Renal replacement therapy in acute poisonings--one center experience.

The authors described three groups of patients after acute poisonings. In the first group were 60 patients after carbon tetrachioride poisoning, the second group consisted of 81 patients after mushroom poisoning and 20 patients after ethylene glycol poisoning were in the third group. Besides two patients with rare poisonings after potassium dichromate and after paraquat poisoning were analysed. All groups of patients with the kidney damage were presented from the diagnostic, differential diagnostic, conservative, ntra- and extracorporeal elimination treatment point of view. In the group of patients suffering from acute carbon tetrachloride poisoning and with acute renal failure following therapy was used: conservative treatment, exchange blood transfusion--in 4 patients in hepatic coma, renal replacement therapy (peritoneal dialysis, haemodialysis, plasmapheresis). From the total number of 60 patients 58 survived and 2 patients died in liver coma. Survival of patients after mushroom poisoning depended on amount of oral use of mushroom (Amanita phalloides), on early admission in dialysis centre and on early beginning of renal replacement therapy within 24 hr after acute poisoning. Twenty four patients from 81 patients of this group died. Main clinical signs of ethylene glycol poisoning were various neurological symptoms (cramps, hemiparesis, coma), severe metabolic acidosis (pH = 7.06 +/- 0.14), leucocytosis (26.4 +/- 5.5x 10(9)/L) and the signs of acute toxic hepatitis and of acute renal failure. Calcium oxalic crystals in urine were present in 17 patients and leucocytosis was observed in every patient. In the first 4 patients we administered intravenously ethylalcohol as an antidotum and later in other patients we used ethylalcohol in dialysis solution. The concentration of ethylalcohol in dialysis solution was 100 mg%. Severe metabolic acidosis improved in 17 patients using bicarbonate haemodialysis and 3 patients died before the possibility to use bicarbonate haemodialysis. Eighty-four hours after acute potassium dichromate poisoning and 24 hours after exchange blood transfusion during haemodialysis a 41-year old man died in haemorhagic shock, which developed after the extensive chemical burns of mucous membrane of gastrointestinal tract caused by this poison. Our patient after paraquat poisoning was treated by repeated charcoal haemoperfusion and haemodialysis. Despite of that therapy the patient died in severe respiratory insufficiency.

The strip patch test--indication in occupational dermatology demonstrated with a case history.

In occupational dermatology, repeat patch testing is a frequent occurrence when an expert opinion is required. As a result, discrepancies in test results may affect the legal position in respect of insurance and a reduction in the level of disability. The strip patch test (SPT) supports the diagnosis of allergic contact dermatitis when a weak sensitization is present or when a weak sensitizer with poor epidermal penetration is involved leading to a false-negative patch test result. We report on a 30-year-old man working as an industrial mechanic from 1995 to 2006. After approval of an occupational disease no. 5101 of the German ordinance on industrial disease in 2007, he went to court claiming compensation. The sensitization with clinical and occupational relevance to potassium dichromate that was decisive for the evaluation for insurance purposes was first confirmed in a patch test in 2005. Succeeding tests in 2006 in the context of an expert opinion and in 2008 in the context of our decisive expert opinion remained negative. We could reconfirm the potassium dichromate sensitization only by the SPT performed in the proposed standardized manner. The potassium dichromate allergy was the determining factor in the assessment for insurance purposes. This resulted in an adjustment in the severity of disability and a pension entitlement. From this case it is obvious that the detection of a SPT-positive and patch test-negative sensitization may have a significant impact on the situation with respect to the legal and insurance position.

Time course study of oxidative and nitrosative stress and antioxidant enzymes in K2Cr2O7-induced nephrotoxicity.

