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Anion gap serum

Increased Serum Anion Gap Normal Serum Anion Gap/Hyperchloremic States... [Pg.855]

Gabow PA, Kaehny WD, Fennessey PV, Goodman SI, Gross PA, Sclirier RW. Diagnostic importance of an increased serum anion gap. N Engl J Med 1980 303 854-8. [Pg.1776]

Winter SD, Pearson JR, Gabow PA, Schultz AL, Lepoff RB. The fall of the serum anion gap. Arch Intern Med 1990 150 311-3. [Pg.1776]

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). [Pg.236]

The serum anion gap (SAG), as defined below, may be used to infer whether an organic or mineral acidosis is present. [Pg.987]

Kraut, J. A., and N. E. Madias. 2007. Serum anion gap Its uses and limitations in clinical medicine. Clinical Journal of the American Society of Nephrology 2 162-174. [Pg.136]

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. [Pg.392]

Metabolic acidosis is characterized by a decrease in serum HC03. The anion gap is used to narrow the differential diagnosis, as this acidosis may be caused by addition of acids (increased anion gap) or loss of HC03 (normal anion gap). The compensation for metabolic acidosis is an increase in ventilation with a decrease in arterial C02. [Pg.419]

It is important to realize that the serum HCO, concentration may be affected by the presence of unmeasured endogenous acids (lactic acidosis or ketoacidosis). Bicarbonate will attempt to buffer these acids, resulting in a 1 mEq loss of serum HCO, for each 1 mEq of acid titrated. Because the cation side of the equation is not affected by this transaction, the loss of serum HC03 results in an increase in the calculated anion gap. Identification of an increased anion gap is very important for identifying the etiology of the acid-base disorder. The concept of the increased anion gap will be applied later in the case studies section. [Pg.424]

Any time an ABG is analyzed it is wise to concurrently inspect the serum chemistry values to calculate the anion gap. The body does not generate an anion gap to compensate for a primary disorder. As such, if the calculated anion gap exceeds 12 mEq/L (mmol/L) there is a primary metabolic acidosis regardless of the pH or the serum HC03 concentration. The anion gap may be artificially lowered by decreased serum albumin, multiple myeloma, lithium intoxication, or a profound increase in the serum potassium, calcium, or magnesium. [Pg.424]

Acid-base disturbances are common clinical problems that are not difficult to analyze if approached in a consistent manner. The pH, PaC02, and HCO, should be inspected to identify all abnormal values. This should lead to an assessment of which deviations represent the primary abnormality and which represent compensatory changes. The serum electrolytes should always be used to calculate the anion gap. In cases in which the anion gap is increased, the excess anion gap should be added back to the measured HC03 . The anion gap and the excess... [Pg.429]

None unless symptoms present => Consider lactate concentrations in patients with 4- serum bicarbonate or T anion gap... [Pg.1269]

Etoposide Blood pressure, respiratory rate, serum pH, serum bicarbonate with arterial blood gases, and evaluation of anion gap if necessary... [Pg.1464]

Frequently monitor both ethylene glycol levels and acid-base balance, as determined by serum electrolyte (anion gap) or arterial blood gas analysis... [Pg.532]

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. [Pg.503]

The major concern of the emergency department physicians was the lethargy, hypotonia, and seizure activity. Initial laboratory studies revealed that the child had a normal complete blood count and smear. Other blood tests revealed metabolic acidosis with a bicarbonate concentration of 11 mEq/L (normal is 20-25 mEq/L) and an anion gap of 22 mEq/L (normal is < 15 mEq/L). His serum glucose, calcium, and magnesium concentrations were normal. To exclude the diagnosis of meningitis, a spinal tap was performed. The cell counts and chemistries of the cerebrospinal fluid were normal. The physicians considered that the child might have sepsis and administered antibiotics and intravenous fluids. Prior to administration of antibiotics, blood, urine, and cerebrospinal fluid were sent for bacterial culture. [Pg.134]

At presentation, the patient was hemodynami-cally unstable. She had a rapid heart rate and exhibited orthostatic hypotension (a fall in blood pressure on assuming an upright posture) and slow mentation. Her fluid deficit was greater than 4 L. Her lab work revealed hyponatremia (low serum sodium), hyperkalemia (high serum potassium), and a severe anion gap metabolic acidosis with dehydration. Her anion gap was 28, and her corrected serum Na+ was 135 mEq/L. [Pg.358]

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. [Pg.259]

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. [Pg.260]

Constable P D, Gohar H M, Morin D E et al 1996 Use of hypertonic saline-dextran solution to resuscitate hypovolemic calves with diarrhea. American Journal of Veterinary Research 57 97-104 Constable P D, Hinchcliff K W, Muir W W 1998 Comparison of anion gap and strong ion gap as predictors of unmeasured strong ion concentration in plasma and serum from horses. American Journai of Veterinary Research 59 881-887... [Pg.359]


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