Year : 2009 | Volume
: 20 | Issue : 1 | Page : 106--111
Selenium intoxication with selenite broth resulting in acute renal failure and severe gastritis
P Kamble1, N Mohsin1, A Jha1, A Date2, A Upadhaya3, E Mohammad1, M Khalil1, A Pakkyara1, M Budruddin1,
1 Department of Nephrology, Royal Hospital, Muscat, Oman
2 Department of Pathology, Sultan Qaboos University Hospital, Muscat, Oman
3 Department of Gastro-Enterology, Royal Hospital, Muscat, Oman
Sr. Consultant and Head of Nephrology, Royal Hospital, P.O. Box 1331, PC 111, Muscat
Selenium (Se) is an essential trace element in human and animal nutrition. It is also widely utilized in industrial processes. Reports of acute selenium toxicity in humans are rare. We report a case of a 23-year-old female who consumed about 100 mL of liquid selenite broth and presented with severe nausea, vomiting, abdominal pain, hematemesis and acute renal failure (ARF). The serum selenium level was significantly increased. Gastro-duodenoscopy revealed severe corrosive gastritis. Renal biopsy showed features of acute tubular necrosis (ATN), affecting primarily the proximal tubules. The patient was managed with gastric lavage, blood transfusions, infusion of fresh frozen plasma (FFP) and platelet concentrates and hemodialysis. The patient was discharged five weeks after admission and her renal functions recovered completely by eight weeks after admission. She continues to be on regular follow-up for any possible sequelae of mucosal corrosive damage. This case highlights a case of selenium intoxication from selenite broth resulting in ARF and corrosive gastritis. The recovery was complete.
|How to cite this article:|
Kamble P, Mohsin N, Jha A, Date A, Upadhaya A, Mohammad E, Khalil M, Pakkyara A, Budruddin M. Selenium intoxication with selenite broth resulting in acute renal failure and severe gastritis.Saudi J Kidney Dis Transpl 2009;20:106-111
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Kamble P, Mohsin N, Jha A, Date A, Upadhaya A, Mohammad E, Khalil M, Pakkyara A, Budruddin M. Selenium intoxication with selenite broth resulting in acute renal failure and severe gastritis. Saudi J Kidney Dis Transpl [serial online] 2009 [cited 2023 Feb 4 ];20:106-111
Available from: https://www.sjkdt.org/text.asp?2009/20/1/106/44715
Selenium (Se) is an ubiquitous element which is essential to the human organism and is also widely utilized in industrial processes. As an essential trace element, it plays an important role in many biochemical and physiological pathways, particularly in the activation of glutathione peroxidase (an enzyme involved in preventing oxidative damage of the cells).  It has been used in cancer patients to improve nutritional and immunological status. Also, it has been shown to have a protective role in preventing liver cancer and nuclear cataract. ,,,
Despite its beneficial effects, excessive doses of this element result in intoxication. Cases of acute Se intoxication occur due to excessive industrial exposure, overdose in demented patients or suicidal patients and in toddlers. Depending on the quantity and the form, symptoms and signs may vary and include excessive salivation, garlicky breath odor, nausea, vomiting, abdominal pain, tachycardia, hematemesis, necrosis of the liver and the kidneys, cerebral and pulmonary edema, coma and death. Currently, there are no known antidotes and the treatment remains mainly symptomatic and supportive. 
The selenite broth, also known as selenite enrichment culture media, is used for the isolation of Salmonella bacilli in urine and blood samples. These media contain four grams of sodium selenite (a highly toxic form of Se) dissolved in one liter base of a mixture of polypeptones.
We report a case, probably the first, of a young and previously healthy female, who consumed about 100 mL of selenite broth. She presented with manifestations of corrosive gastritis and acute renal failure (ARF). She received a multidisciplinary management following which, made complete recovery.