BACKGROUND: Potassium dichromate (K2Cr2O7)-induced nephrotoxicity is associated with oxidative and nitrosative stress. In this study we investigated the relation between the time course of the oxidative and nitrosative stress with kidney damage and alterations in the following antioxidant enzymes: Cu, Zn superoxide dismutase (Cu, Zn-SOD), Mn-SOD, glutathione peroxidase (GPx), glutathione reductase (GR), and catalase (CAT). METHODS: Nephrotoxicity was induced in rats by a single injection of K2Cr2O7. Groups of animals were sacrificed on days 1,2,3,4,6,8,10, and 12. Nephrotoxicity was evaluated by histological studies and by measuring creatinine clearance, serum creatinine, blood urea nitrogen (BUN), and urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG) and total protein. Oxidative and nitrosative stress were measured by immunohistochemical localization of protein carbonyls and 3-nitrotyrosine, respectively. Cu, Zn-SOD, Mn-SOD, and CAT were studied by immunohistochemical localization. The activity of total SOD, CAT, GPx, and GR was also measured as well as serum and kidney content of chromium and urinary excretion of NO2 -/NO3-. Data were compared by two-way analysis of variance followed by a post hoc test. RESULTS: Serum and kidney chromium content increased reaching the highest value on day 1. Nephrotoxicity was made evident by the decrease in creatinine clearance (days 1-4) and by the increase in serum creatinine (days 1-4), BUN (days 1-6), urinary excretion of NAG (days 1-4), and total protein (day 1-6) and by the structural damage to the proximal tubules (days 1-6). Oxidative and nitrosative stress were clearly evident on days 1-8. Urinary excretion of NO2-/NO3- decreased on days 2-6. Mn-SOD and Cu, Zn-SOD, estimated by immunohistochemistry, and total SOD activity remained unchanged. Activity of GPx decreased on days 3-12 and those of GR and CAT on days 2-10. Similar findings were observed by immunohistochemistry of CAT. CONCLUSION: These data show the association between oxidative and nitrosative stress with functional and structural renal damage induced by K2Cr2O7. Renal antioxidant enzymes were regulated differentially and were not closely associated with oxidative or nitrosative stress or with kidney damage. In addition, the decrease in the urinary excretion of NO2-/NO3- was associated with the renal nitrosative stress suggesting that nitric oxide was derived to the formation of reactive nitrogen species involved in protein nitration.

Evidence of hexavalent chromium ingestion.

We describe the application of histochemical demonstration of chromium in a case of fatal ingestion of potassium dichromate in a suicide attempt. Using 2-(8-quinolylazo)-4,5-di-p-tolylimidazole (QTI), we could demonstrate chromium in the erythrocyte of the victim, in situ. This finding provides a means of proving the hexavalent chromium ingestion.

Successful treatment of a patient suffering from severe acute potassium dichromate poisoning with liver transplantation.

BACKGROUND: Oral ingestion of potassium dichromate produces a complex spectrum of complications. It has an extremely poor prognosis and usually leads to rapid death. METHODS: We report the case of a 16-year-old male patient who was admitted to hospital after oral ingestion of potassium dichromate with suicidal intention. RESULTS: The patient's condition deteriorated, and he became comatose within 5 days in spite of immediate attempts at detoxification. Because of irreversible liver failure, which occurred within 2 days after admission, and because of cerebral edema, the decision to perform a liver transplantation was made. On day 6 after admission, a compatible donor liver was transplanted. The course of liver transplantation and the patient's subsequent recovery were uneventful. CONCLUSION: The rationale for the delayed transplantation was to avoid damage of the new organ because of high serum chromium levels. Despite severe organ damage, the chromium content of the liver was increased. To the authors' knowledge, this is the first case report of acute toxic liver failure, caused by potassium dichromate poisoning, treated successfully by means of liver transplantation.

Acute potassium dichromate poisoning: a toxicokinetic case study.

