Magnesium Sulfa-WPS Office
Magnesium Sulfa-WPS Office
Magnesium Sulfa-WPS Office
eclamptic seizures. It is also utilized for prophylactic treatment in all patients with severe preeclampsia.
The mechanism of action of magnesium sulfate is thought to trigger cerebral vasodilation, thus reducing
ischemia generated by cerebral vasospasm during an eclamptic event. The substance also acts
competitively in blocking the entry of calcium into synaptic endings, thereby altering neuromuscular
transmission.
Identification
Pharmacology
Indication
Associated Conditions
Associated Therapies
Contraindications & Blackbox Warnings
Pharmacodynamics
Mechanism of action
Absorption
Volume of distribution
Protein binding
Metabolism
Route of elimination
Half-life
Clearance
Adverse Effects
Toxicity
Affected organisms
Pathways
Pharmacogenomic Effects/ADRs
Interactions
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Chemical Identifiers
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Clinical Trials
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Properties
Spectra
Targets (1)
Magnesium sulfate
IDENTIFICATION
Name
Magnesium sulfate
Accession Number
DB00653
Description
A small colorless crystal used as an anticonvulsant, a cathartic, and an electrolyte replenisher in the
treatment of pre-eclampsia and eclampsia. It causes direct inhibition of action potentials in myometrial
muscle cells. Excitation and contraction are uncoupled, which decreases the frequency and force of
contractions. (From AMA Drug Evaluations Annual, 1992, p1083)
Type
Small Molecule
Groups
Structure
Thumb
Weight
Average: 120.368
Monoisotopic: 119.936771076
Chemical Formula
MgO4S
Synonyms
Magnesium sulphate
magnesium(II) sulfate
Magnesiumsulfat
MgSO4
PHARMACOLOGY
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Indication
Used for immediate control of life-threatening convulsions in the treatment of severe toxemias (pre-
eclampsia and eclampsia) of pregnancy and in the treatment of acute nephritis in children. Also
indicated for replacement therapy in magnesium deficiency, especially in acute hypomagnesemia
accompanied by signs of tetany similar to those of hypocalcemia. Also used in uterine tetany as a
myometriat relaxant.
Associated Conditions
Constipation
Convulsions
Hypomagnesemia
Torsades de Pointes
Barium poisoning
Associated Therapies
Pharmacodynamics
Magnesium sulfate is a small colorless crystal used as an anticonvulsant, a cathartic, and an electrolyte
replenisher in the treatment of pre-eclampsia and eclampsia. It causes direct inhibition of action
potentials in myometrial muscle cells. Excitation and contraction are uncoupled, which decreases the
frequency and force of contractions. Magnesium sulfate is gaining popularity as an initial treatment in
the management of various dysrhythmias, particularly torsades de pointes, and dyrhythmias secondary
to TCA overdose or digitalis toxicity.
Mechanism of action
Magnesium is the second most plentiful cation of the intracellular fluids. It is essential for the activity of
many enzyme systems and plays an important role with regard to neurochemical transmission and
muscular excitability. Magnesium sulfate reduces striated muscle contractions and blocks peripheral
neuromuscular transmission by reducing acetylcholine release at the myoneural junction. Additionally,
Magnesium inhibits Ca2+ influx through dihydropyridine-sensitive, voltage-dependent channels. This
accounts for much of its relaxant action on vascular smooth muscle.
Toxicity
LD50 = 1200 mg/kg (rat, subcutaneous). May be harmful if swallowed. May act as an irritant. Adverse
reactions include hypotension, ECG changes, diarrhea, urinary retention, CNS depression and respiratory
depression.
magnesium sulfate
Available forms
Parenteral injection for I.V. use: 1% (1 and 10 g) in D5W; 2% (10 and 20 g) in D5W
Hypomagnesemic seizures. Adults: 1 g I.V. or I.M. Or, 1 to 2 g (as 10% solution) I.V. over 15 minutes;
then 1 g I.M. q 4 to 6 hours, based on patient’s response and magnesium blood levels.
