Syncope and Methemoglobinemia Preceded by Amyl Nitrite 'Popper' Inhalation.

INTRODUCTION: Methemoglobinemia represents an uncommon but potentially serious cause of presentation to the emergency department, resulting in hypoxemia and even death. The symptoms and clinical findings in this condition can be nonspecific and therefore methemoglobinemia can be easily missed if the clinician is not familiar with it. This report presents a case caused by recreational drug use which has rarely been documented previously. CASE REPORT: A 23-year-old male with a history of asthma presents to the emergency department for an episode of syncope after inhalation of amyl nitrite "poppers". He had normal vitals other than tachycardia but was found to have nailbed and perioral cyanosis, a classic but uncommon presentation that is demonstrated in the included clinical image. He was found to have methemoglobinemia caused by his use of amyl nitrite and received supportive care but did not require methylene blue. CONCLUSION: Emergency physicians should familiarize themselves with the classic physical exam findings in methemoglobinemia in order to identify and treat this condition promptly. While this patient had a good outcome with only supportive care and observation, his presentation and the etiology of his condition offer an important teaching point. The possibility of methemoglobinemia after recreational "popper" use should be considered when working up a patient who presents with cyanosis and hypoxemia.

[A Case of Methemoglobinemia Caused by Toluidine Revelation with Dyspnea and Cyanosis].

Toluidine is a known cause of bladder cancer, but it is less widely recognized as a cause of methemoglobinemia because methemoglobinemia is rare. We herein report a case of methemoglobinemia caused by toluidine in a 50-year-old man. A solution of toluidine overflowed from its container during transportation and adhered to the man's clothes, but he drove to his workplace 100 km away without changing his clothes or undergoing decontamination. Before arriving at his workplace, he developed dyspnea and called emergency services, and he was then transported to a local hospital. He had significant cyanosis upon arrival, and arterial blood gas analysis revealed a high methemoglobin level of 44%. He was diagnosed with toluidine-induced methemoglobinemia and was transported to our hospital, where he was admitted to the intensive care unit. Treatment for methemoglobinemia was started immediately after hospitalization, and the patient's symptoms and methemoglobin level improved. Methemoglobinemia should be considered in workers who handle toluidine and develop cyanosis and dyspnea.

Methemoglobinemia due to use of poppers: a case report.

BACKGROUND: Methemoglobinemia is an excess of oxidized hemoglobin in the blood, affecting oxygen transportation. It is characterized by central cyanosis that does not respond to oxygen therapy. Prognosis is excellent when treated adequately and rapidly. We present a case report of a 38-year-old Caucasian man suffering from methemoglobinemia due to the use of poppers. CASE PRESENTATION: A 38-year-old Caucasian man known as a smoker and addicted to cocaine was admitted to the emergency department with dyspnea, agitation, and central cyanosis that started approximately 3 hours before admission. The persistent hypoxia despite high-flow oxygen therapy and a history of poppers use helped to reveal a condition known as methemoglobinemia. CONCLUSIONS: Our case highlighted a typical clinical presentation of methemoglobinemia. This possible life-threatening condition can occur after ingestion or inhalation of poppers, commonly sold in sex shops for recreational purposes. This can be easily confirmed by the methemoglobin level of the blood gases, provided the emergency physician considers this diagnosis. Rapid treatment with intravenous methylene blue is effective and leads to a favorable prognosis.

Two cases of fatal methemoglobinemia caused by self-poisoning with sodium nitrite: A case report.

