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: A case series.

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.

A Rare Case of Methemoglobinemia after Ifosfamide Infusion in a 3-Year-Old Patient Treated for T-ALL.

Methemoglobinemia is a potentially life-threatening, rare condition in which the oxygen-carrying capacity of hemoglobin is diminished. We present the case of a 3-year-old boy treated for T-cell acute lymphoblastic leukemia (T-ALL) who developed methemoglobinemia (MetHb 57.1%) as a side effect of ifosfamide administration. Due to his critical condition, the patient was transferred to the intensive care unit (ICU). The therapy included methylene blue administration, an exchange transfusion, catecholamine infusion, and steroids. Improving the general condition allowed for continuing chemotherapy without ifosfamide and completion of the HR2 block. Vigilance for methemoglobinemia as a very rare side effect should be widespread when using ifosfamide in the treatment protocols.

Acquired methemoglobinemia due to nitrobenzene poisoning: An unusual acquaintance.

Key Clinical Message: Nitrobenzene poisoning is a rare yet life-threatening contention. The ensuing acute methemoglobinemia has a high fatality rate, hence early prompt intervention is required. Methylene blue (intravenous or oral) and ascorbic acid are the cornerstones of management. They must be administered to suspected patients without tardiness. Abstract: An aromatic organic chemical used in paints and the printing industry is nitrobenzene. Its poisoning causes potentially fatal methemoglobinemia. One aspect of its management involves reducing the iron moiety from its ferric to ferrous form by administering intravenous methylene blue. A 23-year-old man who had deliberately consumed nitrobenzene presented to us with a history of headache and vomiting. He was diagnosed to have methemoglobinemia on the basis of clinical grounds and was managed successfully with intravenous methylene blue and vitamin C.

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.

Causes of acquired methemoglobinemia - A retrospective study at a large academic hospital.

Methemoglobinemia is a potentially life-threatening condition caused by the formation of methemoglobin, a form of hemoglobin that cannot bind oxygen. While there are some rare congenital causes of methemoglobinemia, most cases are acquired from the effects of specific drugs or environmental exposures. In this retrospective study, we analyzed a large data set of whole blood samples analyzed for methemoglobin at an academic medical center in Midwestern United States that provides both pediatric and adult services. For a 14 year timeframe (May 2009- June 2023), we performed detailed chart analysis of all patients with a methemoglobin concentration of 3.1 % or higher. For an earlier 13 year timeframe (January 1996-April 2009), we performed chart review for all patients with a methemoglobin concentration of 10.0 % or higher. For the 2009-2023 data, dapsone was the most frequent cause of methemoglobinemia (methemoglobin 3.1 % or higher) in both pediatric (73.3 %, 115 clinical encounters, 105 unique patients) and adult (65.3 %, 195 clinical encounters, 190 unique patients) populations. Inhaled nitric oxide as medical therapy was the next most frequent cause in both pediatric (18.1 %) and adult (13.2 %) populations. Causes associated with two or more unique episodes with methemoglobin concentrations of 10.0 % and higher included the following: dapsone (n = 40 episodes), benzocaine (n = 10), recreational use of amyl or isobutyl nitrite (n = 3), suicide attempt with sodium nitrite (n = 3 with 1 fatality; all 3 cases within last 3 years), food contaminated with nitrates (n = 2), and sepsis (n = 2). A total of 18 patients received treatment with methylene blue including 5 cases associated with benzocaine and all of the cases associated with amyl nitrite, isobutyl nitrite, sodium nitrite, and contaminated food. Only 3 patients with dapsone-associated methemoglobinemia received methylene blue, reflecting primary management by dose reduction or discontinuation of drug. Overall, our data reinforce previous studies showing dapsone, inhaled nitric oxide, and nitrites as common agents causing methemoglobinemia in a patient population seen at a medical center. Our data also are consistent with recent epidemiology trends showing increase in suicide attempts using sodium nitrite.

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.

Zopiclone-Induced Methemoglobinemia: A Case Report Highlighting How the Treatment Differs in Patients on Serotonergic Medication.

Zopiclone is a sedative-hypnotic that is increasingly being used for insomnia, especially among patients with depression. The side effects of zopiclone include nausea, vomiting, headache, giddiness, sedation, altered mental status, and coma. Here, we describe a rare case of a patient with underlying depression who overdosed on zopiclone, resulting in a presentation of drowsiness and dyspnea. A diagnosis of methemoglobinemia was made only through astute observation of the presence of a saturation gap, poor oxygen saturation despite high flow oxygen supplementation, and the arterial blood gas sample appearing chocolate brown in color. Treatment of such patients usually includes the gold standard of methylene blue. However, in our case, there was a risk of serotonin syndrome as the patient was on a serotonergic antidepressant prior. As such, an alternative treatment with ascorbic acid was utilized instead. Methemoglobinemia, while uncommon, should always be suspected in patients who present with zopiclone overdose as it can be life-threatening and is easily treatable.

Familial Psychomotor Delay of an Uncommon Cause: Type II Congenital Methemoglobinemia.

