Anion gap elevated

In any patient with an elevated anion gap, also check the osmolar gap a combination of elevated anion and osmolar gaps suggests poisoning by methanol or ethylene glycol. Note Combined osmolar and anion gap elevation may also be seen with severe alcoholic ketoacidosis and even diabetic ketoacidosis. 

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. 

It is critical that the blood methanol level be determined as soon as possible if the diagnosis is suspected. Methanol concentrations higher than 50 mg/dL are thought to be an absolute indication for hemodialysis and treatment with fomepizole or ethanol, although formate blood levels are a better indication of clinical pathology. Additional laboratory evidence includes metabolic acidosis with an elevated anion gap and osmolar gap (see Chapter 59). A decrease in serum bicarbonate is a uniform feature of severe methanol poisoning. 

Normally, the sum of the cations exceeds the sum of the anions by no more than 12-16 mEq/L (or 8-12 mEq/L if the formula used for estimating the anion gap omits the potassium level). A larger-than expected anion gap is caused by the presence of unmeasured anions (lactate, etc) accompanying metabolic acidosis. This may occur with numerous conditions, such as diabetic ketoacidosis, renal failure, or shock-induced lactic acidosis. Drugs that may induce an elevated anion gap metabolic acidosis (Table 58-1) include aspirin, metformin, methanol, ethylene glycol, isoniazid, and iron. 

Metabolic acidosis follows, and an increased anion gap results from accumulation of lactate as well as excretion of bicarbonate by the kidney to compensate for respiratory alkalosis. Arterial blood gas testing often reveals this mixed respiratory alkalosis and metabolic acidosis. Body temperature may be elevated owing to uncoupling of oxidative phosphorylation. Severe hyperthermia may occur in serious cases. Vomiting and hyperpnea as well as hyperthermia contribute to fluid loss and dehydration. With very severe poisoning, profound metabolic acidosis, seizures, coma. 

Provide a biochemical explanation for this person s disorder. What is the difference between this patient and that in Problem 21.1 What is the significance of "Kussamaul" breathing What is the significance of the elevated "anion gap" and glycosylated hemoglobin Can you estimate this patient s blood pH and some electrolytes How would you treat him ... 

Intoxication may present as inebriation and drowsiness similar to ethanol use. Other symptoms are vomiting, diarrhea, delirium and agitation, back and abdominal pain, and clammy skin. Toxic effects usually follow a latent period of several hours. Formate inhibits mitochondrial cytochromes resulting in neurotoxicity. Ocular signs include blurred vision, dilated pupils, and direct retinal toxicity with optic disc hyperemia and ultimately permanent blindness [91]. Cerebral hemorrhagic necrosis has been reported [92]. Severe poisoning may result in Kussmaul respiration, inspiratory apnea, coma, and death. Urine samples may have the characteristic smell of formaldehyde. An elevated serum osmolal gap from methanol will be evident early in presentation but may disappear after approximately 12 hours. At this time, an elevated anion gap metabolic acidosis from retained formate may be evident. 

Early laboratory findings include a high serum osmolal gap from the ethylene glycol. An extreme metabolic acidosis with greatly elevated anion gap follows, principally from glycolic acid [100]. Hypocalcemia and hyperkalemia may be evident and urinalysis may reveal calcium oxalate crystalluria, hematuria, and proteinuria. 

Benzyl alcohol is a preservative that may be present in multidose vials of bacteriostatic sodium chloride and bacteriostatic water for injection and pharmaceuticals available in multidose vials for parenteral use. An association between the presence of benzyl alcohol in solutions used for flushing intravascular catheters and to reconstitute medications and a gasping syndrome and deaths in neonates was first reported in the early 1980s.The neonates also displayed clinical findings such as an elevated anion gap, metabolic acidosis, CNS depression, seizures, respiratory failure, renal and hepatic failures, cardiovascular collapse, and death. Those at highest risk were premature infants who weighted less... 

Kidney damage results from precipitation of oxalate crystals in the convoluted tubules. The elevated anion-gap metabolic acidosis is caused by glycolic acid and lactic acid. The latter is formed from pyruvate due to a shift in the redox potential favoring the production of lactate. The treatment is the same as that for methanol intoxication. 

