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Modalities of detection of sentinel nodes in lymphatic mapping
Published in Charles F. Levenback, Ate G.J. van der Zee, Robert L. Coleman, Clinical Lymphatic Mapping in Gynecologic Cancers, 2022
Blanca Segarra, Nuria Agusti, Pedro T. Ramirez
SLN mapping procedures are feasible in pregnant patients. SLN should be considered the standard of care for melanoma and breast cancer in the clinically negative axilla. Isosulfan blue should only be given during pregnancy when benefits outweigh the risks because it is systemically absorbed after sub-cutaneous injection.40 Methylene blue has not been found to be safe and effective in pregnant women according to the FDA, and this labeling has not been approved. It can cause fetal harm when administered to a pregnant woman. Intraamniotic injection during the second trimester has been associated with neonatal intestinal atresia and fetal death. This drug also caused adverse developmental outcomes in animals when administered orally during organogenesis.41
Preterm Prelabor Rupture Of Membranes
Published in Vincenzo Berghella, Obstetric Evidence Based Guidelines, 2022
Anna Locatelli, Sara Consonni, Annalisa Inversetti
Transabdominal amnioinfusion of dye (indigo carmine, Evans blue, fluorescein) can be used as a confirmatory test in doubtful cases at low gestational ages. Methylene blue must be avoided, as it can cause fetal meta-hemoglobinemia [7].
Prelabor rupture of the membranes
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Roberto Romero, Lami Yeo, Francesca Gotsch, Eleazar Soto, Sonia S. Hassan, Juan Pedro Kusanovic, Ray Bahado-Singh
When the diagnosis of preterm PROM is not clear, a transabdominal injection of dye (indigo carmine, Evans blue, fluorescein) into the amniotic cavity may be used for confirmation (174–177). Methylene blue should not be used as it may cause fetal methemoglobinemia (178–180). A tampon in the vagina can document subsequent dye leakage in cases of PROM.
Rising incidence and high mortality in intentional sodium nitrite exposures reported to US poison centers
Published in Clinical Toxicology, 2021
Sean D. McCann, Marit S. Tweet, Michael S. Wahl
Sodium nitrite is a highly water-soluble salt commonly used in industrial chemistry, pharmaceutical production, food processing, and as a therapeutic agent in the treatment of cyanide poisoning [1,2]. The reported lethal dose of ingested nitrite salts in humans is highly variable with a broad range reported between 0.7 and 6 g of nitrite component [3]. Nitrites and nitrates are strong oxidizing agents that, when ingested, can lead to profound and potentially fatal methemoglobinemia [4]. Most cases of acquired methemoglobinemia are mild and morbidity and mortality are rare outcomes [5]. However, in severe cases, the resulting impaired oxygen delivery to tissues can lead to significant end organ damage. The clinical manifestations of impaired hemoglobin function can be further compounded by underlying medical conditions that may affect blood oxygenation and oxygen delivery to tissues, such as anemia, cardiac disease, and pulmonary pathology [4]. Presenting symptoms can include cyanosis, decreased oxygen saturation, hypotension, and central nervous system (CNS) depression, among many others. Methylene blue, while also an oxidizing agent, is used to treat xenobiotic induced methemoglobinemia. Methylene blue is reduced to leukomethylene blue, which then reduces methemoglobin to hemoglobin [4,6]. Early recognition of sodium nitrite associated methemoglobinemia and prompt treatment with methylene blue is important when caring for these patients in the emergency department.
Fatal Sodium Nitrite Poisoning: Key Considerations for Prehospital Providers
Published in Prehospital Emergency Care, 2021
Matthew R. Neth, Jennifer S. Love, B. Zane Horowitz, Michael D. Shertz, Ritu Sahni, Mohamud R. Daya
Methylene blue (methylthioninium chloride) is the treatment of choice for symptomatic methemoglobinemia. It works by accelerating the enzymatic reduction of ferric (Fe3+) iron to the ferrous (Fe2+) state through its metabolic product leukomethylene blue, ultimately converting methemoglobin to hemoglobin (41,42). The usual dose of methylene blue is 1 to 2 mg/kg of a 1% solution IV administered over five minutes (41). The dose can be repeated in 30 to 60 minutes if the patient is still symptomatic or methemoglobin levels are greater than 30% (41). The maximum total dose of methylene blue is 7 mg/kg, in most situations, but more may be needed in severe cases. There is the possibility that oxidation back to methemoglobin will reoccur at higher doses of methylene blue (41). Methylene blue is ineffective in patients with G6PD deficiency, NADPH methemoglobin reductase deficiency, sulfhemoglobinemia, and hemoglobin M disease (41,42). Recent evidence suggests that methylene blue may also inhibit the downstream effect of nitric oxide and may assist in the treatment of refractory distributive shock (43).
Comparative effectiveness of methylene blue versus intravenous lipid emulsion in a rodent model of amlodipine toxicity
Published in Clinical Toxicology, 2019
Intravenous lipid emulsion (ILE) is a relatively new treatment modality that antagonizes the cardiotoxic effects of local anesthetic agents and possibly other cardiotoxic drugs [13]. In addition, ILE may sequester some drugs in the lipid phase (an effect referred to as the “lipid sink”). Methylene blue is the antidote for drug-induced methemoglobinemia [14]. Methylene blue has other actions, including inhibiting the nitric oxide-cyclic guanosine monophosphate (NO-cGMP) pathway, decreasing vasodilation and increasing responsiveness to vasopressors. Consequently, it may improve hemodynamics in refractory distributive shock from various causes e.g., post-cardiac surgery and septicemia [10,15].