Methemoglobinemia is due to oxidization of divalent ferro-iron of hemoglobin to ferri-iron of methemoglobin (MetHb) which is incapable of transferring oxygen to tissues. This disease may be acquired by intoxication with oxidizing agents or inherited with a mutation of CYB5R3, the gene coding for the methemoglobin reductase or cytochrome B5 reductase 3 responsible for the reduction of MetHb to hemoglobin. We report the case of 2 sisters aged respectively of 15 and 8 months. They were born to a second-degree consanguineous marriage with a history of precocious and unexplained deaths in 3 relatives. Both sisters presented neurological features including psychomotor retardation, microcephaly, and axial hypotonia. Cerebral magnetic resonance imaging revealed cerebral atrophy in both cases associated with hypoplasia of the corpus callosum in the younger child. The association of neurological disability, cyanosis, and hypoxemia prompted a search for methemoglobinemia, with MetHB levels respectively of 26% and 15.8%in the 2 sisters. Initial treatment was based on methylene blue, then ascorbic acid. The genetic study revealed a c.463+8G>C mutation of CYB5R3 confirming the diagnosis of methemoglobinemia type II. The diagnosis of methemoglobinemia, although rare, should be considered in the presence of psychomotor retardation with cyanosis and subacute onset hypoxemia, especially in the presence of a family history.

Methaemoglobinaemia Associated With Mixed Cocaine and Amphetamine Overdose: A Case Report.

Methaemoglobinaemia is a rare disorder characterized by increased levels of methaemoglobin, a form of haemoglobin with oxidized iron that cannot efficiently bind oxygen. This leads to inadequate oxygen delivery to tissues with various clinical manifestations from asymptomatic to severe persistent hypoxia, CNS symptoms, and cardiovascular collapse. Acquired methaemoglobinaemia is typically a sudden condition, often resulting from poisoning by specific drugs and compounds, which can potentially have fatal consequences. We present a case of a patient who came with severe methaemoglobinaemia due to intoxication with cocaine and amphetamine.

Dapsone-Induced Methemoglobinemia Presenting Concomitantly With COVID-19 Pneumonia and Pulmonary Embolism: A Case Report.

Acquired methemoglobinemia is a treatable condition that is often clinically subtle and can be missed on routine clinical assessment. We present a 73-year-old male who was evaluated in the emergency department with worsening respiratory symptoms requiring oxygen. He tested COVID-19 positive and had new pulmonary emboli evident on his CT chest. The patient was on dapsone therapy as a treatment for bullous pemphigoid. The discrepancy between his oxygen levels on the pulse oximeter and blood gas was noted and was treated with 3% methylene blue for dapsone-induced methemoglobinemia. The patient received treatment for COVID-19 pneumonia and pulmonary emboli. Our case demonstrates that dapsone-induced methemoglobinemia can present concomitantly with other more common causes of acute hypoxic respiratory failure. It is noteworthy for physicians to maintain a high index of suspicion for oxygen level discrepancy in hypoxic patients and consider the possibility of acquired methemoglobinemia. Hence, earlier detection and treatment of the etiology of tissue hypoxia.

First case of congenital methemoglobinemia in Nepalese population: a case report.

Introduction and importance: Congenital methemoglobinemia is a rare hereditary disorder that leads to decreased oxygen delivery to the tissues. The severity of symptoms is directly proportional to the methemoglobin levels in the blood. Furthermore, this is the first case of congenital methemoglobinemia reported in the Nepalese population. Case presentation: We herein present a case of a 33-year-old male with congenital methemoglobinemia, the first reported case among the Nepalese population. His peripheral oxygen saturation level did not improve despite increasing the oxygen supplementation, and a saturation gap of more than 5% was present. The dark brown color of the blood was noted on the blood sample. On investigations, the methemoglobin level was 9%. Clinical discussion: Congenital methemoglobinemia can occur due to a deficiency of an enzyme known as cytochrome b5 reductase, which primarily converts methemoglobin to hemoglobin. There are two types of congenital methemoglobinemia, type I and type II which can be distinguished clinically by the presence of neurological impairment and mental retardation, which can be seen in type II congenital methemoglobinemia. Conclusion: Congenital methemoglobinemia is a rare syndrome and has not been previously reported in the Nepalese population. Although there are various diagnostic clues including relevant medical history, saturation gap of more than 5%, dark brown coloration of blood, and investigations such as methemoglobin level, healthcare services like cytochrome b5 reductase enzymatic activity and molecular genetic testing regarding congenital methemoglobinemia is recommended.

Recurrent Acute Methemoglobinemia in an Infant With Persistent Gastroenteritis: A Case Report.

Acute toxic methemoglobinemia is a rare and fatal condition with increased levels of oxidized hemoglobin. The clinical presentation of methemoglobinemia varies primarily based on total methemoglobin levels in the blood. Patients sometimes have significant cardiopulmonary compromise, but the majority are asymptomatic, with only cyanosis as the most prevalent sign. We report the case of a 41-day-old male who developed methemoglobinemia and persistent gastroenteritis after consumption of well water. In this case, we believe that the recurrence of acute methemoglobinemia episodes resulted from multifactorial reasons such as age at presentation, infection with nitrate-producing organisms, and consumption of nitrite-containing well water. The rationale for prophylactic therapy was implemented, aiming to prevent further episodes. This case report demonstrates the potential of prophylactic therapy as part of the management of infants with recurrent acute methemoglobinemia episodes.

