Venkat magnesium

Magnesium
The eighth most abundant element
in the earth’s crust
Dr. Nandyala Venkateshwarlu
SVS Medical College

Magnesium
N Venkateshwarlu MBBS (Kurnool), MD(AIIMS/Lady Hardinge)
Professor,
Department of Internal Medicine
SVS Medical College Mahabubnagar A.P.

Magnesium
• The eighth most abundant element in the
earth’s crust
• 4th abundant cation in the body
• 2nd most abundant cation in the cell after
potassium
• Plays an important role in PTH regulation
• Magnesium lowers B.P. and alters peripheral
resistence
SVS Medical College

About magnesium
• Approximately 60% of total body magnesium
is found in bone. 20% in muscle and 20% in
soft tissue and Liver. Only 1% of magnesium is
found in blood, but the body works very hard
to keep blood levels of magnesium constant.
• Total body magnesium in average human is
about 25 Grams
• Total plasma magnesium levels in humans is
1.7 mg to 2.5 mg
SVS Medical College

About magnesium
• Magnesium helps regulate blood sugar levels,
promotes normal blood pressure, and is known
to be involve in energy metabolism and protein
synthesis.
• Magnesium is excreted through the kidneys.
• Magnesium is needed for more than 300
biochemical reactions in the body.
• Helps maintain normal muscle and nerve
function, keeps heart rhythm steady, supports a
healthy immune system, and keeps bones strong
SVS Medical College

Synthesis
• Magnesium is a mineral, so therefore just like
calcium, magnesium must be absorbed
through dietary intake.
SVS Medical College

Regulation
• About 30-40% of dietary magnesium (140–360 mg/d) is absorbed,
principally in the jejunum and ileum.
• Absorption is stimulated by 1,25(OH)2 D.
• Magnesium excretion in urine usually matches net intestinal
absorption (100 mg/d).
• Serum magnesium concentration is regulated by renal magnesium
re-absorption.
• Parathyroid hormone increases magnesium re-absorption in the
cTAL, whereas hypercalcemia and hypermagnesemia inhibit
magnesium reabsorption.
SVS Medical College

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.
SVS Medical College

THICK ASCENDING LIMB OF LOOP OF HENLE
• Para-cellular Mg transport is driven by a favorable
lumen positive electrochemical gradient which is
generated by a trans-cellular 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
SVS Medical College

DISTAL CONVOLUTED TUBULE
• The transport 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- co-transporter, which is exclusively
present in the DCT is important for active
reabsorption of Mg
 Approx 3% of filtered Mg is excreted in the
urine
SVS Medical College

In plasma
60% of Mg 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
SVS Medical College

Food sources
• Green vegetables such as spinach because the
center of the chlorophyll molecule(which gives
green vegetables their color)
• Legumes(beans and peas)
• Nuts and seeds
• Unrefined grains
• Tap water (varies according to the water
supply)
SVS Medical College

Food sources
• Magnesium is abundant in nature. It can be found
in green vegetables,
chlorophyll, cocoa derivatives, nuts, wheat,
seafood, and meat. It is absorbed primarily in the
duodenum of the small intestine.
• The rectum and sigmoid colon can absorb
magnesium.
• Forty percent of dietary magnesium is absorbed.
• Hypomagnesemia stimulates and
hypermagnesemia inhibits this absorption
SVS Medical College

Food
• Foods high in Magnesium:
- Green leafy vegetables
SVS Medical College

Food rich in magnesium
- Nuts
- Legumes
SVS Medical College

Food rich Magnesium
• Seafood
• Chocolate
SVS Medical College

Recommended Daily allowances
RDA
• The recommended daily intake of magnesium
varies by age and gender, but 400 mg is a good
round number for adults.
• The kidneys provide homeostasis, typically
excreting 120 mg/day.
• Since the 1960s, we have known that
consumption of alcohol, even in modest
amounts, can double or even quadruple the
excretion of magnesium.[1]
• Many over-the-counter and prescription drugs,
such as proton pump inhibitors, can lower body
magnesium levels.
SVS Medical College