The diagnosis of D-lactic acidosis is suspected in patients with disorders of the small intestine causing malabsorption and when the serum anion gap (Chapter 39) is elevated in the presence of normal serum levels of L-lactate and other organic acids. Measurement of serum D-lactate requires special enzymatic procedures utilizing D-lactate dehydrogenase and NADH. As D-lactate is converted to pyruvate, NADH is oxidized to NAD+ which is detected spectrophotometrically (Chapter 8). 

Acid-base disturbances frequently coexist with two or more simple disorders (Table 39-2). In these settings, blood pH is either severely depressed (e.g., a patient with metabolic acidosis and respiratory acidosis) or normal. Both plasma HCOj and pH may be within normal limits when metabolic alkalosis and metabolic ketoacidosis coexist, as in a patient with diabetic ketoacidosis who is vomiting. In this situation, an elevated anion gap may be the initial abnormality that can be detected in the underlying mixed acid-base disturbance. 

I 07. A child presents with severe vomiting, dehydration, and fever. Initial blood studies show acidosis with a low bicarbonate and an anion gap (the sum of sodium plus potassium minus chloride plus bicarbonate is 40 and larger than the normal 20 to 25). Preliminary results from the blood amino acid screen show two elevated amino acids, both with nonpolar side chains. A titration curve performed on one of the elevated species shows two ionizable groups with approximate pKs of 2 and 9.5. The most likely pair of elevated amino acids consists of... 

Laboratory tests on a sick child reveal a low white blood cell count, metabolic acidosis, increased anion gap, and mild hyperammonemia. Measurement of plasma amino acids reveals elevated levels of glycine, and measurement of urinary organic acids reveals increased amounts of propionic acid and methyl citrate. Which of the following processes is most likely ... 

The answer is d. (Murray, pp 238-249. Scriver, pp 2165-2194. Sack, pp 121-144. Wilson, pp 287-324.) Propionic acidemia (232000) results from a block in propionyl CoA carboxylase (PCC), which converts propionic to methylmalonic acid. Excess propionic acid in the blood produces metabolic acidosis with a decreased bicarbonate and increased anion gap (the serum cations sodium plus potassium minus the serum anions chloride plus bicarbonate). The usual values of sodium (-HO meq/L) plus potassium ( 4 meq/T) minus those for chloride (-105 meq/L) plus bicarbonate (—20 meq/L) thus yield a normal anion gap of -20 meq/L. A low bicarbonate of 6 to 8 meq/L yields an elevated gap of 32 to 34 meq/L, a gap of negative charge that is supplied by the hidden anion (propionate in propionic acidemia). Biotin is a cofactor for PCC and its deficiency causes some types of propionic acidemia. Vitamin B deficiency can cause methylmalonic aciduria because vitamin Bn is a cofactor for methylmalonyl coenzyme A mutase. Glycine is secondarily elevated in propionic acidemia, but no defect of glycine catabolism is present. 

Arterial blood gases and serum electrolytes should be measured regularly in patients with CKD. These patients should also have a complete medical history and review of medications to determine if there are other potential causes of acid-base disturbances (e.g., diabetic ketoacidosis, ingestion of toxins, or GI disorders). The anion gap, indicating the differences in unmeasured anions and cations, should also be calculated (see Chap. 51). An elevated anion gap (>17 mEq/L) is often present in those with CKD due to the accumulation of organic anions, phosphates, and sulfates. 

Lactic acidosis can occur in patients with SBS and may result in symptoms of ataxia and dehrium. D-Lactic acid is produced by the fermentation of malabsorbed carbohydrates by colonic bacteria, and increased concentrations are associated with small bowel bacterial overgrowth. " The diagnosis of D-lactic acidosis should be considered in patients with a functional colon who have an unexplained metabolic acidosis and an elevated anion gap. ... 

Initial laboratory studies showed a relatively large anion gap of 34 mmol/L (reference range = 9-15 mmol/L). An arterial blood gas analysis confirmed the presence of a metabolic acidosis. Mr. Martini s blood alcohol level was only slightly elevated. His serum glucose was 68 mg/dL (low normal). 

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