Inhalation Injury
Stephen M. Cohn, Matthew O. Dolich, Kenji Inaba in Acute Care Surgery and Trauma, 2016
Diagnosis of CN poisoning is difficult because a rapid assay is not available; CN and CO poisoning share many features to include signs and symptoms related to the central nervous and cardiovascular systems [68]. Three types of antidote are available for CN. The Cyanide Antidote Kit in the United States contains amyl nitrite for inhalation, and sodium nitrite and sodium thiosulfate for IV injection. The nitrites oxidize hemoglobin to methemoglobin (MetHb), which chelates CN. Sodium thiosulfate combines with CN to form thiocyanate, which is excreted in the urine. We do not recommend the use of nitrites in patients with II and suspected CN poisoning. They can cause severe hypotension, and the MetHb does not transport oxygen [69]. This is problematic, particularly in patients with burn shock and impaired oxygen transport and utilization from CO and CN. Certainly, nitrites should not be used in II victims without knowledge of the COHb and MetHb levels [70]. Sodium thiosulfate has slower onset [71] and lacks efficacy compared to hydroxocobalamin [72].
Toxicity and morbidity of IP drug therapy
Wim P. Ceelen, Edward A. Levine in Intraperitoneal Cancer Therapy, 2015
Sodium thiosulfate was identified in the 1980s as an antidote to cisplatin. Sodium thiosulfate neutralizes cisplatin by irreversible binding of the drug and also acts as a diuretic that is believed to speed elimination of the drug. The concentration of active cisplatin in plasma and kidney tissue is significantly decreased in the presence of sodium thiosulfate [36]. The addition of sodium thiosulfate to cisplatin-containing regimens has reduced the incidence of nephrotoxicity and allows for higher doses of cisplatin to be administered. Without sodium thiosulfate, a dose of cisplatin 90 mg/m2 produces nephrotoxicity, but with the addition of sodium thiosulfate, the dose of cisplatin can be escalated to 270 mg/m2 without evidence of nephro- or myelotoxicity [37]. Sodium thiosulfate may also reduce ototoxicity. The incidence of either tinnitus or hearing loss in a large Southwest Oncology Group study was 12% in the group receiving IP cisplatin (vs. 29% in the IV group), in the absence of sodium thiosulfate [21]. A more recent review of patients undergoing HIPEC with cisplatin, who also received IV sodium thiosulfate, found no significant change in hearing sensitivity on audiometric testing [38]. While systemic exposure to cisplatin is limited with IP therapy, the sodium thiosulfate provides further protection for patients receiving cisplatin and should be incorporated into the treatment regimen.
Corrosives
Bev-Lorraine True, Robert H. Dreisbach in Dreisbach’s HANDBOOK of POISONING, 2001
The following sulfur oxides occur as atmosphere contaminants: sulfur dioxide (SO2) and sulfur trioxide (SO3) along with the products of their reactions with water, sulfurous acid (H2SO3), and sulfuric acid (H2SO4), respectively. Sulfur monochloride (S2Cl2) and thionyl chloride (SOCl2) are used in industrial processes. A number of salts of sulfur oxides are used as bleaches, oxidizers, reducing agents, and cleaning agents. Their estimated fatal doses and exposure limits (if established) are as follows: sodium hydrogensulfate (sodium bisulfate, NaHSO4), 10 g; sodium sulfite (Na2SO3), 10 g; sodium hydrosulfite (sodium sulfoxylate, Na2S2O4), 30 g; sodium hydrogensulfite (sodium bisulfite, NaHSO3), 10 g, 5 mg/m3; sodium metabisulfite (Na2S2O5), 10 g, 5 mg/m3; sodium, potassium, or ammonium persulfate (Na2S2O8, K2S2O8, [NH4]2S2O8), 10 g, 0.5 mg/m3; sodium thiosulfate (Na2S2O3), 50 g. Sodium hydrosulfite releases sulfur dioxide on contact with acids. Persulfate salts release ozone and sulfuric acid on contact with water.
