Metabolic lactic acidosis

Severe metabolic lactic acidosis often develops secondary to tissue ischemia and causes localized vasodilation, which further exacerbates the impaired cardiovascular state. 

Lactic acid is the cause of one of many possible disorders in human acid-base metabolism. Lactic acidosis represents an accumulation of lactic acid in the blood and tissues. This condition gradually depletes the natural buffers in the body and there is a consequent lowering of pH. As described in the entry on Glycolysis, lactic acid is the end product til (hat pmcess. Lactic acid blood levels are determined by at least Tour factors. The rate of generation of lactic acid the rate of transport from tissues to plasma and from plasma to the liver (point of utilization of lactic acid) the rate uf utilization and excretion of lactic acid by the kidneys. Normally, all of these funclions are maintained in balance to give a normal blood lactate concentration of about I niFq/l. 

Metabolic Lactic acidosis, worsening renal function... 

B. Cyanide toxicity, manifested by altered mental status and metabolic (lactic) acidosis, may occur with rapid high-dose infusion (> 10-15 mcg/kg/min) for periods of 1 hour or longer. Patients with depleted thiosulfate stores (eg, malnourished) may have elevated cyanide levels at lower infusion rates. Continuous intravenous infusion of hydroxocobalamin, 25 mg/h (see p 453 note caution with preservative), or thiosulfate (p 505) has been used to limit cyanide toxicity. If severe cyanide toxicity occurs, discontinue the nitropmsside infusion and consider antidotal doses of thiosulfate and sodium nitrite (p 476) or high-dose hydroxocobalamin (p 453 note concentrated fona not available in the United States). 

D. Propofol infusion syndrome, a condition of metabolic (lactic) acidosis, renal failure, rhabdomyolysis, and cardiovascular collapse, has been reported after prolonged hIgh-dose infusion in both pediatric and adult populations. 

One of serious complications of thiamine deficiency caused by the impairment of pyruvate utilization by PDHC is metabolic lactic acidosis. This is recognized as the sole condition responsible for lethal outcome of some misdiagnosed or lately treated thiamine-deficient patients (Klein et al. 2004) (Figure 33.1). 

Under certain circumstances, and very rarely, the inhibition of gluconeogenesis by metformin may suppress lactic acid metabolism and precipitate a potentially fatal lactic acidosis. Impairment of renal function, liver disease, alcoholism, conditions that give rise to increased lactate production (e.g. congestive heart failure, infections) are therefore contraindications for the application of metformin. 

Inhibition of Pyruvate Metabolism Leads to Lactic Acidosis... 

This isotonic volume expander contains sodium, potassium, chloride, and lactate that approximates the fluid and electrolyte composition of the blood. Ringer s lactate (also known as lactated Ringer s or LR) provides ECF replacement and is most often used in the perioperative setting, and for patients with lower GI fluid losses, burns, or dehydration. The lactate component of LR works as a buffer to increase the pH. Large volumes of LR may cause metabolic alkalosis. Because patients with significant liver disease are unable to metabolize lactate sufficiently, Ringer s lactate administration in this population may lead to accumulation of lactate with iatrogenic lactic acidosis. The lactate is not metabolized to bicarbonate in the presence of liver disease and lactic acid can result. 

Lactic acidosis A condition caused by build-up of lactic acid in the body. It leads to acidification of the blood (acidosis), and is a form of metabolic acidosis. 

Metabolic acidosis An acid-base disorder caused by overproduction or accumulation of acid (often lactic acid see lactic acidosis) or a deficit of base (i.e., bicarbonate). 

Alkali therapy can be used to treat patients with acute severe metabolic acidosis due to hyperchloremic acidosis, but its role is controversial in patients with lactic acidosis. Therapeutic options include sodium bicarbonate and tromethamine. 

Cyanide ion exerts an inhibitory action on certain metabolic enzyme systems, most notably cytochrome oxidase, the enzyme involved in the ultimate transfer of electrons to molecular oxygen. Because cytochrome oxidase is present in practically all cells that function under aerobic conditions, and because the cyanide ion diffuses easily to all parts of the body, cyanide quickly halts practically all cellular respiration. The venous blood of a patient dying of cyanide is bright red and resembles arterial blood because the tissues have not been able to utilize the oxygen brought to them. Cyanide intoxication produces lactic acidosis, the result of an increased rate of glycolysis and production of lactic acid. ... 

Metabolic acidosis In severe renal disease uncontrolled diabetes circulatory insufficiency due to shock, anoxia, or severe dehydration extracorporeal circulation of blood cardiac arrest and severe primary lactic acidosis where a rapid increase in plasma total CO2 content is crucial. Treat metabolic acidosis in addition to measures designed to control the cause of the acidosis. Because an appreciable time interval may elapse before all ancillary effects occur, bicarbonate therapy is indicated to minimize risks inherent to acidosis itself. 

Lactic acidosis Lactic acidosis is a rare, but serious, metabolic complication that can occur because of metformin accumulation during treatment when it occurs, it is fatal in approximately 50% of cases. Lactic acidosis also may occur in association with a number of pathophysiologic conditions, including diabetes mellitus, and whenever... 

Suspect lactic acidosis in any diabetic patient with metabolic acidosis lacking evidence of ketoacidosis (ketonuria and ketonemia). 

Lactic acidosis is a rare, but serious, metabolic complication that can occur because... 

T Pancreatic insulin release Metformin Peripheral insulin sensitivity hepatic glucose output/production i intestinal glucose absorption Dose Ist-line (naive pts), 1.25/250 mg PO daily-bid 2nd-line, 2.5/500 mg or 5/500 mg bid (max 20/2000 mg) take w/ meals, slowly T dose hold before 48 h after ionic contrast media Caution [C, -] Contra SCr >1.4 mg/dL in females or >1.5 mg/dL in males hypoxemic conditions (sepsis, recent MI) alcoholism metabolic acidosis liver Dz Disp Tabs SE HA, hypoglycemia, lactic acidosis, anorexia, N/V, rash Additional Interactions T Effects W/ amiloride, ciprofloxacin cimetidine, digoxin, miconazole, morphine, nifedipine, procainamide, quinidine, quinine, ranitidine, triamterene,... 

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