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Hemoglobin (Hb) Chile, a variant of Hb M, is produced by a point mutation of CTG→ATG on codon 29 (legacy codon 28) of the Hb ß locus gene, which results in an amino acid substitution of Leu→Met. It has been identified in two families worldwide and is inherited in an autosomal dominant manner. Here, we report a case of Hb Chile in which a de novo mutation was detected in the proband. A 17-year-old male presented to the outpatient clinic with a pale appearance. There was cyanosis on his lips and fingers. Blood tests indicated the existence of hemolysis, but complete blood counts revealed no anemia. Peripheral arterial oxygen saturation on pulse oximetry was 80% on room air and did not improve with oxygen supplementation. The level of methemoglobin was 15.4%. Targeted next-generation sequencing identified a heterozygous NM_000518.4(HBB):c.85C > A mutation, indicating Hb Chile. The Hb Chile mutation, on the other hand, was not discovered in his parents, implying that it arose as a result of a de novo mutation. This case highlights the necessity of suspecting Hb gene mutations in patients with unexplained chronic methemoglobinemia, even if there is no family history.

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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.

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Resumen La metahemoglobinemia ocasionalmente causa cianosis, particularmente cuando es congénita. Debido a sus vías enzimáticas deficientes y a la disminución de la capacidad de transporte de oxígeno, para los pacientes con metahemoglobinemia congénita es importante evitar la exposición a agentes oxidantes. A continuación, presentamos un paciente pediátrico con metahemoglobinemia congénita no diagnosticada preoperatoriamente que fue sometido a cateterismo con diagnóstico probable de hipertensión pulmonar bajo anestesia general. El paciente pediátrico era un niño de 10 años que presentaba una lectura de oximetría de pulso (SpO2) 92% antes de la inducción de la anestesia. La metahemoglobinemia se sospechó intraoperatoriamente por primera vez debido a un desajuste de la SpO2 de la oximetría de pulso digital y la SaO2 (saturación arterial de oxígeno), y luego se confirmó mediante múltiples longitudes de onda con la CO-oximetría. Se discuten la fisiopatología, etiología, manifestaciones clínicas, consideraciones anestésicas y opciones de tratamiento de la metahemoglobinemia.

Abstract Methemoglobinemia occasionally causes cyanosis particularly in congenital methemoglobinemia. Avoidance of exposure to oxidizing agents is important for patients with congenital methemoglobinemia because of their deficient enzymatic pathways and decreased oxygen-carrying capacity. Here, we present a pediatric patient with preoperatively undiagnosed congenital methemoglobinemia who underwent catheterization with probably diagnosis of pulmonar hypertension under general anesthesia. The pediatric patient was a 10-year-old who displayed a low pulse oximetry reading of 92% prior to induction of anesthesia. Methemoglobinemia was first suspected intraoperatively because of a mismatch of SpO2 of finger pulse oximetry and SaO2 of arterial blood, and was later confirmed by multiplewavelength CO-oximetry. The pathophysiology, etiology, clinical manifestations, anesthetic considerations, and treatment options of methemoglobinemia are discussed.

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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.

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.

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BACKGROUND: Hemoglobin (Hb) Chile [ß28(B10) Leu > Met; HBB: c.85 C > A] is a rare hemoglobin variant caused by a missense mutation in the HBB gene. Only one case of Hb Chile has been reported worldwide so far. It is an unstable hemoglobin, characterized by cyanosis associated with chronic methemoglobinemia and hemolytic anemia induced by sulfonamides or methylene blue. CASE PRESENTATION: A 9-year-3-month-old girl had mild anemia of unknown etiology for more than 6 years. She had a slight pallor without other symptoms or signs. The complete blood count revealed normocytic normochromic anemia with a sometimes-elevated reticulocyte count, and the bone marrow cytology showed marked erythroid hyperplasia, but the tests related to hemolysis were normal. Therefore, the whole exome sequencing was performed and showed a heterozygous mutation for HBB: c.85 C > A. With asymptomatic methemoglobinemia confirmed later, she was eventually diagnosed with Hb Chile. CONCLUSIONS: This is the first report of Hb Chile in China and the second worldwide. This case shows that Hb Chile is clinically heterogeneous and difficult to diagnose and expands our understanding on the clinical and hematological traits of the disease.

