Failure of dialysis therapy in potassium dichromate poisoning

Iserson, Kenneth V.; Banner, William; Froede, Richard C.; Derrick, Michele

doi:10.1016/0736-4679(83)90048-3

Cited by 19 publications

(13 citation statements)

References 7 publications

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“…83 Additionally, the ingestion of large doses hexavalent chromium causes vertigo, thirst, abdominal pain, bloody diarrhea, and in severe cases, coma and death. A hepatorenal syndrome, 43 severe coagulopathy, 41 or intravascular hemolysis 88 may occur. If the patient survives the initial phase of shock, hepatic and renal failure may still develop within 1-2 days.…”

Section: Acute Systemic Toxicitymentioning

confidence: 99%

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Chromium

Barceloux¹

1999

Journal of Toxicology: Clinical Toxicology

468

304

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Chromium occurs primarily in the trivalent state (III), which is the most stable form, or in the hexavalent state (VI), which is a strong oxidizing agent. Elemental chromium (0) does not occur naturally on earth. Trivalent chromium (III) is an essential trace metal necessary for the formation of glucose tolerance factor and for the metabolism of insulin. Commercial applications of chromium compounds include tanning (III), corrosion inhibition, plating, glassware-cleaning solutions, wood preservatives (VI), manufacture of safety matches, metal finishing (VI), and the production of pigments (III, VI). Hexavalent chromium (VI) contaminated local soil when chromium waste slag was part of the fill material present in residential, public, and industrial areas. In some urban areas, about two-thirds of the chromium in air results from the emission of hexavalent chromium from fossil fuel combustion and steel production. The remaining chromium in air is the trivalent form. The residence time of chromium in air is < 10 days, depending on the particle size. Trivalent compounds generally have low toxicity and the gastrointestinal tract poorly absorbs these compounds. Hexavalent chromium is a skin and mucous membrane irritant and some of these hexavalent compounds are strong corrosive agents. Hexavalent chromium compounds also produce an allergic contact dermatitis characterized by eczema. Sensitivity to trivalent compounds is much less frequent, but some workers may react to high concentrations of these compounds. Hexavalent chromium is recognized by the International Agency for Research on Cancer and by the US Toxicology Program as a pulmonary carcinogen. The increased risk of lung cancer occurs primarily in workers exposed to hexavalent chromium dust during the refining of chromite ore and the production of chromate pigments. Although individual studies suggest the possibility of an excess incidence of cancer at sites outside the lung, the results from these studies are inconsistent.

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Section: Acute Systemic Toxicitymentioning

confidence: 99%

“…40 A 17-year-old male died after the reported ingestion of 29 mg Cr (VI)/kg (i.e., about 2 g). 41 An 18-year-old man ingested approximately 5 g of potassium dichromate by history. 41 On admission, he was hypotensive and cyanotic (22% methemoglobinemia) and shortly thereafter a coagulopathy, hemorrhage, and a cardiac arrest occurred.…”

Section: Chromic Acidmentioning

confidence: 99%

Chromium

Barceloux¹

1999

Journal of Toxicology: Clinical Toxicology

468

304

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“…Accidental ingestion has been reported for Cr(VI) compounds including chromic acid (Fristedt et al, 1965;Saryan and Reedy, 1988;Loubières et al, 1999), potassium chromate (Goldman and Karotkin, 1935;Partington, 1950;Kaufman et al, 1970;Sharma et al, 1978;Iserson et al, 1983;Clochesy, 1984;Hanston et al, 2005), and ammonium dichromate (Reichelderfer, 1968;Hasan, 2007) resulting in a large variety of clinical presentations such as abdominal pain, nausea, and vomiting; hematemesis and bloody diarrhea; caustic burns of the mouth, pharynx, esophagus, stomach, and duodenum and GI hemorrhage; anemia, decreased blood Hb, abnormal erythrocytes, and intravascular hemolysis; hepatotoxicity (hepatomegaly, jaundice, elevated blood bilirubin, and liver enzymes activities); renal failure (oliguria and anuria); cyanosis; and metabolic acidosis, hypotension, and shock (see also ATSDR, 2012). Fatty degeneration in the liver and tubular degeneration and necrosis in the kidney were observed in biospies (Reichelderfer, 1968;Kaufman et al, 1970;Sharma et al, 1978;Loubières et al, 1999).…”

Section: Acute Oral Toxicitymentioning

confidence: 99%

Scientific Opinion on the risks to public health related to the presence of chromium in food and drinking water

2014

EFS2

101

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EFSA received a request from the Hellenic Food Authority for a scientific opinion on estimation of the risk to human health from the presence of chromium (Cr) in food, particularly in vegetables, and Cr(VI) in bottled water. The CONTAM Panel derived a TDI of 0.3 mg/kg b.w. per day for Cr(III) from the lowest NOAEL identified in an NTP chronic oral toxicity study in rats. Under the assumption that all chromium in food is Cr(III), the mean and 95th percentile dietary exposure across all age groups were well below the TDI and therefore does not raise concerns for public health. In the case of drinking water, the Panel considered all chromium in water as Cr(VI). For non‐neoplastic effects the lowest BMDL10 for diffuse epithelial hyperplasia of duodenum in female mice and the lowest BMDL05 for haematotoxicity in male rats in a 2‐year NTP study were selected as reference points. The MOEs indicate that for non‐neoplastic effects the current exposure levels to Cr(VI) via drinking water are of no concern for public health. For neoplastic effects, the CONTAM Panel selected a lowest BMDL10 for combined adenomas and carcinomas of the mouse small intestine as the reference point. Overall, the calculated MOEs indicate low concern regarding Cr(VI) intake via drinking water (water intended for human consumption and natural mineral waters) for all age groups when considering the mean chronic exposure values with the exception of infants at the upper bound (UB) exposure estimates. MOEs below 10 000 were calculated at the UB 95th percentile exposure estimates, particularly for ‘Infants’, ‘Toddlers’ and ‘Other children’, which were highly influenced by the relatively high occurrence values under the UB assumption. To improve the risk assessment, there is a need for data on the content of Cr(III) and Cr(VI) in food and drinking water.

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“…5 Other treatment modalities like hemodialysis and charcoal hemoperfusion have been tried but not with much success. 6 A case successfully treated with peritoneal dialysis has been reported. 7 Liver tranplantation has been successfully used in cases where hepatic failure is predominant feature of dichromate poisoning.…”

Section: Discussionmentioning

confidence: 99%

Acute Potassium Dichromate Poisoning Presenting With Myocarditis and Uretheral Injuries: A Case Report

Neki¹,

Singh²,

Shergill³

et al. 2017

Int. J. Curr. Res. Med. Sci.

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Acute potassium dichromate poisoning may be accidental or suicidal. The potassium dichromate is highly toxic and is lethal to humans in relatively smaller doses. There is no specific antidote to it and the treatment is symptomatic. Many experimental modalities of treatment have been tried with variable success. We report a case of 33 year old young man who upon ingestion of potassium dichromate, presented to us with myocarditis and severe uretheral injuries along with multi-organ failure.

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Failure of dialysis therapy in potassium dichromate poisoning

Cited by 19 publications

References 7 publications

Chromium

Chromium

Scientific Opinion on the risks to public health related to the presence of chromium in food and drinking water

Acute Potassium Dichromate Poisoning Presenting With Myocarditis and Uretheral Injuries: A Case Report

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