Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Magnesium and anaesthesia


Published on

Dr Manjit George
Thirumalai Mission Hospital

Published in: Health & Medicine
  • Be the first to comment

Magnesium and anaesthesia

  1. 1. Magnesium and Anaesthesia Dr Manjit George
  2. 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. 3. Physiology
  4. 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. 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. 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. 7. Pharmacology
  8. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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