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INTRODUCTION: Hemodialysis uses municipal water that must be strictly purified and sterilized to be used for that procedure. Large amounts of decontaminants are often used, such as chlorine, and if these compounds are not subsequently removed they can be transferred to the blood of patients causing complications including methemoglobinemia. METHODS: In this case series study, dialysis patients in one unit were evaluated. We reviewed clinical characteristics and laboratory findings obtained on the day when the water supply was disinfected with chlorine, with the aim to quantify methemoglobin concentrations. Our objective was to characterize the clinical presentation and management of patients who presented with methemoglobinemia on a specific index day. We also reviewed reported cases in the literature regarding this underreported complication. RESULTS: Eight patients who presented with chlorine intoxication were evaluated. The methemoglobin concentrations were between 1.3% and 7.9% (reference value 0-1%). We believe this to be caused by water containing 0.78 mg/L of total chlorine. Seven patients presented with cyanosis, 4 with dizziness, 6 with dark brown blood, 4 with dyspnea, and 4 with headache and hemolytic anemia. Subjects were treated with supplemental oxygen, methylene blue, intravenous vitamin C, blood transfusions, and increased doses of erythropoietin. No patient died, and all continued with their usual hemodialysis sessions. CONCLUSION: Acute chlorine intoxication transferred by the water used during hemodialysis sessions can present with methemoglobinemia accompanied by cyanosis, oxygen desaturation, and hemolytic anemia. Chlorine levels should be carefully monitored in the water used for hemodialysis treatment.

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Las intoxicaciones por herbicidas propanil son frecuentes en las diferentes áreas agrícolas, sobre todo en los campos de cultivos de arroz. Se presenta el caso de un paciente agricultor, sin factores de riesgo, quien sufrió una intoxicación moderada por propanil. Pese a las limitaciones diagnósticas en cada centro hospitalario, la sospecha y los datos clínicos al ingreso pueden ser suficientes para la elaboración diagnóstica y su respectivo manejo.

Poisoning by propanil herbicides are common in different agricultural areas, especially in rice fields. We present the case of a farmer patient, without risk factors, who suffered a moderate intoxication by propanil. Despite the diagnostic limitations in each hospital, the suspicion and clinical data on admission may be sufficient for the diagnosis and its respective management.

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Cyanosis is typically a sign of a potentially life-threatening condition in the emergency department and requires immediate workup and treatment. This case report highlights the diagnostic reasoning and clinical approach to cocaine- and volatile nitrite-induced methemoglobinemia (MHG). MHG is a rare, life-threatening cause of cyanosis. The diagnosis must be suspected in the emergency department in the presence of hypoxia and cyanosis disproportionate to cardiopulmonary repercussions and refractory to oxygen supplementation. Acquired causes are more prevalent than genetics, and recreational drugs should be highly suspected. Despite the rarity of this situation, cyanosis precipitants and the specificities of each hemoglobinopathy are reviewed in this article.

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Introducción: La metahemoglobina es una forma de hemoglobina en la que el grupo hemo, usualmente en forma ferrosa, es oxidado a forma férrica, lo que afecta el transporte de oxígeno. El incremento por encima de los valores de referencia se denomina metahemoglobinemia. Objetivo: Actualizar conceptos como prevención, manifestaciones clínicas, diagnóstico de laboratorio y tratamiento de elección de esta enfermedad, con la información disponible de la última década. Métodos: Se realizó una revisión de la literatura en inglés y español, a través del sitio web PubMed, el motor de búsqueda Google académico y Scielo, de artículos publicados en los últimos 10 años. Los términos de búsqueda usados incluyeron metahemoglobinemia, déficit de citocromo b5 reductasa, cianosis y cooximetría. Análisis y síntesis de la información: La metahemoglobinemia se puede clasificar en congénita y adquirida, esta última es la más frecuente. Es importante el diagnóstico de esta enfermedad que aunque es un padecimiento poco común, puede cursar con complicaciones graves e incluso la muerte. Puede ser evitable con diagnóstico temprano y tratamiento oportuno para reducir las complicaciones asociadas a este cuadro. Conclusiones: El diagnóstico y el tratamiento, profiláctico y terapéutico de la metahemoglobinemia en su etapa aguda o de mantenimiento, requieren la adecuada actualización del profesional de la salud(AU)