Recommended Daily allowances
RDA
• ADULT MEN 19 to 30 400mg
• 31 yrs and older 420mg
• ADULT WOMEN 19 to 30 310mg
• 31 yrs and older 320mg
SVS Medical College

Fun facts
• “HARD” water contains more magnesium than
“Soft” water
• Craving chocolate? Take some magnesium to
help take the cravings away
SVS Medical College

Some facts about prevalence
• There has been no large systematic study of the
adequacy of magnesium body stores in Americans.
• In 2009, the World Health Organization published a
report[2] that stated that 75% of Americans consumed
less magnesium than needed.
• Some say that we have a nationwide magnesium
deficiency.
• Certainly, those named illnesses are common.
Obviously, the National Institutes of Health or the
Centers for Disease Control and Prevention should fund
serious work to ascertain the status of Americans'
magnesium body stores.
SVS Medical College

Eat Your Spinach, Take Supplements
• Foods with high magnesium content include dark
leafy greens, especially kale, chard, and spinach;
tree nuts and peanuts; seeds; oily fish; beans,
lentils, legumes, and whole grains; avocado,
yogurt, bananas, and dried fruit; dark chocolate;
and molasses.
• Supplemental magnesium is available over the
counter in many forms: citrate, amino acid
chelate, chloride, glycinate, malate, taurate,
carbonate, and others, which vary in absorption,
concentration, and bioavailability.
SVS Medical College

Causes
SVS Medical College

Causes
- Starvation
- Chronic Alcoholism
- Diarrhea, or any disruption in small bowel function
SVS Medical College

Causes
- TPN
- Diabetic ketoacidosis
SVS Medical College

Causes of hypomagnesaemia
1. Increased excretion
2. Decreased intake/ mal absorption
3. Miscellaneous
SVS Medical College

Causes of Hypo-Magnesium
1. Related to redistribution of Mg from ECF to ICF
2. Renal excretion
– Alcoholism, diuretics, Amphotericin B
2. Related to redistribution of Mg from ECF to ICF
3. GI Losses
– Diarrhea, mal absorption, acute pancreatitis, DKA,
primary hyperaldosteronism, fistulas, ostomies
4. Poor p.o. intake
– Starvation, alcoholism, prolonged use of IVF, TPN
5. Related to renal Mg loss
SVS Medical College

DRUGS
 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
SVS Medical College

OTHERS
 Hypercalcemia
 Chronic metabolic acidosis
 Volume expansion
 Primary hyperaldosteronism
 Recovery phase of acute tubular necrosis
 Postobstructive diuresis
SVS Medical College

Decreased magnesium intake
• Alcoholics and individuals on magnesium-
deficient diets or on parenteral nutrition for
prolonged periods can become
hypomagnesaemic without abnormal
gastrointestinal or kidney function.
• The addition of 4-12 mmol of magnesium per
day to total parenteral nutrition has been
recommended to prevent hypomagnesaemia.
SVS Medical College

REDISTRIBUTION OF MAGNESIUM FROM ECF TO
ICF
1. Hungry bone syndrome
2. Treatment of diabetic keto-acidosis
3. Alcohol withdrawal syndromes
4. Re-feeding syndrome
5. Acute pancreatitis
SVS Medical College

ICF
• 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
• Hypomagnesaemia may also occur following
insulin therapy for diabetic keto-acidosis and may
be related to the anabolic effects of insulin
driving magnesium, along with potassium and
phosphorus, back into cells.
SVS Medical College

ICF
• Hyper adrenergic states, such as alcohol withdrawal,
may cause intracellular shifting of magnesium and may
increase circulating levels of free fatty acids that
combine with free plasma magnesium.
• Re-feeding syndrome is a condition in which previously
malnourished patients are fed high carbohydrate loads,
resulting in a rapid fall in phosphate, magnesium, and
potassium, along with an expanding extracellular fluid
space volume, leading to a variety of complications.
SVS Medical College

