Magnesium4th most common cation in the body 2nd most abundant intracellular cation after K plays a fundamental role

in many functions of the cell Involved in regulation of PTH secretion Systemically, Mg lowers blood pressure and alters peripheral vascular resistance

The total body magnesium level of an average adult is 25 g Approximately 60 is present in bone, 20 in muscle, and 20 in soft tissue and the liver Approximately 99 of the total body magnesium is intracellular Normal plasma magnesium concentration is 1.7-2.1 mg/dL

The main determinates are gastrointestinal absorption and renal excretion Healthy individuals need to ingest 0.15-0.2 mmol/kg/d to stay in balance Extracellular magnesium is in equilibrium with that in the bone, kidneys, intestine, and other soft tissues There is no hormonal modulation of urinary magnesium excretion Bone, the principal reservoir of magnesium, does not readily exchange with circulating magnesium in the extracellular fluid space

Malabsorption of Mg in the ileum Loss of GI secretions in large amounts Malnutrition with low dietary intake of Mg Renal losses from primary renal disorders or secondary causes Extracellular volume expansion Redistribution of Mg into cells (Insulin) Pregnant women have been found to be Mg depleted (esp those who experience PTL) Hyper calcemia Hyper aldosteronism

Primary renal disorders cause hypomagnesemia by decreased tubular reabsorption of magnesium by the damaged kidneys Endocrine disorders may cause hypomagnesemia Osmotic diuresis results in magnesium loss in the kidney

Chronic alcoholism Vomiting Drugs (loop,thiazidediuretics,cyclosporine cis plastin,digitalis) Rapid administration of citrate blood Poorly controlled DM Protein calorie malnutrition Acute pancreatitis Antibiotics block resorption in the loop of henle(aminoglycoside) Acute Miwithin 48 hrs of after heart attack Contributing factors are sepsis,burns,hypothermia

History Physical Labs EKG and Cardiac Monitoring Other tests as needed

Mg+ deficiecy usualy occur along with low serum K+ and low Ca+

Hallucination depression Neuromuscular irritability -Hyperactive deep tendon reflexes -Muscle cramps -Muscle fibrillation -Trousseau and Chvostek signs -Dysarthria and dysphagia from esophageal dysmotility

CNS hyperexcitability -Irritability and combativeness -Disorientation -Psychosis -Ataxia, vertigo, nystagmus, and seizures Cardiovascular -Atrial Fibrillation -Ventricular arrhythmias -Repolarization Alternans -Coronary Artery Vasospasm -Sudden Death

ConsiderationsBody stores of magnesium may be depleted markedly before the serum level drops, so a deficiency of Mg is clearly present if the serum level is low Because extracellular magnesium is protein bound, the patients protein status is an important consideration in interpreting magnesium levels Hypocalcemia is caused by magnesium depletion, but the reason is not known Hypophosphatemia has been found in patients with hypomagnesemia

16 EKG and Cardiac monitoringFindings 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 of Mild or Chronic HypomagnesemiaTreated with 240mg elemental Mg PO qd-bid Mg oxide preparations include Mag-Ox 400 and Uro-Mag The major side effect of these is diarrhea Singer G Fluid and electrolyte management. In The Washington Manual of Therapeutics. Lippencott. 30th edition, 2001. p68-69.

Treatment of Severe Symptomatic HypomagnesemiaTreated with 1-2g Mg sulfate (4mEq/ml) IV over 15 min, followed by infusion of 6g Mg sulfate in 1L or more IV fluid over 24hrs B/c of the need to replenish intracellular stores, the infusion should be continued for 3-7 days Serum Mg should be measured q24h and the infusion rate adjusted to maintain a serum Mg level of lt2.5 mEq/L Singer G Fluid and electrolyte management. In The Washington Manual of Therapeutics. Lippencott. 30th edition, 2001. p68-69. 19 Considerations with Mg ReplacementIn pt with normal renal function, excess Mg is readily excreted, and there is little risk of causing hypermagnesemia with recommended doses. However, Mg must be given with extreme care in renal failure b/c of the risk of hypermagnesemia Reduced doses and more frequent monitoring must be used even in mild renal failure Tendon reflexes should be tested frequently as hyporeflexia suggests hypermagnesemia

History Clues to the presence of hypomagnesemia can be found by obtaining a history of potential causes Historical complaints related to hypomagnesemia are nonspecific Altered mental status may be present in severe cases

DONT FORGETHYPOKALEMIA CANNOT BE CORRECTED UNLESS HYPOMAGNESEMIA HAS BEEN CORRECTED

GI Prolonged nasogastric suction Malabsorption Bowel resection Diarrhoea Fistulas Acute pancreatitis Decreased intake Chronic vomiting Redistribution DKA Hungry bone disease

Renal loss Chronic TPN Osmotic diuresis (DM/mannitol) Hypercalcaemia Alcohol Drugs diuretics/aminoglycosides /cisplatin/cardiac glycosides Metabolic acidosis (DKA/ETOH/starvation) Renal disease