Penile calciphylaxis with extragenital gangrene
Published in Baylor University Medical Center Proceedings, 2021
Marcus Zaayman, Annika Silfvast-Kaiser, Edgar Rodriguez, Andrew J. DeCrescenzo, Alan Menter
A more conservative approach advocates the use of sodium thiosulfate, wound care, bisphosphonates, cinacalcet, vitamin K, and hemodialysis modification to control calcium and phosphate levels.4,6,7,16,17 Sodium thiosulfate treatment effectiveness likely relies on the chelation of calcium and possible dissolution of calcium deposits. Sodium thiosulfate has shown efficacy in patients with PC and systemic calciphylaxis.6,7,16,17 Cinacalcet is a calcimimetic agent, sensitizing parathyroid cells to calcium and causing increased suppression of parathyroid hormone. It is approved for use in patients with secondary hyperparathyroidism undergoing hemodialysis.4 In calciphylaxis, it also has some success improving lesions in ESRD patients. More data are necessary to determine true efficacy and dosing.4
Intramuscular dimethyl trisulfide: efficacy in a large swine model of acute severe cyanide toxicity
Published in Clinical Toxicology, 2019
Tara B. Hendry-Hofer, Alyssa E. Witeof, Dennean S. Lippner, Patrick C. Ng, Sari B. Mahon, Matthew Brenner, Gary A. Rockwood, Vikhyat S. Bebarta
Nithiodote®, an FDA approved therapy for cyanide poisoning, contains sodium nitrite and sodium thiosulfate [3]. Sodium thiosulfate acts as a sulfur donor, converting cyanide to the less toxic, renally excreted compound thiocyante [4–6]. Thiosulfate relies on the sulfur transferase rhodanese, which is primarily found in the mitochondria of the liver and kidneys. Furthermore, thiosulfate is minimally lipophilic, limiting its ability to penetrate the cell and blood–brain barrier, a target organ of cyanide toxicity [4,7]. Dimethyl trisulfide (DMTS), like the FDA approved drug sodium thiosulfate, has been found to be therapeutic following cyanide poisoning [8]. Similar to sodium thiosulfate, DMTS, a sulfur-based molecule found in garlic, onion and other plants, acts as a sulfur donor making it an antagonist for cyanide, converting cyanide to the less toxic compound thiocyanate [9,10]. However, compared to thiosulfate, DMTS has been shown to clear cyanide with greater efficiency, making it a potentially ideal candidate drug for cyanide toxicity [8,9].
A meta-analysis of preclinical studies using antioxidants for the prevention of cisplatin nephrotoxicity: implications for clinical application
Published in Critical Reviews in Toxicology, 2020
Alfredo G. Casanova, M. Teresa Hernández-Sánchez, Carlos Martínez-Salgado, Ana I. Morales, Laura Vicente-Vicente, Francisco J. López-Hernández
In preclinical models, thiol-containing molecules (e.g. sodium thiosulfate; N-acetylcysteine, NAC) ameliorate cisplatin nephrotoxicity for their antioxidant properties (Dickey et al. 2005), and for preventing aquation inside the cells [a critical step of cisplatin cytotoxicity (Perez 1998; Sancho-Martínez et al. 2018)], without interfering with the chemotherapeutic effect (Hirosawa et al. 1989; Muldoon et al. 2015; Visacri et al. 2019). However, at the clinical level, sodium thiosulfate has been proved effective (Markman et al. 1985; Hirosawa et al. 1989; Malmström et al. 1993; Alvarado et al. 1997; Balm et al. 2004), with minor side effects (Si et al. 1992); whereas the utility of NAC has been questioned (Visacri et al. 2019). This means that additional barriers emerge in vivo for specific compounds that limit their action. Interestingly, thiols are effective but not outstanding nephroprotectants in this meta-analysis, which supports further exploration for the better preclinical candidates identified.
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