Acidosis metabohc

Solutions of weak acids or bases and their conjugates exhibit buffering, the abihty to resist a change in pH following addition of strong acid or base. Since many metabohc reactions are accompanied by the release or uptake of protons, most intracellular reactions are buffered. Oxidative metabohsm produces CO2, the anhydride of carbonic acid, which if not buffered would produce severe acidosis. Maintenance of a constant pH involves buffering by phosphate, bicarbonate, and proteins, which accept or release protons to resist a change... 

Venkatesha SL, Umamaheswara Rao GS. Metabohc acidosis and hyperventilation induced by acetazolamide in patients with central nervous system pathology. Anesthesiology 2000 93(6) 1546-8. 

Farag E, Deboer G, Cohen BH, Niezgoda J. Metabohc acidosis due to propofol infusion. Anesthesiology 2005 102 697-8. 

The most common side effects are ataxia, impaired concentration, confusion, memory difficulties, dizziness, fatigue, paresthesias, and somnolence. Nephrohthiasis occurs in 1.5% of patients. It has also been associated with acute narrow-angle glaucoma, oligohidrosis, and metabohc acidosis. 

Arterial blood gas (ABC) to assess for metabohc and respiratory acidosis... 

Propofol is very lipid soluble, has a large volume of distribution, and has a rapid onset of action. It has comparable efficacy to midazolam for refractory GCSE. It has been associated with metabohc acidosis, hemodynamic instability, and bradyarrhythmias that are refractory to treatment. 

Fanous MM, MarenT. Does metabohc acidosis contribute to the lOP effect of acetazolamide Invest Ophthalmol Vis Sci 1992 33(suppl) 1246. 

Henger A, Tntt P, Hnlter HM, Krapf R. Acid-base effects of inhibition of aldosterone and angiotensin II action in chronic metabohc acidosis in humans. J Am Soc Nephrol 1999 10 121A. 

Four preterm neonates with posthemorrhagic ventricular dilatation developed severe metabohc acidosis after being given acetazolamide (12). The acidosis suddenly disappeared after a transfusion of packed erythrocytes, which was attributed to the citrate contained in the blood. 

Accidental poisoning with acetazolamide should be included in the differential diagnosis of metabohc acidosis. 

Momblano P, Pradere B, Jarrige N, Concina D, Bloom E. Metabohc acidosis induced by cetrimonium bromide. Lancet 1984 2(8410) 1045. 

Because of its adverse effects, it is logical to omit iodine from all pharmaceutical formulations whenever possible, and at least clearly label its presence when it is necessary. The adverse effects of iodine include goiter and hypothyroidism (19,21), hyperthyroidism (SEDA-18,176), neutropenia (22), metabohc acidosis (23), and generalized iododerma (16). 

One case of hjrperlactatemic metabohc acidosis together with hemolytic anemia dne to glncose-6-phosphate dehydrogenase deficiency has been reported (40). 

Ohsuga S, Ohsuga H, Takeoka T, Ikeda A, Shinohara Y. [Metabohc acidosis and hypoglycemia during calcium hopantenate administration—report on 5 patients.] Rinsho Shinkeigaku 1989 29(6) 741-6. 

Paraldehyde can cause a metabohc acidosis, due to inability of the renal tubules to acidify the urine several cases have been described (9-15). 

Sawada M, Tsurumi H, Kara T, Goto H, Yamada T, Oyama M, Moriwaki H. Graft failure of autologous peripheral blood stem cell transplantation due to acute metabohc acidosis associated with total parenteral nutrition in a patient with relapsed breast cancer. Acta Haematol 2000 102(3) 157-9. 

Nakasaki H, Ohta M, Soeda J, Makuuchi H, Tsuda M, Tajima T, Mitomi T, Fujii K. Clinical and biochemical aspects of thiamine treatment for metabohc acidosis dnring total parenteral nutrition. Nutrition 1997 13(2) 110-17. 

