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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
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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]
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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
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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]
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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
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Almost always associated with advanced stages of CKD and a history of chronic intake of magnesiumcontaining drugs
General Considerations
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
Clinical Findings
A Symptoms and Signs
Muscle weakness, decreased deep tendon reflexes, mental obtundation, and confusion are characteristic manifestations Weakness even flaccid paralysis ileus, urinary retention, and hypotension are noted There may be respiratory muscle paralysis or cardiac arrest
B Laboratory Findings
Serum Mg2+ is elevated In the common setting of CKD, concentrations of BUN and of serum creatinine, phosphate, and uric acid are elevated; serum K+ may be elevated Serum Ca2+ is often low The ECG shows increased PR interval, broadened QRS complexes, and peaked T waves, probably related to associated hyperkalemia
If precise measurements of oxygenation are not needed or if oxygen saturation obtained from the pulse oximeter is adequate, venous blood gases generally provide useful information for assessment of acid base balance and can be used interchangeably with arterial blood gases since the arteriovenous differences in pH and PCO2 are small and relatively constant Venous blood pH is usually 003 004 units lower than that of arterial blood, and venous blood PCO2 is 7 or 8 mm Hg higher Calculated HCO3 concentration in venous blood is at most 2 mEq/L higher than that of arterial blood Serum HCO3 measurement also provides equivalent information to the arterial base deficit in surgical intensive care unit patients An important exception to the rule of interchangeability between arterial and venous blood gases for determination of acid base balance is during cardiopulmonary arrest In this setting, arterial pH may be 741 and venous pH 715, and arterial blood PCO2 can be 32 mm Hg with a venous blood PCO2 of 74 mm Hg
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