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central nervous system damage In alcoholic ketoacidosis, thiamine should be given together with glucose to avoid the development of Wernicke s encephalopathy The amount of HCO3 deficit can be calculated as follows: Amount of HCO3 deficit = 05 body weight (24 HCO3 ) Half of the calculated deficit should be administered within the first 3 4 hours to avoid overcorrection and volume overload In methanol intoxication, ethanol has been used as a competitive substrate for alcohol dehydrogenase, which metabolizes methanol to formaldehyde Recently, successful treatment of methanol intoxication through direct inhibition of alcohol dehydrogenase by fomepizole has been reported
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Evaluate effective circulating volume by physical examination and check urinary chloride concentration This will help differentiate saline-responsive metabolic alkalosis from saline-unresponsive alkalosis
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Metabolic alkalosis is characterized by high HCO3 The high HCO3 is also seen in chronic respiratory acidosis (see below), but pH differentiates the two disorders Abnormalities that generate HCO3 within the body are called initiation factors of metabolic alkalosis, whereas abnormalities that promote renal conservation of HCO3 are called maintenance factors Metabolic alkalosis may remain even after the initiation factors have disappeared It is useful to classify the causes of metabolic alkalosis into two groups based on saline responsiveness or urinary Cl , which are markers for volume status (Table 21 16) Saline-responsive metabolic alkalosis is a sign of extracellular volume contraction, and saline-unresponsive alkalosis implies a volume-expanded state It is rare for a compensatory increase in PCO2 to exceed 55 mm Hg A higher value implies a superimposed respiratory acidosis
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Treatment of RTA is mainly achieved by administration of alkali (either as bicarbonate or citrate) to correct metabolic abnormalities and prevent nephrocalcinosis and renal failure Large amounts of alkali (10 15 mEq/kg/d) may be required to treat proximal RTA because most of the alkali is excreted into the urine, which exacerbates hypokalemia Thus, a mixture of sodium and potassium salts, such as KShohl solution, is preferred The addition of thiazides may reduce the amount of alkali required, but hypokalemia may develop Correction of type 1 distal RTA requires a smaller amount of alkali (1 3 mEq/kg/d) and potassium supplementation as needed For the treatment of type IV RTA, dietary potassium restriction may be needed and potassium-retaining drugs should be withdrawn Fludrocortisone may be effective in cases with hypoaldosteronism, but should be used with care, preferably in combination with loop diuretics In some cases, alkali supplementation (1 3 mEq/kg/d) may be required
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Casaletto JJ Differential diagnosis of metabolic acidosis Emerg Med Clin North Am 2005 Aug;23(3):771 87 [PMID: 15982545] Eledrisi MS et al Overview of the diagnosis and management of diabetic ketoacidosis Am J Med Sci 2006 May;331(5):243 51 [PMID: 16702793] Forni LG et al Circulating anions usually associated with the Krebs cycle in patients with metabolic acidosis Crit Care 2005 Oct 5;9(5):R591 5 [PMID: 16277723] Matin MJ et al Use of serum bicarbonate measurement in place of arterial base deficit in the surgical intensive care unit Arch Surg 2005 Aug;140(8):745 51 [PMID: 16103283] Moe OW et al Clinical acid-base pathophysiology: disorders of plasma anion gap Best Pract Res Clin Endocrinol Metab 2003 Dec;17(4):559 74 [PMID: 14687589] Rosival V Metabolic acidosis Crit Care Med 2004 Dec;32(12): 2563 4 [PMID: 15599180]
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Saline-responsive metabolic alkalosis is by far the more common disorder It is characterized by normotensive extracellular volume contraction and hypokalemia Less frequently, hypotension or orthostatic hypotension may be seen In vomiting or nasogastric suction, for example, loss of acid (HCl) initiates the alkalosis, but volume contraction from loss of Cl sustains the alkalosis because the decline in GFR causes avid renal Na+ and HCO3 reabsorption Because there is Cl depletion from loss of HCl, NaCl, and KCl from the stomach, the available anion is HCO3 , whose reabsorption is increased proximally, and urine pH may remain acidic despite alkalemia (paradoxic aciduria) Renal Cl reabsorption (as well as Na+ reabsorption) is high, and the urinary Cl is therefore low (< 10 20 mEq/L) In alkalosis, bicarbonaturia may force Na+ excretion as the accompanying cation even if volume depletion is present Therefore, urinary Cl is preferred to urinary Na+ as a measure of extracellular volume An exception to the usefulness of urinary Cl is in patients who have recently received diuretics Their urine may contain high Na+ and Cl despite extracellular volume contraction If diuretics are discontinued, the urinary Cl will decrease Metabolic alkalosis is generally associated with hypokalemia This is due partly to the direct effect of alkalosis per se on renal potassium excretion and partly to secondary hyperaldosteronism from volume depletion Hypokalemia induced in this fashion further worsens the metabolic alkalosis by increasing bicarbonate reabsorption in the proximal tubule and hydrogen ion secretion in the distal tubule Administration of KCl will correct the disorder Repletion of KCl is important to reverse the disorder 1 Contraction alkalosis Diuretics can acutely decrease extracellular volume from urinary loss of NaCl and water There is no associated bicarbonaturia, so that body HCO3
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