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![MANAGEMENT
Diet- The normal recommended daily allowance of Mg is 420 mg for
men and 320 mg for women
Green vegetables such as spinach are good sources of magnesium
(which is contained in the chlorophyll molecule)
Some legumes (beans and peas), nuts and seeds, and whole,
unrefined grains are also good sources of magnesium
Hypokalemia,hypocalcemia,andhypophosphatemiaareoftenpresent
withseverehypomagnesemiaandmustbe monitoredcarefully. Hypocalcemia
Doesnot developuntil[Mg]fallsbelow1.2 milligrams/dL.](https://image.slidesharecdn.com/magnesiumdisorders-200828072718/75/Magnesium-disorders-22-2048.jpg)
![MANAGEMENT
Immediate cessation of Mg administration is required. If renal failure
is not evident, dilution by IV fluids followed by Furosemide (40 to 80
milligrams IV) may be indicated. Calcium directly antagonizes the
[Mg2+].
cardiac effects of magnesium because it reverts the calcium channel
blockade provoked by elevated [Mg]. Severe symptomatic
hypermagnesemia can be treated with 10 mL of 10% calcium
chloride IV over 2 to 3 minutes.
Further infusion of 40 to 60 mL during the next 24 hours can be
administered. Patients with renal failure may benefit from dialysis
using a decreased [Mg2+] bath that lowers serum [Mg2+].](https://image.slidesharecdn.com/magnesiumdisorders-200828072718/75/Magnesium-disorders-34-2048.jpg)
Uploaded byDr.Ashutosh Kumar Singh
Magnesium disorders
This document discusses hypo and hypermagnesemia, detailing the body's magnesium stores, mechanisms of absorption, causes, clinical presentation, and management strategies for magnesium disorders. Hypomagnesemia is characterized by low serum magnesium levels and can occur due to various factors including dietary deficiencies and certain medical conditions, while hypermagnesemia is often related to renal failure or excessive intake. Guidelines for treatment include dietary interventions, oral or intravenous supplementation, and monitoring for complications like hypocalcemia or cardiac issues.
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Introduction to hypomagnesemia and hypermagnesemia by Dr. Ashutosh Kumar Singh.
Magnesium body stores range from 21-28g in a 70kg adult; normal serum levels are 1.7-2.5 mg/dL.
60% of magnesium is ionized, 30% protein-bound, and 10% complexed with plasma anions.
30-40% diet Mg absorbed mainly in jejunum; urine excretion matches absorption.
Reabsorption: 60% in the cTAL, 20% in proximal tubule, 5-10% in distal convoluted tubule.
Definition of hypomagnesemia as low blood magnesium levels, not always indicating deficiency.
Decreased intake, redistribution, GI loss, and certain medications lead to hypomagnesemia.
Prevalence: 2% in general population; higher (10-80%) in hospitalized and alcohol-dependent patients.
Symptoms include hypokalemia, hypocalcemia, and multiple biochemical abnormalities.
Hypomagnesemia can cause serious cardiovascular issues like arrhythmias and ECG changes.
Neuromuscular and psychiatric disturbances are early signs; includes tremors, convulsions.
Serum magnesium measurement and acute loading tests to evaluate deficiency.
Treatment involves diet, oral replacement, or IV magnesium for severe cases.
Risk of hypermagnesemia from excessive magnesium replacement; side effects detailed.
Hypermagnesemia is rare; linked to renal insufficiency and specific treatments.
Most common cause is renal failure; other causes include excessive intake and certain diseases.
Symptoms range from nausea to potentially life-threatening conditions like cardiac arrest.
ECG changes and cardiovascular complications associated with elevated magnesium levels.
Diagnosis through serum magnesium levels; management includes fluid management and calcium.
Wrap-up of the presentation.
