Plasmapheresis in Severe Methemoglobinemia Following Naphthalene Ball Poisoning: A Case Report.

Naphthalene is a widely used industrial and household chemical in the form of mothballs, but it has rarely been an agent of poisoning worldwide. We describe a case of ingestional naphthalene poisoning with a good outcome after proper management. A 20-year-old boy with a history of seizure disorder and mental retardation presented with abdominal pain, vomiting, burning micturition, and blood in the urine for 2-3 days. On examination, it was found that he had ingested six to eight mothballs and presented 2 days later with hemolysis and methemoglobinemia. He was given intravenous methylene blue, N-acetylcysteine, and ascorbic acid, besides supportive treatment, but the condition did not improve. The patient then underwent plasmapheresis. After two sessions, he showed improvement in the form of decreasing hemolysis. Renal replacement therapy in the form of hemodialysis was performed. Gradually, his condition improved, and concurrent psychiatric assessment and treatment were also provided. The patient was discharged after 15 days.

Concomitant oxidative haemolysis and methaemoglobinaemia following inhaled nitric oxide in a patient with G6PD deficiency.

We report the case of a man in his 50s who developed acute respiratory distress syndrome and right heart failure, necessitating intubation and initiation of inhaled nitric oxide (iNO) to decrease right ventricular afterload and improve the right heart function. The course was complicated by acute anaemia, with a diagnostic workup revealing methaemoglobinaemia and evidence of oxidative haemolysis indicated by blister and bite cells on peripheral blood film. The patient received conservative management, including successive red blood cell transfusion and gradual iNO weaning due to suspected glucose-6-phosphate dehydrogenase (G6PD) deficiency. Discontinuation of iNO led to the resolution of both oxidative haemolysis and methaemoglobinaemia. Subsequent enzymatic assay, conducted 4 months later, confirmed G6PD deficiency. This case highlights a rare instance of concurrent methaemoglobinaemia and oxidative haemolytic anaemia following iNO in a patient with underlying G6PD deficiency.

Management of isopropyl nitrate-induced methaemoglobinaemia in pregnancy.

A pregnant female in her early 30s presented with cyanosis and oxygen saturation of 78%. She ingested isopropyl nitrate mistaking it for cannabidiol. Her arterial blood gas showed a methaemoglobin of >30% (outside the measuring range). She was treated with 120 mg of methylthioninium chloride (2 mg/kg) and symptoms improved. Her pregnancy progressed but was induced at 36 weeks because her child was small for gestational age. Methaemoglobinaemia is a rare presentation in pregnancy. There have been no reported cases of isopropyl nitrate-induced methaemoglobinaemia in pregnancy. Historically, intra-amniotic methylthioninium chloride was used in amniocentesis but use stopped after links to fetal malformations and neonatal death were made. There is no evidence outlining the risks of isopropyl nitrate in pregnancy and limited data on fetal effects from maternal exposure to intravenous methylthioninium chloride. This case adds to the evidence that treating methaemoglobinaemia may outweigh the risks of maternal exposure to methylthioninium chloride.

[Methemoglobinemia]. / Méthémoglobinémie.

Methemoglobinemia (MetHb) refers to the state of oxidation of the iron ion "ferrous" (Fe2+) to iron "ferric" (Fe3+) within the heme molecule that makes up hemoglobin (Hb). This state is physiological if its level remains controlled. The ferrous state of the heme molecule occurs in the event of significant oxidative stress. The pathophysiology of MetHb involves NADH, NADPH and glucose cycle enzymes such as cytochrome-b5-reductase. MetHb can be acquired or more rarely, congenital. Acquired causes include drug-induced effects such as topical anesthetics, or toxic effects such as nitrites. Primary causes are linked to enzyme deficiencies or constitutional Hb abnormalities. Excessively high MetHb causes symptoms of varying intensity, depending on the level of MetHb and associated comorbidities. Clinical signs are dominated by cyanosis, indicative of tissue hypoxia, which can be complicated by severe metabolic disorders leading to death. Diagnosis can be complex, as the resulting biological abnormalities may go undetected. Treatment is mainly based on identifying the etiology and restoring the heme molecule to its physiological state. Methylene blue is the main antidote in cases of elevated MetHb, but precautions must be taken in its use, and its physico-chemical effects must be understood. We provide an update on methemoglobinemia, summarizing its pathophysiology and clinical presentations, complementary tests and therapeutic principles.

Seizures and severe methaemoglobinaemia following accidental ingestion of amyl nitrite.

We present a case of a man in his late 40s presenting with generalised tonic-clonic seizures and profound methaemoglobinaemia shortly after inadvertent ingestion of amyl nitrite. Arterial blood gas analysis demonstrated methaemoglobin levels exceeding the upper detection threshold of our analyser, accompanied with profound cyanosis despite apparent oxygen saturations of 94%. Prompt administration of intravenous methylene blue led to a rapid and complete recovery. This case highlights the importance of swift recognition and treatment of methaemoglobinaemia particularly when the precipitating factor may be unknown at the time of presentation. This case also demonstrates the potential limitations of bedside blood gas analysers in diagnosis.

