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INTRODUCTION Magnesium, the fourth most common cation in the body approx 1 mole(24g). 53% in bone, 46% in muscle and other soft tissue and <1% in circulation. Previously underappreciated, this ion is now established as a central electrolyte in a large number of cellular metabolic reactions, including DNA and protein synthesis, neurotransmission, and hormone-receptor binding. It is a component of over 300 enzymes e.g. GTPase and a cofactor for Na+/K+–ATPase, adenylate cyclase, and phosphofructokinase. Magnesium also is necessary for the production of parathyroid hormone..

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Magnesium is present in greatest concentration within the cell and is the second most abundant intracellular cation after potassium. The total body content of magnesium is 2000 mEq. The intracellular concentration of magnesium is 40 mEq/L, while the serum concentration is 1.5-2 mEq/L. Most of the body's magnesium is found in bone. Only 1% of the total body magnesium is extracellular. Of this amount, one half is ionized, and 25-30% is protein bound, 5% compelxed with other ions( PO4 and citrate).

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Magnesium, a component of chlorophyll, is absorbed in the small bowel by active and passive transport mechanisms. Also found in dried cereal, nuts, meats, fruits.Absorption of dietary magnesium takes place mainly in the ileum(20-65%). It is excreted in stool and urine, but regulation of serum magnesium is under renal control. Most renal reabsorption of magnesium occurs in the (25-30%) proximal tubule and the thick ascending limb of the loop of Henle (50-60%), (2-5%) in DCT. Renal threshhiold is 0.6- 0.85mmol/l and this is close to normal serum conc. Only 6% of filtered Mg is excreted/day. In hypomagnesemic patients, the kidney may excrete as little as 1 mEq/L of magnesium. Additionally, magnesium may be removed from bone stores in times of deficiency.

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PTH increases the renal absorption and GIT absorption, while Aldosterone and thyroxine have the opposite Effect.


HYPOMAGNESEMIA Causes: The causes of hypomagnesemia are numerous. Most causes are related to renal and GI losses. GI losses Malabsorption of magnesium in the ileum results in hypomagnesemia. Situations of decreased absorption include malabsorption syndromes (eg, celiac sprue), radiation injury to the bowel, bowel resection, or small bowel bypass. GI secretions in large amounts may cause hypomagnesemia. Upper GI secretions contain 1 mEq/L of magnesium, while lower GI secretions contain 15 mEq/L of magnesium. Significant losses of magnesium that result in hypomagnesemia may result from chronic diarrhea, laxative abuse, inflammatory bowel disease, or neoplasm.


HYPOMAGNESEMIA Malnutrition leads to hypomagnesemia when dietary intake of magnesium is low.. Alcoholics are classically hypomagnesemic in part due to poor nutrition. Diabetic patients who are not receiving magnesium supplements may have dietary deficiencies in magnesium.


HYPOMAGNESEMIA Renal losses from primary renal disorders or secondary causes (eg, drugs, hormones, osmotic load) may result in magnesium wasting and subsequent hypomagnesemia. Primary renal disorders cause hypomagnesemia by decreased tubular reabsorption of magnesium by the damaged kidneys. This condition occurs in the diuretic phase of acute tubular necrosis, postobstructive diuresis, and renal tubular acidosis. Drugs may cause magnesium wasting. Diuretics (eg, thiazide, loop diuretics) decrease the renal threshold for magnesium reabsorption in addition to wasting of potassium and calcium. Cisplatin causes dose-dependent kidney damage in 100% of patients receiving this drug. Pentamidine and some antibiotics also cause renal magnesium wasting. Fluoride poisoning similarly causes hypomagnesemia.

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Endocrine disorders may cause hypomagnesemia. Primary aldosteronism decreases magnesium levels by increasing renal flow. Hypoparathyroidism and hyperthyroidism may cause renal wasting. Osmotic diuresis results in magnesium loss in the kidney. Diabetic patients, especially those with poor glucose control, develop hypomagnesemia from a glucose-induced osmotic diuresis. Alcoholics become hypomagnesemic partially by an osmotic diuresis from alcohol. Urinary losses have been reported to be 2-3 times control values.


HYPOMAGNESEMIA Miscellaneous Extracellular volume expansion, as in cirrhosis or intravenous (IV) fluid administration, may decrease magnesium levels. Redistribution of magnesium into cells may cause lower magnesium levels. Insulin causes this effect. Excessive lactation may create a significant amount of magnesium loss. Hungry bone syndrome may lead to lower serum magnesium concentrations. Pregnant women have been found to be magnesium depleted, especially those women who experience preterm labour.


HYPOMAGNESEMIA Physical: The primary clinical findings are neuromuscular irritability, CNS hyperexcitability, and cardiac arrhythmias. This is due to impaired NaK ATPase activity affecting K+ and Ca2+ levels. The severity of symptoms is not related directly to the magnesium level. The reference range for serum magnesium level is 1.8-3 mEq/L. Usually, patients become symptomatic at 1.8 mEq/L. However, the physical findings may not be present in all cases.