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Similar to Magnesium disorders
Magnesium disorders
- 1. HYPO & HYPERMAGNESEMIA DR.ASHUTOSH KUMAR SINGH
- 2. The total bodystores of magnesium are between 21 and 28 g in the average 70 kg adult. Normal serum magnesium usually has a range of 1.7 to 2.5 mg/dL. Most of the body's magnesium is in the skeletal bone mass, which accounts for more than 50% of the body's stores. The remainder is located in soft tissue, of which only 1% is located extracellularly. INTRODUCTION
- 3. • 60% ofMg exists as physiologically active ionised form • 30% is protein bound mainly to albumin • remaining 10 % forms complexes with plasma anions such as phosphates and citrates IN PLASMA
- 4. • About 30-40%of dietary magnesium (140– 360 mg/d) is absorbed, principally in the jejunum and ileum. • Magnesium excretion in urine usually matches net intestinal absorption (100 mg/d). • Serum magnesium concentration is regulated by renal magnesium reabsorption. • Parathyroid hormone increases magnesium reabsorption in the cTAL, whereas hypercalcemia and hypermagnesemia inhibit magnesium reabsorption. METABOLISM
- 5. RENAL HANDLING About 60%of magnesium is reabsorbed in the cortical thick ascending limb of loop of Henle (cTAL), whereas 20% of filtered magnesium is reabsorbed in the proximal tubule, and another 5– 10% in the distal convoluted tubule. PROXIMAL TUBULE Mg absorption in the proximal tubule is dependant on the filtered load as well as net salt and water reabsorption.
- 6. THICK ASCENDING LOOP Paracellular Mg transport is driven by a favorable lumen positive electrochemical gradient which is generated by a transcellular reabsorption of NaCl It is dependant on the activity of Na+-k & -cl co-transporter, renal outer medullary channel, Na+-k +-ATPase pump and renal Cl- channel Claudins are the major components of tight junction strands in the TAL, where the reabsorption of magnesium occurs
- 7. DISTAL CONOLUTED TUBULES Thetransport rate in this segment defines the final urinary Mg+ concentration as no reabsorption takes place beyond this level The cells in this nephron segment have highest energy consumption of the nephrons Na+-cl- cotransporter, which is exclusively present in the DCT is important for active reabsorption of Mg Approx 3% of filtered Mg is excreted in the urine
- 8.
- 9. WHAT IS IT?? Hypomagnesemiais an electrolyte disturbance in which there is an abnormally low level of magnesium in the blood. Hypomagnesemia is not necessarily magnesium deficiency. Hypomagnesemia can be present without magnesium deficiency and vice versa.
- 10. CAUSES Related to decreasedMg intake • Starvation • Alcohol dependence • Total parenteral nutrition II. Related to redistribution of Mg from ECF to ICF • Hungry bone syndrome • Treatment of diabetic ketoacidosis • Alcohol withdrawal syndromes • Acute pancreatitis
- 11. Related to GIMg loss •Diarrhea •Vomiting and nasogastric suction •Gastrointestinal fistulas. •Hypomagnesemia with secondary hypocalcemia (HSH)
- 12. • Diuretics -Loop diuretics, osmotic diuretics, and chronic use of thiazides • Antimicrobials - Amphotericin B, aminoglycosides, pentamidine, capreomycin, viomycin, and foscarnet • Chemotherapeutic agents - Cisplatin • Immunosuppressants - Tacrolimus and cyclosporine • Proton-pump inhibitors • Ethanol DRUGS
- 13. REDISTRIBUTION FROM ICFTO ECF Hungry bone syndrome, in which magnesium is removed from the extracellular fluid space and deposited in bone following parathyroidectomy or total thyroidectomy or any similar states of massive mineralization of the bones Hypomagnesemia may also occur following insulin therapy for diabetic ketoacidosis and may be related to the anabolic effects of insulin driving magnesium, along with potassium and phosphorus, back into cells.