Acquired methemoglobinemia induced by indoxacarb poisoning: a case report.

Indoxacarb, a large-spectrum non-organophosphorus oxadiazine insecticide, is broadly used in farming whose mechanism of action is the blockage of voltage-gated sodium channels of insects. There is restricted data on human poisoning. We report a case of an 18-year-old male patient without comorbidities presented with unconsciousness and cyanosis after the intentional ingestion of indoxacarb in a suicide attempt. Methemoglobinemia was clinically suspected and was successfully treated after methylene blue injection, associated with supportive and symptomatic management. This case emphasizes the importance of considering methemoglobinemia after indoxacarb ingestion in addition to its early recognition and timely injection of methylene blue which led to complete recovery without sequelae.

A rare case of methemoglobinemia in a preterm newborn with unclear etiology.

 Cyanosis is a bluish discoloration of the tissues due to increased levels of deoxygenated hemoglobin in capillaries. It is a common finding in newborn infants that can be caused by different diseases, including pulmonary, cardiac, infectious, and hematological disorders. Methemoglobinemia is a rare cause of cyanosis, in which hemoglobin is oxidized, changing its heme iron configuration from the ferrous (Fe2 +) to the ferric (Fe3 +) state, creating methemoglobin (Met-Hb), a form that does not bind oxygen, leading to decreased oxygen delivery to the tissues and cyanosis. We report a rare case of a preterm newborn, who developed cyanosis and worsening hypoxemia on day ten of life, she was found to have elevated Met-Hb percentage in blood gas analysis that required treatment with intravenous methylene blue. Her symptoms resolved after a period of maintenance treatment with oral methylene blue and ascorbic acid, and the etiology of her disease remains unclear.

Methemoglobinemia screening and treatment in tank warfare survivors.

INTRODUCTION: Methemoglobinemia, characterized by the conversion of functional hemoglobin to methemoglobin, can significantly impede tissue oxygenation. Prompt diagnosis and treatment of methemoglobinemia are critical to optimizing clinical outcomes. Although the underlying etiology of methemoglobinemia is often attributed to a medication reaction or chemical exposure, its association with battlefield trauma remains underexplored. This case series explores the presence of methemoglobinemia in nine soldiers evacuated from tanks targeted by explosives, shedding new light on screening needs and treatment strategies. CASES DESCRIPTION: Nine combat trauma patients with methemoglobinemia were admitted to Soroka Medical Center over a two-month period. Detailed case descriptions illustrate the diverse presentations and treatment responses. Notably, the administration of methylene blue resulted in rapid methemoglobin reductions and an improvement in oxygenation without any observed side effects. DISCUSSION: This series highlights an unexpected consequence of an explosion within an armored fighting vehicle and the challenges related to standard pulse oximetry interpretation and accuracy in the presence of methemoglobinemia, emphasizing the need for vigilant monitoring and co-oximetry utilization. Additionally, the coexistence of carboxyhemoglobin further warrants attention due to its synergistic and deleterious effects on oxygen delivery. Collaborative efforts with military authorities should aim to explore the underlying mechanisms associated with trauma and methemoglobinemia and optimize battlefield care. CONCLUSION: This case series underscores the significance of methemoglobinemia screening in combat trauma patients, and advocates for systematic co-oximetry utilization and methylene blue availability in combat zones. Early detection and intervention of methemoglobinemia in combat soldiers are often difficult in the context of battlefield injuries but are necessary to mitigate the potentially fatal consequences of this condition.

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.

Indoxacarb poisoning causing methemoglobinemia treated with parenteral vitamin C: a case report.

INTRODUCTION: This case study reports on a suicide attempt involving indoxacarb and vitamin C. Indoxacarb is a neurotoxic insecticide used in agriculture and as a flea controller in pets. Cotton, vegetables, and fruits are treated with indoxacarb, an insecticide that can be applied both indoors and outdoors. It causes skin allergies, methemoglobinemia, and hemolytic anemia. It is also attributed to allergic reactions through ingestion, inhalation, physical contact, and translaminar action. This case report highlights use of vitamin C in methemoglobinemia caused by indoxacarb poisoning. Indoxacarb poisoning has the potential to be extremely serious and even lethal. In this instance, the patient initially had no symptoms after ingesting a substance containing indoxacarb in an attempt at suicide. However, further tests revealed methemoglobinemia and low oxygen levels. CASE PRESENTATION: A 28-year-old south-east Asian female patient ingested an insecticide containing 5.25% novaluron, 4.5% indoxacarb, and 25% thiamethoxam, and reported that she noticed muddy brown urine but presented with no active signs or symptoms of poisoning. Upon examination, the patient was fully conscious, alert, and hemodynamically stable, but had an oxygen saturation of 84%. Gastric lavage was performed, and blood investigations revealed a muddy-brown-colored blood sample and methemoglobin levels of 12%. The patient was treated with high-dose vitamin C and showed significant improvement, with a drop in methemoglobin levels to 1.2% and an increase in oxygen saturation to 97%. DISCUSSION: Indoxacarb poisoning can cause severe methemoglobinemia. Vitamin C may be a useful treatment option for methemoglobinemia caused by indoxacarb, particularly in cases in which traditional treatment with methylene blue is contraindicated or not tolerated. Hence high doses of ascorbic acid, that is, vitamin C, were administered to the patient, which lowered their methemoglobin levels and improved oxygen levels without much safety concerns. CONCLUSION: This example emphasizes the significance of early indoxacarb poisoning detection and treatment as well as the possible advantages of utilizing ascorbic acid in the management of methemoglobinemia, and highlights the use of vitamin C in the treatment of methemoglobinemia caused by indoxacarb poisoning. Therefore, it is important for healthcare professionals to be aware of the potential for indoxacarb to cause methemoglobinemia and to consider vitamin C as a treatment option.

