M

M



Magnesium



DEFINITION


Essential nutrient and major divalent cation. Serum total magnesium includes protein-bound (30%), anioncomplexed (15%), and ionized (55%) fractions.



SYNONYMS


Mg, Mg2+



TYPICAL NORMAL RANGE


Range: 1.5-2.7 mg/dL. Unit conversion: mg/dL × 0.4114 = mmol/L; mEq/L × 0.5 = mmol/L.



PHYSIOLOGY


Sources: dietary; commercial foods are fortified. Absorbed in small intestine; vitamin D may enhance absorption. Excreted in urine, feces, milk. Extracellular fluids contain <2% of total, bone contains 50%-60%, remainder is intracellular. Shifts from extracellular to intracellular compartments. Ionized Mg2+ is the biologically active form.



CLINICAL APPLICATIONS


CAUSES OF ABNORMALLY HIGH LEVELS: Decreased urinary excretion (decreased glomerular filtration rate, renal failure). Uncommon: excess oral administration (antacids, laxatives), intravenous Mg.


NEXT DIAGNOSTIC STEP TO CONSIDER IF LEVELS HIGH: Evaluate renal function, review oral and parenteral supplements.



CAUSES OF ABNORMALLY LOW LEVELS



• Hypoproteinemia: decreases protein-bound Mg; no effect on ionized Mg

• Excess urinary excretion: fluid diuresis; diuretic drugs; renal tubular disease

• Inadequate gastrointestinal absorption: chronic diarrhea, malabsorption syndromes, binding to other nutrients (excess fatty acids, oxalate, phosphate, fiber)

• Shifts from extracellular to intracellular compartments: treatment for diabetic ketoacidosis (insulin, bicarbonate infusions)

• Diabetes mellitus, hyperparathyroidism, hyperthyroidism, pancreatitis, trauma, sepsis may predispose


NEXT DIAGNOSTIC STEP TO CONSIDER IF LEVELS LOW



• Measure serum albumin; measure serum ionized magnesium.

• Evaluate for renal, gastrointestinal disease as a primary or contributing cause.


SPECIMEN AND PROCESSING CONSIDERATIONS



DRUG EFFECTS ON LEVELS



• Renal excretion increased by loop and osmotic diuretics, and drug-induced renal tubular injury (e.g., aminoglycosides, cisplatin, amphotericin B)

• Insulin, glucose, or bicarbonate infusions promote intracellular shifting, decreasing serum Mg.

• Administration of Mg-containing laxatives, antacids causes increases.


LAB ARTIFACTS THAT MAY INTERFERE



• Falsely increased by hemolysis or delayed removal of serum from clot

• Falsely decreased if anticoagulants that bind Mg are used (EDTA [lavender-top tube], citrate [blue-top tube], oxalate)

SPECIMEN: Serum preferred (red-top tube); heparinized plasma (green-top tube) may be used. Remove serum from erythrocytes promptly after centrifugation.


RELATIVE COST: $



PEARLS


Concurrent hypocalcemia, hypokalemia may be refractory to therapy until hypo-magnesemia is corrected.


AUTHOR: ROBIN W. ALLISON



Methemoglobinemia, Methemoglobinuria



DEFINITION


Methemoglobinemia: accumulation of methemoglobin in blood. Methemoglobinuria: presence of methemoglobin in urine. Methemoglobin has an iron moiety that has been oxidized to the ferric (Fe 3+) state from the normal ferrous (Fe2+) state in hemoglobin.



SYNONYM


MetHb



TYPICAL NORMAL RANGE



• Methemoglobin spot test: drop of venous blood on a white paper towel normally is bright red; if methemoglobin concentration is >10%, spot remains dark with a brown tinge.

• Blood/urine levels: methemoglobin normally represents <1% of total hemoglobin.


PHYSIOLOGY


Increased production of methemoglobin results from exposure to oxidant chemicals, drugs, plants, or decreased reduction of methemoglobin due to a hereditary deficiency of erythrocyte methemoglobin reductase. Methemoglobin cannot bind and carry oxygen to tissue. If sufficient amounts of methemoglobin are present, low blood oxygen tension (hypoxemia) results.



CLINICAL APPLICATIONS


CAUSES OF ABNORMALLY HIGH LEVELS: Hereditary deficiency of methemoglobin reductase or exposure to oxidant chemicals (nitrite, copper), drugs (e.g., acetaminophen, benzocaine, phenazopyridine, zinc), or plants


NEXT DIAGNOSTIC STEP TO CONSIDER IF LEVELS HIGH


• If spot test is positive, consider arterial blood gas, pulse oximetry, and if available, cooximetry analysis. Cooximetry measures concentrations of methemoglobin as a percentage of the total hemoglobin concentration in the blood sample.

• CBC to determine if hemolytic anemia is present, because it is a common sequela to oxidant injury of erythrocytes

• Evaluation of red blood cell morphology for Heinz bodies and eccentrocytes (hallmarks of oxidant injury)

• Methemoglobin reductase level determination if hereditary deficiency is suspected


SPECIMEN AND PROCESSING CONSIDERATIONS



SPECIMEN



• Anticoagulated whole blood collected in EDTA (lavender-top tube) for spot test; 0.5 mL minimum

• Methemoglobin reductase level determination: prior arrangements must be made with a laboratory before submitting samples. Whole blood (1 mL in EDTA [lavender-top tube]) should be refrigerated and sent chilled (not frozen) to a laboratory allowing assay to be done the same day the specimen is collected. One or more samples collected from normal animals should be submitted with the patient samples for use as controls. Not offered by most veterinary reference labs; may be run in human lab if erythrocyte lysing agent does not cause methemoglobin formation.


PEARLS



• Severe methemoglobinemia produces chocolate brown discoloration of the blood.

• Most chemicals producing methemoglobinemia also produce Heinz body hemolytic anemia.
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Jul 24, 2016 | Posted by in SMALL ANIMAL | Comments Off on M

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