Metahemoglobinemia y hemólisis intravascular aguda después de una intoxicación por naftaleno en un paciente pediátrico / Methemoglobinemia and acute intravascular hemolysis after naphthalene poisoning in a pediatric patient

La intoxicación por naftaleno es poco frecuente en los niños. Es causada por la ingesta, la inhalación o el contacto con la piel de sustancias que contienen naftaleno. Los pacientes suelen tener orina de color marrón oscuro, diarrea acuosa y vómito bilioso. Los signos incluyen fiebre, taquicardia, hipotensión y valores bajos en la oximetría de pulso, incluso con oxigenoterapia. Los análisis de sangre detectan anemia hemolítica, metahemoglobinemia, insuficiencia renal e hiperbilirrubinemia. Además del tratamiento sintomático, se hacen transfusiones de eritrocitos y se les administran ácido ascórbico, azul de metileno y N-acetilcisteína. En este artículo, presentamos el caso de un paciente masculino de 23 meses de edad con metahemoglobinemia y hemólisis intravascular aguda que recibió atención en la unidad de cuidados intensivos durante cinco días por intoxicación por naftaleno. Si bien la intoxicación por naftaleno es muy poco frecuente, tiene consecuencias mortales y se debe ejercer precaución con su uso y venta.

Poisoning by naphthalene is uncommon in children. It is a type of poisoning brought on by ingesting, inhaling, or coming into touch with naphthalene-containing substances on the skin. Patients typically present with an initial onset of dark brown urine, watery diarrhea, and bile vomit. The signs include fever, tachycardia, hypotension, and low pulse oximetry readings even with oxygen support. Hemolytic anemia, methemoglobinemia, renal failure, and hyperbilirubinemia are all detected in blood tests. Erythrocyte transfusion, ascorbic acid, methylene blue, and N-acetylcysteine (NAC) therapies are provided to inpatients in addition to symptomatic treatment. We present a 23-month-old male patient who developed methemoglobinemia and acute intravascular hemolysis, who was followed up in the intensive care unit for five days due to naphthalene intoxication. Although naphthalene poisoning is very rare, it should be known that it has fatal consequences, and more care should be taken in its use and sale.

Sulfohemoglobinemia secundaria a zopiclona. Casos clínicos / Sulfhemoglobinemia secondary to the use of zopiclone. Report of two cases

Sulfhemoglobin (SulfHb) is formed by hemoglobin (Hb) oxidation by sulfur compounds. Sulfhemoglobinemia is mainly associated with drugs or intestinal bacterial overgrowth. Patients present with central cyanosis, an abnormal pulse oximetry and normal arterial oxygen partial pressure. These features are shared with methemoglobinemia (MetHb) whose diagnosis requires an arterial co-oximetry. Depending on the device used, SulfHb may produce interference with this technique. We report two females aged 31 and 43 years, consulting at the emergency room with cyanosis. Both had a history of acute and chronic, high dose zopiclone ingestion. Pulse oximetry showed desaturation but with normal arterial oxygen partial pressure. Cardiac and pulmonary diseases were ruled out. Co-oximetry in two different analyzers showed interference or normal MetHb percentages. No other complications ensued, and cyanosis decreased over days. Since MetHb was discarded among other causes of cyanosis in a compatible clinical context, the diagnosis of sulfhemoglobinemia was made. The confirmatory method is not available in Chile. The presence of SulfHb is difficult to diagnose, confirmatory tests are not readily available, and it frequently interferes with arterial co-oximetry. This is attributed to a similar absorbance peak of both pigments in arterial blood. Venous co-oximetry can be useful in this context. SulfHb is a self-limited condition in most cases, however it must be differentiated from methemoglobinemia to avoid inappropriate treatments like methylene blue.

