Dr Manjit George Anaesthetist Thirumalai Mission Hospital Ranipet India

1. Magnesium and
Anaesthesia
Dr Manjit George

2. Introduction
 4th most plentiful cation in humans (after Na, K, and Ca)
 2nd most important intracellular cation (after K)
 Distribution- bones(53%), muscles(27%), soft tissues(19%) and
in serum and RBCs(less than 1%)
 S. Mg – 3 forms- ionised(62%), protein bound( 33%), complexed
to anions such as citrate, PO4( 5%)
 Ionised fraction is physiologically active

3. Physiology

4. Physiological role
 Physiological antagonist of Ca
 Involvement of Mg in Na K ATPase- essential in maintaining
transmembrane Na and K gradients and normal K conc.
 Determinant of electric potential across cell membranes
 Generation of C-AMP is Mg dependant
 Activation of many enzyme systems, including those involved in
energy metabolism
 Essential role in production of ATP
 Synthesis of DNA, RNA and protein

5. Physiological role
 Direct effect on myocardium and vascular smooth muscle- depress
contractility, block catecholamine receptors, inhibits release of
catecholamines from adrenal medulla, peripheral adrenergic receptors
 Blunts response of vascular tissue to vasoconstrictors
 Bronchodilator, decreases PVR
 Decreases release of acetylcholine at neuromuscular junction
 Decreases excitability of nerves and muscles, involved in contraction
and relaxation of muscles
 Suppress epileptic foci and reverse cerebral vasospasm
 Tocolytic
 Inhibits platelet activity, increases bleeding time

6. Mg homeostasis
 Body stores regulated by hormonal and metabolic effects on
gi absorption and renal excretion
 Normal levels- 0.7- 1.05mmol/l
 GI absorption- ileum and colon, inversely proportional to intake
 Absorbed Mg excreted primarily by kidney
 Majority of reabsorption in ascending limb of Henle’s loop
 Aldosterone increses renal excretion
 PTH enhances gut absorption, reduces renal excretion of Mg

7. Pharmacology

8. Pharmacology
 2ml, 5ml and 10 ml ampoules, clear solution for infusion
 Not to be stored above 25 degrees celsius
 Active substance - Magnesium sulphate heptahydrate
 2ml= 1g MgSO4= 4mmols= 8 meq= 98 milligram elemental Mg
 Too rapid administration- hypotension and even asystole
 Reduced dose in elderly and in renal failure- use with caution
 Use with caution in Myasthenia gravis, muscular dystrophy
 Contraindications- Heartblock, obstetrics- within 2 hours of delivery
 Drug interactions- Digoxin , Beta blocker and CCB, NDMR
 Antidote- resp depression or HB- iv calcium
hypotension- calcium/ dopamine

9. Hypomagnesemia
 Plasma Conc < 0.7mmol/l
 Plasma Mg is less than 1% of total body Mg
 Overall deficiency may exist even with normal plasma levels
 Low serum Mg generally indicates low total body Mg, exceptions-
following massive crystalloid infusion, hypoalbuminemia
 Suggestions that hypomagnesemia may be the most
underdiagnosed electrolyte deficiency
 Relatively common disorder

10. Hypomagnesemia - causes
 Decreased intake- elderly, chronic alcoholics, pancreatic
insufficiency, short bowel syndrome, TPN with insufficient Mg
 Excessive renal loss- loop diuretics, ACEI, Gentamicin, interstitial
nephritis, diuretic phase of ATN, hyperaldosteronism
 Extra renal losses- prolonged diarrhoea, long term NG drainage
 Redistribution- treatment of DKA with insulin dextrose, massive
transfusion with citrated blood

11. Hypomagnesemia-Clinical manifestations
 CVS- HTN, Angina, Arrythmias, digoxin toxicity, ECG changes
 Neuromuscular- myoclonus, cramps, stridor, Chovstek’s and
Trousseau’s signs, convulsions and coma
 Psychiatric disturbances- confusion, psychosis including
Wernicke’s encephalopathy
 Co existing electrolyte disturbances- hypokalemia, hypocalcemia

12. Hypomagnesemia- Treatment
 Normal homeostasis of Mg requires daily intake of 10-20 mmol
 Mg replacement therapy particularly important in critically ill
 Emergency- 10-20 mmol in 50 ml 5% D iv over 15-30mins,
followed by 40 mmol over 4 hrs iv
 Critically ill(c/c deficiency)- 40 mmol iv on day 1 and
10-20 mmols on days 2-5
 Less severely ill- 15 mmols/day, NG/PO
 Renal function should be adequte before Mg administration
 IV administration should be stopped if hypotension/ bradycardia,
if plasma conc. > 2.5 mmol/l or if DTR disappear

13. Hypermagnesemia
 Iatrogenic- overdose in treatment of preeclampsia/eclampsia
 End stage renal disease
 High intake of antacids and use of purgatives
 Adverse effects enhanced by hypocalcimea
 GI- Nausea, vomiting, diarrhoea
 CVS- Prolongation of PR interval, QRS complex and QT interval,
hypotension and bradycardia, Complete HB and cardiac arrest
(10-12.5mmol/l) can also occur
 CNS- Disappearance of DTR (levels> 4-5 mmol/l), depressed
respiration and apnoea due to paralysis of voluntary muscles
(5-7.5mmol/l)
Treatment-
 Stop medications
 iv calcium gluconate 2.5-5mmol bolus
 Diuretics/ dialysis

