Management of a patient with thermal burns and para-chloronitrobenzene poisoning.

Para-chloronitrobenzene (p-CNB), a hazardous and toxic substance, is widely used as an intermediary in chemical industries. p-CNB can cause methaemoglobinaemia due to electron-withdrawing properties of the nitro and chlorine groups. We present a case of a 23-year-old man suffering from thermal burns and p-CNB poisoning. In this case, severe methaemoglobinaemia was caused by the absorption of p-CNB through the burn wounds. Despite active treatment, such as the antidote of methylene blue, the patient's methaemoglobinaemia progressed, with slowly increasing methaemoglobin (MetHb) level. This case highlights the complexity and difficulty of managing this type of injury. To our knowledge, this case can be the first case report describing methaemoglobinaemia induced by p-CNB in a patient with thermal burns.

A fatal case of severe methaemoglobinemia due to nitrobenzene poisoning.

An acute poisoning with nitrobenzene presenting as methaemoglobinemia is an uncommon medical emergency. A young girl with nitrobenzene induced methaemoglobinaemia died despite use of mechanical ventilator, administration of oral methylene blue and parenteral ascorbic acid. Here author highlights the rare occurrence of such cases, methaemoglobin induced severe oxidative stress, unexplained splenomegaly and leucocytosis and the ineffectivity of oral methylene blue and other supportive measures in evading death due to nitrobenzene poisoning.

Acute cardiogenic pulmonary oedema with multiorgan dysfunction--still to learn more about nitrobenzene poisoning.

Nitrobenzene is a nitrite compound often used in polishes or solvents. Its toxic effects are due to its ability to induce methaemoglobinaemia. The clinical presentation of this poisoning varies according to the concentration of methaemoglobin level in blood. The importance of early identification of the compound on the basis of clinical suspicion corroborative with methaemoglobin level with timely intervention is required to prevent fatal outcome. It is also important to take care of the secondary cycling of nitrobenzene from body stores to prevent secondary recurrence of symptoms in patients after heavy exposure. Here author reports a rare case of accidental poisoning with nitrobenzene presented with respiratory distress and cyanosis. On investigation, he was diagnosed to have cardiogenic pulmonary oedema and multiorgan dysfunction. The urgent institution of methylene blue as specific antidote along with haemodynamic and ventilatory support was proved crucial for life saving of the patient.

A fatal case of severe methaemoglobinemia due to nitrobenzene poisoning.

An acute poisoning with nitrobenzene presenting as methaemoglobinemia is an uncommon medical emergency. A young girl with nitrobenzene induced methaemoglobinaemia died despite use of mechanical ventilator, administration of oral methylene blue and parenteral ascorbic acid. Here author highlights the rare occurrence of such cases, methaemoglobin induced severe oxidative stress, unexplained splenomegaly and leucocytosis and the ineffectivity of oral methylene blue and other supportive measures in evading death due to nitrobenzene poisoning.

Acute nitrobenzene poisoning with severe associated methemoglobinemia: identification in whole blood by GC-FID and GC-MS.

A rare fatal case of self-poisoning with nitrobenzene following oral ingestion is reported. On presentation to the hospital, severe methemoglobinemia (70%) was observed in an 82-year-old male who had ingested 250 mL of an unknown substance in the previous 24 h. Methylene blue and exchange transfusion were the therapeutic methods applied in the treatment of the methemoglobinemia. Forty-eight hours after ingestion, a blood sample was collected in ICU and sent to our laboratory. We detected that the blood contained 3.2 microg/mL of nitrobenzene. The determination of nitrobenzene was performed using the combination of GC-FID for screening analysis and quantitation and GC-MS for confirmation of the obtained results.

Methaemoglobinaemia in nitrobenzene poisoning--a case report.

A 24-year-old female of nitrobenzene poisoning presented with features of methaemoglobinaemia. She was treated with oral methylene blue and intravenous ascorbic acid and responded favourably from 3rd day onwards. The case is reported in details.

[The protective action of tocopherol acetate in simultaneous administration with nitrobenzene and its chloro derivatives]. / Zashchitnoe deistvie tokoferola atsetata pri odnovremennom vvedenii s nitrobenzolom i ego khlorproizvodnymi.

In experiments in albino rats, effects were studied of nitrobenzene and its chloro derivatives in intragastric administration with tocoferolum acetatum. Changes in the process of lipid peroxidation in blood serum, liver, and spleen which were characteristic of xenobiotics themselves have been shown to be less pronounced in this setting. Tocoferolum acetatum being administered at the same time is actively drawn into the metabolism. Normalization of the antioxidant activity of the tissues under investigation was to be observed, with lipid peroxidation and the antioxidant system being in equilibrium. Tocoferolum acetatum administered with xenobiotics has been shown to have a protective action. Tocoferolum acetatum is recommended to be included into diets for workers engaged in chemical industry on a prophylactic basis.

