Survival after severe acute chromic acid poisoning complicated with renal and liver failure.

Chromic acid is a strong metal acid and acute poisoning is very rare, but very serious with severe skin injury, renal and liver failure. The majority of published cases were suicide attempts with lethal outcomes. We describe the case of a 55-year-old man who had accidentally taken a sip of 20% chromic acid (estimated chromium intake: 2.3 g). Renal and liver failure were not present at presentation, but appeared later in the course of disease. He was treated with hemodialysis, no chelating agents or other methods for enhancing elimination were used. Liver and renal function improved over the next 30 days and the patient was discharged after 45 days of hospitalization with no need for dialysis. In the follow-up period of eight months his renal function remained depressed, but stable.

Acute, fatal, oral chromic acid poisoning.

CASE REPORT: We report a 35-year-old woman who developed severe acidosis, massive gastrointestinal hemorrhage, acute renal failure, and hepatic injury following ingestion of chromic acid (50 mL) and died 12 hours after ingestion. Postmortem liver biopsy revealed a fatty degeneration with chromium concentration 3.6 mumol/g. The kidney, with chromium concentration 2.6 mumol/g, had extensive necrosis and ischemic lesions. Erythrocyte chromium was 1903 mumol/L at 3 hours declining to 865 mumol/L at 11 hours.

Unusual findings in a fatal case of poisoning with chromate compounds.

An interesting case of acute poisoning by chromate compounds is reported. A 51-year-old man committed suicide by ingesting a fatal dose of sodium chromate solution. He unexpectedly lost consciousness 6 h after the ingestion and died approximately 20.5 h later. An examination of the blood showed noticeable hepatic damage and thrombocytopenia. The postmortem examination revealed extensive bleeding in the alimentary tract and a severe hepatic lesion due to hepatocellular necrosis. However, the renal disorder was unusually light in the microscopic and clinical findings. Moreover, the renal lesion was observed mainly in the distal tubules instead of the proximal tubules which is more typical in cases of acute poisonings by diverse heavy metals including chromium. The patient's death was assumed to have been caused by circulatory collapse due to internal bleeding and the direct toxicity of chromate compounds with hepatic malfunction and possibly disseminated intravascular coagulation (DIC).

Acute ammonium dichromate poisoning.

We report the ingestion of ammonium dichromate by a child that resulted in multiple-organ-system failure and death. Exchange transfusion and hemodialysis were ineffective in removing significant amounts of chromium or causing sustained clinical improvement. We suggest that immediate, large doses of the reducing agent ascorbic acid would allow effective reduction of hexavalent chromium with less cellular toxicity.

Acute renal failure in a case of fatal chromic acid poisoning.

Despite its frequent use in industry, acute poisoning by chromic acid has very rarely been reported. We report a patient who developed massive gastrointestinal hemorrhage, acute renal failure, and hepatic injury following chromic acid ingestion, and subsequently died. Postmortem liver and kidney biopsies revealed centrilobular necrosis and severe acute tubular necrosis, respectively.

Lung cancer mortality among a cohort of male chromate pigment workers in Japan.

In 1975, five manufacturers of chromate pigment in Japan were examined in a study of the carcinogenicity of chromates. These companies were producing lead chromate, zinc chromate, molybdate orange and/or strontium chromate. The current study covers a cohort of 666 workers involved in the manufacture of chromate pigment for at least 1 year between 1950 and 1975. The workers were followed up for 15-40 years, until 1989. Many previous reports have found an excess lung cancer risk among workers involved in the manufacture of chromate pigments and chromate chemicals. In the current study, subjects were classified on the basis of years worked, years of observation, characteristics of company, type of work engaged in for the longest period of time, and involvement in the manufacture of zinc chromate. Mortality was compared with that of all Japanese males by means of the person-year method. The route of exposure was primarily inhalation through the respiratory system. None of the results showed statistically significant differences that would suggest an excess risk for malignant neoplasms, particularly lung cancer, among workers engaged in the manufacture of chromate pigment in Japan.

[Chronic chromate intoxication with renal tubular damage--report of a case].