CASE REPORT: A 48-year-old man drank 150 mL of an aqueous solution containing potassium dichromate 22.5 g in a suicidal attempt and was admitted 7 hours after the ingestion. Hemodialysis was promptly undertaken and chromium concentrations in serum, erythrocytes, and dialysate were determined during the treatment. Chromium elimination in urine was monitored during hemodialysis and the subsequent 400 hours. The total chromium eliminated via hemodialysis and urine was calculated as 36.7 mg or 0.16% of the ingested dose. Spontaneous urinary elimination proceeded according to an open one-compartment model. The elimination half-life was 71.37 hours +/- 17.13 hours (95% CI). Chromium elimination from serum followed an open two-compartment model, with the half-lives of 3.16 hours +/- 2.63 hours for phase 1 and 50 hours +/- 27 hours (95% CI) for phase 2. Calcium-EDTA therapy had no influence on erythrocyte, serum, or urine chromium level. It contributed, however, to a significant increase in chromium elimination rate in the dialysate. Serum zinc was very low at admission and serum zinc, copper, and magnesium were controlled during the initial 30 hours.

[Severe potassium dichromate poisoning after accidental nasal introduction]. / Intoxication grave au dichromate de potassium après introduction nasale accidentelle.

BACKGROUND: Nasal foreign body (NFB) is a common situation in pediatrics. Poisoning is a rare complication of NFB insertion. We report a case of acute potassium dichromate poisoning secondary to NFB insertion. CASE REPORT: Six days after insertion of a NFB, progressive occurrence of diarrhea, vomiting, nasal obstruction, acute renal failure, pancreatitis, hepatitis and drowsiness justified hospitalization of a 3-year-old girl in the pediatric intensive care unit. Acute potassium dichromate poisoning was confirmed by high plasma chromium level and by the spectrophotometric analysis of the crystal. Recovery was satisfactory with supportive treatment. An official survey allowed to discover that the crystal was freely sold and that its toxicity was unknown by dealers, while no information was given to the customers. CONCLUSION: Transmucosal absorption of toxics is an unusual severe potential hazard that should be evoked to allow a rapid management. After the discovery and withdrawal of a NFB, occurrence of systemic symptoms, even trivial, must make one suspect a poisoning. In this circumstance, analysis of the foreign body should be done, associated with toxicologic dosages. This case report illustrates that potassium dichromate poisoning is a severe medical condition and that its clinical presentation assume a large widespread of symptoms due to multiple organ involvement.

Níveis plasmáticos e eritrocitário de cromo após intoxicaçäo aguda por dicromato de potássio / Levels of Chromium in plasma and red blood cells after acute poisonning by postassium dichromate

Foram coletadas amostras de sangue, durante 23 dias consecutivos, e nos 26§, 29§ e 40§ dias, de um indivíduo do sexo masculino, após tentativa de suicídio, ao ingerir cerca de 10 gramas de K2 Cr2 O7. Utilizando-se EAA-Zeeman, realizaram-se as determinaçöes de cromo total e de cromo (VI), no plasma (Cr-P) e nos eritrócitos (Cr-E). Os percentuais de Cr (VI) e as relaçöes Cr-P/Cr-E permitiram obter informaçöes quanto à distribuiçäo de cromo no compartimento sangüíneo, e aos processos de reduçäo, durante intoxicaçäo aguda

[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.

Poisoning with a traditional remedy containing potassium dichromate.

A fatal case of potassium dichromate ingestion is documented. A retrospective review of serum and organ levels of chromium demonstrates that charcoal haemoperfusion, peritoneal and haemodialysis are ineffective therapies for the toxin. Other treatments for this poisoning are reviewed, the poor prognosis of dichromate ingestion, and the paucity of effective therapy underlined. The application of dichromates in traditional medications is briefly discussed; this is a toxin which may be more prevalent than previously thought. It is proposed that the exposure limits of dichromate be more widely publicised.

Acute renal failure in a child after chewing of match heads.

A few days after ingestion of 40 match heads, a 3-year-old boy was admitted to hospital with oliguric acute renal failure (ARF) requiring peritoneal dialysis during 9 days. A renal biopsy showed acute tubulointerstitial nephritis; the outcome was rapidly favorable and the child recovered normal GFR. It seems to be the first published case of ARF after match poisoning, probably because of the presence of potassium bichromate.

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.