To test the feasibility and safety of a randomized controlled trial (RCT) delivering nitric oxide into the sweep gas of extracorporeal membrane oxygenation (ECMO) circuits (sNO) in critically ill children. Second, we explored whether use of sNO may influence clinical outcomes. Prospective pilot single-center open-label RCT (trial registration number ACTRN12619001518156). Single-center, tertiary PICU with enrollment between July 2020 and July 2023. Patients from birth to 16 years requiring venoarterial or venovenous ECMO support were enrolled. Randomization to sweep flow with an oxygen/nitrogen mix vs. a mix of oxygen, nitrogen and sNO (20 parts per milliion). Randomization was stratified by type of ECMO support (venoarterial vs. venovenous). Of 60 eligible patients 53 underwent randomization. The median (interquartile range [IQR]) was 1 month (0.1-33.5 mo) and 6.2 months (0.5-120.2 mo) for the intervention and control arms, respectively. Venoarterial and venovenous support were used in 35 of 53 (65%) and 18 of 53 (35%) patients, respectively. In all, 17 of 53 (32%) received pulmonary, 23 of 53 (43%) cardiac and 13 of 53 (25%) extracorporeal cardiopulmonary resuscitation support. Median (IQR) survival free of ECMO and survival free of PICU censored at 30 and 90 days were similar: 18.2 days (0-25.2 d) and 69.1 days (0-85.2 d) vs. 20.8 days (0-26.3 d) and 77.7 days (0-85.9 d) with an effect estimate of -3.2 days (-16.6 to 10.1 d) and -8.8 days (-54.2 to 36.6 d) between the intervention and standard care arm. Blood product use, circuit duration to replacement, free plasma hemoglobin, degree of oxygenator thrombus, and incidence of methemoglobinemia were similar between the two groups. No major adverse events occurred related to the treatment allocation or intervention. This single-center pilot RCT of sNO vs. standard sweep flow in the ECMO circuit demonstrated that such a trial is safe and feasible. However, given no effect of sNO on clinical outcomes was detected further exploration of dose and route of administration of NO should be undertaken before larger, definitive trials are conducted.

Introduction: Metal phosphides are highly effective insecticides and rodenticide. They are used as a cheap and effective rodenticide in developing countries. Hemolysis and methemoglobinemia are rare but reported complications of phosphide poisoning Aim of the work: The aim of this study was to detect the incidence of methemoglobinemia and intravascular hemolysis in some cases of acute phosphide poisoning. Patients and methods: A cross sectional study was conducted on 50 cases suffering from acute metal phosphide poisoning admitted to Tanta toxicology unit, from the start of October 2014 till the end of March 2015. For each case, the following were done: history taking, physical examination and laboratory investigations (including measurement of methemoglobin (Met-Hb) level, arterial blood gas analysis, routine investigations, lactate dehydrogenase enzyme and complete blood picture with reticulocytic count). Results: Eight cases (16%) had combined methemoglobinemia and hemolysis. Aluminum phosphide was the toxic agent in seven of them and zinc phosphide in only one. Three cases (6%) had methemoglobinemia alone; one of them was poisoned by aluminum phosphide and the other two by zinc phospide. Another three cases had hemolysis alone; one of them was due to aluminum phosphide toxicity and the other two were due to zinc phospidetoxicity. So the present study included a total of eleven cases (22%) of methemoglobinemia. Their median age was 27 years old, while it was 24 years for patients with normal Met-Hb level. The median delay time was 4 hours for them and 2 hours for cases with normal Met-Hb level with significant statistical differences between both. The mean Met-Hb level was 14.45 ± 9.32% and1.63 ± 0.45% in cases with high and normal Met-Hb level respectively, with a significant statistical difference between both. Furthermore, the mean oxygen saturation showed a significant statistical difference between both. In addition, the present study included a total of eleven cases (22%) of hemolysis. Their median age was 27 years old, while it was 24 years for patients with no hemolysis. The median delay time was 3 hours in them and 2 hours in cases with no hemolysis. Conclusion: It was concluded that methemoglobinemia and hemolysis can complicate the course of acute phosphide poisoning. Recommendations: Further studies on a large scale of cases of acute phosphide poisoning with assessment of the outcome of cases presented with methemoglobinemia and hemolysis and the efficacy of the available treatment for such cases are recommended. Furthermore, it is important that health care professionals be aware of these rare presentations of phosphide poisoning.