G.I. Loss
• When the small bowel is involved, due to
disorders associated with mal absorption,
chronic diarrhea, or steatorrhea, or as a result
of bypass surgery on the small intestine.
• Patients with ileostomies can develop
hypomagnesaemia as there is some degree of
magnesium absorption in the colon
SVS Medical College

Association with hypocalcaemia
• Hypomagnesaemia with secondary hypocalcaemia (HSH) is a rare
autosomal-recessive disorder characterized by profound
hypomagnesaemia associated with hypocalcaemia.
• Pathophysiology is related to impaired intestinal absorption of
magnesium accompanied by renal magnesium wasting as a result of
a reabsorption defect in the DCT.
• Mutations in the gene coding for TRPM6, a member of the transient
receptor potential (TRP) family of cation channels, have been
identified as the underlying genetic defect.
• Patients usually present within the first 3 months of life with the
neurologic symptoms of hypomagnesaemic hypocalcaemia,
including seizures, tetany, and muscle spasms.
SVS Medical College

Renal losses
• Familial hypomagnesaemia with hypercalciuria
and nephrocalcinosis (FHHNC), an autosomal-
recessive disorder, there is profound renal
magnesium and calcium wasting.
• The hypercalciuria often leads to
nephrocalcinosis, resulting in progressive renal
failure.
• Other symptoms reported in patients with
FHHNC include urinary tract infections,
nephrolithiasis, incomplete distal tubular
acidosis, and ocular abnormalities
SVS Medical College

Renal losses
• Autosomal-dominant hypocalcaemia with
hypercalciuria (ADHH) is another disorder of
urinary magnesium wasting.
• Individuals who are affected present with
hypocalcaemia, hypercalciuria, and polyuria
• About 50% of these patients have
hypomagnesaemia
• ADHH is produced by mutation of CaSR gene
(calcium-sensing receptor) which is involved in
renal calcium and magnesium reabsorption
SVS Medical College

Renal losses
• Isolated dominant hypomagnesaemia (IDH) with hypocalciuriais an
autosomal-dominant condition associated with few symptoms
other than chondrocalcinosis.
• Patients always have hypocalciuria and variable (but usually mild)
hypomagnesaemic symptoms
• Isolated recessive hypomagnesaemia (IRH) with normocalcemia is
an autosomal-recessive disorder in which the individuals who are
affected present with symptoms of hypomagnesemia early during
infancy.
• Hypomagnesemia due to increased urinary magnesium excretion
appears to be the only abnormal biochemical finding.
IRH is distinguished from the autosomal-dominant form by the lack of
hypocalciuria
SVS Medical College

Renal causes
Bartter’s syndrome
• Autosomal recessive disorder involving impaired
Thick Ascending Limb salt reabsorption
Gitelman syndrome
• autosomal recessive disorder involving loss of
function of the thiazidesensitive sodium-chloride
symporter located in the distal convoluted tubule
SVS Medical College

Drugs
 Drugs like loop diuretics (including furosemide,
bumetanide, and ethacrynic acid), produce large
increases in magnesium excretion through the
inhibition of the electrical gradient necessary for
magnesium reabsorption in the TAL.
 Long-term thiazide diuretic therapy also may
cause magnesium deficiency due to enhanced
magnesium excretion, it specifically reduces renal
expression levels of the epithelial magnesium
channel TRPM6
SVS Medical College

Drugs
• Aminoglycosides are thought to induce the action of
the CaSR on the TAL and DCT, producing magnesium
wasting
• Cisplatin and amphotericin B induced magnesium
deficiency is associated with hypocalciuria, which
suggests injury to the DCT
• Many nephrotosic drugs also cause hypomagnesemia
by increased urinary magnesium excretion, but the
causes are still unknown
SVS Medical College