A 23-year-old, unmarried, employed female, with no past history of any psychiatric or medical illness, was admitted to our hospital through the accident and emergency department. Her chief complaints were nausea, vomiting, (4 to 5 times without hematemesis or garlicky smell) and epigastric pain of one day's duration. She also gave history of passing two to three loose stools with mucus but, without blood. The patient denied any history of intake of any illicit drugs or chemicals at the time of admission. On examination, she was conscious, well oriented with stable vitals. There was mild epigastric tenderness. The remainder of the systemic examination was unremarkable. The laboratory investigations on admission showed a white blood cell count of 5.9 × 10 9 /L, hemoglobin of 12.8 gm/dL and platelet count of 270 × 10 9 /L. The blood urea was 3 mmol/L and the serum creatinine was 51 µmol/L. Serum electrolytes and liver function tests (LFT) were normal. The patient was treated as a case of gastro-enteritis with intravenous fluids, antiemetics and histamine-2 receptor antagonists (ranitidine). The patient's condition did not improve over the next 36-48 hours as the abdominal pain and vomiting increased. She did not have hematemesis. She remained conscious and oriented, but she appeared slightly apprehensive and had developed tachycardia. She also developed oligo-anuria with impairment of renal functions. The serum creatinine rose to 692 µmol/L and the blood urea to 25.8 mmol/L. The serum sodium (Na) was 142 mmol/L, potassium (K) 5.1 mmol/L and chloride (Cl) 115 mmol/L. The hemogram, LFT and coagulation profile were within normal limits. The electrocardiogram showed sinus tachycardia without ST segment and T wave changes. The patient was taken into confidence by a lady physician and on detailed enquiry, it was revealed that the patient had "accidentally" consumed about 100 mL of selenite broth from a local hospital laboratory, one day prior to her hospital admission. The patient said that she hid the information for fear of social stigma and medico-legal enquiry. Blood samples showed elevated Se levels at 1.7 µmol/L (normal: 0.75 to 1.51 µmol/L). Urine samples were not available as the patient was anuric. Hemodialysis was initiated with the continuation of supportive treatment. A kidney biopsy was performed which showed 10 glomeruli under light microscopy, all of which looked grossly normal. The proximal tubules showed epithelial necrosis with eosinphilic cell debris filling the tubular basement membrane area. The distal tubular epithelium was largely preserved except for some intraluminal debris which was probably washed down from the proximal segments. The interstitium and the vascularture were unremarkable [Figure 1]. Tissue for immunofluorescence contained four glomeruli; none showed positive staining.
During the course of her stay in the hospital, the patient developed hematemesis. Her vitals remained stable. The coagulation profile was mildly deranged. The patient received blood transfusions, fresh frozen plasma (FFP) and platelet infusions. A gastro-duodenoscopy (OGD) was performed and showed severe hemorrhagic gastritis. She was started on proton pump inhibitors (PPI) and sucralfate. Hemodialysis was continued without heparin. She had another bout of hematemesis 48hours later. A second OGD was performed and showed large clots on the gastric greater curvature along with diffuse mucosal and submucosal hemorrhages. The esophagus was relatively spared. The findings were suggestive of severe corrosive hemorrhagic gastritis [Figure 2]. Intravenous PPI, octreotide, FFPs and blood were administered. The bleeding stopped and the condition of the patient improved progressively. Dialysis was discontinued in the fourth week of hospitalization and she was discharged a week later. Renal functions recovered completely by the eighth week of her illness. Periodic follow-up up to six months from discharge did not reveal any possible late sequelae of Se toxicity such as alopecia, abnormality of the fingernails or gastric strictures.
Selenium (Se) is an essential dietary trace element with anti-oxidant properties due to its role in activation of glutathione peroxidase, an enzyme involved in preventing oxidative damage to cells. It also plays an important role in many biochemical and physiological processes including the biosynthesis of coenzyme Q (a component of mitochondrial electron transport system), regulation of the ion fluxes across membranes, maintenance of integrity of keratins and stimulation of antibody synthesis.  There is some evidence suggesting that adequate dietary supplementation of Se may provide protection against some cancers. Se is currently used in hyperalimentation and total parenteral nutrition. ,
There appears to be a relatively narrow range between levels of Se intake resulting in deficiency and those causing toxicity.  The recommended daily allowance (RDA), for adults, by the Federal Drug Administration (FDA) is 50-200 µg.
Selenium is a grey metalloid element of the sulfur group discovered in 1817 by Berzelius who named it after Selene, the Greek Goddess of the moon. It is widely used in many commercial applications, thus constituting a common source of human exposure. , Industrial uses include solar energy, semi-conductor processing and the manufacturing of electronics and ceramics. ,,,, It is present in steel and copper alloying, metal pigmentation in photographic cells, glass and paint manufacturing, rubber vulcanization, nutritional supplements and Selsun TM shampoo. Also, it is mixed with various compounds utilized for polishing and bluing the exterior metallic surfaces of handguns. , In selenite enrichment media (selenite broth), selenium is used to selectively isolate Salmonella bacilli from urine and blood samples. 