RATIONALE: Sodium nitrite intoxication reportedly causes severe methemoglobinemia. Recent studies reported that most clinically significant cases resulted from intentional exposure in suicidal attempts. We describe 2 cases of severe methemoglobinemia secondary to intentional sodium nitrite intoxication in suicidal attempts. PATIENTS CONCERNS: A 26-year-old man and 20-year-old woman attempted suicide by taking sodium nitrite, and were brought to the emergency department. DIAGNOSIS: The male patient collapsed at the scene. He ingested approximately 18 g of sodium nitrate, and his methemoglobin level was 90.3%. The female patient was conscious, but was cyanotic. She ingested approximately 12.5 g of sodium nitrite, and her methemoglobin level was 54.6%. INTERVENTIONS: The male patient received advanced cardiac life support in the emergency department. Methylene blue was immediately administered for the female patient. OUTCOMES: The male patient died despite aggressive resuscitation. The female patient's cyanosis resolved, and her methemoglobin level decreased to 1.2% 3 hours later. LESSONS: The immediate administration of methylene blue in severe methemoglobinemia patients prevented fatal consequences. The public should be informed about the accessibility and toxicity of sodium nitrite.

[Unexplained cyanosis in two newborns: neonatal methemoglobinemia after maternal perineal infiltration of prilocaine]. / Onbegrepen cyanose bij twee neonaten.

BACKGROUND: Methemoglobinemia is a rare cause of neonatal cyanosis in the newborn. It is considered a medical emergency. Failure of recognition or appropriated treatment could result in serious disease and neonatal death. Neonatal methemoglobinemia can be caused by both hereditary and acquired factors. CASE DESCRIPTION: We present two cases of newborns who developed severe cyanosis a few hours after birth due to methemoglobinemia. This was thought to be related to the local maternal perineal infiltration of prilocaine during childbirth. Though rare, prilocaine is the most potent agent to induce methemoglobinemia compared to other local aneasthetics. After intravenous administration of methylene blue, both newborns fully recovered. CONCLUSION: Neonatal methemoglobinemia is a rare and potentially fatal complication of local anesthetics, particularly prilocaine, administered to the mother during childbirth. Midwives, obstetricians, gynecologists and pediatricians should be aware of this complication. The use of other local anesthetics, including lidocaine, should be considered.

Use of terlipressin in critically ill children with liver disease.

BACKGROUND: Terlipressin, a long-acting synthetic analogue of vasopressin has been used in the adult population for various indications including hepatorenal syndrome (HRS-AKI), esophageal variceal hemorrhage (EVH) and shock, but its use in pediatrics is still limited to individualized cases and data on safety and efficacy is scant. METHODS: We reviewed the patient records of children with liver disease and Acute Kidney Injury requiring terlipressin admitted to the Paediatric Intensive Care Unit (PICU) of King's College Hospital, London from January 2010-December 2017, with special emphasis on its effect on renal parameters and adverse event profile. RESULTS: Twenty-one terlipressin administration records in a total of 16 patients (median) (IQR) 10 years (6.1-14.4) were included. The drug was initially given as a bolus dose in all cases, followed by either bolus or infusion with median dosage being 5.2 (3.8-6.7) mcg/kg/hour. After administration, a sustained increase of mean arterial pressure was observed. There was an improvement in serum creatinine (Cr) (at 24 h; p = 0.386) and increase in urine output (UO), especially in the hepatorenal syndrome subgroup (HRS-AKI). We found minimal evidence of gastrointestinal side effects including feeding intolerance and vasoconstrictive side effects including cyanosis / ischaemia of extremities. CONCLUSION: Terlipressin was found to be safe in critically sick children with liver disease with positive impact on renal parameters which might be taken as a surrogate marker of HRS reversal, though effects on outcomes are difficult to ascertain. It is important to be aware of all its side-effects and actively watch for them. Future prospective studies are warranted to validate these findings.

A Case of Dapsone-induced Mild Methemoglobinemia with Dyspnea and Cyanosis.