Causes of Hypo-Magnesium
5. Related to renal loss of magnesium
• Gitelman syndrome
• Classic Bartter syndrome (Type III Bartter syndrome)
• Familial hypomagnesemia with hypercalciuria and
nephrocalcinosis (FHHNC)
• Autosomal-dominant hypocalcemia with hypercalciuria
(ADHH)
• Isolated dominant hypomagnesemia (IDH) with
hypocalciuria
• Isolated recessive hypomagnesemia (IRH) with
normocalcemia
SVS Medical College

Increased excretion
1. Medications: diuretics, antibiotics( Ticarcillin,
Amphoterecin B, Aminoglycosides), Cis-platinum,
Cyclosporin, PPI(Pantoprazole mostly)
2. Alcoholism
3. Diabetes mellitus – patients being treated for DKA
4. Renal tubular diseases – magnesium wasting
5. Hypercalcemia/ Hypercalcuria
6. Hyperaldosteronism/ Barter’s syndrome
7. Marked diaphoresis
8. Excess lactation
SVS Medical College

Decreased intake/ mal absorption
1. Starvation – most common cause
2. Bowel bypass/ resection
3. TPN
4. Chronic malabsorption syndrome – chronic
pancreatitis
5. Chronic diarrhea
SVS Medical College

Miscellaneous
1. Acute pancreatitis
2. Hypoalbuminemia
3. Vitamin D therapy – hypercalcuria
SVS Medical College

Differential diagnosis
• Hypocalcaemia: Similar signs and symptoms.
Both coexist in one patient. Hypocalcaemia
does not correct if hypomagnesaemia is not
corrected
• Hypokalemia: Hypokalemia often coexists.
Correction of hypokalemia does not show any
improvement. More weakness and more
arrhythmias.
SVS Medical College

Hypomagnesaemia
• Hypomagnesaemia is an electrolyte
disturbance in which there is an abnormally
low level of magnesium in the blood.
• Hypomagnesaemia is not necessarily
magnesium deficiency. Hypomagnesaemia can
be present without magnesium deficiency and
vice versa.
SVS Medical College

The risk of hypomagnesaemia 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
SVS Medical College

Associated
• Hypokalemia is a common event in patients with
hypomagnesaemia, occurring in 40-60% of cases
• Partly due to underlying disorders that cause
magnesium and potassium losses, including diuretic
therapy and diarrhea
• The mechanism for hypomagnesaemia-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.
SVS Medical College

• The classic sign of severe hypomagnesaemia (< 1.2 mg/dL)
is hypocalcaemia.
• The mechanism is multifactorial.
• Impaired magnesium-dependent adenyl cyclase mediates
the decreased release of PTH causing hypocalcaemia.
• Skeletal resistance to this hormone in magnesium
deficiency has also been implicated.
• Hypomagnesaemia also alters the normal heteroionic
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.
SVS Medical College

Clinical features
• Magnesium deficiency has been blamed for
various arrhythmias, hypertension, attention-
deficit/hyperactivity disorder, anxiety,
seizures, leg cramps, restless legs syndrome,
kidney stones, myocardial infarction,
headaches, premenstrual syndrome,
fibromyalgia, chest pain, osteoporosis,
altitude sickness, diabetes, fatigue, weakness,
and other maladies.[1]
SVS Medical College

Clinical features
• Clinical manifestations are anorexia, nausea, vomiting,
lethargy, weakness, personality change, tetany (eg, positive
Trousseau or Chvostek sign or spontaneous carpopedal
spasm, hyperreflexia), and tremor and muscle
fasciculations.
• The neurologic signs, particularly tetany, correlate with
development of concomitant hypocalcemia, hypokalemia,
or both.
• Myopathic potentials are found on electromyography but
are also compatible with hypocalcemia or hypokalemia.
• Severe hypomagnesemia may cause generalized tonic-
clonic seizures, especially in children.
SVS Medical College