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.

Modern suicide trend from internet.

INTRODUCTION: The most common suicide methods vary slightly from country to country, partly related to the availability of effective means. Societal development over the years and especially the advent of the Internet has enabled the sudden spread of new suicide methods. Recently, especially since 2019, intentional sodium nitrite poisoning has appeared on many social networks as an increasingly popular method of suicide. MATERIAL AND METHODS: There was performed a retrospective-prospective study of the autopsy protocols of the Medico-Legal Departments of the Healthcare Surveillance Authority in Slovakia, in a period of 15 years (2008-2022). We performed the analysis of cases of death due to nitrite poisoning, focusing on cases of intentional self-harm. In all selected cases, we present complete information, including photo documentation from the place of death, as well as the results of the performed autopsy and the results of additional laboratory examinations. RESULTS: We did not record any fatal cases of unintentional, accidental consumption of sodium nitrite in Slovakia, nor any fatal cases of homicidal poisoning by this substance. However, there were three cases of intentional self-harm (completed suicide) by sodium nitrite poisoning (in 2019, 2020 and 2022). CONCLUSIONS: The correct diagnosis of the cases of sodium nitrite poisoning deaths is possible only based on evaluating all the information obtained, a thorough examination of the body and the crime scene, and the correct interpretation of the findings found during a subsequent autopsy and the results of the toxicological analysis.

Severe Hemolytic Anemia After Mothball Ingestion Complicated by an Undiagnosed Enzyme Deficiency: A Case Report.

Ingestion of mothballs containing naphthalene or paradichlorobenzene is known to cause hemolysis and methemoglobinemia secondary to severe oxidative stress, affecting the oxygen delivery system of the body. The gradual accumulation of oxidizing radicals in the setting of restricted glutathione availability leads to the oxidization of hemoglobin and other body proteins, ultimately causing cell destruction. In the setting of glucose-6-phosphate dehydrogenase deficiency (G6PDD), more pronounced symptoms and poor prognosis are anticipated as adequate nicotinamide adenine dinucleotide phosphate is not generated to protect red blood cells from oxidative injury, potentiating the hemolytic process further. Here, we report the case of a young male with mothball ingestion whose presentation and management were complicated by underlying undiagnosed G6PDD.

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.

Methemoglobinemia in the Era of COVID-19: A Potential Confounder of Glycemic Control.

Glycated hemoglobin A1c (HbA1c) is frequently used as a measure of glycemic control but can be inaccurate in certain clinical scenarios leading to poor estimates of insulin requirements. We present the case of a 76-year-old man with diabetes and COVID infection. HbA1c was measured at 5.7%, though the patient reported home glucose readings of 200 to 300 mg/dL (11.1-16.65 mmol/L). Pulse oximetry on presentation was 50% to 60%, which initially improved to 93% with supplemental oxygen of 15 L via nonrebreather face mask. Treatment with remdesivir and dexamethasone was initiated, but the patient was again found to have low oxygen saturations requiring bilevel positive airway pressure and transfer to the intensive care unit. The patient was started on 1.1 U/kg of insulin daily in a basal-bolus regimen. The patient developed severe hyperglycemia requiring 2.4 U/kg to achieve glycemic control. Co-oximeter analysis of an arterial blood gas sample revealed methemoglobinemia. Exchange transfusion was performed with clinical improvement. Subsequent measurement of fructosamine was 360 umol/L (360 000 µmol/L), correlating with reported home glucose measurements. Methemoglobinemia may impair glycation of hemoglobin or interfere with measurement of HbA1c, thereby compromising the use of this molecule as a marker for glycemic control in patients with this condition.

A Chest Pain Conundrum: Dapsone-Induced Methemoglobinemia in a Heart Transplant Patient.

We present the case of a 39-year-old male with a past medical history of orthotopic heart transplantation who presented with chest pain and dyspnea on exertion. He was diagnosed with dapsone-induced methemoglobinemia toward the end of his hospital course, and his condition clinically improved with the discontinuation of the offending agent. This case highlights the importance of medication review and history-taking. Clinicians should be mindful of dapsone-induced methemoglobinemia, especially when encountering patients with dyspnea and a history of dapsone intake.

Pyrogallol Toxicosis in Horses.

Plants in the maple genus, Acer, and pistachio genus, Pistacia, have been reported to cause acute hemolysis in horses. The cause of hemolysis seems to be metabolism of gallic acids to the potent oxidant pyrogallol by enteric bacteria of the horse. Diagnosis is often tentative and circumstantial. Treatment is symptomatic and supportive and can include detoxification, fluid and electrolyte therapy, supplemental oxygen, and pain control. Corticosteroid and antioxidant therapies do not improve prognosis. Prognosis is guarded to poor but horses that survive 6 days postexposure are expected to recover.