14. PIH and Eclampsia
 Major cause of maternal mortality and fetal loss
 Uteroplacental ischaemia
 Multisystem disorder affecting CVS, resp, hepatic, renal,
haemostatic and CNS
 Control BP and abnormal haemodynamic state, prevent
convulsions, ensure safe delivery
 MgSO4 is the most widely used anti convulsant

15. MgSO4 in Preeclampsia
 Magpie Trial- Lancet 2002- “ MgSO4 halves the risk of eclampsia
and probably reduces the risk of maternal death with no
substantive harmful effects to mother or baby in short term”
 Intense cerebral vasospasm with increased sensitivity to pressor
agents
 Reduction in cerebral blood flow causing convulsions
 MgSO4 in PIH- reduces intracerebral vasospasm, as measured by
Doppler examination of MCA

16. MgSO4 in Eclampsia
 Collaborative Eclampsia trial ( Lancet,1995)– superiority of MgSO4
over Diazepam & Phenytoin in prevention of reccurent convulsions in
eclampsia
 Reduction in incidence of eclamptic convulsions in women with PIH
 Alters cardiovascular response to endotracheal intubation(40mk/kg
after induction agent, 30mg/kg in a patient on Magnesium therapy)
 Less foetal depression than Alfentanil
 For very severe preeclampsia- combination of MgSO4 and Alfentanil
superior to MgSO4 alone

17. MgSO4 in PIH
 MgSO4 is the DOC for prevention and treatment of eclamptic
seizures
 Loading dose of 4 g( some centres use 5g) iv over 5 mins
followed by iv infusion at 1-2g/hr for 24 hrs after last convulsion
 If further convulsion occurs, another 2-4 g given iv over 5 mins
 Therapeutic range of 2-3.5mmol/l recommended
 IM route- painful, less predictable plasma concentrations
 5 g im, then 2.5g im every 4 hrs until 24 hrs after last seizure
 Plasma conc of 2-4 mmol/l usually acceptable

18. MgSO4 in cardiovascular anaesthesia
 Hypomagnesemia is common after CPB- Mg widely accepted in
treatment and prophylaxis of arrythmias after CPB
 Anti arrythmic agent- post MI, torsades de pointes, intractable VT/
VF, digoxin induced arrythmias, multifocal atrial tachycardia
 Component of some cardioplegic solutions- protects ischemic
myocardium especially during reperfusion
 Aortic cross clamping- NMDA antagonsit- protection to spinal
cord during repair of supra renal anuerysms
 Control of hypertensive responses to laryngoscopy and intubation-
suppress stress response at a dose of 40mg/kg

19. Mg and anaesthesia
 Both hypo and hyper magnesemia- anaesthetic implications
 Frequently accompanied by other electrolyte disturbances
 If not urgent, postpone procedure
 Increased risk of perioperative arrythmias
 High chances of stridor provoked by airway stimulation, upon
induction of hypomagnesemic patients
 Avoid hyperventilation, as it further lowers Mg levels
 Vasodilation produced by volatile agents, narcotics may be
exacerbated by Mg leading to hypotension

20. Mg and anaesthesia
 It decreases presynaptic release of acetylcholine and reduces
sensitivity of post junctional membrane
 NDMR potentiated by Mg
 MgSO4 causes dose related depression of acetylcholine release
 Mg decreases twitch response without TOF fade, unlike NDMR
 Pancuronium, rocuronium and vecuronium are potentiated by Mg
 Reduced dose of muscle relaxant
 Use peripheral nerve stimulator

21. Other clinical uses of Magnesium
 Phaeochromocytoma crisis -bolus dose of 2-4 g followed by infusion at 1g/hr-
marked anti adrenergic effect, inhibition of release of catecholamines and calcium
channel blocking property allied to its effect on release of acetylcholine
 Anaesthetic management of phaeochromocytoma resection
 Asthma- bronchodilator- calcium antagonism, inhibitory action on smooth muscle
contraction, on Histamine release from mast cells and Acetylcholine release from
cholinergic nerve terminals. IgE stimulation increases calcium conc intracellularly,
leading to Histamine release
 Tetanus- MgSO4 in conjunction with sedation eg: clonidine, reduce cardiovascular
(autonomic) instability and inhibits release of catecholamines, reduces spasms
 Sub arachnoid haemorrhage- neuroprotective mechanisms- inhibition of release
of excitatory aminoacids, blockade of NMDA glutamate receptors, non competitive
antagonist of voltage dependant Ca channel, cerebrovascular dilatory activity

22. From the journals
 MgSo4 attenuates arterial pressure increase during lap
cholecystectomy - BJA (2009)103(4)
 MgSO4 as an adjuvant to intrathecal bupivacaine in mild pre
eclampsia undergoing CS- reduces post op analgesic requirements-
IJOA 2010;19
 MgSO4 in severe tetanus improves muscle spasm and cardiovascular
stability- Anaesthesia 2008;63
 Intra articular inj of MgSO4 enhances analgesic effect of intra
articular Bupivacaine- Anaesth Analg 2008;106

23. References
 Cations- Pottasium, Calcium, Magnesium BJA CEACCP 2012 Vol 12,No 4
 Magnesium: an emerging drug in anaesthesia- Editorial, BJA (2009)103(4)
 Magnesium and the anaesthetist BJA CEACCP 2001,Vol 1 No 1
 Magnesium- Physiology and pharmacology, BJA 1999;83:302-20
 Clinical uses of Magnesium infusions in Anaesthesia,
Anaesth Analgesia 1992;74:129-136