Features
• Sx: neuromuscular and CNS hyperactivity i.e.
exaggerated deep tendon reflexes (alcohol
withdrawal), tremors, delirium, seizures; even status
epilepticus, nystagmus, psychosis, depression and
agitation
• Sx similar to hypercalcemia
• Associated with hypokalemia
– Prolonged QT and PR intervals
– ST segment depression
– Flattened or inversion of p waves
– Torsades de pointes
– arrhythmias
SVS Medical College

Features
• Sx similar to hypercalcemia
• Associated with hypokalemia
• EKG:
– Prolonged QT and PR intervals
– ST segment depression
– arrhythmias
SVS Medical College

Features
• Heart: cardiac arrhythmias, atrial and ventricular ectopics,
supraventricular tacycardia, ventricular tacycardias, and
ventricular fibrillations hypotension
• Abdomen: pancreatitis absent bowel sounds, and tenderness,
stigmata of cirrhosis of liver – hepatosplenomegaly, caput
medusea ascites, palmar erythema, spider angiomas, - alcohol
induced
SVS Medical College

Diagnosis
• High degree of suspicion clinical assessment and estimation
of serum magnesium.
• It is important to recognize the levels of serum magnesium
do not correlate with intracellular magnesium levels.
• It is possible to have total body or intracellular magnesium
depletion with normal or even high magnesium levels.
• For this reason initial urine collection for magnesium, or
urinary retention test after parenteral administration of
magnesium to be done to determine the magnesium
depletion.
• Though such tests are useful in specific occasions, an
acutely ill patient is treated based on serum levels and
clinical judgement.
• Lab error – repeat
SVS Medical College

Measurement of serum magnesium
Its use in evaluating total body stores is limited
SVS Medical College
Mg++ Normal
sMg 1.7 – 2.5 mg/dl
RBC Mg 4.04 – 6.9 mg/dl
24 hr urinary Mg 120 – 150 mg

• Measurement of serum magnesium
• Its use in evaluating total body stores is
limited
SVS Medical College

Diagnosis
GOLD STANDARD
• A surrogate for direct 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.
SVS Medical College

Excretion Analysis
FEMg = [(UMg x PCr) / (PMg x UCr x 0.7)]
• Distinction between gastrointestinal and renal losses
can be made by measuring the 24-hour urinary
magnesium excretion or the FE of magnesium on a
random urine specimen
• Daily excretion of more than 24 mg or calculated FE of
magnesium above 3% in a subject with normal renal
function indicates renal magnesium wasting.
SVS Medical College

Lab tests
• Serum electrolytes
• Blood glucose
• Serum calcium and phosphorus
• ABG
• Hypocalcemia, hypokalemia and alkalosis coexist.
• If alcoholic hypophosphatemia is likely
• Diabetics more prone to hypomagnesemia especially with the
treatment of DKA
• 24 hour urine for magnesium – renal magnesium wasting or the
diagnosis is doubtful.
• Magnesium retention test: using parenteral or oral magnesium –
the diagnosis is doubtful or mal absorption syndrome
• Miscellaneous: LFT, Serum Amylase And Lipase, USG Abdomen
SVS Medical College

Electrocardiogram
• EKG:
– Prolonged QT, QRS and PR intervals
– ST segment depression mimic hypokalemia, hypocalcemia
– Arrhythmias – atrial tacycardia, atrial fibrillation ventricular
tachycardia , ventricular fibrillation
SVS Medical College

EKG
SVS Medical College

Management
• Medical/Nursing management
- IV/PO Magnesium replacement, including
Magnesium Sulfate
- Give Calcium Gluconate if accompanied by
hypocalcaemia
- Monitor for dysphagia, give soft foods
- Measure vital signs closely
SVS Medical College

Management
• Urgency of treatment depends on the clinical
features
• Intravenous therapy is indicated in patients
with neurological and cardiac complication
and serum magnesium <1mEq/L
SVS Medical College