Metahemoglobinemia, una entidad de diagnóstico complejo. Reporte de un caso

Methemoglobinemia is a rare condition with serious consequences if not diagnosed. We report the case of a 64-year-old woman with a history of allergy to sulfa drugs and a recent diagnosis of a small vessel vasculitis (ANCA-p) who started induction therapy with corticosteroids and rituximab. Due to the need for infectious prophylaxis, and considering her history, dapsone was administered instead of cotrimoxazole after ruling out glucose-6-phosphate dehydrogenase deficiency. During the admission to the hospital for her second dose of rituximab, and while being asymptomatic, she persistently presented a pulse oximetry ≪ 90% despite the administration of O2. Therefore, the infusion was postponed to study the patient. The arterial gasometric study by direct potentiometry revealed an O2 saturation of 98%, with a saturation gap > 5%. Considering the use of dapsone, a methemoglobinemia was suspected and confirmed by co-oximetry (methemoglobinemia 9%). Dapsone was suspended and one week later, her methemoglobinemia was absent.

Metahemoglobinemia inducida por dapsona: presentación de un caso pediátrico / Methemoglobinemia due to Dapsone: a pediatric case report

La metahemoglobinemia es una patología caracterizada por la presencia de altas concentraciones de metahemoglobina en sangre. Esta es una forma oxidada de la hemoglobina, muy afín al oxígeno, que es incapaz de cederlo a los tejidos. Es una entidad poco frecuente, con baja sospecha diagnóstica. Aunque puede ser congénita en recién nacidos con cianosis, es más frecuente la adquirida por fármacos y tóxicos. En la Argentina, no se conoce la incidencia real de esta patología. El objetivo es comunicar un caso de metahemoglobinemia en una paciente pediátrica que ingresó al Hospital Magdalena V. de Martínez con cianosis en la cara y las extremidades, en mal estado general, con el antecedente de ingesta de varios comprimidos de dapsona, y se constató concentración sérica de metahemoglobina del 35%. El tratamiento consistió en la administración endovenosa de azul de metileno. Su evolución fue favorable.

Methemoglobinemia is a condition characterized by a high blood concentration of methemoglobin. Methemoglobinemia is a disorder that occurs when hemoglobin in the blood is oxidized to form methemoglobin, rendering it unable to transport oxygen. Although it can be congenital in cyanotic newborn, it is more often an adverse medication effect. The aim is to report a pediatric methemoglobinemia case, assisted in Magdalena V. de Martínez Hospital, with cyanosis in face and limb, in poor condition, that consumed dapsone accidentally. Her methemoglobin concentration was 35%. Intravenous methylene blue was administered with favorable outcome.

Metahemoglobinemia adquirida inducida por fármacos antipalúdicos / Acquired methemoglobinemia induced by antymalaric drugs

Clásicamente se describe cianosis como niveles de hemoglobina desoxigenada en sangre periférica por encima de 5g/dl; sin embargo se ha dejado a un lado, que dicha expresión clínica no sólo responde a esta condición, sino también a la acumulación distal de pigmentos anómalos producto de la alteración en la morfología habitual de la molécula de hemglobina o el estado químico de ésta. Por tal motivo, se presenta un interesante caso clínico en paciente masculino de 35 años de edad, quien consulta por cuadro febril agudo y diagnóstico de Paludismo por Plasmodium vivax, iniciando tratamiento antipalúdico. Posteriormente presenta, en ausencia de fiebre, cianosis peribucal y acral acompañada de disminución de la saturación a 83% por oximetría de pulso. El diagnóstico se basó en la evidencia clínica y la oximetría de pulso, el manejo terapéutico consistió en la administración de oxígeno húmedo y bolos de azul de metileno, notando franca mejoría clínica(AU)

Methemoglobinemia has traditionally been described in multiple studies. Cyanosis, and deoxygenated hemoglobin levels in peripheral blood above 5g / dL, not only responds to this condition, but also to the distal accumulation of anomalous pigments as products of an alteration in the normal morphology of the haemoglobin molecule or chemical state of this. An interesting case report is presented in a male, who after the diagnosis of Plasmodium Vivax Malaria and malaria treatment presenteded perioral the and distal cyanosis, as well as desaturation of 83% by oximetry. The diagnosis was based on clinical evidence and pulse oximetry, and therapeutic approach was based on the administration of wet oxygen and methylene blue bowling, showing marked clinical improvement(AU)