- 14. The risk ofhypomagnesemia can be summarized as follows: • 2% in the general population • 10-20% in hospitalized patients • 50-60% in intensive care unit (ICU) patients • 30-80% in persons with alcoholism • 25% in outpatients with diabetes
- 15. CLINICAL PRESENTATION A carefulfamily history is important, particularly when acquired causes of hypomagnesemia have to be excluded Often associated with multiple biochemical abnormalities, including hypokalemia, hypocalcemia, and metabolic acidosis. As a result, hypomagnesemia is sometimes difficult to attribute solely to specific clinical manifestations
- 16. RELATED METABOLIC CONDITIONS Hypokalemia isa common event in patients with hypomagnesemia, occurring in 40-60% of cases Partly due to underlying disorders that cause magnesium and potassium losses, including diuretic therapy and diarrhoea The mechanism for hypomagnesemia-induced hypokalemia relates to the intrinsic biophysical properties of renal outer medullary K+ (ROMK) channels mediating K+ secretion in the TAL and the distal nephron.
- 17. The classic signof severe hypomagnesemia (< 1.2 mg/dL) is hypocalcemia. The mechanism is multifactorial. • Impaired magnesium-dependent adenylcyclase mediates the decreased release of PTH causing hypocalcemia. • Skeletal resistance to this hormone in magnesium deficiency has also been implicated. • Hypomagnesemia also alters the normal hetero-ionic exchange of calcium and magnesium at the bone surface, leading to an increased bone release of magnesium ions in exchange for an increased skeletal uptake of calcium from the serum.
- 18. EFFECT ON CVS Thecardiovascular effects of magnesium deficiency include effects on electrical activity, myocardial contractility, potentiation of digitalis effects, and vascular tone Hypomagnesemia is also recognized to cause cardiac arrhythmia like Monomorphic ventricular tachycardia, Torsade de pointes, Ventricular fibrillation. Changes in ECG are non specific like prolongation of conduction and slight ST depression, Nonspecific T-wave changes, U waves may b seen, Prolonged QT seen
- 19. NEUROMUSCULAR MANIFESTATION The earliest manifestationsof magnesium deficiency are usually neuromuscular and neuropsychiatric disturbances, the most common being hyper excitability. Neuromuscular irritability, including tremor, fasciculation's, tetany, Chvostek and Trousseau signs, and convulsions, may be present. Other manifestations include Apathy, Muscle cramps, Hyper- reflexia, Acute organic brain syndromes, Depression, Generalized weakness, Anorexia, Vomiting
- 20. INVESTIGATION Measurement of serummagnesium Its use in evaluating total body stores is limited
- 21. A surrogate fordirect intracellular magnesium is the measurement of magnesium retention after acute magnesium loading An infused magnesium load - 2.4 mg/kg of lean body weight over the initial 4 h is given A magnesium deficiency is indicated if a patient has reduced excretion (< 80% over 24 h) Patients with malnutrition, cirrhosis, diarrhea, or long-term diuretic use typically have a positive test, whether or not they have signs or symptoms referable to magnesium depletion. GOLD STANDARD
- 22. MANAGEMENT Diet- The normalrecommended daily allowance of Mg is 420 mg for men and 320 mg for women Green vegetables such as spinach are good sources of magnesium (which is contained in the chlorophyll molecule) Some legumes (beans and peas), nuts and seeds, and whole, unrefined grains are also good sources of magnesium Hypokalemia,hypocalcemia,andhypophosphatemiaareoftenpresent withseverehypomagnesemiaandmustbe monitoredcarefully. Hypocalcemia Doesnot developuntil[Mg]fallsbelow1.2 milligrams/dL.