A Case Report of Primaquine Associated Methemoglobinemia in a Man With Pneumocystis Jirovecii Pneumonia Following Cardiac and Renal Transplantation.

We describe the case of a 51-year-old Caucasian man with a background of a cardiac and renal transplant who developed Enterocytozoon bieneusi colitis and pneumocystis jirovecii (PJP) pneumonia following treatment for suspected rejection. The patient developed methemoglobinemia which was attributed to primaquine. He was treated with intravenous methylene blue leading to clinical and biochemical resolution. We describe in detail the pathophysiological mechanism for methemoglobinemia and its treatment, in particular with methylene blue.

Pediatric popper intoxication: Case report of intoxication in a 3-month-old infant.

We present the case of a 3-month-old boy who accidentally ingested poppers. The patient presented with refractory hypoxemia and compensated circulatory failure associated with severe methemoglobinemia. He made a full recovery after treatment with the specific antidote methylene blue. This is the first report of popper poisoning in a child - a rare case of poisoning in pediatrics.

Detection of methaemoglobinaemia in a COVID-19 patient on dapsone.

Methaemoglobinaemia occurs when iron in haemoglobin is oxidised into a form that cannot transport oxygen. At low levels, it is asymptomatic, though at rising levels symptoms arise from impaired oxygenation, and it can ultimately be fatal. While uncommon, it is important to consider in hypoxaemic COVID-19 patients, especially if they are not clinically improving on standard treatments and workup for other causes does not explain the ongoing hypoxaemia. It is often diagnosed through a mismatch in peripheral and arterial oxygen, with the former typically less than the latter. We present the case of a COVID-19 patient who was found to have methaemoglobinaemia due to dapsone use for Pneumocystic jirovecii pneumonia (PJP) prophylaxis while on chemotherapy. Dapsone was stopped and supplemental high-flow nasal cannula was provided, and methaemoglobin levels improved over a 5-day period. She was discharged to follow-up with her haematologist in the clinic.

Acquired methaemoglobinaemia in infancy associated with acute diarrhoea: A case series.

Acute diarrhoeal illness remains a common medical problem in children with nearly 1.7 billion cases globally every year. We report five infants who, following severe diarrhoea, developed methaemoglobinemia. This is an altered state of haemoglobin presenting with cyanosis and can pose a diagnostic dilemma. It should be suspected in young infants without cyanotic heart disease presenting with severe diarrhoea, sepsis and cyanosis disproportionate to their clinical status. Its outcome depends on prompt treatment, the severity of underlying sepsis and co-morbidity.

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

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.

[Methemoglobinemia Induced by Sildenafil Tablets Ordered in the Darknet - Importance of Syncopes' Causes]. / Methämoglobinämie durch Sildenafil-Tabletten aus dem Darknet.

Drug-induced methemoglobinemia is a well-known phenomenon as well as induction by poppers (alcylnitrites substance group). Usually, suspicion is thrown in the right direction by a thorough medical history and environmental survey. But if intoxication is unintended and happens within the very private environment diagnosis might be very tricky. We report on an unusual case of accidental intoxication with probably contaminated tablets which were bought in the darknet. Finally, diagnosis was made by blood gas analysis' methemoglobine values.

The first Chinese with Hb Chile leading to chronic anemia and methemoglobinemia: a case report.

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.

Impact of methemoglobin on carboxyhemoglobin saturation measurement in fatal sodium nitrate and sodium nitrite cases.

An increase in suicide cases by sodium nitrate and sodium nitrite ingestion has been noted in the scientific literature. We report on the possible impact of nitrate/nitrite-caused methemoglobinemia on carboxyhemoglobin measurement by spectrophotometric methods. Elevated methemoglobin saturation may result in insufficient reducing agents to convert methemoglobin into deoxygenated hemoglobin, affecting the measured total hemoglobin and carboxyhemoglobin saturation. We highlight four cases where the cause of death was attributed to sodium nitrate or sodium nitrite ingestion. The possible impact of the nitrate/nitrite-caused methemoglobinemia on the carboxyhemoglobin saturation as measured by spectrophotometry is discussed. Further studies are needed to identify a causal relationship between nitrate/nitrite-caused methemoglobinemia and carboxyhemoglobin saturation as measured by spectrophotometric methods.