Introduction: Methemoglobin is a form of hemoglobin in which the heme group, usually in the ferrous form, is oxidized to the ferric form, which affects oxygen transport. The increase above the reference values ​​is called methemoglobinemia. Objective: To update concepts such as prevention, clinical manifestations, laboratory diagnosis and treatment of choice for this disease, with the information available from the last decade. Methods: A review of the literature in English and Spanish was carried out, through the PubMed website, the academic Google search engine and Scielo database, of articles published in the last 10 years. Search terms used included methemoglobinemia, cytochrome b5 reductase deficiency, cyanosis, and co-oximetry. Analysis and synthesis of information: Methemoglobinemia can be classified into congenital and acquired, the latter being the most common. It is important to diagnose this disease, which, although it is a rare condition, can cause serious complications, and even death, which are avoidable with early diagnosis and timely treatment that reduce the complications associated with this condition. Conclusions: The diagnosis and treatment, prophylactic and therapeutic, of methemoglobinemia, in its acute or maintenance stage, require adequate updating of the health professional(AU)

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BACKGROUND: The optimum second-line treatment or best sequence of treatments for immune thrombocytopenia (ITP) are yet to be determined. Our institution has accumulated extensive experience regarding the use of dapsone as second-line therapy for ITP. OBJECTIVES: We aimed to assess the efficacy rate and safety of dapsone treatment in ITP patients. PATIENTS/METHODS: Here we report our experience in a retrospective study, including 122 patients, with a median treatment duration with dapsone of 6 months and a median follow-up period of 3.4 years. RESULTS: The overall response rate in this cohort was 66%, including 24% of complete responses. Among responders, in 24% a relapse occurred while on treatment. Therefore, a sustained response was observed in 51% of patients. Interestingly, 81% of the responders maintained the response after the interruption of treatment, for a median time of 26 months. Side effects were reported in 16% of the patients in this cohort and treatment was interrupted due to side effects in 11% of patients. The main cause in these cases was hemolytic anemia and methemoglobinemia. Reductions in hemoglobin levels during the use of dapsone were seen in 94% of the patients. Responders presented significantly greater reductions in their hemoglobin levels than nonresponders did: median hemoglobin drop of 1.9 g/dl vs. 1.2 g/dl (p = .004). CONCLUSIONS: Our findings suggest that dapsone has adequate efficacy and is well tolerated. Although the mechanism of action is still unclear, our observation that the degree in the drop of hemoglobin is greater in responders suggest a possible role of the blockage of the reticuloendothelial system in the therapeutic effect of the drug.

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We report a second case of methemoglobinemia and non-autoimmune hemolytic anemia after contracting the SARS-CoV-2 infection in the absence of an identifiable eliciting drug. A 35-year old male without previous known comorbidities was admitted after he was diagnosed with the COVID-19 infection and had large pulmonary involvement. Seven days later, he desaturated but was without any signs of respiratory distress. A check of arterial blood gas revealed normal partial pressure of oxygen and follow-up tests confirmed a methemoglobinemia diagnosis. Over the next few days, hemolysis was established after decreased levels of hemoglobin and increased levels of indirect bilirubin and lactate dehydrogenase. A hemolytic anemia investigation panel came back normal, including G6PD. A second G6PD test was ordered at the 5-month follow-up appointment and revealed decreased levels. Clinicians should thus be aware of possible false negative tests when testing for G6PD during hemolytic crisis. In addition, whether the COVID-19 infection alone would be responsible for this chain of events remains a challenging question.

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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.

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El nitrito de amilo, conocida como "poppers", se ha masificado como droga recreacional en parte por sus efectos con objetivos sexuales. Su consumo se asocia a complicaciones psiquiátricas y médicas. Reportamos el caso de un paciente que se presenta con metahemog-lobinemia moderada secundaria a la inhalación de nitrito de amilo asociado a alcohol. Al ingreso presenta cianosis peribucal y en extremidades, disociación entre oximetría de pulso y presión parcial de oxígeno en gases arteriales, además de metahemoglobinemia 29,9%. Se descartan otras intoxicaciones y causas primarias de metahemoglobinemia. Se maneja con oxigenoterapia, hidratación y ácido ascórbico, presentando una evolución favorable. Presentamos el primer caso en Chile de metahemoglobinemia secundaria al consumo de nitrito de amilo con fines recreativos.