Dear Editor, Dapsone is a dual-function drug with antimicrobial and antiprotozoal effects and anti-inflammatory features (1). In dermatology, it is a first choice for conditions such as leprosy, IgA pemphigus, dermatitis herpetiformis, and linear IgA bullous dermatosis, or an adjunctive treatment for, e.g. bullous pemphigoid (BP) and pemphigus vulgaris (1). However, dapsone is associated with some adverse effects, including methemoglobinemia (1). Methemoglobin (MetHb) concentrations of less than 15% usually cause no symptoms in patients with normal hemoglobin concentrations (2). Herein, we report the case of a patient with BP who developed dyspnea because of dapsone-induced methemoglobinemia that was as mild as 4.7%. A 93-year-old man was diagnosed with BP based on skin manifestations (Figure 1, a and b), histopathological findings (Figure 1, c and d), and anti-BP180 NC16A antibody titer determined by chemiluminescence enzyme immunoassay (279 U/mL) 3 years earlier. His comorbidities included diabetes mellitus, chronic heart failure, right pleural effusion, and brain infarction. The patient had been successfully treated with oral prednisolone, so the steroid was tapered to 4 mg/day. The blisters recurred, however, and new ones kept developing even though the prednisolone was increased to 25 mg/day. Dapsone (75 mg/day) was begun as adjunctive treatment, and new blister formation ceased. At one week from dapsone initiation, the patient developed dyspnea, and his oxygen saturation as measured by pulse oximetry decreased to 88% on room air. At presentation, his blood pressure was 118/78 mmHg, the heart rate was 95 beats/minute, and axillary temperature was 36.3 °C. Neurological examination and consciousness findings remained unchanged compared with findings before dyspnea onset. Chest examination showed normal breath and heart sounds, but lip and peripheral cyanosis was present. Blood tests revealed a white blood cell count of 12,920/µl; red blood cells, 370×104/µl; hemoglobin, 11.7 g/dl; and CMV antigenemia (or C7-HRP), negative. Chest CT and echocardiography indicated no remarkable change compared with imaging from one year earlier. Arterial blood gas analysis showed a pH of 7.454, PaO2 63.1 mmHg, PaCO2 35.4 mmHg, HCO3- 24.3 mmol/L, SaO2 92.4%, and MetHb of 4.7%. These findings indicated a saturation gap (difference between SpO2 and SaO2) induced by MetHb. Upon cessation of dapsone, MetHb levels and SpO2 returned to normal and the dyspnea resolved, implicating dapsone in the methemoglobinemia (Figure 1, e). Differential diagnoses were pulmonary disease, heart disease, neuromuscular disease, sepsis, and drug intoxication. These possibilities were ruled out by the physical examination, drug history, vital signs, blood tests, and chest CT and echocardiography. In normal individuals, MetHb levels are less than 1% (2). Healthy patients with normal hemoglobin concentrations develop cyanosis at MetHb level of 15-20%, dyspnea at 20-50%, and coma at 50-70%, and die at more than 70% (2). However, patients with hematologic disease, acidosis, or cardiopulmonary diseases, for example, present with symptoms even with MetHb levels less than 15% (2,3). We inferred that our patient presented with dyspnea even under mild methemoglobinemia because he had anemia, chronic heart failure, and right pleural effusion. The occurrence of dapsone-induced methemoglobinemia with obvious symptoms is rare (1,4). Clinicians should be aware that methemoglobinemia symptoms are influenced not only by MetHb concentrations but also by comorbidities.

Higher naloxone dosing may be required for opioid overdose.

PURPOSE: Carfentanil is a synthetic opioid with an estimated potency that is 10,000 times more than that of morphine and 100 times more than that of fentanyl. Although there is a paucity of evidence, when considering the potency of carfentanil, it is reasonable to speculate that larger doses of naloxone may be required to resuscitate patients after carfentanil ingestion. This case report discusses the use of high-dose naloxone in 2 patients with suspected carfentanil overdose presenting to a small community hospital. SUMMARY: Two patients with suspected carfentanil overdose presented to a 30-bed emergency department at a community hospital in New Hampshire. Cyanosis and respiratory distress were noted in both instances, and airway intervention was ultimately deemed necessary. Patient 1 required a total of 12 mg of naloxone to be successfully resuscitated, while patient 2 required a total of 10 mg for resuscitation. Both patients were successfully resuscitated with high doses of naloxone. The use of high-dose naloxone prevented the need for intubation in these patients. CONCLUSION: While more robust studies should be considered, emergency personnel should be comfortable using higher-than-standard doses of naloxone in appropriate cases.