A 46-year-old male chromium plating worker visited our hospital due to rhinorrhea, sneezing and cough with blood-tinged sputum for more than 10 years. He also had skin ulceration and chronic dermatitis on both hands Medical therapy was inefficient. Physical examinations revealed nasal septum perforation, severe inflammation of the nasopharynx cavity, and eczema of both hands. Laboratory investigations showed significant tubule proteinuria, enzymuria, hypercalciuria, etc. It is evident that renal tube damage was present in this patient. The blood chromium level was 25 ng/mL, and the 24-hour urine chromium excretion level was 2.8 mg/day. A pulmonary function test showed reduced functional residual capacity (FRC), which may be due to either long-term smoking or chromate acid exposure. To our knowledge this is the first case of renal tubal damage induced by chronic chromate intoxication Taiwan. Further evaluation of the occupational safety and health of chromium plating workers is needed on this island.

[Clinical and toxicologic problems related to acute poisoning with chromium]. / Zagadnienie kliniczne i toksykologiczne ostrych zatruc chromem.

Clinical course and toxicological findings in 18 patients intoxicated with ingested chromium salts are presented. Seventeen of these patients ingested potassium and sodium dichromate while the remaining patient--chromic acid. The first stage of 6-valent chromium is characterized by its irritating effect on the gastro-intestinal mucous membrane manifested by diarrhoea, vomiting often with blood, leading to severe water-electrolyte disorders, acidosis and shock. Lesions to kidneys, liver and myocardium may develop in the next stage. Probably endothelium is also in injured with resulting increase in its permeability. Acute renal failure is not seen even with high levels of chromium in the urine provided, that the recovery from the shock is prompt, and adequate diuresis induced with mannitol and/or furosemide is maintained. All patients with blood chromium concentration exceeding 1 mg/100 g died. This level is of prognostic and diagnostic value indicating an ingestion and absorption of the high doses of this metal.

Chromic acid burns; beware, be aggressive, be watchful.

Two cases involving the development of systemic toxicity and prolonged wound healing in small percentage area burns to chromic acid are reported. The treatment of chromic acid burns is reviewed and a protocol of management suggested.

Acute dichromate poisoning after use of traditional purgatives. A report of 7 cases.

Seven cases of dichromate poisoning after the use of purgative solutions obtained from nyanga (traditional township healers) are reported. The patients all presented in established renal failure requiring dialysis, and all had abnormal liver function tests. One patient who took dichromate orally died from massive gastro-intestinal haemorrhage. Six patients took dichromate solutions as rectal enemas, 2 were left with impaired renal function and 1 required a permanent colostomy as a result of extensive peri-anal necrosis. The clinical presentation of acute renal failure, gastro-intestinal haemorrhage and hepatocellular dysfunction should alert the physician to the possibility of dichromate poisoning. The diagnosis, management and the role of dialysis in dichromate poisoning are reviewed.

[Study of Ag-NOR, SCE and micronucleus in peripheral blood lymphocyte of chromate producers].

Ag-NOR, SCE and micronucleus test of peripheral blood lymphocyte obtained from 31 chromate producers had been studied. We found that (1) in the workers who had been exposed over eight years, the frequency of Ag-NOR, Ag-AA and SCE were 6.905 +/- 1.100, 0.380 +/- 0.652 and 8.190 +/- 3.727, but in the control group, 6.512 +/- 1.595, 0.215 +/- 0.529 and 7.171 +/- 2.683, respectively. So there was considerably significant difference between the exposed and the unexposed (P less than 0.01); (2) the frequency of micronuclei was 3.71 +/- 1.419% in the exposed group; however, in the control group it was 0.333 +/- 0.479%. So there was also remarkably significant difference between them (P less than 0.001). The observations lead the authors to conclude that the genetic material of the workers who have been working over eight years may be damaged because of being exposed to chromate.

Chromium determinations in a case of chromic acid ingestion.

A fatal case of acute chromic acid ingestion is reported. The case history and biological fluid concentrations of chromium are presented and discussed. Previous cases of acute chromium intoxication are reviewed and recommendations for the management of such patients are presented.