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Thread: [Laboratory] Electrolytes, Other Minerals, and Trace Elements

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    PharmD Year 1 TomHsiung's Avatar
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    Default [Laboratory] Electrolytes, Other Minerals, and Trace Elements

    Serum or plasma electrolyte concentrations are among the most commonly used laboratory tests by clinicians for assessment of a patient's clinical conditions and disease states.

    Sodium, potassium, and chloride are among the most commonly monitored electrolytes in clinical practice. Magnesium, calcium, and phosphate are also monitored as determined by the patient's disease states and/or clinical indication.

    Table 1 Normal Daily Dietary Nutrient Intake
    Nutrient Intake
    Sodium Variable; average 3.4 g (148 mEq)
    Potassium 50-100 mEq
    Chloride Varies with potassium and sodium intake
    Magnesium 300-400 mg
    Calcium ~1000 mg
    Phosphate 800-1500 mg
    Copper 2-5 mg
    Zinc 4-14 mg
    Manganese 3-4 mg
    Chromium 50-100 mcg


    Table 2 Conversion Factors to SI Units
    Nutrient Traditional Units Conversion Factors to SI Units SI Units
    Sodium mEq/L 1 mmol/L
    Potassium mEq/L 1 mmol/L
    Chloride mEq/L 1 mmol/L
    Magnesium mEq/L 0.5 mmol/L
    Calcium mg/dL 0.25 mmol/L
    Phosphate mg/dL 0.3229 mmol/L
    Copper mcg/dL 0.1574 umol/L
    Zinc mcg/dL 0.1530 umol/L
    Manganese mcg/L 18.2 umol/L
    Chromium mcg/L 19.2 nmol/L
    Last edited by TomHsiung; Sat 10th December '16 at 11:58am.
    B.S. Pharm, West China School of Pharmacy, Class of 2007, Health System Pharmacist, RPh. Hematology, Infectious Disease.

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    PharmD Year 1 TomHsiung's Avatar
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    Default Re: [Laboratory] Electrolytes, Other Minerals, and Trace Elements

    Sodium
    Normal range: 136-142 mEq/L or 136-142 mmol/L
    Sodium is the most abundant cation in the extracellular fluid and is the major regulating factor for bodily water balance. Extracellular (i.e., intravascular and interstitial) and intracellular sodium contents are closely affected by the body fluid status. Thus, an accurate interpretation of serum sodium concentration must include an understanding of body water homeostasis and the inter-relationship between the regulation of sodium and water.

    Hyponatremia
    Hyponatremia is loosely defined as a serum sodium concentration less than 136 mEq/L (<136 mmol/L). Hyponatremia may occur when total body water status is low (i.e., dehydration), normal, or high (i.e., fluid overload). Therefore, natremic status cannot be assessed without first assessing the fluid and water status of the patient.

    Fluid status should be evaluated based on vital signs; other supportive laboratory findings if available; recent changes in body weight; recent medical, surgical, and nutrition history; and findings from the physical examination. More importantly, the patient's renal function, hydration status, and fluid intake and output must be carefully assessed and closely monitored.

    The most common causes of hyponatremia can be broken down into two types: sodium depletion in excess of total body water loss and dilutional hyponatremia. Dilutional hyponatremia can be further categorized into five subtypes: 1) primary dilutional hyponatremia (e.g., SIADH and renal failure); 2) neuroendocrine (e.g., adrenal insufficiency and myxedema); 3) psychiatric disorder (e.g., psychogenic polydipsia); 4) osmotic hyponatremia (e.g., severe hyperglycemia); and 5) thiazide diuretic-induced.

    Hyponatremia associated with total body sodium depletion reflects a reduction in total body water, with an even larger reduction in total body sodium. This condition is primarily caused by depletion of extracellular fluid, which stimulates ADH release to increase renal water reabsorption even at the expense of causing a transient hypo-osmotic state.

    In addition, low serum sodium can also result when a large quantity of an osmotically active substance enters the bloodstream, resulting in a dilutional hyponatremia. This situation can occur with the use of mannitol, as well as in the presence of hyperglycemia.

    In hyperglycemia, the elevated serum glucose concentration results in high serum osmolarity, thus creating an osmolar gradient between the plasma compartment and the extracellular fluid leading to a shift of water into the intravascular space. The net effect is a dilution of the serum sodium concentration resulting in hyponatremia. In the absence of other causes impairing sodium homeostasis, the effect should be transient and should be reversed once serum glucose is normalized. However, hyperglycemia also leads to fluid loss through an osmotic diuretic effect. Hence, dilutional hyponatremia occurs as long as the rate of water moving from the cells into the blood is greater than the volume of water excreted through the urine. As cellular water diminishes and diuresis continues, plasma sodium may increase progressively.

