAkg i.m. every
4 to 12 hours until the symptoms abate or another chelator is substituted. One author
recommends tapering the dose but continuing administration of dimercaprol until the urinary
excretion is less than 50mcg/24 hours1. Dimercaprol is an effective chelator but has some
disadvantages. The intramuscular injections can be painful, and there are many adverse effects
such as mild systemic shock, tachycardia, hypertension, vomiting, convulsions, headache,
nausea, vomiting and anorexia. A prior injection with epinephrine might alleviate some of
systemic effects25. D-Penicillamine is an oral chelator found to be effective. The usual dose is
25 mg/kg given 4 times a day up to one gram/day. The 3 short-term adverse effects have not
been reported, but long-term effects of penicillamine have included fever, leukopenia,
thrombocytopenia, eosinophilia and renal toxicity. Another agent, 2,3-dimercaptosuccinic acid
(DMSA), appears to be a promising method of treatment, although currently it is approved only
for use in lead-poisoning in children. DMSA for adult arsenic treatment is still under
investigation and, therefore, must be obtained from the Regional Poisons Unit27.

Source:

Cao, N. T., Tran, T. B., Huynh, N. P., Nguyen, N. T., & Wu, M. (2020). Arsenic Poisoning from

Repeated Exposure to Burning Herbal Products Containing Realgar: A Case Report. Journal of

Clinical Toxicology, 10(2), 1–5. https://doi.org/10.35248/2161-0495.20.10.435