Amyl nitrite, known as "poppers", has become popular as a recreational drug for sexual purposes. Its consumption is associated with psychiatric and medical complications. We report the case of a patient presenting with moderate methemoglobinemia secondary to amyl nitrite inhalation associated with alcohol. At admission, perioral and extremities cyanosis, a dissociation between pulse oximetry and partial pressure of oxygen in arterial gases, and methemoglobinemia 29.9% were present. Other intoxications and primary causes of methemoglobinemia were ruled out. The patient receives oxygen therapy, hydration, and ascorbic acid, presenting a favorable evolution. We report the first Chilean's case of methemoglobinemia secondary to amyl nitrite consumption for recreational purposes

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Ochronosis is the blue-gray discoloration of collagen-containing tissues due to homogentisic acid (HGA) deposition, secondary to endogenous alkaptonuria or exogenous enzyme inhibition. In renal disease, accumulation of HGA in serum can cause methemoglobinemia. A 60-year-old woman with renal disease and anemia presented with 3 days of weakness and months of gray skin discoloration. Her hemoglobin was 8.1g/dl with 24.5% methemoglobin. Despite treatment with methylene blue, exchange transfusion, and continuous renal replacement therapy, the patient died. Autopsy revealed gray discoloration and ochronotic pigment in the ribs and cartilage. Based on these findings, the patient was diagnosed with ochronosis, suggestive of alkaptonuria, complicated by methemoglobinemia. The differential diagnosis for blue-gray skin discoloration includes argyria, methemoglobinemia, and ochronosis. This patient's clinical and autopsy findings suggested alkaptonuria complicated by methemoglobinemia due to progressive renal dysfunction. Development of methemoglobinemia in the setting of chronic skin discoloration and renal failure should prompt consideration of alkaptonuria.

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Three outbreaks of poisoning by Portulaca oleracea were reported in sheep and goats in Northeast Brazil. In the first outbreak, 8 out of 20 sheep were affected and later died. In the second outbreak, three goats and one sheep died out of a flock of 30 animals that included both species. In the third outbreak, two out of 19 sheep were affected, and they recovered after a treatment of 2% methylene blue at a dose of 4 mg/kg body weight. In the first and second outbreaks, the animals ingested P. oleracea after it was cut and offered in feeders. In the third outbreak, the flock was grazing in an area that had been invaded by the plant. To determine the toxicity, P. oleracea was administered experimentally at a dose of 80g/kg of body weight to seven sheep, weighing 19-30 kg. One control sheep received green grass. One to four hours after P. oleracea ingestion, the animals showed clinical signs of poisoning characterized by cyanotic mucous membranes, bloat, ruminal pH of 8-9, pollakiuria, aerophagia, involuntary movements of the upper lip, apathy, tachypnea and tachycardia. Five animals recovered, including one that was treated with 1% methylene blue, and two animals died. During necropsy, the mucous membranes were brownish, and the blood was dark brown. Diphenylamine tests of the plant and of rumen contents were positive for nitrates. Positive results for nitrates were also found in 24 samples of P. oleracea that were collected in different places in the states of Pernambuco and Paraíba. We conclude that P. oleracea accumulates nitrates at toxic levels and may cause poisoning in sheep and goats.(AU)

Relatam-se três surtos de intoxicação por Portulaca oleracea em ovinos e caprinos no Nordeste do Brasil. No primeiro surto morreram oito de 20 ovinos. No segundo morreram três caprinos e um ovino de um total de 30 animais das duas espécies. No terceiro surto foram afetadas duas ovelhas de um rebanho de 19 animais, que se recuperaram após o tratamento com azul de metileno a 2% na dose de 4 mg/kg/vivo. Nos surtos 1 e 2 os animais ingeriram P. oleracea cortada e oferecida no coxo e no surto 3 estavam pastoreando em uma área invadida pela planta. Para determinar a toxicidade de P. oleracea foram utilizados oitos ovinos, sendo sete experimentais e um controle, com peso entre 19 e 30 kg. A planta foi administrada por via oral, na dose de 80 g/kg/peso corporal. O animal controle recebeu capim verde e concentrado. Entre uma a quatro horas após a ingestão da planta os animais apresentaram sinais clínicos caracterizados por mucosas cianóticas, timpanismo gasoso, pH ruminal de 8-9, polaquiúria, aerofagia, movimentos involuntários do lábio superior, apatia, taquipnéia e taquicardia. Cinco animais se recuperaram, incluindo um que foi tratado com azul de metileno a 2%, e dois morreram. Na necropsia observaram-se mucosas de coloração marrom e sangue marrom escuro. O teste de difenilamina realizado na planta e no conteúdo ruminal foi positivo para nitratos. Resultados positivos para nitratos foram detectados em 24 amostras coletadas em diferentes locais dos estados de Pernambuco e Paraíba. Conclui-se que P. oleracea acumula nitratos em níveis tóxicos, e quando ingerida por ovinos e caprinos pode provocar intoxicação e morte.(AU)