Metemoglobinemia em pacientes com malária por Plasmodium vivax em uso oral de primaquina / Methemoglobinemia in patients with Plasmodium vivax receiving oral therapy with primaquine

INTRODUÇÃO: A primaquina pode acarretar sérios eventos adversos, com destaque para a toxicidade ao sangue. O objetivo deste trabalho é determinar a metemoglobinemia de 20 pacientes com malária por Plasmodium vivax tratados com primaquina, comparando-os segundo o sexo e a expressão da glicose-6-fosfato desidrogenase. MÉTODOS: Quantificação da metemoglobina por espectrofotometria visível e avaliação qualitativa da glicose-6-fosfato desidrogenase. RESULTADOS: A metemoglobinemia variou de 2,85 a 5,45 por cento nos pacientes do sexo masculino e de 3,77 a 7,34 por cento no feminino. CONCLUSÕES: A instituição da terapia aumentou de maneira significativa os teores de metemoglobina, sem manifestação clínica evidente e independente do sexo e da atividade enzimática.

INTRODUCTION: Primaquine can produce adverse reactions as toxicity to blood when used in the treatment of vivax malaria. This work aimed to determine methemoglobinemia in patients with vivax malaria receiving oral therapy with primaquine. METHODS: Spectrophotometric quantification of methemoglobinemia and qualitative assay for glucose-6-phosphate dehydrogenase. RESULTS: Methemoglobinemia ranged from 2.85 to 5.45 percent in male patients and 3.77 to 7.34 percent in female patients. CONCLUSIONS: A statistically significant increase in methemoglobinemia was observed following oral therapy with primaquine, with no clinical manifestations, and independent of sex and the qualitative expression of glucose-6-phosphate dehydrogenase.

Methemoglobinemia and dapsone levels in patients with leprosy

The objective of this work was to determine the methemoglobinemia and correlate with dapsone levels in multibacillary leprosy patients under leprosy multi-drug therapy. Thirty patients with laboratory and clinical diagnosis of multibacillary leprosy were enrolled. Dapsone was analyzed by high performance liquid chromatography and methemoglobinemia by spectrophotometry. The mean dapsone concentrations in male was 1.42 g/mL and in female was 2.42 g/mL. The mean methemoglobin levels in male was 3.09 µg/mL; 191 percent, and in female was 2.84 ± 1.67 percent. No correlations were seen between dapsone levels and methemoglobin in male and female patients. Our results demonstrated that the dosage of dapsone in leprosy treatment does not promote a significant methemoglobinemia.

Thinner intoxication manifesting as methemoglobinemia.

Lacquer thinner, commonly used for removing household paints is known to contain mixture of various arometic hydrocarbons; halogenated hydrocarbons and naptha, if ingested may rarely cause methemoglobinemia. We report a 3 year old child who presented to us with history of accidental ingestion of thinner, used for removing household paint. Child was having cyanosis with minimal tachypnoea & the colour of his blood was chocolate brown. Later methemoglibulin level estimations were also done, which were suggestive of this diagnosis. Child was managed conservatively with oxygen therapy & vital monitoring, which lead to complete recovery and discharge from hospital later.

Metoclopramid methemoglobinemia: a rare cause of neonatal cyanosis

The authors report three cases of methemoglobinemia diagnosed in premature. The new-borns presented isolated cyanosis. All explorations were normal. Diagnosis of methemoglobinemia was confirmed by a high blood rate of methemoglobin. Over dose of metoclopramid related to an error of its administration was noted. The authors recall physio-pathology, diagnosis, causes and treatment of acquired methemoglobinemia, while insisting on necessity of primary prevention

Dapsone induced methemoglobinemia : Intermittent vs continuous intravenous methylene blue therapy.

