|
| Article Access Statistics | | | Viewed | 11171 | | | Printed | 302 | | | Emailed | 1 | | | PDF Downloaded | 150 | | | Comments | [Add] | | | Cited by others | 2 | | |
|
Click on image for details.
|
|
| LETTER TO EDITOR |
|
|
|
| Year : 2003 | Volume
: 49
| Issue : 3 | Page : 286-287 |
Fatal Potassium Dichromate Ingestion
Sharma N, Chauhan S, Varma S
Department of Internal Medicine, Postgraduate Institute of Medicine Education and Research, Chandigarh - 160 012
Correspondence Address:
Department of Internal Medicine, Postgraduate Institute of Medicine Education and Research, Chandigarh - 160 012
How to cite this article:
Sharma N, Chauhan S, Varma S. Fatal Potassium Dichromate Ingestion
. J Postgrad Med 2003;49:286-7 |
Sir,
Potassium dichromate, a hexavalent compound of chromium, is used as a furniture stainer and as a disinfectant for cleaning swimming pools.[1] Ingestion of this compound is fatal but a few patients have survived.[1] We report a case of potassium dichromate poisoning with a fatal outcome. A 32-year-old male presented to the medical emergency services after consuming 73.46 mg/kg of hexavalent chromium as potassium dichromate powder. He had vomited 5-6 times and had a burning sensation in the throat. The pulse was 120 per minute and blood pressure was 80/60 mm Hg. On investigating, his haemoglobin level was 18.5 gm%, bilirubin level 11.9 mg/dL (conjugated fraction - 6.3 mg/dL), serum albumin 2.0 mg/dL, aspartate aminotransminase 112 IU/L and alanine aminotransminase 92 IU/L. The level of plasma haemoglobin was raised. Arterial blood gas analysis revealed the presence of combined metabolic acidosis and respiratory alkalosis with an oxygen saturation of 93%. The prothrombin time index was 48%.
Hypotension was managed with fluid resuscitation using crystalloids and steroid therapy. Four days after admission, signs of bronchopneumonia and acute liver failure appeared, which were managed with administration of antibiotics, pantoprazole, vitamin K, lactulose, bowel washes and daily fresh frozen plasma. On day 6, he developed acute renal failure, for which haemodialysis was instituted. The investigations revealed a blood urea level of 124 mg/dL and serum creatinine concentration of 7.4 mg/dL. Other metabolic and biochemical abnormalities that were detected at this stage included hyperbilirubinaemia (serum bilirubin concentration 10.7 mg/dL with conjugated fraction accounting for 7.0 mg/dL), hypoalbuminaemia (serum albumin 1.2 mg/dL), raised levels of hepatic transaminases (aspartate aminotransminase level of 133 IU/L, alanine aminotransminase concentration of 82 IU/L) and severe metabolic acidosis. The prothrombin time index was 20%. Despite treatment the hepatorenal syndrome worsened and the patient succumbed to his illness.
The chromium moiety in potassium dichromate exists as a hexavalent ion. It is taken up by the red blood cells and platelets and it exhibits non-specific binding to nucleoproteins. It gets reduced to trivalent chromium and causes free radical damage to the mitochondria, particularly in the kidney tubules and hepatocytes.[1] The clinical features of poisoning consist of gastrointestinal irritation followed by a phase of severe systemic toxicity presenting with coagulopathy, intravascular haemolysis, severe acidosis and hepatorenal syndrome with fulminant hepatic failure.[2], [3] The treatment of this uncommon poisoning consists of gut decontamination using an ascorbic acid solution that reduces the hexavalent chromium compound to the less toxic trivalent compound. Although animal experimentation has shown some role for parenteral ascorbate,[4] as yet, clinical evidence or studies favouring its use in humans, are lacking. The efficacy of haemodialysis for the effective removal of dichromate is controversial with only one case report supporting its use.[3] In the case reported, (Kolacinski et al[3]), haemodialysis was credited for patient survival although the 5-hour haemodialysis was shown to have removed only 5 mg chromium. Other studies have doubted the efficacy of haemodialysis in removing dichromate.[5] Recently, orthotopic liver transplantation has been carried out successfully for acute liver failure in a case of dichromate poisoning.[6]
Thus, potassium dichromate ingestion should be suspected in any patient presenting with hepatorenal syndrome after alleged suicidal consumption. If presenting early, selective gut decontamination with ascorbate solution can be attempted and for persons presenting late, referral to a centre equipped with facilities for orthotopic liver transplantation is the only option available.
| 1. | Michie CA, Hayhurst M, Knobel GJ, Stokol JM, Hensley B. Poisoning with traditional remedy containing potassium dichromate. Hum Exp Toxicol 1991;10:129-31.  [PUBMED] |
| 2. | Chemicals-chromium. In: Ellenhorn MJ, Schonwald S, Ordog G, Wasserberger J, eitors. Ellenhorn's Medical toxicology: Diagnosis and treatment of Human Poisoning. 2nd edn. Baltimore: Williams and Wilkins; 1997:1551-3. |
| 3. | Kolacinski Z, Kostrzewski P, Kruszewska S, Razniewska G, Mielczarska J. Acute potassium dichromate poisoning: a toxicokinetic case study. J Toxicol Clin Toxicol. 1999;37:785-91. [PUBMED] |
| 4. | Bradberry SM, Vale JA. Therapeutic review: is ascorbic acid of value in chromium poisoning and chromium dermatitis? J Toxicol Clin Toxicol 1999;37:195-200. [PUBMED] |
| 5. | Iserson KV, Banner W, Froede RC, Derrick MR. Failure of dialysis therapy in potassium dichromate poisoning. J Emerg Med 1983;1:143-9. [PUBMED] |
| 6. | Stift A, Friedl J, Langle F, Berlakovich G, Steininger R, Muhlbacher F. Successful treatment of a patient suffering from severe acute potassium dichromate poisoning with liver transplantation. Transplantation 2000;69:2454-5. [PUBMED] |
 |
 |
|
|
|
|