Acute poisoning with Se or its compounds, especially the fatal ones, occurs extremely rarely in humans. Marco Polo gave the first account of Se toxicity which he observed during his travel in western China in the 13 th century. He linked the sloughing off of the hooves of horses to their consumption of certain plants rich in very high concentration of Se.  In humans, acute Se intoxication can occur due to industrial exposure, accidental overdose in demented or suicidal patients and in toddlers. Acute oral exposure can result in excessive salivation, garlicky breath odor, shallow breathing, diarrhea, continuous vomiting, mucosal irritation, hematemesis, abdominal pain, tachycardia, hemolysis, necrosis of the liver and the renal tubules (resulting in ARF), cerebral and pulmonary edema, paralysis, convulsions, coma and death. ,,,
Selenium occurs in several valency states; -2 (hydrogen selenide, sodium selenide, dimethyl selenium, selenomethionine); 0 (elemental selenium); +4 (selenium dioxide, selenious acid and sodium selenite); and +6 (selenic acid and sodium selenate). Toxicity of Se varies according to the valency state and the water solubility of the compound. The more soluble compounds such as sodium selenate are more toxic than the less soluble elemental selenium. Absorption is also more efficient after a single dose than after repetitive daily doses. Gastrointestinal absorption of the various Se compounds ranges from about 44 to 95 %. It is widely distributed in the body. Relatively high concentrations are seen in the gastric mucosa, heart, liver, kidneys, lungs, pancreas, spleen and testes. Excretion is primarily via the urine (0-15 µg/L). ,,
Multi-organ system involvement is known to occur in acute oral Se intoxication. The severity depends upon the dose and the type of Se compound ingested. Nantel AJ et al reported a case in which a two-year-old male child presented with severe corrosive gastritis and moderate renal, hepatic and pulmonary dysfunction after consuming 15 mL of GunBlue solution containing selenious acid. Plasma Se concentration was raised to 285 µg/L. The patient died after 17 days.  In another instance, where the patient presented after fatal suicidal ingestion of Gun-Blue solution, post-mortem examination revealed pulmonary edema with pleural effusion and congestion of the kidney. Necrosis of proximal tubules was noted in the kidney on histological examination. The selenium levels in the tissues were 9 to 90-fold higher than in normal subjects, with highest tissue levels found in the lungs, kidneys and stomach.  In animal studies, a dose dependent acute tubular necrosis (ATN) of the kidney and centrilobular liver injury is well documented. 
Our patient developed severe ARF requiring dialysis support. Her renal biopsy revealed proximal tubular necrosis consistent with toxic ATN [Figure 1]. The biochemical mechanism of toxicity of Se and related compounds is not fully understood. However, potential mechanisms of toxicity include: ,
substitution of Se for sulfur in sulfhydrylcontaining enzymes necessary for oxidative reactions in cellular respiration via effects on the mitochondrial and microsomal electron transport.mediation of oxidative stress mechanism, interference with the normal redox-regulating activities of glutathione peroxidase,mediation of apoptotic and free radical formation.
Our patient also had severe hematemesis due to corrosive gastritis [Figure 2] which required aggressive management with multiple transfusions of blood, FFPs, platelet concentrates, PPI and octreotide. Kise Y, et al reported a case of oral Se intoxication in a 48-year-old female who had hematemesis with severe corrosive mucosal injury of the oral cavity, esophagus and stomach with deep gastric ulcers. The patient had consumed 2000 mg of selenium dioxide (from the bottle of glassblue). She recovered with symptomatic and supportive care.  Highly toxic Se compounds like sodium selenite and selenium dioxide, upon contact with water, form a weak acid (selenic acid) which is a strong oxidant and is responsible for the corrosive mucosal injury. 
Se clearance in humans appears to follow a two-compartment model characterized by an initial distribution phase of six hours and a final elimination half- life phase of 17.5 hours. ,, In humans, toxic effects have been re-ported at blood levels ranging from 0.1797.5 µg/mL.  It was calculated that the patient under discussion consumed about 400 mg of sodium selenite. Her serum Se level was 1.71 µmol/L, which was moderately but significantly higher than the normal level, in a sample collected 3-4 days after Se ingestion. Hemodialysis is not an established mode of treatment for Se intoxication, but was indicated for the treatment of the ARF. Nevertheless, a decrease in serum Se concentration has been reported with dialysis. ,
The principal treatment strategy in acute Se intoxication is to remove the patient from the source of Se and to provide symptomatic and supportive care, as currently there are no antidotes available. Few pharmaceutical agents such as bromobenzene, arsenic compounds and glutathione have been suggested as possible antidotes, but require confirmation before putting them into practical use. ,
The terminal half-life of selenite is about four months. Hence, care should be taken to avoid further exposure to Se and to observe any late sequelae of Se toxicity such as changes in hair, skin and nails or any persistent gastric symptoms. ,, After six months of follow-up, our patient is doing fine and looks healthy. An OGD at six years is suggested, as corrosive gastritis may cause late complications like strictures or stenosis. 
