Organic acidosis

The chloride (CD) ion is the most abundant anion in the ECF (see Table 46-2), In the absence of acid-base disturbances, Cr concentrations in plasma will generally follow those of Na. However, determination of plasma CD concentration is useful in the differential diagnoses of acid-base disturbances and is essential for calculating the anion gap (see Increased Anion Gap Acidosis [Organic Acidosis] section later in this chapter). Fluctuations in serum or plasma Cl have little clinical consequence, but do serve as signs of an underlying disturbance in fluid and acid-base homeostasis and can be an aid in differentiating the cause of these disturbances. 

The presence of mild elevations in the SAG caimot be antomat-ically attribnted to the presence of a high SAG metabolic acidosis. Elevations in the SAG are commonly seen in hospitalized patients, especially those who are critically iU. A variety of factors may con-tribnte to this nonspecific elevation in the SAG, inclnding the presence of alkalemia, which increases the anionic charge of albnmin and other plasma proteins. The nsefnlness of the SAG as a marker of acid-base status is dependent on proper interpretation of a patient s clinical status. Despite these limitations, when the SAG exceeds 20 to 25 mEq/L a significant organic acidosis is likely to be present. 

Excessive bicarbonate therapy of an organic acidosis Mild/moderate potassium deficiency Sodium chloride-resistant (urinary chloride concentration >20 mEq/L)... 

Serum electrolytes should be monitored in patients with CKD for the development of metabolic acidosis. Metabolic acidosis in patients with CKD is generally characterized by an elevated anion gap greater than 17 mEq/L (17 mmol/L), due to the accumulation of phosphate, sulfate, and other organic anions. 

Sepsis The systemic inflammatory response syndrome and documented infection (culture or Gram stain of blood, sputum, urine, or normally sterile body fluid positive for pathogenic microorganisms Severe sepsis Sepsis associated with organ dysfunction, hypoperfusion, or hypotension (systolic blood pressure less than 90 mm Hg). Hypoperfusion and perfusion abnormalities may include, but are not limited to, lactic acidosis, oliguria, or acute alteration in mental status. 

Acidosis occurs during cardiac arrest because of decreased blood flow and inadequate ventilation. Chest compressions generate only about 20% to 30% of normal cardiac output, leading to inadequate organ perfusion, tissue hypoxia, and metabolic acidosis. Furthermore, the lack of ventilation causes retention of carbon dioxide, leading to respiratory acidosis. The combined acidosis reduces myocardial contractility and may cause arrhythmias because of a lower fibrillation threshold. 

Sepsis associated with organ dysfunction, hypoperfusion, or hypotension. Hypoperfusion and perfusion abnormalities may include, but are not limited to, lactic acidosis, oliguria, or acute alteration in mental status. 

Progression of uncontrolled sepsis leads to evidence of organ dysfunction, which may include oliguria, hemodynamic instability with hypotension or shock, lactic acidosis, hyperglycemia or hypoglycemia, possibly leukopenia, disseminated intravascular coagulation, thrombocytopenia, acute respiratory distress syndrome, GI hemorrhage, or coma. 

Metabolic acidosis is characterized by decreased pH and serum HC03 concentrations, which can result from adding organic acid to extracellular fluid (e.g., lactic acid, ketoacids), loss of HC03 stores (e.g., diarrhea), or accumulation of endogenous acids due to impaired renal function (e.g., phosphates, sulfates). 

Tromethamine, a highly alkaline solution, is a sodium-free organic amine that acts as a proton acceptor to prevent or correct acidosis. However, no evidence exists that tromethamine is beneficial or more efficacious than sodium bicarbonate. The usual empiric dosage for tromethamine is 1 to 5 mmol/kg administered IV over 1 hour and an individualized dose can be calculated as follows ... 

A Add-base abnormalities Metabolic acidosis resulting from the accumulation of organic and inorganic... 

Clinical chemistry prior to death for both men revealed metabolic acidosis, acute renal and hepatic failure, skeletal muscle necrosis, and damage to other organ systems. Autolysis of viscera prevented complete characterization of lesions associated with mortality from these... 

Methanol is a solvent, which is added to ethanol and sometimes used in antifreeze. The main target organ is the optic system resulting from metabolic inhibition and systemic toxicity due to metabolic acidosis from formate and lactate. Toxicity is due to metabolism to formic acid via alcohol dehydrogenase and insufficient detoxication via tetrahydrofolate. The overall result is circulus hypoxicus. Treatment involves blockade of metabolism with ethanol and treatment of metabolic acidosis (NaHCC>3). 

Experience with metformin in a large American health organization in 9875 patients has been presented (68). There was one probable case of lactic acidosis in an 82-year-old woman who developed renal impairment while taking metformin 500 mg/day. 

A non-diabetic 25-year-old woman died after 2 days of lactic acidosis and multiple organ failure, having taken an unknown amount of her father s metformin (58,131). 

Acetazolamide can produce severe lactic acidosis, with an increased lactaterpyruvate ratio, ketosis with a low beta-hydroxybutyrateracetoacetate ratio, and a urinary organic acid profile consistent with pyruvate carboxylase deficiency. The acquired enzymatic injury that results from inhibition of mitochondrial carbonic anhydrase V, which provides bicarbonate to pyruvate carboxylase, can damage the tricarboxylic acid cycle. 

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