- 23. oral replacement shouldbe given in the asymptomatic patient, preferably with a sustained-release preparation Bioavailability of oral preparations is assumed to be 33% in the absence of intestinal malabsorption • Mag-Ox 400, containing magnesium oxide • Slow-Mag, containing magnesium chloride • Mag-Tab, containing magnesium lactate These preparations provide about 60 – 84 mg of Mg per tablet 500mg of magnesium gluconate contain 27 mg of elemental magnesium & 1gm of magnesium sulfate contains 98 mg of elemental magnesium
- 24. The hypocalcemic-hypomagnesemic patientwith tetany or the patient who is suspected of having hypomagnesemic-hypokalemic ventricular arrhythmias are given 50 mEq of intravenous magnesium, given slowly over 8-24 hours This dose can be repeated as necessary to maintain the plasma magnesium concentration above 1.0 Non emergency cases 64 mEq in first 24 hrs and 32 mEq daily for 2 to 6 days, should be continued for 1 – 2 days after serum Mg level normalises
- 25. ADVERSE EFFECT The mainadverse effect of Mg replacement is hypermagnesemia due to administration at an excessive rate or excessive amount Side effect include facial flushing, loss of deep tendon reflex, hypotension, AV block May precipitate tetany as well in cases of hypocalcemia by increasing urinary calcium excretion antidotes for hypermagnesemia is Intravenous calcium chloride or gluconate (1-2 ampules should be administered immediately )
- 26.
- 27. Hypermagnesemia is rarelyencountered in emergency medicine practice, because the kidney can Increase the fractional excretion of Mg up to nearly 100%. A small elevation in serum concentration has little clinical significance. The most common cause for hypermagnesemia can be found in patients with renal insufficiency or renal failure who ingest Mg2+ - containing drugs. Hypermagnesemia is more commonly seen in the perinatal setting secondary to the treatment of preeclampsia or eclampsia.
- 28. CAUSES The most commoncause of hypermagnesemia is renal failure. Other causes include the following: • Excessive intake(Antacids, Laxatives) • Lithium therapy • Hypothyroidism • Addison disease • Familial hypocalciuric hypercalcemia • Milk alkali syndrome • Depression
- 29. SYMPTOMS Plasma magnesium concentration4 to 6 mEq/L (4.8 to 7.2 mg/dL or 2 to 3 mmol/L) – nausea, flushing, headache, lethargy, drowsiness, and diminished deep tendon reflexes. Plasma magnesium concentration 6 to 10 mEq/L (7.2 to 12 mg/dL or 3 to 5 mmol/L) – somnolence, hypocalcemia, absent deep tendon reflexes, hypotension, Bradycardia, and ECG changes.
- 30. Plasma magnesium concentrationabove 10 mEq/L (12 mg/dL or 5 mmol/L) – muscle paralysis, respiratory paralysis, complete heart block, and cardiac arrest. In most cases, respiratory failure precedes cardiac collapse.
- 31. Magnesium is aneffective calcium channel blocker both extracellularly and extracellularly; in addition, intracellular magnesium profoundly blocks several cardiac potassium channels . These changes can combine to impair cardiovascular function ECG Changes: prolongation of the P-R interval, an increase in QRS duration, and an increase in Q-T interval. CARDIOVASCULAR EFFECTS Complete heart block and cardiac arrest may occur at a plasma magnesium concentration above 15 mEq/L.
- 32. Moderate hypermagnesemia caninhibit the secretion of parathyroid hormone, leading to a reduction in the plasma calcium concentration However this fall is usually transient and produces no symptoms HYPOCALCEMIA
- 33. DIAGNOSIS Hypermagnesemia usually resultsfrom a combination of excess magnesium intake and a coexisting impairment of renal function. Diagnosis is usually straightforward and involves measuring serum magnesium levels, as many cases are unsuspected. If a magnesium level is not immediately available, a clue to the existence of hypermagnesemia would be the disease context (preeclampsia, renal failure), the presence of magnesium-containing preparations, or a decreased anion gap.
- 34. MANAGEMENT Immediate cessation ofMg administration is required. If renal failure is not evident, dilution by IV fluids followed by Furosemide (40 to 80 milligrams IV) may be indicated. Calcium directly antagonizes the [Mg2+]. cardiac effects of magnesium because it reverts the calcium channel blockade provoked by elevated [Mg]. Severe symptomatic hypermagnesemia can be treated with 10 mL of 10% calcium chloride IV over 2 to 3 minutes. Further infusion of 40 to 60 mL during the next 24 hours can be administered. Patients with renal failure may benefit from dialysis using a decreased [Mg2+] bath that lowers serum [Mg2+].
- 35.