Topiramate lowers serum bicarbonate by inhibiting carbonic anhydrase. In 20 of 29 children there was a greater than 10% fall in serum bicarbonate after starting topiramate (mean absolute reduction 4.7 mmol/1), but none had significant sjmptoms of metabohc acidosis, except possibly for anorexia in one (44). In another report, mild to moderate metabolic acidosis (bicarbonate concentrations, 16-21 mmol/1) developed in three topiramate-treated patients aged 25-51 years the condition was not considered clinically significant, but it led to diagnostic tests to exclude other causes (45). 

A 16-month-old girl developed increasing irritability associated with topiramate it resolved promptly on withdrawal. Venous blood showed a metabohc acidosis. 

Metabohc acidosis developed in eight of nine infants and toddlers aged 5 months to 2.3 years, weights 8.2-26... 

Takeoka M, Hohnes GR, Thiele E, Bourgeois B, Hehners SL, Duffy FH, Riviello JJ Jr. Topiramate and metabohc acidosis in pediatric epilepsy. Epilepsia 1999 40(Suppl 7) 126. 

Sethi PP, Tulyapronchote R, Faught E, GiUiam F. Topiramate-induced metabohc acidosis. Epilepsia 1999 40(Suppl 7) 148. 

Stowe CD, Bollinger T, James LP, Haley TM, Griebel ML, Farrar HC 3rd. Acute mental status changes and hyperchloremic metabohc acidosis with long-term topiramate therapy. Pharmacotherapy 2000 20(l) 105-9. 

Philippi H, Boor R, Reitter B. Topiramate and metabohc acidosis in infants and toddlers. Epilepsia 2002 43(7) 744—7. 

Flanagan RJ, Mant TGK. Coma and metaboHc acidosis in severe acute paracetamol poisoning. Human Toxicol 1986 5 179-82. 

The finding of a hyperchloremic metabohc acidosis in a patient without evidence of gastrointestinal bicarbonate losses and with no obvious pharmacological cause should prompt suspicion of an RTA. The presence of suggestive clinical (e.g., nephrocalcinosis in dRTA) or biochemical (e.g., hypophosphatemia and hypouricemia as a result of proximal tubular wasting in pRTA) features should also be considered. 

Increased plasma Cl" concentration, Uke increased Na concentration, occurs with dehydration, RTA, acute renal failure, metabohc acidosis associated with prolonged diarrhea and loss of sodium bicarbonate, DI, states of adrenocortical hyperfimction, and overtreatment with saline solutions. A slight rise in Cl" concentration may also be seen in respiratory alkalosis due to the renal compensation of excreting... 

Hyperventilation in lactic acidosis is more intense than in other forms of metaboHc acidosis. It is believed that this is because of the participation of the respiratory center in lactic acid production and the resulting greater local acidification of the respiratory center. During exercise, lactate levels may increase significantly, from an average normal concentration of -0.9 mmol/L to 12 mmol/L. However, under normal conditions, the lactate is rapidly metabolized so that the "acidosis is only transient. 

This generally occurs with blood salicylate concentrations above 30 mg/dL. Salicylate, itself an unmeasured anion, alters peripheral metabolism, leading to the production of various organic acids without dominance of any specific acid. The processes eventually result in a metabohc acidosis with a high anion gap. Saficylate also stimulates the respiratory center to increase the rate and depth of respiration, resulting in a low PCO2, low HCOj, and respiratory alkalosis (see the section entitled Respiratory Alkalosis). In adults, mijced respiratory aUcalosis and metabolic acidosis are more common, whereas in children, metabolic acidosis predominates. 

Acidosis seen during cardiac arrest results from decreased blood flow and inadequate ventilation. Chest compressions generate approximately 20% to 30% of normal cardiac output, leading to inadequate organ perfusion, tissue hypoxia, and metabohc acidosis. In addition, the lack of ventilation causes retention of carbon dioxide, leading to respiratory acidosis. This combined acidosis produces not only reduced myocardial contractility and negative inotropic effect but also the appearance of arrhythmias because of a lower fibrillation threshold. In early cardiac arrest, adequate alveolar ventilation is the mainstay of control to limit the accumulation of carbon dioxide and control the acid-base imbalance. With arrests of long duration, buffer therapy often is necessary. 

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