Seizures secondary to hypomagnesemia in acute nephritis. Children: 0.2 ml/kg of 50% solution I.M. q 4
to 6 hours, p.r.n., or 100 to 200 mg/kg as a 1% to 3% solution I.V. given slowly over 1 hour with the first
half of dose in the first 15 to 20 minutes. Also, 0.1 to 0.2 ml/kg of 20% solution (20 to 40 mg/kg) I.M.
Adjust dosage according to magnesium blood levels and seizure response.
Life-threatening arrhythmias. Adults: For patient with sustained ventricular tachycardia or torsades de
pointes, give 1 to 6 g I.V. over several minutes followed by 3- to 20-mg/minute I.V. infusion for 5 to 48
hours depending on patient response and serum magnesium levels. For patient with paroxysmal atrial
tachycardia, give 3 to 4 g I.V. over 30 seconds.
Prevention or control of seizures in preeclampsia or eclampsia. Adults: Initially, 4 g I.V. in 250 ml D5W
and 4 to 5 g deep I.M. into each buttock (using undiluted 50% magnesium sulfate injection); then 4 to 5
g deep I.M. into alternate buttock q 4 hours, p.r.n. Or, 4 g I.V. as a loading dose followed by 1 to 3 g
hourly as an I.V. infusion. Maximum daily dose is 30 to 40 g. Or, 8 to 15 g depending on weight of patient
(8 g for 45-kg [100-lb] patient and 15 g for 90-kg [198-lb] patient); 4 g of magnesium sulfate (as
magnesium sulfate injection or magnesium sulfate in D5W) is given I.V. and the remaining dose is given
I.M. using undiluted 50% magnesium sulfate injection. Dosage over next 24 hours based on serum level
and urinary excretion of magnesium following initial dose. Later doses should be sufficient to replace
magnesium excreted in urine, about 65% of the initial dose given I.M. q 6 hours.
≡ Dosage adjustment. For patients with severe renal insufficiency, maximum dose is 20 g in 48 hours.
Management of preterm labor ◇. Adults: 4 to 6 g I.V. over 20 minutes as a loading dose, followed by
maintenance infusions of 2 to 4 g/hour for 12 to 24 hours as tolerated after contractions subside.
Mild hypomagnesemia. Adults: 1 to 3 g I.M. q 6 hours for four doses. Or, 5 g in 1 L of D5W or dextrose
5% in normal saline solution I.V. over 3 hours.
Reduction of CV morbidity and mortality caused by acute MI. Adults: 2 g I.V. over 5 to 15 minutes,
followed by infusion of 18 g over 24 hours (12.5 mg/minute). Start therapy as soon as possible, and no
longer than 6 hours after MI.
Pharmacodynamics
Anticonvulsant action: Magnesium sulfate has CNS and respiratory depressant effects. It acts
peripherally, causing vasodilation; moderate doses cause flushing and sweating, whereas high doses
cause hypotension. It prevents or controls seizures by blocking neuromuscular transmission.
Drug is sometimes used in pregnant women to prevent or control preeclamptic or eclamptic seizures; it
also is used to treat hypomagnesemic seizures in adults, and in children with acute nephritis.
Pharmacokinetics
Metabolism: None.
Excretion: Excreted unchanged in urine; some appears in breast milk.
Parenteral administration of drug contraindicated in patients with heart block or myocardial damage.
Use cautiously in patients with impaired renal function and in women in labor. Don’t give to patients
with toxemia of pregnancy during the 2 hours preceding delivery.
Interactions
Cardiac glycosides: Changes in cardiac conduction in digitalized patients may lead to heart block if I.V.
calcium is administered. Avoid use together, if possible.
Succinylcholine, tubocurarine: Potentiates and prolongs neuromuscular blocking action of these drugs.
Use cautiously.
Drug-lifestyle. Alcohol use: Increases CNS depressant effects. Discourage alcohol use.
Adverse reactions
Metabolic: hypocalcemia.
Skin: diaphoresis.