Treatment
• Oral if asymptomatic: each tablet contains 60-84mg, give 2-4 tabs/day
in mild cases, 6-8 tabs for severe depletion
-Slow Magnesium (magnesium chloride)
-Magnesium-Tab SR (magnesium lactate)
-Magnesium Oxide (formulary at the VA) 20 mEq of magnesium per 400
mg tablet. 1-2 tablets/day
• Avoid replacement in patients with reduced GFR
• Treat underlying disease (PPI, diuretics, alcohol, uncontrolled
diabetes)
• Diarrhoea in high doses
SVS Medical College

I.V. Magnesium sulphate
• Magnesium sulphate 1G(2ml of 50% solution
of magnesium sulphate) equals to 98 mg of
elemental magnesium = 8 mEq MgSO4 or 4
Mg2+.
SVS Medical College

Treatment
• IV if symptomatic (magnesium sulfate)
– 1.5-1.9mg/dL 2g magnesium sulfate IV over 10-20 minutes (tetany,
cardiac involvement)
– 1.2-1.4mg/dL4g
– .8-1.1mg/dL 6g
– <.8mg/dL 8g
– Torsades: 2g IV push over 2 minutes
– Low K/Ca w/ tetany / arrhythmia: 50meq (~6g) of IV Mg given slowly
over 8-24 hrs
SVS Medical College

Acute myocardial infarction
• Therapeutic magnesium may prevent
arrhythmias limit damage from reperfusion
arrhythmias and have a favourable impact on
hemodynamics.
• Dispute
• 2 G i.v. Over 5 mts followed by 16 G i.v.
Infusion/ 24 hrs
• Monitor deep tendon reflexes, blood pressure,
and respiratory depression
SVS Medical College

• Over dosage occurs in a setting of renal
insufficiency
• Treatment for over dosage: respiratory arrest
shock, cardiac asystole – i.v. 1 – 2 G of Calcium
gluconate( 100 – 200 mg of elemental calcium)
over 3 mts followed by 15mg/kg over 4 hrs.
• Physostigmine 1 mg over 1 minute
• Forced diuresis
• Dialysis
SVS Medical College

Intramuscular magnesium
• 1 – 2 G IM Q 4 hrs – 5 doses first day
• 1G IM – 6 hrly for 2 – 3 days.
• Pain at IM sites
SVS Medical College

Miscellaneous
Treatment of the following conditions
• Hypocalcaemia
• Hypokalemia
• Hypophosphateamia
• Underlying condition
SVS Medical College

Deficiency and treatment
• Osteoporosis
• Bone fractures
• Convulsion
• Muscle spasms
• Heart failure
• Bleeder’s disease
SVS Medical College

• The hypocalcemic-hypomagnesemic patient with
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
SVS Medical College

• The main adverse 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 )
SVS Medical College

Potassium sparing diuretics
• Patients with diuretic-induced hypomagnesemia who
cannot discontinue diuretic therapy may benefit from the
addition of a potassium-sparing diuretic
• Amiloride, spirolonolactone and triamterene can be used.
• Also useful in patient with hypomagnesemia refractory to
oral therapy or in cases where oral therapy result in
diarrhoea
• Passive reabsorption of Mg in late distal convoluted tubule
• These drugs may decrease magnesium excretion by
increasing its reabsorption in the collecting tubule.
• These drugs also may be useful in Bartter and Gitelman
syndrome or in cisplatin nephrotoxicity.
SVS Medical College

Hypermagnesemia
• Serum Magnesium level greater than 2.5
mEq/L
SVS Medical College

Causes
- Renal failure
- Untreated diabetic ketoacidosis
- Excessive use of antacids and laxatives
SVS Medical College

Clinical manifestations
SVS Medical College
- Flushed face and skin warmth
- Mild hypotension

Clinical manifestations
- Heart block and cardiac arrest
- Muscle weakness and even paralysis
SVS Medical College