OBJECTIVE: The study compares the decline in blood methemoglobin (MetHb) level in children of dapsone intoxication treated with intermittent and continuous methylene blue therapy. METHODS: Eleven children with history of accidental dapsone ingestion and suggestive clinical features of dapsone intoxication were studied. Patients were randomized into two groups: Gr I (n=5) received intermittent methylene blue therapy, while Gr II (N=6) as continuous infusion. The dose of methylene blue was same in both groups. MetHb level in blood was assessed by spectrophotometer at admission and thereafter 12hrly up to 72 hrs. The decline in MetHb was statistically analyzed with student t-test. RESULTS: Six patients had history of seizure and altered sensorium. Severe anemia was observed in 2 patients. The mean levels of MetHb in Gr II was statistically significant after 12, 24, 36, 48 and 72 hrs of methylene blue therapy as compared to Gr I. CONCLUSION: Continuous I.V methylene blue therapy causes significant decline in MetHb level and is more effective in treatment of methemoglobinemia as compared to intermittent regimen.

Acute methemoglobinemia induced by dapsone / Metahemoglobinemia aguda induzida por dapsona: relato de caso no tratamento para hanseníase

Acute methemoglobinemia is an uncommon but potentially treatable disorder in witch patient can present with dramatic signs and symptoms. The early diagnostic and treatment are essentials to prevent this fatal medicine reaction.

Associação de metemoglobinemia e deficiência de glicose-6-fosfato desidrogenase em pacientes com malária tratados com primaquina / Association of methemoglobinemia and glucose-6-phosphate dehydrogenase deficiency in malaria patients treated with primaquine

Este estudo teve como objetivo verificar a ocorrência de metemoglobinemia em indivíduos deficientes da glicose-6-fosfato desidrogenase durante o tratamento da infecção malárica com primaquina. Foram selecionados pacientes com diagnóstico para malária por Plasmodium vivax ou mista V+F (Plasmodium vivax + Plasmodium falciparum), Grupo 1: com 74 indivíduos com diagnóstico clínico de metemoglobinemia e Grupo 2: 161 indivíduos sem diagnóstico clínico de metemoglobinemia. Quanto à deficiência da G6PD, nos Grupos 1 e 2, houveram 51,3 por cento (38) e 8,7 por cento (14) de indivíduos enzimopênicos, respectivamente, demonstrando através de tais dados, significância estatística na associação com a metemoglobinemia somente nos indivíduos do Grupo 1 (p<0,05). A comparação da relação da metemoglobinemia à deficiência da G6PD mostrou haver uma possível associação de indivíduos enzimopênicos desenvolverem metemoglobinemia com maior freqüência.

This study had the aim of investigating occurrences of methemoglobinemia among individuals with glucose-6-phosphate dehydrogenase deficiency during treatment for malaria infection using primaquine. Patients with a diagnosis of malaria caused by Plasmodium vivax or the V+F mixture (Plasmodium vivax + Plasmodium falciparum) were selected. Group 1 consisted of 74 individuals with a clinical diagnosis of methemoglobinemia and Group 2 consisted of 161 individuals without a clinical diagnosis of methemoglobinemia. The glucose-6-phosphate dehydrogenase deficiency rates (numbers of enzymopenic individuals) in Groups 1 and 2 were 51.3 percent (38) and 8.7 percent (14) respectively. These data demonstrated a statistically significant association with methemoglobinemia only among the individuals in Group 1 (p<0.05). Investigation of the relationship between methemoglobinemia and glucose-6-phosphate dehydrogenase deficiency showed that there was a possible association such that enzymopenic individuals may develop methemoglobinemia more frequently.

Hepatic and haematological adverse reactions associated with the use of multidrug therapy in leprosy--a five year retrospective study.

This study analyses retrospectively some of the risks associated with the use of WHO-multidrug therapy (MDT) in Sri Lanka. Case records of 3,333 new cases of leprosy attending the Central Leprosy Clinic in Colombo during 1991-1995, were analysed for adverse drug reactions involving the liver and blood. There were 81 reports of suspected hepatic or haematological adverse reactions associated with the use of MDT, of which 39 were classified as haemolytic anaemia, 25 as toxic hepatitis, 2 as methaemoglobinaemia and 15 as anaemia. Dapsone, was incriminated in the majority of adverse reactions (72%). Adverse drug reactions were more common in female than male subjects (55% vs 45%; P < 0.5), but there was no significant differences between the age groups. Majority of adverse reactions was seen within the first three months of initiation of MDT. This study in no way undermines the benefits of MDT but highlights the risks and suggests measures to minimize these risks.