Lab Studies: : 

Lab Studies: Serum magnesium, calcium, potassium, and phosphorus levels The serum magnesium level is not a reliable way to determine total body magnesium depletion because only a small fraction of magnesium in the body is extracellular. Consider obtaining an ionized magnesium level. Body stores of magnesium may be depleted markedly before the serum level drops. Nevertheless, a deficiency of magnesium is clearly present if the serum level is low.

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In one study, alcoholics were found to have total body magnesium depletion (via measurement of their 24-hour urinary magnesium excretion) despite having normal serum levels. Because extracellular magnesium is protein bound, the patient's protein status is an important consideration in interpreting magnesium levels. Hypomagnesemia contributes to hypokalemia. This condition may be due to defective membrane ATPase or urinary losses of potassium. Hypocalcemia is caused by magnesium depletion, but the reason is not known. Some studies link hypomagnesemia to decreased parathyroid hormone levels and end-organ resistance to parathyroid hormone. Alterations in vitamin D metabolism contribute to hypocalcemia. Hypophosphatemia has been found in patients with hypomagnesemia.

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BUN and creatinine levels Blood glucose level ECG Findings in hypomagnesemia are nonspecific. Findings include ST segment depression; tall, peaked T waves; flat T waves or depression in the precordium; U waves; loss of voltage; PR prolongation; and widened QRS.


TREATMENT Oral intake of Mg-lactate, Mg-oxide of Mg-CL or antacid that contains Mg. Severely ill, IV MgSO4.


HYPERMAGNESEMIA Hypermagnesemia is a rare electrolyte abnormality because the kidney is very effective in excreting excess magnesium. Pathophysiology: Magnesium excess affects the CNS, neuromuscular, and cardiac organ systems. It most commonly is observed in renal insufficiency and in patients receiving intravenous (IV) magnesium for treatment of a medical condition.


CAUSES Most cases of hypermagnesemia are due to iatrogenic interventions and administration, especially errors in calculating appropriate infusions. Ingestion of magnesium-containing substances such as vitamins, antacids, or cathartics by patients with chronic renal failure Acute renal failure Excessive intravenous infusions of magnesium in patients being treated for eclampsia, asthma, torsade de pointes, or other cardiac arrhythmias


CAUSES In neonates, treatment of maternal eclampsia with magnesium, which passes through the placental circulation Decreased GI elimination and increased GI absorption of magnesium due to intestinal hypomotility from any cause GI medications that decrease motility, including narcotics and anticholinergics Hypomotility disorders such as bowel obstruction and chronic constipation Tumor lysis syndrome, by releasing massive amounts of intracellular magnesium Adrenal insufficiency (secondary hypermagnesemia)


CAUSES Rhabdomyolysis, like tumor lysis syndrome, by releasing significant amounts of intracellular magnesium Milk-alkali syndrome Hypothyroidism Hyperparathyroidism Neoplasm with skeletal muscle involvement Lithium intoxication Extracellular volume contraction, as in diabetic ketoacidosis


PHYSICAL FINDINGS Related to the serum magnesium levels. Serum magnesium levels of 3.5-5.0 mEq/L are associated with the following: Disappearance of deep tendon reflexes Muscle weakness Serum magnesium levels of 5.0-6.0 mEq/L are related to the following: Hypotension Vasodilatation


PHYSICAL FINDINGS Serum magnesium levels of 8.0-10.0 mEq/L are associated with the following: Arrhythmia, including atrial fibrillation Intraventricular conduction delay Levels of serum magnesium greater than 10.0 mEq/L are related to the following: Asystole Heart block Ventilatory failure Stupor or coma Death Elevated levels of magnesium also are associated with the following: Delayed thrombin formation Platelet clumping

Lab Studies : 

Lab Studies Electrolytes, including potassium, magnesium, and calcium levels A test for ionized magnesium is not clinically available. Elevation in magnesium level is usually not found as an isolated electrolyte abnormality. Hyperkalemia and hypercalcemia are often present concurrently. BUN and creatinine levels Obtain renal function tests and calculate creatinine clearance to assess the ability of the kidney to excrete magnesium. Serum magnesium levels rise when creatinine clearance is less than 30 mL/min. Check serum creatine phosphokinase (CPK) level or urine myoglobin level in patients in whom rhabdomyolysis is suspected. Arterial blood gases (ABG) may reveal a respiratory acidosis.

Lab Studies : 

Lab Studies Thyroid function tests Hypothyroidism is a rare cause of hypermagnesemia. Check these tests in the absence of any other good explanation. An ECG and cardiac monitor may show prolongation of the PR interval or intraventricular conduction delay, which are nonspecific findings. The ECG findings may reflect other electrolyte abnormalities such as hyperkalemia.


TREATMENT Supportive treatment for cardiac, neuromuscular, respiratory and neurological abnormalities. Treatment of the underlying disorder.

Determination of magnesium : 

Determination of magnesium Specimen: non-hemolyzed serum or lithium heparin plasma used. EDTA and citrate bind to the Mg. 24hr urine may be used and should be acidified to avoid Ppt. Colorimetric method/photometric; Mg binds to calmagite, formazen dye and methylthymol blue to form a chromogen that is measure at 532- 600nm. Ca2+ should be eliminated from the sample AAS- absorbance at 285.2nm ISE- free Mg with neutral carrier inonophores.

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