Ischemic Skin Necrosis in Hepatorenal Syndrome Patient Secondary to Terlipressin.

Hepatorenal syndrome and variceal bleeding are two serious complications of chronic liver disease. Terlipressin is commonly used for reversal of these conditions. Besides its clinical advantages, it often causes serious ischemic complications. These complications are seen in patients at risk. Ischemic events, typically involve peripheries, but gastrointestinal mucosa, coronary arteries, trunk, and scrotum are also rarely involved. We observed extensive skin necrosis of right hand and forearm of a 50-year female patient treated with terlipressin for hepatorenal syndrome. Since this event was never noticed earlier in tertiary care hospitals of our province; to the best of authors' knowledge, this is the first case in medical literature from this part of the country.

Terlipressin-Induced Peripheral Cyanosis in a Patient with Liver Cirrhosis and Hepatorenal Syndrome.

BACKGROUND Hepatorenal syndrome (HRS), which is a type of functional renal impairment, is one of the most serious complications in patients with liver cirrhosis. Terlipressin can induce splanchnic vasoconstriction, which increases the renal blood flow and has beneficial effects on HRS. However, terlipressin administration may cause serious ischemic complications such as skin ischemia, peripheral gangrene, and ischemic bowel necrosis. Here, we report a case of peripheral cyanosis following terlipressin administration in a cirrhotic patient with HRS. CASE REPORT The patient was a 65-year-old male. He was considered to have type-1 HRS, and thus, terlipressin was administered. However, peripheral cyanosis involving the fingers, toes, area around an umbilical hernia, and scrotum was noted. Thus, terlipressin administration was discontinued. Subsequently, his condition rapidly improved. CONCLUSIONS We reported a case of peripheral cyanosis following terlipressin administration, which resolved after discontinuation of terlipressin administration. It is important to recognize the early signs of side effects and discontinue the administration of the suspected drug immediately.

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.

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

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.

Nitrite-induced acute kidney injury with secondary hyperparathyroidism: Case report and literature review.

RATIONALE: Acute kidney injury (AKI) with hyperparathyroidism caused by nitrite was rare, and renal function and parathyroid hormone (PTH) decreased to normal range after therapy. PATIENT CONCERNS: Acute kidney injury was diagnosed in a 40-year-old male with hyperparathyroidism and cyanosis of his hands and both forearms. DIAGNOSES: The patient ate some recently pickled vegetables, and he experienced nausea, vomiting and diarrhoea without oliguria or anuria; Additionally, his hands and both forearms had a typical blue ash appearance. After admission, the laboratory findings indicated theincreasing serum creatinine (Scr) and parathyroid hormone (PTH). He was diagnosed as acute kidney injury with hyperparathyroidism caused by nitrite. INTERVENTIONS: The patient stopped eating the pickled vegetables and was given rehydration, added calories and other supportive therapy without any glucocorticoids. OUTCOMES: According to his clinical manifestations, laboratory findings and imaging results, the patient was diagnosed with acute kidney injury with secondary hyperparathyroidism. He was given symptomatic supportive care therapy. After one week, the serum creatinine, parathyroid hormone (PTH), hypercalcemia, hyperphosphatemia, proteinuria, and urine red blood cell values decreased to normal range. LESSONS: Nitrite-induced acute kidney injury with secondary hyperparathyroidism was relatively rare. After therapy, the function of the kidney and parathyroid returned to normal. This case suggests that detailed collection of medical history, physical examination and correct symptomatic treatment is very important.

Fenómeno de Raynaud secundario a un colirio antiglaucomatoso / Raynaud's phenomenon secondary to anti-glaucoma eye drops

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