Methaemoglobinaemia in epidemic proportions.

Five cases of methaemoglobinaemia, following exposure to industrial waste, are examined, investigated and managed successfully. The condition is discussed in detail.

Methaemoglobinaemia in areas with high nitrate concentration in drinking water.

BACKGROUND: An epidemiological investigation was undertaken in all age groups to assess the prevalence of methaemoglobinaemia in areas with high nitrate concentration in drinking water. METHODS: Five areas were selected with an average nitrate concentration (as nitrate) of 26, 45, 95, 222 and 459 mg nitrate ions/litre in drinking water. These areas were visited and the house schedule (containing name, age, sex and weight of the family members) prepared in accordance with the statistically designed protocol. In all, 178 persons, matched for age and weight, were selected and arranged in five age groups. They constituted 10% of the total population of each of these areas. A detailed history of the selected population was taken, medical examination conducted and blood samples taken to ascertain the level of methaemoglobin. The collected data were subjected to statistical analysis to ascertain a relationship between nitrate concentration and methaemoglobinaemia. RESULTS: High nitrate concentrations cause severe methaemoglobinaemia (7%-27% of Hb) in all age groups, especially in the age group of less than 1 year and above 18 years. The lower levels of methaemoglobin in the age group of 1-18 years is probably due to better reserve of cytochrome b5 reductase activity and its adaptation to increasing nitrate concentration in water to compensate for methaemoglobinaemia in this age group. CONCLUSION: We conclude that high nitrate ingestion causes methaemoglobinaemia in all age groups. Cytochrome b5 reductase activity and its adaptation with increasing water nitrate ingestion plays a role in compensating for the methaemoglobinaemia.

Methemoglobinemia in aluminium phosphide poisoning in rats.

Aluminium phosphide (AlP) a grain fumigant is the leading cause of intentional poisoning in North India. The mechanisms involved in toxicity are not known and there is no antidote till date. The present study was carried out to investigate the oxygen free radical generation, methemoglobinemia and effect of methylene blue treatment on survival time in rat model of AlP poisoning. AlP (50 mg/kg, intragastric) was administered in one group and the other group received AlP + Methylene Blue (MB) (0.1%, 1 mg/kg/5 min, i.v.). Malonyldialdehyde (MDA) and methemoglobin (MeHb) levels were measured at 10 and 30 min intervals. Blood MDA levels increased at 10 and 30 min after AlP exposure with simultaneous rise in MeHb levels suggesting methemoglobinemia could be due to increased oxygen free radical generation. Methylene blue caused a significant fall in both the parameters with prolongation of survival time. It is concluded that AlP causes methemoglobinemia responding to methylene blue treatment.

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.

A case of methemoglobinemia after ingestion of an aphrodisiac, later proven as dapsone

Methemoglobin (MetHb) is an oxidation product of hemoglobin in which the sixth coordination position of ferric iron is bound to a water molecule or to a hydroxyl group. The most common cause of acquired MetHb-emia is accidental poisoning which usually is the result of ingestion of water containing nitrates or food containing nitrite, and sometimes the inhalation or ingestion of butyl or amyl nitrite used as an aphrodisiac. We herein report a case of MetHb-emia after ingestion of an aphrodisiac, later identified as dapsone by gas chromatograph/mass selective detector (GC/MSD). A 24-year old male was admitted due to cyanosis after ingestion of a drug purchased as an aphrodisiac. On arterial blood gas analysis, pH was 7.32, PaCO2 26.8 mmHg, PaO2 75.6 mmHg, and bicarbonate 13.9 mmol/L. Initial pulse oxymetry was 89%. With 3 liter of nasal oxygen supplement, oxygen saturation was increased to 90-92%, but cyanosis did not disappear. Despite continuous supplement of oxygen, cyanosis was not improved. On the fifth hospital day, MetHb was 24.9%. Methylene blue was administered (2 mg/kg intravenously) and the patient rapidly improved. We proved the composition of aphrodisiac as dapsone by the method of GC/MSD.