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Serum concentration of magnesium may not be decreased even in the presence of magnesium depletion Check urinary magnesium excretion if renal magnesium wasting is suspected Causes neurologic symptoms and arrhythmias Impairs release of PTH



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Urinary excretion of magnesium exceeding 10 30 mg/d or a fractional excretion more than 2% indicates renal magnesium wasting In calculating fractional excretion of magnesium, since only 30% is protein bound, it follows that 70% of circulating magnesium is filtered by the glomerulus In addition to hypomagnesemia, hypocalcemia and hypokalemia are often present The ECG shows a prolonged QT interval, due to lengthening of the ST segment PTH secretion is often suppressed (see Hypocalcemia, above)





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Causes of hypomagnesemia are listed in Table 21 12 Normomagnesemia does not exclude magnesium depletion because only 1% of total body magnesium is in the ECF Nearly 50% of hospitalized patients in whom serum electrolytes are ordered have unrecognized hypomagnesemia Up to 40% of patients with hypomagnesemia have hypokalemia, and up to 50% have hypocalcemia Hypomagnesemia and hypokalemia share many etiologies, including diuretics, diarrhea, alcoholism, aminoglycosides, and amphotericin B Renal potassium wasting also occurs from hypomagnesemia, and is refractory to potassium replacement until magnesium is repleted Hypomagnesemia also suppresses PTH release and causes endorgan resistance to it and to low 1,25-dihydroxyvitamin D3 levels This hypocalcemia is also refractory to calcium replacement until the magnesium is repleted In addition, molecular

Magnesium oxide, 250 500 mg orally once or twice daily, is useful for repleting stores in patients with chronic hypomagnesemia Treatment of symptomatic hypomagnesemia can include an infusion of 1 2 g of magnesium sulfate, followed by an infusion of 6 g magnesium sulfate in at least 1 L of fluids over 24 hours, repeated for up to 7 days to replete magnesium stores Magnesium sulfate may also be given intra-

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muscularly in a dosage of 200 800 mg/d (8 33 mmol/d) in four divided doses Serum levels must be monitored daily and dosage adjusted to keep the concentration from rising above 25 mmol/L Tendon reflexes may also be checked, since hypermagnesemia causes hyporeflexia K+ and Ca2+ replacement may be required as well, but patients with hypokalemia and hypocalcemia of hypomagnesemia do not recover without magnesium supplementation Patients with normal renal function can excrete excess magnesium and hypermagnesemia should not develop with replacement dosages In patients with CKD, replacement of magnesium should be done cautiously to avoid hypermagnesemia Reduced doses (50 75% dose reduction) and more frequent monitoring (at least twice daily) are indicated

P4 = s P 4 ( f nl4 f sys )

Figure 3-11

Mouw DR et al Clinical inquiries What are the causes of hypomagnesemia J Fam Pract 2005 Feb;54(2):174 6 [PMID: 15689296] Tong GM et al Magnesium deficiency in critical illness J Intensive Care Med 2005 Jan-Feb;20(1):3 17 [PMID: 15665255]

a rate of 100 mg (45 mmol)/min Hemodialysis or peritoneal dialysis may be necessary to remove the magnesium, particularly when there is severe renal failure Long-term use of magnesium-containing drugs, such as magnesium hydroxylate and magnesium sulfate, should be avoided in patients with advanced stages of CKD

Kraft MD et al Treatment of electrolyte disorders in adult patients in the intensive care unit Am J Health Syst Pharm 2005 Aug 15;62(16):1663 82 [PMID: 16085929] Touyz RM Magnesium in clinical medicine Front Biosci 2004 May 1;9:1278 93 [PMID: 14977544]

To assess a patient s acid base status, measurement of arterial pH, PCO2, and plasma bicarbonate (HCO3 ) is needed Blood gas analyzers directly measure pH and PCO2, and the HCO3 value is calculated from the Henderson Hasselbalch equation: HCO 3 pH = 61 + log ----------------------03 Pco 2 The total venous CO2 measurement is a more direct determination of HCO3 Because of the dissociation characteristics of carbonic acid (H2CO3) at body pH, dissolved CO2 is almost exclusively in the form of HCO3 , and for clinical purposes the total carbon dioxide content is equivalent ( 3 mEq/L) to the HCO3 concentration: H + HCO H 2 CO 3 CO 2 + H 2 O

Almost always associated with advanced stages of CKD and a history of chronic intake of magnesiumcontaining drugs

65 MW = ( 34 MW/Hz ) ( f nl1 - 60 Hz )

Magnesium excess is almost always the result of advanced CKD and the inability to excrete what has been taken in from food or drugs, especially the long-term use of antacids and laxatives Magnesium replacement should be done cautiously in patients with CKD, and dose reductions up to 75% may be needed to avoid hypermagnesemia

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Multiline text (aka Word Wrap) · Issue #8 · MrRio/jsPDF · GitHub
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