In summary, the present case highlights the possibility of acute Se intoxication following the ingestion of selenite enrichment media (selenite broth). The clinical features included acute renal failure and corrosive gastritis with hematemesis. She recovered with multidiscip linary symptomatic and supportive management.
|1||Hammond PB, Beliles RP. Metals. In: Casarett and Doull's Toxicology, The Basic Science of Poisons, 2nd ed ,J.Doull, C.D. Klaassen,, M.O. Amdur, (eds). Macmillam Publ., New York. 1980;409-67.|
|2||Federico A, Iodice P, Federico P, et al. Effects of selenium and zinc supplementation on nutritional status in patients with cancer of digestive tract. Eur J Clin Nutr 2001;55(4): 293-7.|
|3||Kiremidjian-Schumacher L, Roy M, Glickman R, et al. Selenium and immunocompetence in patients with head and neck cancer. Biol Trace Elem Res 2000;73(2):97-111.|
|4||Yu SY, Zhu YJ, Li WG. Protective role of selenium against hepatitis B virus and primary liver cancer in Qidong. Biol Trace Elem Res 1997;56(1):117-24.|
|5||Sperduto RD, Hu TS, Milton RC, et al. The Linxian cataract studies: Two nutrion intervention trials. Arch Ophthalmol 1993;111(9): 1246-53.|
|6||Barceloux DG. Selenium. Clin Toxicol 1999; 37(2):145-72.|
|7||Alaejos MS, Romero FJ, Diaz Romero C. Selenium and cancer: Some nutritional aspects. Nutrition 2000;16(5):376-83.|
|8||Kise Y, Yoshimura S, Akieda K, et al. Acute oral selenium intoxication with ten times the lethal dose resulting in deep gastric ulcer. J Emerg Med 2004;26(2):183-7.|
|9||Lech T. Suicide by selenium tetraoxoselenate (VI) poisoning. Forensic Sci Int 2002;130 (1):44-8.|
|10||Chan S, Gerson B, Subramanium S. The role of copper, molybdenum, selenium and zinc in nutrition and health. In: Gerson B, ed. Clinics in laboratory medicine: Toxicology. Philadelphia: Saunders; 1998:673-85.|
|11||Civil ID, McDonald MJ. Acute selenium poisoning: Case report. N Z Med J 1978;87 (612):354-6.|
|12||Alderman LC, Bergin JJ. Hydrogen selenide poisoning: An illustrated case with review of literature. Arch Environ Health 1986;41(6): 354-8.|
|13||Quadrani DA Spiller HA, Steinhorn D. A fatal case of gun-blue ingestion in a toddler. Vet Human Toxicol 2000;42(2):96-8.|
|14||Osler O, Prelwitz W, Kasper W, Meinertz T. Congestive cardiomyopathy and the selenium content of serum. Clin Chim Acta 1983;128 (1):123-32.|
|15||Shrift A, Boulette RF. Form of selenium in selenite enrichment media for isolation of salmonellae. Appl Microbiol 1974;27(4):814-6.|
|16||Koppel C, Baudisch H, Beyer KH, Kloppel I, Schneider V. Fatal poisoning with selenium dioxide. Clin Toxicol 1986;24(1):21-35|
|17||Matoba R, Kimura H, Uchima E, et al. An autopsy case of acute selenium (selenious acid) poisoning and selenium levels in human tissues. Forensic Sci Int 1986;31(2):87-92.|
|18||US EPA 1993. Toxicity profiles of selenium by Dennis M. Opresko, Ph.D, Chemical Hazard Evaluation Group, Oak Ridge, Tennessee (Online file).|
|19||ATSDR (Agenda For Toxic Substances and Disease Registry). Toxicological Profiles For Selenium. ASTR, US Public Health Services, Atlanta GA; 1989.|
|20||Bopp BA, Sonders RC, Kesterson JW. Metabolic fate of selected selenium compounds in laboratory animals and man. Drug Metab Rev 1982;13(2):271-318.|
|21||Nantel AJ, Brown M, Dery P, Lefebvre M. Acute poisoning by selenious acid. Vet Hum Toxicol 1985;27(6):531-3.|
|22||Cherdwongcharoensuk D, Henrique R, Upatham S, et al. Tubular kidney damage and centrilobular liver injury after intratraceal instillation of dimethyl selenide. Toxicol Pathol 2005;33(2):225-9.|
|23||Hunsaker DM, Spiller HA, William D. Acute selenium poisoning: Suicide by ingestion. J Forensic Sci 2005;50(4):942-6.|
|24||Gasmi A, Garnier R, Galliot-Guilley M, et al. Acute selenium poisoning. Vet Hum Toxicol 1997;39(5):304-8.|
|25||Hogeberg J, Alexander J. Selenium. In: Friberg L, Nordberg GF, Vouk V, eds. Handbook on the toxicology of metals, 2nd ed. Amsterdam: Elsevier Science Publishers B.V.; 1986:482-520.|
|26||Bogye G, Tompos G, Alfthan G. Selenium depletion in hemodialysis patients treated with polysulfone membranes. Nephron 2000;84(2):119-23.|
|27||Gezernik W, Schmaman A, Chappel JS. Corrosive gastritis as a result of ferrous sulphate ingestion. S Afr Med J 1980;57(5):151-4|