In 1976, the combination of cerium nitrate and silver sulfadiazine was introduced as a topical therapy for burn wounds. Experience with a locally prepared combination agent has shown physical change of the eschar and delayed subeschar bacterial colonization. A potential systemic complication of this treatment is the development of methemoglobinemia (Met-Hba) due to the oxidizing nature of Ce(NO(3))(3). Met-Hba has a spectrum of clinical consequences, ranging from headache and cyanosis to cardiac ischemia, hypotension, and even death. Given the frequent use of this combination agent at our burn center, a retrospective review was conducted to evaluate the incidence of Met-Hba. A query of pharmacy records revealed 170 patients from January 2005 to October 2009 that had received this treatment. Eighteen patients (∼10%) developed Met-Hba as noted on arterial blood gas (methemoglobin>3%) and only three patients (∼2%) had methemoglobin levels >10%. In the majority of cases, there were no clinical symptoms of Met-Hba. Most patients' relative hypoxia resolved with cessation of treatment; however, five patients required treatment with methylene blue. The presence of Met-Hba associated with this topical therapy can be diagnosed early by vigilant monitoring, thereby reducing morbidity and mortality. In our experience, cerium combined with silver sulfadiazine is a valuable and safe treatment for deep partial and full-thickness burn wounds.

Methemoglobinemia is a recognized complication of topical anesthesia with benzocaine during transesophageal echocardiography (TEE). Though several risk factors have been described, the importance of individual factors is not known. We performed a retrospective study to identify determinants of the risk of methemoglobinemia. All patients who underwent TEE with benzocaine topical anesthesia between June 2005 and June 2007 were included in this retrospective study. Of the 886 patients who were included in the study, 140 had active infection (15.8%). The incidence of methemoglobinemia in this group was 2.9% (vs. 0%, P < 0.001). Compared to those without infection, patients in the active infection group were more likely to have a lower hemoglobin (P < 0.001), serum albumin level (P < 0.001), glomerular filtration rate less than 60 ml/min per 1.73 m(2) (P < 0.001), higher rates of dialysis (P < 0.001), a higher incidence of malignancy (P = 0.01), and increased use of acetaminophen and sulfa drugs (P < 0.001). However, multivariate logistic regression analysis did not identify any statistically significant covariates. In conclusion, patients with an active systemic infection who undergo TEE are at a higher risk of methemoglobinemia. However, none of the risk factors for methemoglobinemia including active infection reached statistical significance in the regression analysis which has to be interpreted with caution in view of the low event rate.

The potentially life-threatening condition of methemoglobinemia is characterized by cyanosis, low pulse oximetric readings, and normal arterial Po(2) values. Acquired methemoglobinemia has been linked to the use of the topical anesthetic benzocaine in endoscopic procedures, including transesophageal echocardiography (TEE). Yet, the incidence of benzocaine-induced methemoglobinemia with TEE and the clinical factors associated with its development are unclear. All cases of methemoglobinemia complicating TEE at our institution (from January 1, 1999, to July 1, 2006) were identified by a comprehensive review of medical records and echocardiography and pharmacy databases. During 90 months among 28 478 TEEs, 19 cases of methemoglobinemia were identified, with a mean +/- SD methemoglobin level of 32% +/- 15%. All patients were cyanotic, with low oxygen saturations. Eighteen of 19 patients received methylene blue (mean +/- SD dose, 1.3 +/- 0.4 mg/kg of body weight), with resolution of symptoms and signs. One of 19 cases resolved spontaneously. Compared with a random sample of 190 patients undergoing TEE, the age, sex, body mass index, left ventricular systolic function, and dose of sedation (midazolam hydrochloride, fentanyl citrate, or both) were similar in the 2 groups. However, study patients who developed methemoglobinemia were more likely to be hospitalized (89.5% vs 57.6%, P =.005), be anemic (84.2% vs 44.7%, P =.002), and have active systemic infection (68.4% vs 6.8%; P < .001) at the time of TEE compared with the random control cohort. In a large series of patients undergoing TEE, the incidence of methemoglobinemia is low (1 case per 1499 [0.067%; 95% confidence interval, 0.040%-0.100%]) and has a good outcome if promptly recognized and treated. Clinical factors associated with the development of methemoglobinemia include sepsis, anemia, and hospitalization. Minimizing or avoiding the use of benzocaine in these patients is recommended.

Spectrophotometric analysis of arterial blood samples from 695 hospitalized patients revealed a mean methemoglobin value of 0.44% (±0.3%) of total hemoglobin. Since values of methemoglobin greater than one percent exceed two standard deviations from the mean, it is concluded that methemoglobinemia in the hospitalized patient should be defined as a methemoglobin concentration of greater than one percent of total hemoglobin. This study demonstrates that no statistically significant differences exist in the incidence of methemoglobinemia among various populations within the hospital.

The relationship of added nitrate to pigment formation in native pork-sausage ( longaniza)

1945-46 a number of articles by H. H. Comly (1) and other writers (2-4) called attention to the relation between the presence of nitrate in drinking water and the incidence of methemoglobinemia in infants (blue babies) up to six months of age. This infant ailment developed acutely with marked cyanosis when the nitrate nitrogen content of drinking water and water used to make up milk feeding formulas reached a figure of 10-20 ppm. or more. Some of the cases studied in which severe cyanosis developed indicated the nitrate nitrogen content of the water to be over 100 ppm. The presence of nitrates in the human body ordinarily results in a breakdown of the compounds to nitrite and ammonia. Apparently young infants are not able to transform all of