Other: hypothermia.
Signs and symptoms of overdose with magnesium sulfate include a sharp decrease in blood pressure,
respiratory paralysis, ECG changes (increased PR, QRS, and QT intervals), heart block, and asystole.
Treatment requires artificial ventilation and I.V. calcium salt to reverse respiratory depression and heart
block. Usual dose is 5 to 10 mEq of calcium (10 to 20 ml of a 10% calcium gluconate solution).
Special considerations
• Administer by constant infusion pump if possible; maximum infusion rate is 150 mg/minute. Rapid drip
causes feeling of heat.
• Level of magnesium sulfate for I.V. administration shouldn’t exceed 20% and rate shouldn’t exceed
150 mg/minute (1.5 ml of a 10% concentration or equivalent). For I.M. administration in adults, levels of
25% or 50% are generally used; in infants and children, levels shouldn’t exceed 20% (200 mg/ml).
• Respiratory rate must be 16 breaths per minute or more before each dose. Keep I.V. calcium gluconate
20% on hand.
• When giving repeated doses, test knee jerk reflex before each dose; if absent, discontinue magnesium.
Use of drug beyond this point risks respiratory center failure.
• When using drug as a tocolytic agent, monitor patient for magnesium toxicity and monitor I.V. infusion
to avoid circulatory overload.
• After use in toxemic women within 24 hours before delivery, newborn requires observation for signs
of magnesium toxicity, including neuromuscular and respiratory depression.
Breast-feeding patients
• Drug appears in breast milk. In patients with normal renal function, all magnesium sulfate is excreted
within 24 hours of discontinuing drug. Recommend an alternative to breast-feeding during therapy.
Pediatric patients
Patient education
• Inform patient about short-term need for drug, and address any questions or concerns.
5. Begin patient education to increase knowledge and skills concerning preterm labor. Patient education
is individualized but may include the following:
e) Adequate hydration
b) Vital signs
1) Antepartum and Intrapartum: Blood pressure, pulse and respirations at start of bolus and every 15
minutes for the first hour, then hourly x 2 then every 4 hours or as ordered by physician. Pulse oximetry
with same frequency as vital signs. If patient progresses to active labor, VS per labor protocol.
c) Fetal Monitoring
(2) hours after bolus started, then EFM as per physician order.
2) Intrapartum: Continuous fetal monitoring when patient moves into active labor.
CAUTION NOTE: Magnesium Sulfate may depress the central nervous system of the fetus and, therefore,
may diminish variability. Be prepared at delivery to resuscitate any baby with a mother on Magnesium
Sulfate regardless of FHR tracing. Babies may have normal pH values at delivery yet be unable to
breathe independently.
d) Auscultate chest for any adventitious sounds, such as congestion, rales and rhonchi with vital signs.
a) When patient is identified as having pre-term labor, have room prepared for delivery. Oxygen and
suction checked and available.
b) Emergency delivery pack should be available at bedside or case cart set up for delivery in the LDR.
c) Initial NICU notification of patient and fetal status with updates periodically. NICU staff and a
neonatologist should be present at delivery of a preterm infant less than 34 weeks gestation, or as
appropriate.
a) Uterine activity.
b) Decreased baseline variability which may indicate depressed fetal CNS. Presence of fetal HR changes
(i.e., late decelerations and/or accelerations and/or a rise in baseline FHR).
informed
2. Assess physical and mental status of patient. Any change in alertness may be a very important finding
indicating central nervous system irritability or depression.
3. Provide quiet environment when feasible.
4. Position patient on side as much as possible, discourage semi-fowler’s position for extended periods
of time.
a) If significant concern regarding intake/output, obtain order for an indwelling Foley catheter. Notify
the
two hours.
2) +1 = low response.
3) +2 = normal response.
physician.
SULFATE SOLUTION:
sulfate
Pump.
a) Absent DTRs.
respiratory arrest.
c) Chest pain
g) Coma.
dosage changes.
rd edition).
Pregnancies. (5
Livingston