10), and measuring the levels of toxic alcohols (used for confirmation; typically, this testing is not time sensitive, and the treatment should not be withheld in any patient suspected of having toxic alcohol ingestion). Lastly, serious skin injuries can occur in the setting of extravasation of hypertonic bicarbonate solutions, and whenever possible it should be administered through large bore intravenous lines or central venous lines. The potential benefits of exogenous intravenous sodium bicarbonate include the correction of metabolic acidosis with its associated detrimental effects. However, the role of sodium bicarbonate in the management of acute acidosis remains controversial and may even be associated with potential side effects and complications such as volume overload, metabolic alkalosis, hypercapnia, hypokalemia, hypernatremia and hyperosmolality, and ionized hypocalcemia [6, 7]. In rare circumstances (such as acute illness and worsening renal function), metformin administration may result in the development of lactic acidosis that is believed to be secondary to mitochondrial dysfunction, with a shift towards anaerobic glycolysis [60–62]. Nevertheless, it is important to keep in mind that IV sodium bicarbonate represents only a single tool in the management of these toxicities and additional mechanisms of toxicity may account for protean clinical manifestations of these poisonings. A repeat level may sometimes be obtained two hours after hemodialysis to exclude rebound. Sodium bicarbonate is the active ingredient in baking soda. When administered, sodium bicarbonate dissociates into a molecule of sodium and bicarbonate. The Role of Sodium Bicarbonate in the Management of Some Toxic Ingestions, Department of Medicine, University of Kentucky College of Medicine, Lexington, KY, USA, University of Kansas Medical Center, Kansas City, KS, USA, http://www.cdc.gov/nchs/data/hus/hus14.pdf#085, Carbamazepine, Lamotrigine, Zonisamide, Lacosamide, Cocaine, local anesthetics, Thioridazine, Propranolol, Amantadine, Chloroquine, Hydroxychloroquine, Cyclobenzaprine, K. Alka and J. R. Casey, “Bicarbonate transport in health and disease,”, T. Dybvik, T. Strand, and P. A. Steen, “Buffer therapy during out-of-hospital cardiopulmonary resuscitation,”, R. B. Vukmir and L. Katz, “Sodium bicarbonate improves outcome in prolonged prehospital cardiac arrest,”, S. S. Brar, A. Y.-J. The major mechanism of action of aspirin is mediated via inhibition of cyclooxygenase enzyme, resulting in decreased production of thromboxane A2 and various prostaglandins [53]. Salicylic acid (HS) is a weak acid that exists in a charged (deprotonated, sal−) and uncharged (protonated, H+) form: H+ + sal−  ⇔ HS. The development of hypokalemia is particularly detrimental to the patients with salicylate-mediated toxicity because of increase in hydrogen ion urinary excretion resulting in more acidic urine and greater salicylate reabsorption and thus, should be aggressively corrected [55, 56]. Carbon dioxide under normal conditions (intact lung perfusion and ventilation) is exhaled, maintaining delicate acid-base equilibrium. However, according to the consensus guidelines, the therapy with IV sodium bicarbonate should be strongly considered when pH falls below 7.3 with the therapeutic aim of pH normalization. The decrease in the blood pH will favor formation of lipid soluble salicylic acid which easily penetrates blood-brain barrier and undergoes renal reabsorption [55]. Important to review briefly the metabolism of methanol to formaldehyde by hepatic alcohol! 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