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Potassium depletion, which can accompany diarrhea (and surreptitious laxative abuse), may also impair renal acidification Thus, when volume depletion is present, the urinary anion gap is a better measurement of ability to acidify the urine than urinary pH When large amounts of other anions are present in the urine, the urinary anion gap may not be reliable In such a situation, NH4+ excretion can be estimated using the urinary osmolar gap NH4+ excretion (mmol/L) = 05 Urinary osmolar gap = 05 [U osm 2(U Na+ + U K+) + U urea + U glucose] where urinary (U) concentrations and osmolality are in millimoles per liter
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C Dilutional Acidosis
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Rapid dilution of plasma volume by 09% NaCl may cause a mild hyperchloremic acidosis
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D Recovery from Diabetic Ketoacidosis
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See earlier section, Increased Anion Gap Acidosis (Increased Unmeasured Anion)
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decreases and Cl excretion If the respiratory alkalosis is corrected quickly, PCO2 will increase acutely but HCO3 will remain low until the kidneys can generate new HCO3 , which generally takes several days In the meantime, the increased PCO2 with low HCO3 causes metabolic acidosis In prolonged respiratory alkalosis, HCO3 increases from decreased renal NH4+Cl
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Clinical Findings
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Symptoms of metabolic acidosis are mainly those of the underlying disorder Compensatory hyperventilation is an important clinical sign and may be misinterpreted as a primary respiratory disorder; when severe, Kussmaul respirations (deep, regular, sighing respirations) are seen
F Hyperalimentation
Hyperalimentation fluids may contain amino acid solutions that acidify when metabolized, such as arginine hydrochloride and lysine hydrochloride
Assessment of Hyperchloremic Metabolic Acidosis by Urinary Anion Gap
Increased renal NH4+Cl excretion to enhance H+ removal is a normal physiologic response to metabolic acidosis NH3 reacts with H+ to form NH4+, which is accompanied by the anion Cl for excretion The normal daily urinary excretion of NH4Cl of about 30 mEq can be increased up to 200 mEq in response to acid load Urinary anion gap from a random urine sample ([Na+ + K+] Cl ) reflects the ability of the kidney to excrete NH4Cl as in the following equation: Na + K + NH = Cl + 80 where 80 is the average value for the difference in the urinary anions and cations other than Na+, K+, NH4+, and Cl Therefore, urinary anion gap is equal to (80 NH4+), and thus aids in the distinction between gastrointestinal and renal causes of hyperchloremic acidosis If the cause of the metabolic acidosis is gastrointestinal HCO3 loss (diarrhea), the renal acidification ability remains normal and NH4Cl excretion increases in response to the acidosis The urinary anion gap is negative (eg, 30 mEq/L) If the cause is distal RTA, the urinary anion gap is positive (eg, +25 mEq/L), since the basic lesion in the disorder is the inability of the kidney to excrete H+ and thus the inability to increase NH4Cl excretion In proximal (type II) RTA, the kidney has defective HCO3 reabsorption, leading to increased HCO3 excretion rather than decreased NH4Cl excretion Thus, the urinary anion gap is often negative in proximal (type II) RTA Urinary pH may not as readily differentiate between the two causes Despite acidosis, if volume depletion from diarrhea causes inadequate Na+ delivery to the distal nephron and therefore decreased exchange with H+, urinary pH may not be lower than 53 In the presence of this relatively high urine pH, however, H+ excretion continues due to buffering of NH3 to NH4+, since the pK of this reaction is as high as 91
+ + 4+
B Laboratory Findings
Blood pH, serum HCO3 , and PCO2 are decreased Anion gap may be normal (hyperchloremic) or increased (normochloremic) Hyperkalemia may be seen (see above)
Treatment
A Increased Anion Gap Acidosis
Treatment is aimed at the underlying disorder, such as insulin and fluid therapy for diabetes and appropriate volume resuscitation to restore tissue perfusion The metabolism of lactate will produce HCO3 and increase pH The use of supplemental HCO3 is indicated for treatment of hyperkalemia (Table 21 7) and some forms of normal anion gap acidosis but has been controversial for treatment of increased anion gap metabolic acidosis Controversy remains about the efficacy and safety of alkali therapy for severe metabolic acidosis Administration of large amounts of HCO3 may have deleterious effects, including hypernatremia and hyperosmolality Furthermore, intracellular pH may decrease because administered HCO3 is converted to CO2, which easily diffuses into cells There, it combines with water to create additional hydrogen ions and worsening of intracellular acidosis Theoretically, this could impair cellular function, but the clinical significance of this phenomenon is uncertain In addition, alkali administration is known to stimulate phosphofructokinase activity, thus exacerbating lactic acidosis via enhanced lactate production Ketogenesis is also augmented by alkali therapy In salicylate intoxication, however, alkali therapy must be started unless blood pH is already alkalinized by respiratory alkalosis, since the increment in pH converts salicylate to more impermeable salicylic acid and thus prevents
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