Methaemoglobinemia in nitrobenzene poisoning.

A young girl with nitrobenzene induced methaemoglobinaemia was saved by the timely use of mechanical ventilator, administration of oral methylene blue and parenteral ascorbic acid. Though parenteral methylene blue is the antidote of choice, due to its non-availability, the laboratory preparation of methylene blue have been utilized orally. The rare occurrence of such cases, and the efficacy of oral methylene blue and other supportive measures in evading death due to Nitrobenzene poisoning have been highlighted.

Pharmacokinetic study of p-chloronitrobenzene in humans suffering from acute poisoning.

The pharmacokinetics of p-chloronitrobenzene (p-CNB) in human subjects suffering from acute poisoning was studied from the urinary excretion of p-CNB metabolites. The time course for excretion of five metabolites--2-chloro-5-nitrophenol,N-acetyl-S-(4-nitrophenyl)- L-cysteine, 2,4-dichloroaniline, p-chloroaniline, and 2-amino-5-chlorophenol-were determined by reversed-phase HPLC analysis of urine collected from six subjects during their hospitalization after accidental exposure to p-CNB. The cumulative excretion amount at infinite time (X infinity) and mean residence time for each metabolite were estimated by moment analysis of excretion rate vs. the time curve. The rate constants for p-CNB metabolism were calculated by nonlinear least squares fitting of the time course data using a one-compartment model. The results indicated that the average values of the ratio of excreted amount of each metabolite to the total amount of the five metabolites (X infinity metabolite/X infinity Total) and mean residence time in the six subjects were, respectively: 12.2% and 6.7 days for 2-chloro-5-nitrophenol, 48.0% and 7.0 days for N-acetyl-S-(4-nitrophenyl)-L-cysteine, 1.2% and 3.7 days for 2,4-dichloroaniline, 29.9% and 10.0 days for p-chloroaniline, and 8.7% and 6.0 days for 2-amino-5-chlorophenol. The average values of rate constants in the metabolism of p-CNB to 2-chloro-5-nitrophenol, N-acetyl-S-(4-nitrophenyl)-L-cysteine, and p-chloroaniline were 0.021, 0.082, and 0.067 day-1, respectively. Similarly those in further metabolism of p-chloroaniline for C-chlorination, C-hydroxylation, and N-conjugation were 0.205, 1.206, and 3.526 day-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

[Effect of nitrobenzenes on methemoglobin formation and activity of antioxidative enzymes in mouse erythrocytes]. / Vliianie nitrobenzolov na metgemoglobinoobrazovanie i aktivnost' antiokislitel'nykh fermentov éritrotsitov myshi.

The mice intoxication with intraperitoneal introduction of 1,3,5-trinitrobenzene and 2,4,6-trinitrotoluene causes an increase of methemoglobin and a decrease of glutathione level. But intoxication by polynitrobenzenes exerts no effect on the total level of SH-groups. A small increase in total activity of dehydrogenases of the pentose phosphate way in response to 2,4,6-trinitrotoluene intoxication is also revealed. The level of both lipid peroxidation, superoxide dismutase and catalase activity is not influenced by 2,4,6-trinitrotoluene and 1,3,5-trinitrobenzene.

Identification of urinary metabolites of human subjects acutely poisoned by p-chloronitrobenzene.

1. Urinary metabolites from human subjects acutely poisoned with p-chloro-nitrobenzene (p-CNB) were identified by g.l.c.-mass spectrometry. 2. Eight substances, namely, a very large amount of N-acetyl-S-(4-nitrophenyl)-L-cysteine, relatively large quantities of p-chloroaniline, 2-chloro-5-nitrophenol and p-chloroformanilide produced by pyrolysis of a substance originating from p-CNB, small amounts of 2-amino-5-chlorophenol and 2,4-dichloroaniline, and traces of p-chloroacetanilide and 4-chloro-2-hydroxyacetanilide, were detected in urine samples. 3. All of the absorbed p-CNB was metabolized prior to excretion, as the parent compound was not found in urine. 4. N-Acetylated metabolites of p-chloroaniline and 2-amino-5-chlorophenol, resulting from p-CNB by metabolism, were found in only one of eight individuals indicating that this pathway is weak or may be absent in some humans. 5. A scheme for the pattern of metabolic pathways of p-CNB is proposed, and chlorination was considered to be a possible novel metabolic pathway.

[A case of methemoglobinemia due to 4-nitrobenzonitrile exposure]. / Un caso di metaemoglobinemia da esposizione a 4-nitrobenzonitrile.

The paper describes a singular case of acute intoxication by 4-nitrobenzonitrile, a rare intermediate compound produced by pharmaceutical synthesis. The patients subsequently showed an increase in triglycerides and fatty alterations of the liver.