Causes
• The most common cause of hyper-magnesemia is
renal failure. Other causes include the following:
• Excessive intake(Antacids, Laxatives)
• Lithium therapy
• Hypothyroidism
• Addison disease
• Familial hypocalciuric hypercalcemia
• Milk alkali syndrome
• Depression
SVS Medical College

Stages
Stag
e
Serum Magnesium levels Symptoms and signs
I 4 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.
II 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.
III Above 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.
SVS Medical College

Eclampsia
• Note that the therapeutic range for the
prevention of the pre-eclampsic uterine
contractions is: 4.0-7.0 mEq/L. As per Lu and
Nightingale, serum Mg2+ concentrations
associated with maternal toxicity (also
neonate depression - hypotonia and low
Apgar scores) are (vide next slide )
SVS Medical College

Levels of serum Magnesium –
symptoms
• 7.0-10.0 mEq/L - loss of patellar reflex
• 10.0-13.0 mEq/L - respiratory depression
• 15.0-25.0 mEq/L - altered atrioventricular conduction
and (further) complete heart block
• >25.0 mEq/L - cardiac arrest
SVS Medical College

Predisposing factors
• Hemolysis, magnesium concentration in erythrocytes is
approximately three times greater than in serum, therefore
hemolysis can increase plasma magnesium.
Hypermagnesemia is expected only in massive hemolysis.
• Renal failure Kidney insufficiency, excretion of magnesium
becomes impaired when creatinine clearance falls below 30
ml/min. However, hypermagnesemia is not a prominent
feature of renal insufficiency unless magnesium intake is
increased.
• Other conditions that can predispose to mild
hypermagnesemia are diabetic ketoacidosis, adrenal
insufficiency, Hypothyroidism, hyperparathyroidism and lithiu
m intoxication.
SVS Medical College

Neuromuscular symptoms
• Increased magnesium decreases impulse
transmission across the neuromuscular
junction producing a curare-like effect
SVS Medical College

Cardiovascular abnormality
• Magnesium is an effective calcium channel
blocker both extracellularly and intracellularly; in
addition, intracellular magnesium profoundly
blocks several cardiac potassium channels [1].
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. Complete heart block and cardiac arrest
may occur at a plasma magnesium concentration
above 15 meq/L.
SVS Medical College

Hypocalcemia
• Moderate hypermagnesemia can inhibit the
secretion of parathyroid hormone, leading to
a reduction in the plasma calcium
concentration
• However this fall is usually transient and
produces no symptoms.
SVS Medical College

Diagnosis
• Hypermagnesemia usually results from 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.
SVS Medical College

Treatment
• In mild cases, withdrawing magnesium
supplementation is often sufficient.
SVS Medical College

Severe cases
• If Renal Function is adequate, Diuretics can be
used
• IV Calcium Gluconate: Because the actions of
Magnesium are antagonized by Calcium(However,
Calcium should be reserved for patients with life-
threatening symptoms, such as arrhythmia or
severe respiratory depression.)
• In case of Severe Hypermagnesemia, Dialysis
needs to be done( >8mEq/L, poor renal function,
life threatening symptoms)
SVS Medical College

• Prevention of hypermagnesemia usually is possible. In mild cases,
withdrawing magnesium supplementation is often sufficient. In
more severe cases the following treatments are used:
• Intravenous calcium gluconate, because the actions
of magnesium in neuromuscular and cardiac function are
antagonized by calcium.
• Intravenous diuretics, in the presence of normal renal function
• Dialysis, when kidney function is impaired and the patient is
symptomatic from hypermagnesemia
•
SVS Medical College

Referrences
• Brenner and Rector’s THE KIDNEY 9th edition
• Harrison’s principles of internal medicine, 17th
edition
• Medscape.com
SVS Medical College

SVS Medical College

Venkat magnesium

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Viewers also liked

Viewers also liked (20)

Similar to Venkat magnesium

Similar to Venkat magnesium (20)

Recently uploaded

Recently uploaded (20)

Venkat magnesium