    Hyponatremia associated with normal total body sodium, also called euvolemic or dilutional hyponatremia, refers to impaired water excretion without any alteration in sodium excretion. Etiologies include any mechanism that enhances ADH secretion or potentiates its action at the collecting tubules.

    Hyponatremia associated with an increase of total body sodium. This condition implies an increase in total body sodium with an even larger increase in total body water. It is frequently observed in edematous states such as CHF, cirrhosis, nephrotic syndrome, and chronic kidney disease (CKD). In these patients, renal handling of water and sodium is usually impaired.

    Tests for Assessing Fluid Status

    Fractional Excretion of Sodium (FENa)
    Normal range: 1% to 2%
    In most cases, natremic disorders cannot be effectively managed without first optimizing the overall fluid status. Therefore, when a serum sodium value is abnormal, the clinician should first evaluate whether vascular volume is optimal. In addition to physical examinations and history, FENa may help validate these findings, especially in patients whose physical examination results may be limited by other confounders (e.g., the use of antihypertensive drugs, heart failure). The FENa may be determined by the use of a random urine sample to determine renal handling of sodium. FENa, the measure of the percentage of filtered sodium excreted in the urine, can be calculated using the following equation:

    [Laboratory] Electrolytes, Other Minerals, and Trace Elements-screen-shot-2016-12-10-at-2-49-06-pm-png

    Values greater than 2% usually suggest that the kidneys are excreting a higher than normal fraction of the filtered sodium, implying likely renal tubular damage. Conversely, FENa values less than 1% generally imply preservation of intravascular fluid through renal sodium retention, suggesting prerenal causes of renal dysfunction (e.g., hypovolemia and cardiac failure). Since acute diuretic therapy can increase the FENa to 20% or more, urine samples should be obtained at least 24 hours after diuretics have been discontinued.

    Blood Urea Nitrogen (BUN): Serum Creatinine (SCr) Ratio
    Normal range: <20:1
    The BUN:SCr ratio can provide useful information to assess fluid status. When this ratio is higher than 20:1, dehydration is usually present. As extracellular fluid volume is diminished, the kidney increase their reabsorption of urea but not creatinine. Therefore, BUN increases by a larger magnitude than the SCr concentration in dehydrated individuals, leading to a rise in the BUN:SCr ratio.
    Last edited by TomHsiung; Sat 10th December '16 at 2:18pm.
    B.S. Pharm, West China School of Pharmacy, Class of 2007, Health System Pharmacist, RPh. Hematology, Infectious Disease.

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    PharmD Year 1 TomHsiung's Avatar
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    Default Re: [Laboratory] Electrolytes, Other Minerals, and Trace Elements

    Potassium
    Normal range: 3.8-5.0 mEq/L or 3.8-5.0 mmol/L
    Potassium is the primary cation in the intracellular space, with an average intracellular fluid concentration of about 140 mEq/L (140 mmol/L). The major physiological role of potassium is in the regulation of muscle and nerve excitability. It may also play important roles in the control of intracellular volume (similar to the ability of sodium in controlling extracellular volume), protein synthesis, enzymatic reactions, and carbohydrate metabolism.

    Corrected Potassium in Acid-Base Abnormality
    When a severe metabolic acid-base abnormality exists, adjustment of the measured serum potassium concentration may be necessary to more accurately assess the body potassium status. For every 0.1-unit reduction in arterial pH less than 7.4, roughly 0.6 mEq/L (range: 0.2-1.7 mEq/L) could be added to the serum potassium value:

    Kcorr = ([7.4 - pH] / 0.1 x 0.6 mEq/L) + Kuncorr

    where Kcorr is the corrected serum potassium concentration and Kuncorr is the uncorrected or measured serum potassium. It is important to note that Kcorr is a hypothetical value and only reflects what the serum potassium concentration would be if the serum pH is normalized and in the absence of other factors affecting potassium homeostasis. As long as the serum pH remains abnormal, the measured serum potassium concentration (Kucorr) is the true reflection of actual serum potassium concentration.

    The Kcorr value should always be assessed together with the actual serum potassium concentration and the patient's clinical presentation. The clinical value of calculating Kcorr is mostly to avoid overcorrection of potassium based solely on Kucorr, as well as to provide a more complete picture that reflects total potassium stores in the body.

    Clinicians should remember that regardless of the value of Kcorr, a patient with a significantly abnormal measured (uncorrected) serum potassium concentration is still at risk for developing cardiac arrhythmias.
    B.S. Pharm, West China School of Pharmacy, Class of 2007, Health System Pharmacist, RPh. Hematology, Infectious Disease.

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