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Three outbreaks of poisoning by Portulaca oleracea were reported in sheep and goats in Northeast Brazil. In the first outbreak, 8 out of 20 sheep were affected and later died. In the second outbreak, three goats and one sheep died out of a flock of 30 animals that included both species. In the third outbreak, two out of 19 sheep were affected, and they recovered after a treatment of 2% methylene blue at a dose of 4 mg/kg body weight. In the first and second outbreaks, the animals ingested P. oleracea after it was cut and offered in feeders. In the third outbreak, the flock was grazing in an area that had been invaded by the plant. To determine the toxicity, P. oleracea was administered experimentally at a dose of 80g/kg of body weight to seven sheep, weighing 19-30 kg. One control sheep received green grass. One to four hours after P. oleracea ingestion, the animals showed clinical signs of poisoning characterized by cyanotic mucous membranes, bloat, ruminal pH of 8-9, pollakiuria, aerophagia, involuntary movements of the upper lip, apathy, tachypnea and tachycardia. Five animals recovered, including one that was treated with 1% methylene blue, and two animals died. During necropsy, the mucous membranes were brownish, and the blood was dark brown. Diphenylamine tests of the plant and of rumen contents were positive for nitrates. Positive results for nitrates were also found in 24 samples of P. oleracea that were collected in different places in the states of Pernambuco and Paraíba. We conclude that P. oleracea accumulates nitrates at toxic levels and may cause poisoning in sheep and goats.(AU)

Relatam-se três surtos de intoxicação por Portulaca oleracea em ovinos e caprinos no Nordeste do Brasil. No primeiro surto morreram oito de 20 ovinos. No segundo morreram três caprinos e um ovino de um total de 30 animais das duas espécies. No terceiro surto foram afetadas duas ovelhas de um rebanho de 19 animais, que se recuperaram após o tratamento com azul de metileno a 2% na dose de 4 mg/kg/vivo. Nos surtos 1 e 2 os animais ingeriram P. oleracea cortada e oferecida no coxo e no surto 3 estavam pastoreando em uma área invadida pela planta. Para determinar a toxicidade de P. oleracea foram utilizados oitos ovinos, sendo sete experimentais e um controle, com peso entre 19 e 30 kg. A planta foi administrada por via oral, na dose de 80 g/kg/peso corporal. O animal controle recebeu capim verde e concentrado. Entre uma a quatro horas após a ingestão da planta os animais apresentaram sinais clínicos caracterizados por mucosas cianóticas, timpanismo gasoso, pH ruminal de 8-9, polaquiúria, aerofagia, movimentos involuntários do lábio superior, apatia, taquipnéia e taquicardia. Cinco animais se recuperaram, incluindo um que foi tratado com azul de metileno a 2%, e dois morreram. Na necropsia observaram-se mucosas de coloração marrom e sangue marrom escuro. O teste de difenilamina realizado na planta e no conteúdo ruminal foi positivo para nitratos. Resultados positivos para nitratos foram detectados em 24 amostras coletadas em diferentes locais dos estados de Pernambuco e Paraíba. Conclui-se que P. oleracea acumula nitratos em níveis tóxicos, e quando ingerida por ovinos e caprinos pode provocar intoxicação e morte.(AU)

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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.

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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.

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.

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La cianosis es la coloración azulada de la piel y las mucosas debida al aumento de la concentración de hemoglobina reducida en los capilares o a la presencia de metahemoglobina en concentraciones mayores de las normales. Es importante pensar en metahemoglobinemia como diagnóstico diferencial frente a un paciente con cianosis que no responde a la administración de oxígeno cuando no existen causas cardiorrespiratorias que la justifiquen, dado que requiere de otros métodos diagnósticos y de tratamiento específico. Se presenta el caso de un paciente adolescente de 14 años de edad con cianosis secundaria a metahemoglobinemia de probable etiología congénita. Se discuten las causas, forma de presentación, diagnóstico y tratamiento.

The bluish coloration of skin and mucous membranes, called as cyanosis, could be explained by high reduced hemoglobin in the capillaries, or the presence of elevated methemoglobin concentration. It is important to think of methemoglobinemia as a differential diagnosis in a cyanotic patient who does not respond to oxygen administration once cardiorespiratory causes are discarded; since it requires other diagnostic methods and specific treatment. We described a case of cyanosis in a fourteen-year-old adolescent with probable congenital methemoglobinemia. We discussed their probable causes, clinic presentation, diagnosis and treatment.

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